Evidence Report/Technology Assessment 

Number 163 

Carbohydrate and Lipid Disorders and Relevant 

Considerations in Persons with Spinal Cord Injury 

Prepared for: 

Agency for Healthcare Research and Quality 

U.S. Department of Health and Human Services 

540 Gaither Road 

Rockville, MD 20850 

www.ahrq.gov 

Contract No. 290-02-0009, Task Order #1 

Prepared by: 

Minnesota Evidence-based Practice Center, Minneapolis, Minnesota 

Investigators 

Timothy J. Wilt, M.D., M.P.H. 

Kathleen F. Carlson, Ph.D. 

Gary D. Goldish, M.D. 

Roderick MacDonald, M.S. 

Catherine Niewoehner, M.D. 

Indulis Rutks, B.S. 

Tatyana Shamliyan, M.D., M.S. 

James Tacklind, B.S. 

Brent C. Taylor, Ph.D. 

Robert L. Kane, M.D. 

AHRQ Publication No. 08-E005 

January 2008
This report is based on research conducted by the Minnesota Evidence-based Practice Center 

(EPC) under contract to the Agency for Healthcare Research and Quality (AHRQ), Rockville, 

MD (Contract No. 290-02-0009, Task Order #1). The findings and conclusions in this document 

are those of the authors, who are responsible for its content, and do not necessarily represent the 

views of AHRQ. No statement in this report should be construed as an official position of AHRQ 

or of the U.S. Department of Health and Human Services. 

The information in this report is intended to help clinicians, employers, policymakers, and others 

make informed decisions about the provision of health care services. This report is intended as a 

reference and not as a substitute for clinical judgment. 

This report may be used, in whole or in part, as the basis for the development of clinical practice 

guidelines and other quality enhancement tools, or as a basis for reimbursement and coverage 

policies. AHRQ or U.S. Department of Health and Human Services endorsement of such 

derivative products may not be stated or implied. 
ii 

This document is in the public domain and may be used and reprinted without permission except 

those copyrighted materials noted for which further reproduction is prohibited without the 

specific permission of copyright holders. 

Suggested Citation: 

Wilt TJ, Carlson FK, Goldish GD, et al. Carbohydrate & Lipid Disorders & Relevant 

Considerations in Persons with Spinal Cord Injury. Evidence Report/Technology Assessment 

No. 163 (Prepared by the Minnesota Evidence-based Practice Center under Contract No. 290-02-

0009.) AHRQ Publication No. 08-E005. Rockville, MD. Agency for Healthcare Research and 

Quality. January 2008. 

No investigators have any affiliations or financial involvement (e.g., employment, consultancies, 

honoraria, stock options, expert testimony, grants or patents received or pending, or royalties) 

that conflict with material presented in this report. 
iii 

Preface 

 The Agency for Healthcare Research and Quality (AHRQ), through its Evidence-Based 

Practice Centers (EPCs), sponsors the development of evidence reports and technology 

assessments to assist public- and private-sector organizations in their efforts to improve the 

quality of health care in the United States. This report was requested and funded by the Spinal 

Cord Medicine Consortium, Paralyzed Veterans of America. The reports and assessments 

provide organizations with comprehensive, science-based information on common, costly 

medical conditions, and new health care technologies. The EPCs systematically review the 

relevant scientific literature on topics assigned to them by AHRQ and conduct additional 

analyses when appropriate prior to developing their reports and assessments. 

 To bring the broadest range of experts into the development of evidence reports and health 

technology assessments, AHRQ encourages the EPCs to form partnerships and enter into 

collaborations with other medical and research organizations. The EPCs work with these partner 

organizations to ensure that the evidence reports and technology assessments they produce will 

become building blocks for health care quality improvement projects throughout the Nation. The 

reports undergo peer review prior to their release. 

 AHRQ expects that the EPC evidence reports and technology assessments will inform 

individual health plans, providers, and purchasers as well as the health care system as a whole by 

providing important information to help improve health care quality. 

 We welcome written comments on this evidence report. They may be sent to the Task Order 

Officer named below at: Agency for Healthcare Research and Quality, 540 Gaither Road, 

Rockville, MD 20850, or by email to epc@ahrq.gov.

Carolyn M. Clancy, M.D. Jean Slutsky, P.A., M.S.P.H. 

Director Director, Center for Outcomes and Evidence 

Agency for Healthcare Research and Quality Agency for Healthcare Research and Quality 

J. Paul Thomas Beth A. Collins Sharp, R.N., Ph.D. 

Consortium Coordinator Director, EPC Program 

Spinal Cord Medicine Consortium 

Paralyzed Veterans of America Michael Handrigan, M.D., FACEP 

 EPC Program Task Order Officer 

 Agency for Healthcare Research and Quality 
iv 

Acknowledgments 

 We would like to thank Yuying Chen, M.D., Ph.D., James Fitzsimmons, M.D., David Gater, 

M.D., Leonard Pogach, M.D., Suparna Rajan, Ph.D., and Thomas E. Stripling for helpful advice 

throughout the review process, for reviewing the draft, and providing recommendations for 

revisions and clarifications, and James H. Rimmer, M.D., and William A. Bauman, M.D., for 

reviewing the draft and providing recommendations for revisions and clarifications. We would 

also like to thank Maureen Carlyle for assistance with figures and Marilyn Eells for editing and 

formatting this report. 
v 

Structured Abstract 

Objectives: To assess the prevalence of carbohydrate and lipid disorders in adults with chronic 

spinal cord injury and evaluate their risk contribution to cardiovascular diseases and the potential 

impact of exercise and pharmacologic and dietary therapies to alter these disorders and reduce 

cardiovascular disease risk. 

Data Sources: MEDLINE® (PubMed®), Cochrane Database and websites of the American 

Spinal Injury Association, American Paraplegia Society, Paralyzed Veterans of America, 

Consortium of Spinal Cord Medicine, and WorldCat through August 2007. 

Review Methods: English language observational studies addressing prevalence of carbohydrate 

and lipid disorders were included if they evaluated at least 100 adults with chronic spinal cord 

injury or a total of 100 subjects if using a control group. Epidemiologic investigations of more 

than 50 adults with spinal cord injury that were published in English after 1990 and reported 

cardiovascular morbidity and mortality were abstracted. Intervention studies from 1996-2007 

were included regardless of design or size if they assessed exercise, diet, or pharmacologic 

therapies and reported carbohydrate, lipid, or cardiovascular outcomes. 

Results: The quality of evidence regarding the prevalence, impact, and outcomes of 

carbohydrate and lipid disorders in adults with chronic spinal cord injuries is weak. Evidence is 

limited by relatively few studies, small sample size, lack of appropriate control groups, failure to 

adjust for known confounding variables, and variation in reported outcomes. However, the 

existing evidence does not indicate that adults with spinal cord injuries are at markedly greater 

risk for carbohydrate and lipid disorders or subsequent cardiovascular morbidity and mortality 

than able-bodied adults. Body mass index is not reliable for assessing body composition, 

especially percent body fat, in adults with spinal cord injury. There are no high quality studies 

evaluating the impact of exercise, diet, or pharmacologic therapies on these disorders. 

Conclusions: Evidence does not support using different thresholds to define or treat abnormal 

lipid and carbohydrate measures or to incorporate other markers to assess risk (e.g., insulin 

resistance, impaired fasting glucose, or impaired glucose tolerance) for individuals with spinal 

cord injuries compared to able-bodied adults. Due to physiologic differences between adults with 

spinal cord injuries and able-bodied individuals, caution may be required when extrapolating 

findings from studies conducted in able-bodied adults. The role of exercise in individuals with 

spinal cord injuries represents a unique challenge and requires further exploration into the 

benefits, harms, and resource implications of broad-based spinal cord injury exercise programs. 

vii 

Contents 

Executive Summary........................................................................................................................ 1 

Evidence Report

Chapter 1. Introduction ................................................................................................................. 15 

 Overview ................................................................................................................................ 15 

Chapter 2. Methods....................................................................................................................... 19 

 Topic Assessment and Refinement and Literature Review.................................................... 19 

 Literature Search Strategy and Eligibility Criteria........................................................... 22 

 Question 1 .................................................................................................................. 22 

 Question 2 .................................................................................................................. 22 

 Question 3a (exercise)................................................................................................ 22 

 Question 3b ................................................................................................................ 22 

 Data Synthesis .................................................................................................................. 23 

 Strength of Evidence ........................................................................................................ 24 

Chapter 3. Results ......................................................................................................................... 25 

 Study Identification ................................................................................................................ 25 

 Outcomes ................................................................................................................................ 29 

 Question 1......................................................................................................................... 29 

 Overall Description .................................................................................................... 29 

 Hyperinsulinemia (insulin resistance/metabolic syndrome) ...................................... 29 

 Summary.............................................................................................................. 30 

 Abnormalities in carbohydrate metabolism (diabetes mellitus and impaired 

glucose tolerance..................................................................................................... 30 

 Summary .............................................................................................................. 31 

 Abnormalities in lipid metabolism (hyperlipidemia and/or low HDL cholesterol)... 31 

 Summary .............................................................................................................. 32 

 Obesity ....................................................................................................................... 32 

 Summary .............................................................................................................. 33 

 Question 2......................................................................................................................... 43 

 Subject characteristics................................................................................................ 43 

 Cardiovascular prevalence in adults with chronic SCI .............................................. 43 

 Asymtomatic heart conditions in patients with SCI ............................................ 44 

 Cardiovascular mortality............................................................................................ 45 

 Cardiovascular prevalence and mortality in adults with chronic SCI 

compared to the general population according to age, race, and gender ................ 45 

 Interpretation of findings............................................................................................ 47 

 Summary .............................................................................................................. 48 

 Question 3......................................................................................................................... 64 

 Exercise in adults with SCI ........................................................................................ 64 

 Description of exercise intervention studies with carbohydrate-related 

outcomes........................................................................................................... 64 
viii 

 Impact of exercise programs on carbohydrate related measures ......................... 64 

 Description of exercise intervention studies with lipid or cardiovascular 

related outcomes ............................................................................................ 65 

 Impact of exercise programs on lipid or cardiovascular related measures .......... 65 

 Summary .............................................................................................................. 66 

 Dietary and pharmacologic intervention studies with carbohydrate or lipid 

related outcomes in adults with SCI....................................................................... 66 

 Carbohydrate outcomes ....................................................................................... 66 

 Lipid related outcomes......................................................................................... 66 

Chapter 4. Discussion ................................................................................................................... 79 

 Prevalence and Risk Estimates ............................................................................................... 79

 Role of Exercise, Diet, and Pharmacologic Interventions...................................................... 81 

 Conclusions and Policy Implications...................................................................................... 84 

 Future Research ...................................................................................................................... 84 

References and Included Studies .................................................................................................. 89 

List of Acronyms/Abbreviations................................................................................................... 95 

Figures

Figure 1. Conceptual model. Contribution of carbohydrate and lipid disorders to risk 

of cardiovascular disease in adults with chronic posttraumatic SCI.......................... 21 

Figure 2. Flow chart for Question 1 references ......................................................................... 25 

Figure 3. Flow chart for Question 2 references ......................................................................... 26 

Figure 4. Flow chart for Question 3a references (exercise/physical activity interventions)...... 27 

Figure 5. Diabetes prevalence, SCI vs. Control......................................................................... 34 

Figure 6. Prevalence of diagnosed diabetes, undiagnosed diabetes, and impaired fasting 

in men (NHANES 1999-2002)................................................................................... 34 

Figure 7. Weighted mean difference in lipid levels (mg/dL: Spinal cord injured subjects 

vs. controls ................................................................................................................. 35

Figure 8. Mean levels of total cholesterol, SCI studies ............................................................. 37 

Figure 9. Mean levels of LDL cholesterol, SCI studies............................................................. 37 

Figure 10. Mean levels of HDS cholesterol, SCI studies............................................................. 38 

Figure 11. Mean levels of triglycerides, SCI studies ................................................................... 38 

Figure 12. Total cholesterol, LDL-C and triglyceride levels of able-bodied males by age 

(NHANES)................................................................................................................. 39 

Figure 13. HDL cholesterol levels of able-bodied males by age (NHANES) ............................. 40 

Figure 14. Mean BMI, SCI, and Control ..................................................................................... 41 

Figure 15. Prevalence of BMI levels by age group (NHANES 1999-2002) ............................... 42 

Figure 16. Percent of all deaths due to coronary heart disease among adults with SCI .............. 56 

Figure 17. Odds ratios of cardiovascular outcomes in VA users with SCI and diabetes 

vs. SCI but no diabetes............................................................................................... 57 

Figure 18. Adjusted odds ratio of CVD in patients with SCI: Tetraplegia with no functional 

motor preservation compared to paraplegia and no functional motor preservation... 58 
ix 

Figure 19. Hazard ratio of dying based on ECG abnormality vs. normal ECG among 

VA users with SCI and able-bodied VA users........................................................... 59 

Tables

Table 1. Patient characteristics in studies that reported cardiovascular events in 

adults with SCI........................................................................................................... 49 

Table 2. Prevalence of CVD in adults with SCI....................................................................... 51 

Table 3. Prevalence of CVD in adults with SCI by age and years after injury ........................ 52 

Table 4. Prevalence of CVD according to SCI neurological category..................................... 53 

Table 5. Mortality from CVD in patients with SCI.................................................................. 54 

Table 6. Percent of all deaths from CVD among adults with SCI............................................ 56 

Table 7. Odds ratios of diabetes or CVD in adults with SCI compared to able bodied ........... 57 

Table 8. Diabetes management and diabetes complications in VA users with SCI, in 

VA users without SCI, and non-VA general population without SCI ....................... 58 

Table 9. Hazard ratio of dying having ECG abnormality vs. normal ECG among 

patients with SCI and able-bodied veterans ............................................................... 59 

Table 10. Age standardized mortality ratios in adults with chronic SCI compared to 

the general population (no adjustment for other confounding factors)...................... 60 

Table 11. Age standardized mortality ratios for cardiovascular death by gender 

compared to able bodied ............................................................................................ 61 

Table 12. Age standardized mortality ratios from CVD in adults with SCI compared 

to the general population............................................................................................ 62 

Table 13. Description of exercise intervention studies with carbohydrate related 

outcomes in people with SCI ..................................................................................... 68 

Table 14. Description of exercise intervention studies with lipid or cardiovascular 

related outcomes in people with SCI.......................................................................... 71 

Table 15. Diet and pharmacologic therapy studies for prevention and/or treatment of 

carbohydrate and lipid metabolism disorders in people with spinal cord injury 

and disease ................................................................................................................. 77 

Appendixes 

Appendix A: Technical Expert Panel Members and Affiliation 

Appendix B: Exact Search Strings 

Appendix C: Data Abstraction Form 

Appendix D: Excluded Studies 

Appendix E: Evidence Tables 

Appendix F: Conceptual Definition of Outcomes 

Appendixes cited in this report are available at http://www.ahrq.gov/clinic/tp/carbliptp.htm.

1 

Executive Summary 

Introduction 

Spinal cord injuries (SCI) result in 11,000 hospitalizations of new cases annually in the 

United States.5,6 More than 240,000 Americans live with a disability related to SCI and the 

estimated annual cost averages $9.7 billion.5,7,8 Improved quality of care over the last several 

decades has resulted in a 40 percent decline in mortality during the two years following the 

injury.9 However, improvement in long-term survival has been smaller. Cardiovascular diseases 

(CVD) have been reported as the most common cause of death in adults with chronic SCI.2,10-12

CVD risk factors associated with SCI include behavior (smoking, limited exercise) and 

metabolic abnormalities (obesity, metabolic syndrome,13-15 and diabetes11). The prevalence of 

dyslipidemia16,17 and coronary heart disease has been reported to be higher in adults with SCI 

compared to the general population.10,18 The Institute of Medicine recently released two reports 

that emphasized the role of cardiovascular risk assessment and management in adults with 

chronic SCI.6,11 Some evidence suggests that exercise,19 diet,20,21 and pharmacological therapy22

may reduce diabetes and CVD risk in these individuals. Furthermore, markers or thresholds of 

carbohydrate and lipid disorders commonly used in adults without SCI may not apply to the 

population that has sustained SCI. In particular, because adults with SCI lose muscle mass that is 

replaced with fat mass, traditional measures of obesity (weight or body mass index [BMI]) may 

not be appropriate. 

 Accurate estimates of diabetes prevalence and severity in adults with SCI may: 1) be 

underestimated relative to able-bodied controls because individuals with SCI may not undergo 

regular testing, 2) have lower levels of high-density lipoprotein (HDL) cholesterol that go 

unrecognized if providers only assess total cholesterol (TC) levels or base treatment solely on 

low-density lipoprotein (LDL) cholesterol, or 3) they have earlier evidence of impaired glucose 

tolerance or altered insulin sensitivity. Existing guidelines do not include routine evaluation of 

glucose and lipid abnormalities nor do they provide recommendations for threshold definitions of 

abnormality or target levels for interventions to achieve it.23-25 Furthermore, the prevalence, 

morbidity, and mortality associated with carbohydrate and lipid disorders may differ in adults 

with SCI compared to able-bodied individuals. 

 Effective interventions to treat carbohydrate and lipid disorders and reduce cardiovascular 

complications in able-bodied individuals include dietary, pharmacologic, and exercise therapies. 

However, adults with SCI have unique physiologic characteristics that may preclude 

generalization of evidence from able-bodied individuals to those with SCI. Total daily energy 

expenditure for adults with SCI is difficult to calculate but likely much lower than for ablebodied individuals, especially among individuals requiring motorized wheelchairs for mobility. 

Treatment of obesity in SCI remains largely empiric, including guidelines developed for dietary 

intervention in SCI. Pharmacologic therapies to alter carbohydrate and lipid disorders may have 

different effectiveness and adverse effects in individuals with SCI compared to able-bodied 

patients. For example, assessment of hepatic or muscle toxicity in SCI individuals may be 

difficult using traditional serologic measures developed in able-bodied adults because SCI 

individuals have reduced muscle mass and potentially altered hepatic metabolism. 

 Despite the expected benefits of exercise for individuals with SCI, this group also faces 

unique challenges and risks from exercise that are not experienced by the able-bodied 

population.8,26 For one, lack of access to and choices in exercise modes, depending on the 
2 

neurological impact and level of the injury, form physical barriers to obtaining exercise. 

Physiological risks of exercise are also a barrier to improved fitness among those with SCI. 

Depending on the level and completeness of the spinal injury, motor, sensory, and autonomic 

reflexes may still be intact but no longer under control of the brain. Individuals with SCI also 

experience various types of autonomic and circulatory dysregulation.26 Risk of stress-related 

musculoskeletal injury is of concern, given the reliance on a small group of muscles for activities 

of daily living as well as for any physical conditioning. Fractures, joint dislocation, and overuse 

injuries are common for individuals with SCI.27

 We conducted a systematic review of published evidence to address the following questions: 

Question 1a: What proportion of adult patients with chronic posttraumatic spinal cord 

injuries have been diagnosed with: 

a. Insulin resistance syndrome, metabolic syndrome 

b. Diabetes mellitus Type 2, impaired glucose tolerance 

c. Dyslipidemia 

d. Obesity 

Question 1b: Is the prevalence of carbohydrate and lipid disorders higher in the subgroups of 

patients by age, race, and gender compared to the general population? Does the prevalence of 

carbohydrate and lipid disorders differ by the time after trauma, the level of trauma, and 

functional impairment? 

Question 2: For people with SCI, what is the evidence on contribution to risk of 

cardiovascular disease of: 

a. Hyperinsulinemia 

b. Abnormalities in carbohydrate metabolism 

c. Abnormalities in lipid metabolism? 

d. Obesity 

This question was refined as: 

Question 2: Regarding risk of cardiovascular disease for people with SCI: 

a. What is cardiovascular prevalence and mortality in adults with chronic posttraumatic 

spinal cord injuries? 

b. Does cardiovascular incidence and mortality in adults with chronic posttraumatic spinal 

cord injuries differ compared to the general population based on age, race, and gender 

categories? 

c. What is the strength of the association between cardiovascular incidence and mortality 

and abnormalities in lipid and glucose metabolism including Type 2 diabetes mellitus 

after adjustment for possible confounding factors? 

d. Does association vary depending on age, gender, race, the duration after SCI, the level of 

SCI, and functional impairment? 

Question 3: What are the effects on carbohydrate or lipid-related outcomes in adults with SCI 

of: 

a. Exercise 

b. Dietary and pharmacologic interventions 

Methods 

 Studies addressing prevalence of obesity, diabetes, impaired glucose tolerance, insulin 

resistance, and lipid disorders through August 2007 were included if: 
3 

1. adults had chronic SCI; 

2. the total number of spinal cord subjects was at least 100, or totaling at least 100 subjects if a 

control group was included (SCI + controls ≥100); 

3. reported prevalence of obesity, diabetes, impaired glucose tolerance, metabolic syndrome or 

insulin resistance, or lipid disorders or reported mean BMI or lipid levels, 

4. were published in the English language. Abstracts of articles excluded due to small sample 

size were reviewed to assess for study quality and potential impact. 

 For Question 2, original epidemiologic investigations of more than 50 adults with chronic 

SCI and published in English after 1990 were identified in MEDLINE® via PubMed® and the 

Cochrane library. Websites of the American Spinal Injury Association, American Paraplegia 

Society, Paralyzed Veterans of America, Consortium of Spinal Cord Medicine, and the catalog 

WorldCat identified reviews. 

 For exercise interventions, the Endnote library containing original and review articles 

(n=2,212) was searched for abstracts that included the words fitness, physical activity, or 

exercise, resulting in a subset of 303 citations. A MEDLINE® search was conducted of articles 

written in English and published between 1996 and August 2007. Any identified study was 

included regardless of design, sample size, or duration if it reported carbohydrate, lipid, or 

cardiovascular results in adults with chronic SCI. 

 To assess dietary or pharmacologic interventions for treatment of carbohydrate and lipid 

metabolism disorders in the SCI population, studies were identified by searching in MEDLINE®

through October 2007. Reference lists of included studies or reviews were also searched. Since 

no randomized trials were identified, nonrandomized studies were eligible. To be included, 

studies had to: 

1. evaluate adults who had chronic SCI, defined as one year or more since sustaining the injury; 

2. evaluate pharmacologic or dietary interventions; 

3. report carbohydrate and/or lipid-related outcome measures; and 4) be published in the English 

language. 

 Reviewers extracted study and patient characteristics and outcomes onto standardized forms. 

A second reviewer assessed the findings and disagreements, while rare, were resolved by 

discussion. Prevalence estimates of obesity, diabetes, lipid disorders, and cardiovascular 

morbidity and mortality among adults with SCI and, where possible, able-bodied controls, are 

presented. Findings are reported separately where possible according to age, gender, race, and 

level/severity of SCI. For Question 3, carbohydrate and lipid outcomes are described according 

to the exercise, diet, or pharmacologic intervention studied. Due to heterogeneity in populations, 

interventions, comparator groups, and/or reported outcomes, pooled analyses was generally not 

conducted. 

Results 

 For Question 1, 23 studies met the inclusion criteria, two studies for insulin resistance/ 

metabolic syndrome,15,28 12 studies for diabetes mellitus,3,15,28-37 three studies for impaired 

glucose tolerance,28,29,31 seven studies for lipid disorders,16,17,21,31,38-40 and ten studies for obesity 

and body composition.28,31,36,38,40-45 Potentially eligible studies excluded due to small sample size 

that limited generalizability (n=45, number of SCI individuals in each study ranged from 1-77) 

were also of low quality and relevance because they were from a single center, not from the 
4 

United States, lacked controls, and/or did not assess clinically relevant carbohydrate and lipid 

disorders. 

For Question 2, 20 articles of 19 studies met inclusion criteria; most were conducted in the 

United States.1-3,30,32,34,36,37,39,46-56 Studies included more than 50,000 patients with SCI. Males 

(pooled prevalence 86 percent) and Caucasians comprised the majority of individuals. Most used 

general population controls, were uncontrolled, or did not adjust for known confounding 

variables including: age, race, gender, smoking status, exercise, or duration of followup. Wide 

variation existed in the definitions of reported CVD outcomes. 

 For Question 3a, studies evaluating the following types of exercise were identified: Active 

Exercise (AE) (seven studies),57-63 Functional Electrical Stimulation exercise (FES) (five 

studies),64-68 Passive Exercise (PE) (no studies, Self-Reported Physical Activity (six 

studies),13,14,54,69-71 and Other (one study).72

 For Question 3b, only two prospective studies (neither randomized) evaluating dietary and/or 

lifestyle interventions to reduce lipid levels met inclusion criteria.20,72

Prevalence of Carbohydrate and Lipid Disorders 

 The prevalence of insulin resistance, metabolic syndrome, diabetes mellitus, impaired 

glucose tolerance, dyslipidemia, and obesity in a population are all highly dependent upon 

demographics of the population including age, socioeconomic status, and race/ethnicity. The 

dependence of these conditions on population characteristics makes it difficult to conduct 

between-study comparisons since population characteristics varied greatly, both between and 

within studies. 

 Insulin resistance/metabolic syndrome. There was little data on the prevalence of insulin 

resistance/metabolic syndrome in adults with SCI. There are no high-quality data to determine if 

insulin resistance or metabolic syndrome are elevated in adults with SCI compared to similar 

individuals without SCI because no studies included a non-SCI control or comparison group. 

Only two studies assessed the prevalence of insulin resistance. The one study that provided 

results by severity of injury showed increased hyperinsulemia in persons with tetraplegia 

compared to paraplegia following a glucose challenge.28 The only study assessing metabolic 

syndrome was small, uncontrolled, and used definitions for specific metabolic disorders likely to 

increase the estimated prevalence of the disorders and therefore their estimated prevalence of 

metabolic syndrome. Their definitions are not widely recommended.15,73

 Diabetes mellitus or impaired glucose tolerance (IGT). The prevalence of diabetes 

appeared higher on average in SCI populations studied compared to the general population. 

However, there is credible scientific reason to believe that the general population groups selected 

were not appropriate controls for the studied SCI individuals. For example, lifestyle and 

comorbidities, irrespective of SCI, could be quite different. Therefore, the extent to which the 

observed increased prevalence of diabetes is due to a causal relationship between the SCI and the 

development of subsequent diabetes is not known. Overall, control groups comprised of veterans 

using Veterans Affairs (VA) medical centers for health care tended to be similar to VA SCI 

populations in their rate of diabetes. Only when the rate of diabetes in the VA SCI group was 

compared to the general public did the SCI individuals appear to be at higher risk. Users of the 

VA health care system have greater comorbidities than either veterans not using the VA health 

care system or non-VA populations. Therefore, current evidence is insufficient to determine to 

what extent the higher rate of diabetes is independently attributable to SCI or to other factors that 
5 

might be higher in adults who subsequently have a SCI than in the general public. There was 

little evidence suggesting that fasting plasma glucose was elevated in adults with SCI. There was 

some evidence that adults with SCI may be more likely to meet IGT or diabetes diagnostic 

criteria following oral glucose tolerance tests (OGTT). However, no studies reported repeated 

OGTT. 

 Lipid disorders. There is some evidence that individuals with SCI compared to controls may 

possess favorably lower average TC (three studies n = 1,427; weighted mean difference (WMD) 

= -14.3 mg/dL [95 percent CI = -22.2, 6.4]),38-40 LDL cholesterol (two studies, n = 773 WMD = -

10.77 [95 percent CI = -16.0, -5.6]),38,40 and triglyceride levels (two studies n = 773; WMD = -

10.0 mg/dL [95 percent CI = -18.3, 1.6]).38,40 HDL cholesterol was lower in SCI individuals 

compared to controls (three studies n = 1,427; WMD = -7.6 mg/dL [95 percent CI = -10.6, 4.6]), 

though confidence intervals were wide and results not statistically significant.38-40

 Obesity and body composition. While BMI is unlikely to be an accurate measure of obesity 

in the SCI population, it is by far the predominant measure reported in research studies of the 

prevalence of obesity. There is no high quality evidence that obesity defined by BMI is elevated 

in individuals with SCI compared to appropriately matched controls. There is some evidence that 

when obesity is measured as percent body fat, individuals with SCI may be at elevated risk. 

However, the absence of validated measures of body composition in SCI individuals or large 

studies that include accurate measurements of body fat precludes stronger conclusions regarding 

the prevalence of obesity and the impact of injury type and duration on obesity. 

Cardiovascular Prevalence and Mortality in Adults with SCI 

 CVD prevalence among SCI individuals ranged from 1-3 percent in the majority of 

studies,32,50,52,53,55 with an increase to 19 percent in older patients and to 14 percent in those 30 or 

more years after injury.52 The prevalence of cerebrovascular diseases was 1-2 percent3,39,53 and 

coronary heart disease ≤2 percent,32,39,53 being increased to 12 percent among members of 

Paralyzed Veterans of America.37 SCI veterans using VA health care had a higher prevalence of 

myocardial infarction (14 percent37to 25 percent)48 than SCI civilians (<5 percent in three 

studies.3,39,53 The highest prevalence of 33 percent was reported among veterans who were older 

than 50 years at the time of injury.48

 Mortality from CVDs was more consistent than prevalence across five studies that reported 

this outcome;1-3,49,52 0.849 to 1.52

 per 1,000 injured died from diseases of the arteries; 149 -6 

percent1

 to 10 percent52 died from cardiovascular disease. Mortality was higher in men (5.3 

percent) compared to women (1 percent)1 and in older patients, being the highest after 75 years 

(10 percent).52 Less than 1 percent of SCI patients died from cerebrovascular diseases and 

stroke,1,2,49 with higher mortality in men (0.7 percent) than women (0.2 percent).1 Mortality from 

ischemic heart disease was <1 percent in two studies2,3 and 2.5 percent (including 2 percent men) 

in one European study.1 One long-term followup study of VA users reported a two-fold increase 

in mortality from 5 years (0.4 percent) to 20 years (0.9 percent) after injury.3

 Lung embolus 

caused death in 0.7 percent of patients with chronic SCI.1

 Three studies reported that coronary heart diseases constitute approximately 9 percent among 

primary causes of death in SCI patients.1-3 The proportion of deaths attributable to all CVDs 

varied from 18.8 percent for diseases of the heart49 to 24 percent for circulatory system 

disorders.1

 Cardiovascular diseases are among the leading causes of death in patients with 

chronic SCI1,49,52 however, the contribution of age cannot be estimated analyzing crude 
6 

proportion of aging SCI patients who died from heart diseases. One study of 402 veterans with 

chronic SCI followed for 55.6 months36 showed that diabetes (relative risk 2.62, 95 percent CI 

1.19; 5.77) and heart diseases (relative risk 3.66, 95 percent CI 1.77; 7.78) were significant risk 

factors for death after adjustment for age. 

 When compared to able-bodied adults, cardiovascular morbidity in SCI patients did not show 

significant differences.34,39 Inconsistent and limited evidence suggested that patients with chronic 

SCI had lower prevalence of congestive heart failure34 but no differences in the odds of diabetes, 

myocardial infraction, angina pectoris, or cerebrovascular diseases.34,39,55

 Diabetes contributed to a higher risk of CVD in veterans with SCI compared to SCI veterans 

without diabetes. One large study of veterans with SCI, able-bodied veterans, and the general 

population reported a three times higher rate of diabetes in injured veterans compared to the 

general population (20 percent vs. 6.7 percent, odds ratio 3.32, 95 percent CI 1.34; 8.26) but 

similar odds compared to other veterans (21 percent, odds ratio 0.94, 95 percent CI 0.47; 1.87).37

Injured veterans with diabetes had higher adjusted rates of coronary heart disease by 280 percent, 

myocardial infarction by 270 percent, arterial hypertension by 250 percent, and stroke by 230 

percent compared to SCI patients without diabetes.37 Age may modify the association with injury 

and diabetes. For example, odds of diabetes were higher in injured veterans compared to the 

general population in all age groups but higher compared to able-bodied veterans in those ages 

45-59, 55-59, and older than 70 years.37 

 Some evidence suggested that neurological functional status may be associated with 

cardiovascular morbidity.53 Patients with tetraplegia and no functional motor preservation had 

higher age adjusted odds ratio of cerebrovascular diseases, dysrhythmia, and valvular diseases 

and lower odds ratio of coronary heart disease compared to paraplegic patients.53 Injured patients 

with functional motor preservation had higher age adjusted odds of all CVDs, coronary 

atherosclerosis, dysrhythmia, and valvular disease.53 Some electrocardiogram abnormalities 

including left bundle branch block, left ventricular hypertrophy with strain, and atrial fibrillation 

accompanied the higher hazard ratio of death in patients with SCI.34 Furthermore, these 

abnormalities were associated with a greater risk of dying in injured compared to able-bodied 

patients.34

 Cardiovascular mortality in injured patients was compared to a standardized by age mortality 

in the general population in three studies.1,2,36 Mortality from nonischemic heart diseases 

(standardized mortality ratio 5.6, 95 percent CI 4.4; 6.8), artery diseases (standardized mortality 

ratio 4.5 95 percent CI 2.1; 6.9), and lung emboli (standardized mortality ratio 11.4, 95 percent 

CI 4.2; 24.8) was higher in all injured adults compared to the general population.1

Cardiovascular mortality was lower in those injured after 1972 (standardized mortality ratio 2.4 

95 percent CI 1.95; 3.01) compared to those injured from 1953-1971 (7.1, 95 percent CI 2.31; 

9.32).1

 Patients with complete tetraplegia died from ischemic heart disease (standardized 

mortality ratio 2.6, 95 percent CI 1.3; 3.9), nonischemic heart diseases (standardized mortality 

ratio 23.4, 95 percent CI 16.5; 30.3), and cerebrovascular diseases (standardized mortality ratio 

5.4, 95 percent CI 1.8; 9) more often than would be expected from the same age able-bodied 

adults.1,2,36

 The role of lipid disorders to alter the risk of cardiovascular morbidity and mortality in SCI 

adults has not been adequately addressed in the published articles. One study concluded that 

increased blood pressure, elevated blood cholesterol, or smoking could not explain the increased 

cardiovascular prevalence in SCI patients.39 One study showed that diabetes in SCI patients was 

associated with an increased risk of coronary heart disease, myocardial infarction, arterial 
7 

hypertension, high cholesterol, and stroke.37 The relative risk contribution to adults with SCI 

compared to able-bodied individuals was not reported. 

 Diabetes mellitus contributed to an increased risk of cardiovascular diseases compared to 

individuals with SCI but not having a diagnosis of diabetes.37 The relative contribution versus 

able-bodied individuals is not known. The role of metabolic syndrome had not yet been 

investigated. Cardiovascular morbidity varied substantially among studies and was highest in 

injured veterans. Many important confounders might explain such differences beyond the veteran 

status and many veterans do not receive health care from the VA.74 Indirect comparisons of 

cardiovascular morbidity in adults with SCI with the general population were inadequate to 

estimate the relative contribution of metabolic disorders in patients with SCI. 

Exercise to Alter Carbohydrate and Lipid Disorders in Adults with SCI 

 Of the 19 peer reviewed original articles, none were randomized controlled trials 

(RCTs).13,14,54,57-72 The majority consisted of small case series or uncontrolled cross-sectional 

surveys using measures of self-reported physical activity. Six studies (n=57) involved active 

exercise, five (n=32) assessed functional electrical stimulation, and six studies (n=219) evaluated 

self-reported physical activity. No studies evaluated passive exercise. Carbohydrate related 

outcomes were reported in ten studies (n=101) and lipid related measures were reported in 13 

studies of 292 individuals. Variation in study design, intervention, and reported outcomes 

precluded quantitative pooling of results or accurate assessment of efficacy. Evidence on effects 

of exercise on lipid and carbohydrate metabolism disorders is of poor quality and inconclusive in 

findings. Studies to date have been short in duration, have involved few subjects, and have relied 

on study designs highly susceptible to error. None assessed glycosylated hemoglobin. 

Dietary and Pharmacologic Intervention for Carbohydrate or Lipid 

Outcomes in Adults with SCI 

 There were no prospective studies that evaluated dietary and/or lifestyle interventions on 

carbohydrate related outcomes. 

 Only two poor quality prospective studies evaluated dietary and/or lifestyle interventions to 

alter lipid levels.20,72 No studies assessing pharmacologic interventions were identified. The two 

dietary/lifestyle case-series studies included 238 subjects, overwhelmingly male (87 percent). 

 One controlled trial compared the effect of a dietary intervention referral compared to no 

dietary referral20 over a mean of 16 months. Group 1 subjects were older (mean 42.8 versus 35.7, 

p<0.0001) and had a longer post-injury duration (15.6 versus 11.1 years, p<0.0001) compared to 

Group 2 subjects. There were reductions in total and LDL cholesterol levels from baseline in 

Group 1, 234 to 224 (p<0.001) and 159 to 151 (p=0.004), respectively. Levels increased slightly 

but not significantly in Group 2. There were no significant effects on HDL cholesterol or 

triglyceride (TG) levels. An uncontrolled study evaluated a weight management program 

consisting of 12 classes for 12 weeks, primarily led by a registered dietician.72 There were no 

significant changes in total and LDL cholesterol levels from baseline at weeks 12 and 24. HDL 

cholesterol was not different at week 24 compared to baseline value. 

Discussion 
8 

 The present report systematically evaluated published evidence regarding the prevalence of 

lipid and carbohydrate disorders, CVD, and mortality in adults with chronic posttraumatic SCI. 

The overall quality of evidence is low. Most studies were retrospective, small, lacked adequate 

controls, and did not assess or adjust for confounding factors. Outcome measure definitions 

varied widely. However, limited low quality data suggest that adults with SCI are not at 

markedly higher risk of carbohydrate and lipid disorders or CVD than age and gender matched 

able-bodied individuals. Assessment of obesity using BMI is likely to be inaccurate and 

underestimates body fat in adults with SCI. 

 The prevalence of insulin resistance, metabolic syndrome, diabetes mellitus, impaired 

glucose tolerance, dyslipidemia, obesity, and CVD in a population are all highly dependent upon 

the demographics of the population, including, most importantly, the age distribution, but also 

socioeconomic status and race/ethnicity. The dependence of these conditions on population 

characteristics makes it difficult to make between-study comparisons, since the population 

characteristics range greatly both between and within studies. These factors may explain the 

wide variation in study prevalence estimates as well as the relative risk compared to different 

able-bodied control populations. 

 Some potentially eligible studies (n=45) were excluded due to small sample size (i.e., less 

than 100 SCI subjects if lacking controls or less than 100 total subjects if including controls). 

Based on review of published abstracts, the impact of these studies on our overall findings 

regarding carbohydrate, lipid and body composition disorder prevalence, and subsequent clinical 

decisionmaking is likely to be small. The number of SCI individuals in the excluded studies 

ranged from one to 77. Only 17 had control groups. The largest excluded study reporting 

impaired glucose tolerance and insulin resistance in the United States lacked controls, was 

comprised of 57 adults from a single center, and was published in 1983. The largest excluded 

controlled study of lipid disorders was a single center report comprised of 60 young SCI adults 

(mean age = 28 years) and 28 healthy able-bodied controls matched by age and gender. Serum 

LDL cholesterol was higher (109 mg/dL vs. 91 mg/dL; p = 0.04) and HDL cholesterol lower (33 

mg/dL vs. 44 mg/dL; p =0.004) in SCI adults versus controls. The authors concluded that “serum 

lipoprotein levels should not be ignored for the followup of patients with spinal cord injury.”75

We agree with their conclusion. Other excluded studies were of even lower quality and relevance 

to health care in the United States because they were smaller, from a single center, not from the 

United States, lacked controls, and/or did not assess clinically relevant carbohydrate and lipid 

disorders. 

 A previous review76 suggested a high prevalence of CVD in individuals with SCI. However, 

this report included, but did not differentiate between, highly prevalent self-reported signs and 

symptoms, such as leg swelling or palpitations56 and less common but more serious conditions or 

those documented in medical records, such as myocardial infarction (0.28 to 3 percent of SCI 

patients).3,53 Several factors may contribute to the prevalence of undiagnosed CVD in SCI 

individuals, including access and quality of care, asymptomatic angina in patients with diabetes 

or upper level injury,77,78 and metabolic syndrome, unstable blood pressure, and cardiac 

rhythm.79,80 If screening intensity or criteria to detect/define asymptomatic heart diseases, 

including coronary heart disease, arrhythmias, and autonomic dysreflexia, differs in SCI 

compared to able-bodied adults this could bias comparative CVD prevalence estimates. 

 Prevalence of CVD in aging SCI individuals can be attributable to age rather than injury. 

Patients differed by the prevalence of risk factors prior to injury and by age at the time of injury. 

Both could modify the association between SCI and CVD. Indeed, a recently published 
9 

retrospective analysis found that the presence of cardiovascular disease prior to injury was 

associated with a 280 percent increase in risk of death.81 For each additional year of age at 

injury, the relative risk of dying was increased by 8 percent (RR 1.08, 1.06; 1.09).81 Whether the 

reported increased risk of all CVD in tetraplegic compared to paraplegic individuals can be 

interpreted as an evidence of higher morbidity53,76 requires additional studies. Limited evidence 

suggests that cardiovascular mortality may contribute to approximately 20 percent of all deaths 

in SCI patients1,36,49,52 and coronary heart disease to 9 percent of all deaths.1-3 There is 

insufficient evidence to determine whether percentage of deaths due to CVD differs in SCI adults 

compared to appropriately matched able-bodied individuals. One study suggested that presence 

of heart diseases was associated with a 3.7 fold increased risk of death in SCI patients compared 

to SCI patients without CVD, independent of age and other risk factors.52 Limited evidence 

suggests that the contribution of different forms of heart disease (e.g., ischemic vs. nonischemic 

coronary heart disease) to overall CVD mortality in SCI patients may differ from the general 

population. However, proportionate mortality in SCI patients cannot give a valid estimation of 

mortality rates in this population. Standardized mortality ratios from nonischemic heart diseases, 

artery diseases, and lung emboli were higher in all injured adults compared to the general 

population.2

 Mortality from lung emboli contributed the most to the overall differences within 

the total population. However, the inconsistency of results and the multiplicity of outcomes 

assessed makes it very plausible that these are chance findings. 

 Whether the independent contribution of diabetes and impaired glucose tolerance on CVD 

prevalence differs in adults with versus without SCI has not been reported. The association 

between metabolic control and CVD in adults with SCI remains unclear. Prevalence of 

retinopathy was not different in SCI users of the VA health care system who were diabetic 

compared to diabetic able-bodied veterans.37 The impact of lipid disorders on CVD in SCI 

individuals is not well documented and needs future investigation. 

 There is no evidence that diagnostic and treatment threshold for carbohydrate and lipid 

disorders should differ in SCI vs. able-bodied individuals. Assessment of insulin resistance and 

impaired glucose tolerance are not routinely performed in able-bodied individuals. The 

effectiveness of screening to improve clinical outcomes by detection of pre-diabetes (impaired 

fasting glucose or impaired glucose tolerance), insulin resistance, and diabetes in asymptomatic 

adults has not been demonstrated.73 Use of these tests is limited due to their inconvenience, 

complexity of testing requirements, costs, and current lack of accuracy. The OGTT is 

inconvenient and not ordered by most physicians to diagnose diabetes, even among those at risk. 

Additionally, about one-half with IGT or OGTT would have normal tests if repeated. Similar 

concerns exist with the criteria used to define impaired fasting glucose. Because the glucose 

concentration distribution is unimodal, the choice of cutpoints used to designate abnormalities of 

carbohydrate metabolism is arbitrary. A recent systematic review assessed the comparative 

effectiveness and safety of oral medications for Type 2 diabetes mellitus. The authors reported 

that there was no definitive evidence about the comparative effectiveness of oral diabetes agents 

on all-cause mortality, cardiovascular mortality, or morbidity, peripheral arterial disease, 

neuropathy, retinopathy, or nephropathy.82 Two more recent meta-analyses of thiazolidinediones 

have been conducted. Among able-bodied patients with impaired glucose tolerance or Type 2 

diabetes (n=14,291), rosiglitazone use for at least 12 months was associated with an increased 

risk of myocardial infarction and heart failure. There was no difference in increased risk in 

cardiovascular mortality.83 A review of pioglitazone (n=16,390) showed a significantly lower 

risk of death, myocardial infarction, or stroke among patients with Type 2 diabetes and 
10 

inadequate glycemic control. Serious heart failure was increased.84 Existing recommendations to 

assess cardiovascular risk for able-bodied individuals suggest that all adults should have a 

complete lipid profile, including HDL and LDL cholesterol levels, as well as family history, 

smoking status, and gender. The treatment recommendations should be based on that 

comprehensive risk assessment. Future studies are needed to determine if SCI should be included 

as an independent risk factor. 

 The evidence that exercise programs alter carbohydrate and lipid outcomes is of poor quality 

and inconclusive. Only one study examined the effects of exercise on coronary heart disease 

outcomes or survival, with no identified associations. There were relatively few consistent 

findings pertaining to plasma glucose, two-hour post-load glucose, fasting insulin, or two-hour 

post-load insulin. Similarly, little consistency was reported between studies for HDL cholesterol, 

TC/HDL, and TG. Results may have indicated some overall post-training benefits for outcomes 

of TC and LDL cholesterol. While many reported findings are suggested as beneficial in the 

primary papers as well as past reviews,85 caution in warranted. There was a general lack of 

quantity, quality, and consistency in methods and outcomes across studies. Reports were based 

on short-term exercise protocols, often involved carefully recruited hospital- and/or clinic-based 

patients, and failed to consider implementation or sustainability of exercise interventions in 

community-based populations. The exercise described in these papers varied considerably from 

one study to the next. In the cross-sectional surveys, parameters of physical activity were rarely 

reported. 

 Exercise and dietary programs among able-bodied individuals have demonstrated a modest 

improvement in carbohydrate and lipid parameters among selected highly motivated individuals. 

Translation of these findings to community settings of SCI adults has not been demonstrated and 

even the effectiveness in the general able-bodied population is unclear. For example, a recent 

randomized trial evaluated the effects of 22 weeks of aerobic training, resistance training, or both 

(three times per week) on glycemic control in 251 able-bodied adults with Type 2 diabetes.86

Combined training resulted in a 1 percent absolute reduction in glycated hemoglobin values 

versus sedentary controls. Reductions due to either resistance or aerobic training alone were 

about one-half that seen with combination therapy. There was no difference in lipid values, blood 

pressure, lean body mass, fat mass, or percent body fat of any of the exercise programs versus 

controls. Adverse events were more common in the exercise group, and 14 percent of those 

randomized to exercise dropped out. 

Conclusions 

 The available evidence regarding the prevalence, impact, and outcomes of carbohydrate and 

lipid disorders in adults with chronic SCI is weak. Evidence is limited by relatively small sample 

size, lack of appropriate control groups, failure to adjust for known confounding variables, and 

variation in reported outcomes. However, the existing evidence does not indicate that adults with 

SCI are at markedly greater risk for carbohydrate and lipid disorders or subsequent 

cardiovascular sequelae than able-bodied adults. The available evidence does not support 

incorporating SCI status as an independent variable to assess risk of cardiovascular morbidity 

and mortality or to alter diagnostic/treatment thresholds compared to able-bodied adults. 

Individuals with SCI may have unique physiologic differences compared to able-bodied 

individuals. Therefore, caution is advised in attempting to extrapolate findings from studies 

conducted in able-bodied adults evaluating efficacy and harms of interventions to improve 
11 

carbohydrate, lipid disorders, and subsequent CVD. Assessment of obesity and body 

composition by BMI is likely inaccurate and underestimate risks. Alternative methods for 

assessment in SCI populations are needed. However, unless future high-quality studies suggest 

otherwise, current evidence supports the conclusion that detection and treatment of carbohydrate 

and lipid disorders in adults with SCI should be similar to able-bodied individuals.

Future Research 

 A major gap in the evidence is the lack of high-quality prospective epidemiologic studies 

assessing the prevalence and impact of lipid and carbohydrate abnormalities and corresponding 

CVD complications in SCI individuals, especially compared to appropriately matched ablebodied controls. Future research could include a large prospective multicenter cohort study of 

adults with SCI. Risk assessment should be started at the time of injury and continued during 

long-term followup. Prevalence and incidence assessment needs to be objective rather than self 

reported. Inclusion of baseline and followup physiologic and serologic values (e.g. body 

composition measures, actual lipid and carbohydrate laboratory values) and standardized 

outcomes should be made according to well-recognized diagnostic criteria of heart diseases. 

Expansion of existing cohort studies in the VA, a large non-VA cohort study, and future RCTs 

that aim to test whether more aggressive screening or treatment within SCI populations actually 

reduces disease prevalence, morbidity, and mortality could be initiated. Additional information 

on women is needed. 

 If prospective cohort studies identify an increased risk in adults with SCI, RCTs will be 

needed to further extend the information. Techniques for identifying and treating these 

carbohydrate and lipid disorders and CVDs may need to be modified to meet the specific needs 

of those with SCI. 

 The level of injury, neurological impairment, and other known or potential confounders 

including smoking status, hypertension, family history, race, age, diabetes, infections, 

socioeconomic status, and quality of health care should be analyzed as possible effect modifiers 

of the association between well known risk factors and cardiovascular morbidity and mortality. 

 Consistent, higher quality research on exercise and metabolic and cardiovascular health in 

SCI patients is needed. Studies examining effectiveness as well as efficacy of exercise 

interventions are needed. Continued research should be conducted to gain a better idea of the 

important barriers to exercise experienced by individuals with SCI and to develop novel methods 

to overcome these barriers. Preliminary studies may also assess which patients are most in need 

of intervention, the best types of exercise programs and equipment, and how to modify them 

based on characteristics of the injury. Whether qualitative or quantitative, this preliminary work 

would not only inform the development of exercise programs but also the research used to 

evaluate efficacy and effectiveness. 

 Short-term, intermediate outcomes of exercise, as were typically reported in the current 

studies, may not be ideal or definitive measurements for this type of research. Studies ideally 

would focus on long-term clinically relevant outcomes such as prevention of or improvement in 

diabetes mellitus, coronary heart disease, and mortality. Long-term harms and adherence also 

need to be assessed. Key variables to be included in future studies are age, race, and gender; 

comorbid conditions; baseline lipid and carbohydrate related measures; duration, level, and 

completeness of SCI; functional status; baseline physical activity; exercise program type, 
12 

frequency, intensity, and duration; and life satisfaction and other important psychosocial 

variables. 

 An RCT would provide the best evidence for or against the use of exercise to prevent or 

control carbohydrate and lipid disorders among those with SCI, though conducting adequately 

sized studies would be difficult and require cooperative group participation. Further research will 

be needed to translate any findings of exercise efficacy into effective community-based 

interventions. Even if efficacy is promising, it will remain to be seen if these interventions are 

feasible in a community setting and if the interventions, as well as health outcomes, are 

sustainable over time. Further evidence on how best to motivate individuals to sustain exercise, 

while preventing and identifying potential harms, will be needed. 

 RCTs evaluating the potential effectiveness and harms of pharmacologic and dietary 

interventions to alter CVD risk factors (diabetes, lipid abnormalities and/or obesity) and reduce 

CVD incidence, morbidity, and mortality may be needed if there is continued concern that results 

may differ in SCI populations compared to able-bodied adults. 
Evidence Report

15 

Chapter 1. Introduction 

Overview 

Spinal cord injuries (SCI) result in 11,000 hospitalizations of new cases annually in the 

United States.5,6 More than 240,000 Americans live with a disability related to SCI and the 

estimated annual cost averages $9.7 billion.5,7,8 Improved quality of care over the last several 

decades has resulted in a 40 percent decline in mortality during the two years following the 

injury.9

 However, improvement in long-term survival has been smaller. Cardiovascular diseases 

(CVD) have been reported as the most common cause of death in adults with chronic SCI.2,10-12

CVD risk factors associated with SCI include behavior (smoking, limited exercise) and 

metabolic abnormalities (obesity, metabolic syndrome,13-15 and diabetes11). The prevalence of 

dyslipidemia16,17 and coronary heart disease has been reported to be higher in adults with SCI 

compared to the general population.10,18 The Institute of Medicine recently released two reports 

that emphasized the role of cardiovascular risk assessment and management in adults with 

chronic SCI.6,11 Some evidence suggests that exercise,19 diet,20,21 and pharmacological therapy22

may reduce diabetes and cardiovascular disease risk in these individuals. Furthermore, markers 

or thresholds of carbohydrate and lipid disorders commonly used in adults without SCI may not 

apply to the population that has sustained SCI. In particular, because adults with SCI lose muscle 

mass that is replaced with fat mass, traditional measure of obesity (weight or body mass index 

[BMI]) may not be appropriate. 

 Accurate estimates of diabetes prevalence and severity in adults with SCI may: 

1. be underestimated relative to able-bodied controls because individuals with SCI may not 

undergo regular testing, 

2. have lower levels of high-density lipoprotein (HDL) cholesterol that go unrecognized if 

providers only assess total cholesterol (TC) levels or base treatment solely on low-density 

lipoprotein (LDL) cholesterol, or 

3. they have earlier evidence of impaired glucose tolerance or altered insulin sensitivity. 

Existing guidelines do not include routine evaluation of glucose and lipid abnormalities nor do 

they provide recommendations for threshold definitions of abnormality or target levels for 

interventions to achieve.23-25 Furthermore, the prevalence, morbidity, and mortality associated 

with carbohydrate and lipid disorders may differ in adults with SCI compared to able-bodied 

individuals. 

 Effective interventions to treat carbohydrate and lipid disorders and reduce cardiovascular 

complications in able-bodied individuals include dietary, pharmacologic, and exercise therapies. 

However, adults with SCI have unique physiologic characteristics that may preclude 

generalization of evidence from able-bodied individuals to those with SCI. Total daily energy 

expenditure for adults with SCI is difficult to calculate but likely much lower than for ablebodied individuals, especially among individuals requiring motorized wheelchairs for mobility. 

Treatment of obesity in SCI remains largely empiric, including guidelines developed for dietary 

intervention in SCI. Pharmacologic therapies to alter carbohydrate and lipid disorders may have 

different effectiveness and adverse effects in individuals with SCI compared to able-bodied 

patients. For example, assessment of hepatic or muscle toxicity in SCI individuals may be 

difficult using traditional serologic measures developed in able-bodied adults because SCI 

individuals have reduced muscle mass and potentially altered hepatic metabolism. 
16 

 Despite the expected benefits of exercise for individuals with SCI, this group also faces 

unique challenges and risks from exercise that are not experienced by the able-bodied 

population.8,26 For one, lack of access to and choices in exercise modes, depending on the 

neurological impact and level of the injury, form physical barriers to obtaining exercise. 

Physiological risks of exercise are also a barrier to improved fitness among those with SCI. 

Depending on the level and completeness of the spinal injury, motor, sensory, and autonomic 

reflexes may still be intact but no longer under control of the brain. Individuals with SCI also 

experience various types of autonomic and circulatory dysregulation.26 Risk of stress-related 

musculoskeletal injury is of concern, given the reliance on a small group of muscles for activities 

of daily living as well as for any physical conditioning. Fractures, joint dislocation, and overuse 

injuries are common for individuals with SCI.27

In selected highly motivated able-bodied population, exercise, and its resulting improvements 

in aerobic capacity, appear to modestly improve carbohydrate metabolism, lipid profiles, and 

general cardiovascular health.7,87-90 For example, even moderate levels of physical activity, 

defined as three to six metabolic equivalents (METs) sustained for 30 minutes five to six times 

per week, may reduce the risk of cardiovascular disease and all-cause mortality.91 Current 

Centers for Disease Control and Prevention (CDC) and American College of Sports Medicine 

recommendations for exercise in the able-bodied population include 30 minutes of moderate 

physical activity, five to six times per week, or 20 minutes of vigorous (greater than six METs) 

physical activity, three or more times per week.92

 However, translation of these findings to community settings of SCI adults has not been 

demonstrated, and even the effectiveness in the general able-bodied population is unclear. For 

example, a recent randomized trial evaluated the effects of 22 weeks of aerobic training, 

resistance training, or both (three times per week) on glycemic control in 251 able-bodied adults 

with Type 2 diabetes.86 Combined training resulted in a 1 percent absolute reduction in glycated 

hemoglobin values vs. sedentary controls. Reductions due to either resistance or aerobic training 

alone were about one-half that seen with combination therapy. There was no difference in lipid 

values, blood pressure, lean body mass, fat mass, or percent body fat of any of the exercise 

programs vs. controls. Adverse events were more common in the exercise group and 14 percent 

of those randomized to exercise dropped out. 

 Whether this amount of physical activity would produce the same benefits in patients with 

SCI is unknown. However, it is reasonable to assume that similar metabolic responses to exercise 

would occur for these individuals. No evidence-based guidelines for exercise in this population 

currently exist.93 At present, the American College of Sports Medicine’s endurance training 

recommendations for those with SCI are relatively similar to advice directed toward the general 

population. Generally, the recommended exercise prescription, at least for those with paraplegia, 

is three to five weekly sessions of 20 to 60 minutes in duration and at an intensity of 50 to 80 

percent of the individual’s peak heart rate.94 Suggested modes of exercise include arm cranking, 

wheelchair propulsion, swimming, wheelchair sports, circuit resistance training, electricallystimulated cycling, and electrically-stimulated walking. 

 Based on a topic and key questions nominated by the Consortium for Spinal Cord Medicine,

we conducted a systematic review of published evidence to address the following questions: 

Question 1a: What proportion of adult patients with chronic posttraumatic spinal cord 

injuries have been diagnosed with: 

a. Insulin resistance syndrome, metabolic syndrome 

b. Diabetes mellitus Type 2, impaired glucose tolerance 
17 

c. Dyslipidemia 

d. Obesity 

 Question 1b: Is the prevalence of carbohydrate and lipid disorders higher in the subgroups of 

patients by age, race, and gender compared to the general population? Does the prevalence of 

carbohydrate and lipid disorders differ by the time after trauma, the level of trauma, and 

functional impairment? 

 Question 2: For people with SCI, what is the evidence on contribution to risk of 

cardiovascular disease of: 

a. Hyperinsulinemia 

b. Abnormalities in carbohydrate metabolism 

c. Abnormalities in lipid metabolism? 

d. Obesity 

This question was refined as: 

 Question 2: Regarding risk of cardiovascular disease for people with SCI: 

a. What is cardiovascular prevalence and mortality in adults with chronic posttraumatic 

spinal cord injuries? 

b. Does cardiovascular incidence and mortality in adults with chronic posttraumatic spinal 

cord injuries differ compared to the general population based on age, race, and gender 

categories? 

c. What is the strength of the association between cardiovascular incidence and mortality 

and abnormalities in lipid and glucose metabolism including Type 2 diabetes mellitus 

after adjustment for possible confounding factors? 

d. Does association vary depending on age, gender, race, the duration after SCI, the level of 

SCI, and functional impairment? 

 Question 3: What are the effects on carbohydrate or lipid-related outcomes in adults with SCI 

of: 

a. Exercise 

b. Dietary and pharmacologic interventions 

Appendixes cited in this report are available at http://www.ahrq.gov/clinic/tp/carbliptp.htm

19 

Chapter 2. Methods 

Topic Assessment and Refinement and Literature Review 

 A Technical Expert Panel (TEP) was convened, comprised of individuals with expertise in 

rehabilitation/physical therapy/neuromuscular aspects of chronic SCI, primary care relevant to 

patients with chronic SCI, lipid and carbohydrate disorders, dietary intervention, exercise, and 

pharmacotherapy in patients with chronic SCI. Names of individuals who agreed to participate, 

their CVs, and disclosure statements were sent to the Agency for Healthcare Research and 

Quality (AHRQ) for review and approval by the end of January 2007. Those members are 

identified in Appendix A. 

 Based on discussions with our partner and TEP members, we developed inclusion and 

exclusion criteria for study design and size, population, intervention, comparator groups, and 

outcomes. Question 2 was refined to read: 

- What is cardiovascular prevalence and mortality in adults with chronic posttraumatic 

spinal cord injuries? 

- Does cardiovascular prevalence and mortality in adults with chronic posttraumatic spinal 

cord injuries differ compared to the general population based on age, race, and gender 

categories? 

- What is the strength of the association between cardiovascular prevalence and mortality 

and abnormalities in lipid and glucose metabolism including Type 2 diabetes mellitus, 

after adjustment for possible confounding factors? 

- Does association vary depending on age, gender, race, the duration after SCI, the level 

of SCI, and functional impairment? 

 We evaluated, but ultimately did not include, findings from systematic reviews of 

randomized controlled trials (RCTs) related to behavioral, dietary or pharmacologic 

interventions as primary prevention of CVD and carbohydrate and lipid disorders in able-bodied 

adults. The rationale was that little RCT evidence regarding the efficacy and harms of these 

interventions in SCI individuals existed. It was unlikely that outcomes from these interventions 

would markedly differ between SCI and able-bodied individuals. Therefore, findings from these 

intervention studies in able-bodied controls were used to assess baseline lipid and carbohydrate 

characteristics as well as effectiveness and harms in able-bodied individuals. We also sought to 

determine whether evidence from these RCTs or current practice guidelines suggested that 

thresholds for diagnosis or intervention in SCI individuals currently recommended for ablebodied adults should be altered for SCI individuals. 

 Following the initial conference calls, the Minnesota Evidence-based Practice Center (EPC) 

conducted a systematic review and meta-analysis (where feasible) of published evidence of the 

association between lipid and carbohydrate disorders and risk of cardiovascular diseases in adults 

with chronic SCI. The prevalence of insulin resistance, metabolic syndrome, diabetes mellitus, 

impaired glucose tolerance, obesity, and abnormalities in lipid metabolism in patients with 

chronic SCI was estimated from cross-sectional studies that attempted to capture a nationally 

representative sample of adults with SCI. Observational cohort and case-control studies that 

tested the hypothesis of the association between carbohydrate and lipid disorders and risk of 

CVDs in adults with chronic SCI were reviewed. The risk of CVDs among patients with chronic 
20 

SCI was analyzed. We examined case control and cohort studies to determine if risks of 

carbohydrate and lipid disorders and CVDs are greater in adults with SCI than in age/gender 

matched controls without SCI. 

 The role of different forms of exercise (passive and active, person initiated, and due to 

electrical stimulation) and diet in the prevention and treatment of carbohydrate and lipid 

disorders and corresponding sequelae in adults with chronic SCI was evaluated from 

observational studies and clinical trials. Controlled and randomized trials that examined the 

effects of exercise, diet, and pharmacological intervention on cardiovascular risk and outcomes 

in adults with chronic SCI were analyzed. Our preliminary search found few controlled trials of 

these interventions and only one survey report that assessed their impact on major cardiovascular 

endpoints, such as morbidity and mortality. Therefore, we estimated the potential impact of early 

detection and treatment of adults with SCI by evaluating large RCT and systematic reviews of 

treatments for lipid and carbohydrate disorders in adults without SCI. Our comprehensive work 

plan covered the assessment and refinement of study questions, proposed literature search and 

review, inclusion/exclusion criteria, and methods for evaluating the quality of studies and rating 

the strength of evidence. 

 The following conceptual model (Figure 1) was created: 
21 

Figure 1. Conceptual model. Contribution of carbohydrate and lipid disorders to risk of cardiovascular 

disease in adults with chronic posttraumatic SCI 

Insulin resistance Altered functional status 

Compensatory 

hyperinsulinemia 

Insulin resistance 

syndrome 

Metabolic syndrome 

Inadequate insulin 

response 

Type 2 diabetes 

Dyslipidemia: 

Elevated total 

cholesterol, LDL-C, 

Triglycerides 

Decreased HDL-C 

Retinopathy 

Neuropathy 

Nephropathy 

Cardiovascular diseases:

Hypertension 

Stroke 

Myocardial infarction 

Heart failure 

Cardiac arrhythmias 

Death

Sedentary lifestyle 

Obesity 

Reduced/altered exercise 

Altered muscle tone 

Increased fat mass and decreased 

muscle mass

Abnormal blood 

pressure response & 

control

Adapted from American College of Endocrinology statement on insulin resistance4

Bold - eligible outcomes 

Adults with SCI

Age, race, gender, comorbidity, socioeconomic status 

Access to medical care 

Time after injury 

Level/severity of injury 
22 

Literature Search Strategy and Eligibility Criteria 

 The search strategy is presented in Appendix B. The general approach is described below. 

Specific items for each question are based on conference calls with our TEP members. 

 Question 1. A literature search was conducted on Ovid MEDLINE®, using the search term 

spinal cord injury combined with the following terms: hyperinsulinemia or hyperinsulinism or 

insulin resistance or Metabolic Syndrome X or metabolic syndrome; diabetes mellitus or glucose 

intolerance or impaired glucose tolerance; hyperlipidemias or HDL cholesterol or low HDL 

cholesterol; and obesity. The search was limited to articles published from 1990 to May 2007 or 

to articles recommended by peer reviewers through October 2007. 

 Studies were included if: 

1. Adults had chronic SCI, defined as 1 year or more since sustaining the injury; 

2. The total number of spinal cord subjects was at least 100, or totaled at least 100 subjects if a 

control group was included; 

3. Reported outcomes such as the prevalence of obesity, diabetes, impaired glucose tolerance, 

metabolic syndrome or insulin resistance, or lipid disorders or reported mean BMI or lipid levels 

(total cholesterol, HDL cholesterol, LDL cholesterol, or triglycerides); 

4. Were published in the English language. For able-bodied individuals we used nationally 

representative samples from NHANES that reported on obesity, diabetes and glucose intolerance, 

and lipid disorders. In particular, we were interested in results provided according to age categories 

and male gender because nearly 90 percent of reported SCI individuals were male. We also 

included a single uncontrolled study of 93 SCI adults that assessed insulin resistance and metabolic 

syndrome because only one other report for insulin resistance and no studies for metabolic 

syndrome met our predefined eligibility criteria. 

 Question 2. Original epidemiologic investigations of more than 50 patients with traumatic 

chronic (>1 year after injury) SCI published in English after 1990 were identified in MEDLINE®

via PubMed®. The search of the Cochrane library and the websites including the American Spinal 

Injury Association, American Paraplegia Society, Paralyzed Veterans of America, Consortium of 

Spinal Cord Medicine, and the catalog WorldCat identified reviews but not additional original 

studies. 

Question 3a (exercise). The Endnote library containing original and review articles 

(n=2,212) was searched for abstracts that included the words fitness, physical activity, or 

exercise, resulting in a subset of 304 citations. In addition, a University of Minnesota medical 

reference librarian assisted in a MEDLINE® search in response to the question, “What is the role 

of exercise in the prevention/treatment of carbohydrate and lipid metabolism disorders in people 

with spinal cord injury or disease?” This search, limited to human studies written in English and 

published between 1996 and 2007, resulted in 13 original articles as well as one review article. 

Of these, one relevant original article65 and the review article85 were not previously identified in 

the Endnote library. The original article was added to the database, for a total of 305 citations. 

 Question 3b. To identify and evaluate evidence whether pharmacologic or dietary 

interventions play a role in the prevention and/or treatment of carbohydrate and lipid metabolism 

disorders in the SCI population, studies were identified by searching in MEDLINE® through 

May 2007 or by recommendations of peer reviewers through October 2007. Our initial literature 

search used the same search string utilized for Question 1. In addition, reference lists of relevant 

studies or reviews were also searched. Since no randomized trials were identified, 

nonrandomized (controlled or uncontrolled) studies were eligible. To be included, studies had to: 
23 

1. Evaluate adults who had chronic SCI, defined as one year or more since sustaining the injury; 

2. Evaluate pharmacologic or dietary interventions; 

3. Report carbohydrate and/or lipid related outcome measures; 

4. Be published in the English language. 

 To address question 3b regarding the effectiveness of interventions on carbohydrate and lipid 

disorders to prevent CVD outcomes and mortality and diabetes in able-bodied adults, we relied 

on RCTs or systematic reviews of RCTs. Studies were identified using the Cochrane Library and 

searching MEDLINE® through September 2007. The search was limited to the English language. 

Included studies must have enrolled or evaluated separately able-bodied adult subjects without 

pre-existing CVD or Type 2 diabetes and reported clinical outcomes such as mortality, 

myocardial infarction, stroke, or prevalence of Type 2 diabetes. Studies reporting only 

improvements in lipid or glucose values were excluded. To limit the scope of the therapeutic 

interventions, we evaluated primarily clinically proven pharmacologic interventions, with the 

exception of omega-III fatty acids. Results were assessed and summarized but not formally 

included in the final report (they are available from the authors upon request). 

Data Synthesis 

For Questions 1 and 2 related to prevalence, we extracted the percentage of individuals with a 

diagnosis of diabetes, impaired glucose tolerance, insulin resistance, lipid abnormality, obesity 

(including BMI categories), CVD, and mortality according to the definitions provided to the 

authors. Additionally, we extracted mean carbohydrate, lipid, or BMI values. We pooled values to 

estimate the mean total, LDL, HDL cholesterol, and triglyceride (TG) values as well as BMI for 

adults with SCI and displayed these in comparison to a representative sample of U.S. adults from 

NHANES. Where data were available we used age stratified NHANES values for U.S. males 

because nearly 90 percent of SCI subjects were male with mean ages between approximately 30 

and 60. We used a random-effects model to estimate the weighted mean difference with 95 percent 

confidence intervals (CI) in lipid values between SCI adults and able-bodied controls. 

 For Question 2, the results of individual studies were abstracted (see Appendix C for 

abstraction form) and summarized in evidence tables to analyze the level of evidence, differences 

in populations and definitions of the outcomes, and the association between risk factors with 

cardiovascular prevalence and mortality by age and injury status. We analyzed outcomes using 

the exact definitions from the individual studies. Any combinations were possible only for the 

same International Classification of Diseases (ICD) codes. Prevalence was calculated as the 

number of CVD events among the total number of SCI patients in the study; standard error and 

CI for population prevalence were calculated with Wilson estimate.95 We calculated mortality as 

a proportion of the patients who died from CVDs during the time of the data collection among 

the total sample of SCI patients. We could not analyze annual mortality rates because the authors 

did not report this outcome. We calculated crude odds ratios (OR) of the outcomes when the 

author reported rates in SCI patients and able-bodied controls.96 Meta-analysis was used to assess 

the pooled prevalence of CVD with random effects models.97 Assumptions underlying metaanalysis included valid measurements of the outcomes and similarity in study and target 

populations. Chi squared tests and I squared tests were used to assess heterogeneity in study 

results.98-100 Calculations were performed using STATA software.101
24 

 For Question 3, we extracted and reported the individual study outcome results with tests of 

significance for SCI patients as reported by authors. Variation in study design, population, 

intervention, and outcome did not permit pooling. 

 Strength of Evidence 

 The strength of the available evidence was rated according to methods of the U.S. Preventive 

Services Task Force via a three-point scale (high, medium, and low). Confidence in the level of 

evidence from the review of assessing interventions in able-bodied adults is considered high based 

on the consistent results from at least two high-quality studies with long-term followup. For all 

other questions strength is considered low due to serious flaws in study design, inconsistency in 

findings, and subsequent risk of bias in outcome assessment. 
Appendixes cited in this report are available at http://www.ahrq.gov/clinic/tp/carbliptp.htm

25 

Chapter 3. Results 

Study Identification

 Figures 2-4 trace the flow of our literature search. Excluded studies are listed in Appendix D. 

Figure 2. Flow chart for Question 1 references 

Search results = 210 references 

Updated search results = 204 references 

Included studies = 22 references 

Duplicate MEDLINE® listings = 6 references 

Excluded: 

Not adult chronic SCI population = 50 references 

Less than 100 patients in study = 46 references 

No relevant data = 58 references 

Not English language = 19 references 

Review articles = 6 references 

Not human subjects = 3 references 
26 

Figure 3. Flow chart for Question 2 references 

Combined search results 

= 260 references 

Included studies = 19 

references 

Excluded: 

News = 1 reference 

Case report = 2 references 

Case series with less than 50 patients = 16 

references 

Case control with less than 50 patients = 1 

reference 

Legal case = 1 reference 

Not eligible exposure = 4 references 

Not eligible outcomes = 111 references 

Not eligible target population = 104 references 

Review article = 1 reference 

Additional references from citations in reviews = 

17 references 

MEDLINE® search 

results = 243 references 
27 

Figure 4. Flow chart for Question 3a references (exercise/physical activity interventions)

Search results = 304 references 

Combined search results = 305 references 

Included studies = 18 references 

Additional references from UMN 

library search = 1 reference 

Excluded: 

Not adult chronic SCI 

population = 38 references; 

Not exercise program 

intervention = 18 references; 

No relevant outcomes = 231 

references 

Additional references from 

citations in included studies = 

1 reference 

Total included studies = 19 references 
Appendixes cited in this report are available at http://www.ahrq.gov/clinic/tp/carbliptp.htm

28 

 For Question 1, the 210 citations identified through the search were screened for inclusion. 

Exclusions were based on the following reasons: not human subjects (three articles), duplicate 

citation listings (six articles), review articles with no data of interest (six articles), not English 

language (19 articles), studies with less than 100 subjects (45 articles), not adult chronic SCI 

patients (50 articles), and no relevant data (58 articles). The remaining 22 articles meeting the 

inclusion criteria contained data for one or more of the following: metabolic syndrome or insulin 

resistance (one article), glucose intolerance or Type 2 diabetes (12 articles), lipid values (six 

articles), or obesity (nine articles) (Appendix E Table 1). Abstracts of the 45 identified studies 

that were excluded primarily for small sample size (i.e. they contained less than 100 SCI subjects 

if lacking controls or less than 100 total subjects if including controls) were further reviewed to 

determine the potential impact on our results and conclusions. The impact of these studies on our 

overall findings regarding carbohydrate, lipid and body composition disorder prevalence, and 

subsequent clinical decisionmaking is likely to be small. The number of SCI individuals in the 

excluded studies ranged from one to 77. Only 17 had control groups. The largest study reporting 

glucose intolerance and insulin resistance in the United States lacked controls, was comprised of 

57 adults from a single center, and was published in 1983. The largest excluded controlled study 

of lipid disorders was a single center report comprised of 60 young SCI adults (mean age = 28 

years) and 28 healthy able-bodied controls matched by age and gender. Serum LD cholesterol 

was higher (109 mg/dL vs. 91 mg/dL; p = 0.04) and HDL cholesterol lower (33 mg/dL vs. 44 

mg/dL; p = 0.004) in SCI adults versus controls. The authors concluded that “serum lipoprotein 

levels should not be ignored for the followup of the patients with spinal cord injury.”75 We agree 

with their conclusion. Other excluded studies were of even lower quality and relevance to health 

care in the United States because they were smaller, from a single center, not from the United 

States, lacked controls, and/or did not assess clinically relevant carbohydrate and lipid disorders. 

 For Question 2, the library included 260 references after the deletion of duplicates; 18 

references were found with a manual search of the citation lists; 243 were identified in 

MEDLINE®. We excluded 241 references for the following reasons: one review, one legal case, 

one news, two case reports, one case control study with <50 SCI patients, 16 case series with 

<50 patients, four evaluated events after diet, acupuncture, surgery, or drug therapy, 111 (46 

percent) did not report cardiovascular events, and 104 (43 percent) examined patients with acute 

traumatic or not traumatic injuries. We reviewed 20 articles of the 19 studies that reported 

cardiovascular events in adults more than 1 year after traumatic SCI (Appendix E Table 2). 

Observational studies were conducted in the United States,2,3,34,36,37,46-51 United Kingdom,52,53

Canada,54 Denmark,1

 Sweden,55,56 Australia,39 and Japan.30,32 Two publications reported different 

outcomes from the same Stockholm Spinal Cord Injury Study.55,56 The results from the Japanese 

National Livelihood Basic Survey were published twice and were considered as one study.30,32

Several American studies were conducted in the Veteran Affairs Spinal Cord Injury Services but 

differed by location, time, and outcome.3,34,37,48,51 One prospective cohort examined incidence of 

CVD in people with long-term SCI.53 Another prospective study evaluated mortality in patients 

with chronic SCI.36 One case control study compared probability of CVDs in patients with SCI 

compared to age-matched able-bodied persons.46 Retrospective cohorts evaluated prevalence of 

electrocardiogram (ECG) abnormalities,34 cardiovascular morbidity, and mortality in patients 

with chronic SCI1-3,47,49,52 compared to the general population1,2,52 and after adjustment for age, 

gender, level of injury, time after injury,52 race, etiology of injury, neurologic level of injury, 

American Spinal Injury Association Impairment Scale, ventilator dependency, sponsor of care, 

and autopsy.49 Cross-sectional surveys reported prevalence of diabetes after adjustment for age, 
Appendixes cited in this report are available at http://www.ahrq.gov/clinic/tp/carbliptp.htm

29 

race, marital status, duration of injury, employment and education,37 and prevalence of 

cardiovascular diseases after adjustment for age,30,32 gender, education, ethnicity, marital and 

vocational status,50 duration of cigarette use,54 duration of injury and functional status,56 and 

socioeconomic status of the patients.55

 For Question 3, based on the criteria identified above, 304 citations identified through the 

keyword search were reduced to 19 for use as evidence. Exclusions were based on the following: 

38 due to lack of adult, chronic SCI patient population; 18 due to lack of exercise program or 

measure of self-reported physical activity; 231 due to lack of relevant carbohydrate or lipid 

related outcome measures. Upon review of citations from the 18 eligible references and one 

previous review paper, one additional reference was identified and added to the evidence base.69

Thus, results of 19 original studies were synthesized to address this question. 

 For Question 3b, only two prospective studies in adults with SCI evaluated dietary and/or 

lifestyle interventions to reduce lipid levels and met inclusion criteria.20,72

Outcomes 

Question 1 

 Overall Description. The prevalence of insulin resistance syndrome, metabolic syndrome, 

diabetes mellitus Type 2, impaired glucose tolerance, dyslipidemia, and obesity in a population 

are all highly dependent upon demographics of the population, including most importantly the 

age distribution, but also factors such as socioeconomic status and race/ethnicity. The 

dependence of these conditions on population characteristics makes it difficult to conduct 

between-study comparisons, since the population characteristics range greatly both between and 

within studies. For example, one study might include men and women between the ages of 18 

and 70, and within such a study one would expect age and gender stratified proportions of Type 

2 diabetes to vary several fold; however, studies of this sort might only present an overall percent 

that are diabetic. Such an overall value is difficult to interpret and nearly meaningless unless the 

study has an appropriate control group. In the included evidence tables and figures, results have 

been presented stratified by age and other key factors (including severity or duration of injury) 

when such information was reported, but the paucity of consistently stratified results makes 

pooled estimates nearly impossible. Therefore, we have chosen to focus primarily on the higher 

quality studies (largest observational reports with control groups). 

 Hyperinsulinemia (insulin resistance/metabolic syndrome). Little is known regarding the 

extent to which hyperinsulinemia is related to SCI. Only one relatively small observational study 

reported results for metabolic syndrome and insulin resistance syndrome (Appendix E Table 1).15

This study included a convenience sample of 93 SCI subjects (mean age = 50 years) recruited 

from a single VA and local community clinics (86 percent male). Of these 93 subjects, 11 

percent were insulin resistant when relying entirely on mean fasting glucose and insulin values; 

however, when glucose-regulating medications were taken into account, 22 percent of the 

subjects were insulin resistant.15 Metabolic syndrome was defined as the presence of three or 

more metabolic disorders, including hypertension (systolic blood pressure ≥130 mmg/Hg, 

diastolic pressure ≥85 mmg/Hg, or the use of antihypertensive medications), obesity (defined by 

waist circumference), hyperglycemia (fasting glucose ≥110 mg/Dl or presence of glucoselowering medications), hypertriglyceridemia (fasting serum triglycerides ≥150 mg/dL or taking 
Appendixes cited in this report are available at http://www.ahrq.gov/clinic/tp/carbliptp.htm

30 

cholesterol-lowering medications), and low HDL cholesterol (<40 mg/dL). Using this definition, 

metabolic syndrome was noted in 22 percent. This study did not include a control group or 

attempt to present results stratified by age and gender or level and duration of injury. The authors 

definitions for specific metabolic disorders are not widely accepted and are likely to increase the 

estimated prevalence of a given disorder.73 A second study of 201 SCI patients included results 

from an oral glucose challenge and reported rates of hyperinsulinemia by type of SCI injury.28

This study found hyperinsulinemia in 53 percent of people with tetraplegia and 37 percent of 

paraplegics. 

Summary. Currently, there are no high quality studies adequately assessing the prevalence of 

metabolic syndrome and insulin resistance syndrome in a large population of adults with SCI. 

There are also no data to assess if the prevalence of either metabolic syndrome or insulin 

resistance are elevated in adults with SCI compared to similar individuals without SCI. Since 

metabolic and insulin resistance rates are dependent on age, gender, and race/ethnicity, future 

studies are needed that are large enough to report rates stratified by these key factors. 

 Abnormalities in carbohydrate metabolism (diabetes mellitus and impaired glucose 

tolerance). The prevalence of diabetes in SCI subjects has been reported in multiple studies 

(Appendix E Table 1).3,15,28-37 Several of these studies have also reported a comparison between 

SCI individuals and non-SCI subjects (Figure 5).29,32,34,37

 A total of 6,832 persons with SCI and 254,847 controls were included in the reviewed 

studies, of which the vast majority of all of SCI individuals came from two large Veterans Health 

Administration (VHA) studies.34,37 The largest of these studies included a national crosssectional survey of 3,737 SCI adults who were users of the VA health care system, along with a 

control group of 6,413 non-SCI VA health-care user control subjects and data from the CDC 

Behavioral Risk Factor Surveillance System 2003 survey of 221,650 community-dwelling 

adults.37 This large study found a substantially greater portion of VA SCI individuals self 

reported that they had diabetes compared to the general population surveyed by the CDC (20 

percent versus 7.6 percent, p<0.001). However, overall self-reported prevalence of diabetes in 

VA users with SCI was similar to the prevalence of diabetes in the non-SCI VA user population 

(20 percent vs. 21 percent). Another large study also from a VA population found similar rates of 

diabetes in SCI and non-SCI subjects (11 percent vs. 10 percent, respectively).34 Differences in 

the overall prevalence of diabetes between these two studies are likely due in part to differences 

in ascertainment of diabetes status (self-report versus diagnosis in administrative dataset) and 

differences in the ages of the subjects, with the study reporting higher veteran prevalence of 

diabetes including older subjects and self-reported surveys. Results from national representative 

able-bodied populations clearly show that the prevalence of diabetes is highly dependent on 

method of ascertainment or definition (diagnosed vs. undiagnosed diabetes vs. impaired fasting 

glucose (Figure 6). The two other studies that included non-SCI control groups reported 

increased diabetes prevalence among SCI individuals.29,32 Both of these studies found severalfold higher rates of diabetes among the SCI subjects but were published more than a decade 

earlier and had smaller sample sizes. The first of these studies also involved veterans with and 

without SCI from a single institution. This study had a small number of controls (n=50) and only 

three controls had diabetes.29 For this study diabetes was diagnosed using a one-time oral 

glucose tolerance test. There was some evidence that persons with SCI had higher scores on their 

oral glucose tolerance tests than would be expected based on their fasting plasma glucose levels 

compared to non-SCI controls. In the non-SCI control group, people who were categorized as 

diabetics had an average mean fast plasma glucose level of 115 mg/dl while mean levels for 
Appendixes cited in this report are available at http://www.ahrq.gov/clinic/tp/carbliptp.htm

31 

paraplegic and tetraplegic diabetics were 99 mg/dl and 102 mg/dl, respectively. The other study 

presented results from a survey of Japanese subjects with overall diabetes rates much lower than 

those observed in the U.S. population (the control group had a 1.2 percent prevalence of 

diabetes).32 

 The relationship between increased age and increased diabetes prevalence in both ablebodied individuals and those with SCI is strong and clearly demonstrated in the large survey of 

SCI individuals by Lavela and colleagues37 and results from the nationally representative 

NHANES III study (Figure 6).102 However, we found no evidence to suggest that the association 

between age and diabetes was substantially different in SCI compared to non-SCI groups. 

 The prevalence of impaired glucose intolerance (IGT) has been studied less frequently. In the 

three studies that met our inclusion criteria,28,29,31 only one study included a non-SCI control 

group (n=50) (Appendix E Table 1).29 All three studies were of veterans receiving care at a VA 

hospital, and all reported approximately 30 percent SCI patients with IGT, while only 12 percent 

of controls had IGT. The fact that only six control individuals with IGT were included in the one 

study with a non-SCI control group makes it impossible to determine from these data whether 

IGT is increased or not. 

Summary. The prevalence of diabetes appeared higher on average in SCI populations studied 

as compared to the general population. However, there is considerable reason to believe that the 

general population groups used were not appropriate controls for SCI patients. For example, 

lifestyle and comorbidities, irrespective of SCI, could be quite different. Therefore, the extent to 

which this increased the prevalence of diabetes is due to a causal relationship between the SCI 

and the development of subsequent diabetes is not well known. Overall, the VA patient control 

groups tended to be similar to the VA SCI patient populations in their rate of diabetes, and it was 

only when the rate of diabetes in the VA SCI patients was compared to the general public that 

the SCI individuals appeared to be at higher risk. Users of the VA health care system have 

greater comorbidities than either veterans not actively using the VA health care system or nonVA populations. Therefore, current evidence is insufficient to determine to what extent the 

higher rate of diabetes is independently attributable to SCI or to other factors that might be 

higher in adults who subsequently have a SCI than in the general public. While there was not 

consistent evidence that fasting plasma glucose was substantially different in SCI patients, some 

evidence suggests that these individuals may be more likely to meet IGT or diabetes mellitus 

diagnostic criteria following oral glucose tolerance tests. More research is needed to determine 

whether using the oral glucose tolerance test (OGTT) is more likely to diagnose diabetes in SCI 

compared to non-SCI patients, and whether individuals diagnosed with diabetes by OGTT 

benefit from treatment. 

 Abnormalities in lipid metabolism (hyperlipidemia and/or low HDL cholesterol). Lipid 

disorders among SCI populations have been reported in seven included articles,16,17,21,31,38,39,103 of 

which three appear to have included SCI individuals from the same study.16,17,40 There appear to 

be a total of 1,413 SCI individuals in all of these studies. Three studies (n=747 SCI adults) 

included some form of a non-SCI control group (n=680 for controls assuming the Krum et al. 

1992 study included a 1:1 match, even though the number of controls was not reported) 

(Appendix E Table 1 and Figure 7).38,39,103 The pooled results of the three studies with control 

groups (one study only reported total cholesterol) showed that on average individuals with SCI 

had lower TC, LDL cholesterol, HDL cholesterol, and TG. While these differences were 

statistically significant, none were likely to result in differences in clinical decisionmaking. All 
32 

mean values were within less than a half a standard deviation. Furthermore, the mean 7.5 mg/dL 

lower (worse) value of HDL cholesterol among SCI individuals was counterbalanced by 11 

mg/dL lower (better) LDL cholesterol and 10 mg/dL lower TG levels. When the mean lipid 

values from SCI individuals were compared to those of the able-bodied national male age norms 

for the NHANES study, the similarities between SCI and able-bodied lipid values were also 

observed (Figures 8-13). None of the mean lipid values were outside of the threshold established 

for primary prevention among able-bodied adults. Mean lipid values for SCI individuals were: 

total cholesterol (six studies) 194 mg/dL (range 188-205); LDL cholesterol (five studies) 125 

mg/dL (range 120-126); HDL cholesterol (five studies) 42 mg/dL (range 39-46), and 

triglycerides (five studies) 122 mg/dL (range 108-148). Therefore in the absence of evidence that 

SCI status conveys an independent risk for coronary vascular events, detection and treatment 

strategies would be similar compared to able-bodied individuals. 

 The small number of SCI adults with reported lipid values makes it difficult to draw 

conclusions regarding subcategories of SCI adults with respect to age, sex, race/ethnicity, 

severity of SCI injury, and duration of SCI injury. The largest study of ethnicity and lipid levels 

in an SCI population included a total of 600 adults (percentage of whom were male was not 

reported) of whom 27 percent were White, 47 percent were Hispanic, and 27 percent were 

African American.17 While this study reported some racial/ethnic differences in lipid levels, there 

exists almost no evidence regarding whether these possible ethnic differences are unique to SCI 

individuals. Additionally, this study did not report whether the percentage of individuals who 

were male differed by ethnicity. The majority of SCI individuals in the studies were men, and 

even in studies that appeared to contain both men and women, the lipid values were not always 

reported by sex. In the few studies that did report female-specific lipid values,21,39,40 only two 

reported control groups (n=139 SCI women in controlled studies). Therefore, little evidence 

exists for whether women with SCI have different lipid levels than able-bodied women. With 

respect to the type of SCI injury (tetraplegia versus paraplegia, complete versus incomplete), the 

studies did not report a substantial difference in lipid levels.16,31,38,40

Summary. There is some evidence that on average SCI individuals may possess slightly, but 

likely not clinically meaningfully, reduced total cholesterol, LDL cholesterol, triglycerides 

(beneficial) and HDL cholesterol (detrimental). The evidence does not support a policy that lipid 

screening should differ in SCI adults compared to able-bodied adults. 

 Obesity. Reports in the general population have consistently shown that the level of obesity 

is increasing in the United States104 and that this increase in obesity is contributing to an excess 

in mortality.105 BMI is the primary method used for assessing obesity in population-based 

studies. However, several alternative methods for assessing obesity exist, including waist 

circumference, waist-to-hip ratio, percent body fat measured through multiple different 

techniques, percentage of ideal weight, and others. The use of general population cutpoints for 

obesity from BMI (>30 kg/m2

) have been called into question by the finding that SCI individuals 

tend to have lower body fat at a given BMI as compared to non-SCI individuals.42 BMI has been 

and remains the predominant measure of obesity reported in SCI studies. 

 The prevalence of obesity among SCI populations has been reported in multiple 

studies,28,31,36,38,40-45 most of which have included some form of a non-SCI control 

group.38,40,42,43,45

 A total of 10,226 persons with SCI (7,959 from one large VA clinical and administrative 

database study)45 and 246,478 control subjects (246,025 from one national population-based 

survey)43 contributed data to this section. Across these studies, mean BMI between SCI and non-
33 

SCI populations were relatively similar with non-SCI populations consistently having slightly 

elevated mean BMI (Figures 14 and 15). However, differences in mean BMI are difficult to 

interpret, not only because BMI might underestimate obesity in SCI individuals, but also because 

the relationship between BMI and disease is typically U- or J-shaped with those in the middle 

categories of BMI having the lowest risk compared to the lowest extreme and upper levels of 

BMI. Separating out the studies by category of BMI is therefore important. However, whether 

the category cutpoints for underweight, normal, overweight, and obese used in able-bodied 

populations can be applied to adults with SCI, is worthy of greater discussion and cannot be 

addressed based upon the available research. To date, many of the studies have either only 

reported mean BMI or merged underweight and normal weight categories together. Also, the 

extent to which the lower mean BMI findings in SCI populations compared to controls are due to 

an underestimate of obesity by BMI in individuals with SCI is difficult to address. 

 Only one of the included studies directly assessed obesity by means other than algorithms 

based on weight and/or height, primarily recorded as BMI.42 This study of 133 SCI individuals 

and 100 age-, height-, and ethnicity-matched able-bodied male controls measured percent fat 

mass using dual energy x-ray absorptiometry (DXA). This study found that total percent lean 

mass was lower and total percent fat mass higher in SCI individuals for a given level of BMI. 

The findings from this study combined with the prior studies showing no striking difference in 

BMI between SCI and able-bodied populations would suggest that future studies should focus 

less on comparing BMI and should investigate whether other indicators of obesity are more 

relevant for this population and correspondingly more predictive of future adverse health events. 

However, it should be noted that while DXA is a reliable measure of body composition, it is also 

much more difficult and expensive to obtain than BMI. 

 Several studies have attempted to explore whether differences in injury type (paraplegia 

versus tetraplegia or complete versus incomplete) or injury duration are correlated with obesity, 

but as with the overall studies of obesity and SCI, these studies are mostly conducted only with 

BMI measurements of obesity. Studies that have looked at injury type have tended to find a 

slightly higher average BMI in adults with paraplegia versus tetraplegia.28,38,42-45 However, it is 

not clear from these studies the extent to which mean BMI is driven by more underweight 

individuals with tetraplegia or possibly a greater tendency for BMI to underreport obesity in 

people with tetraplegia compared to people with paraplegia. 

 Several clinical and research questions remain to be answered, including what is an 

appropriate definition for obesity in an SCI population? For example, can BMI be used to define 

obesity? If not, what should be used in its place? If so, can current general population cutpoints 

for BMI be used or does the cutpoint need to be different (i.e., either specific for SCI in general 

or even more specific for type of SCI injury)? 

Summary. There is no high-quality evidence that obesity defined by BMI is elevated in SCI 

individuals compared to appropriately matched controls. While several authors have reported 

that BMI might not be an accurate measure of obesity in the SCI population, it is by far the 

predominant measure used in research studies of the prevalence of obesity. There is some 

evidence that when obesity is measured as percent body fat, SCI individuals may be at elevated 

risk; however, the absence of large studies that include accurate measurements of body fat 

preclude stronger conclusions from being made about the burden of obesity on individuals with 

SCI and the impact of injury type and duration on the extent of obesity.
34 

Figure 5. Diabetes prevalence, SCI vs. control 

Figure 6. Prevalence of diagnosed diabetes, undiagnosed diabetes, and impaired fasting glucose in men 

(NHANES 1999-2002)102

0

5

10

15

20

25

30

35

40

45

20 - 39 years 40 - 59 years ≥60 years

Age group

Prevalence (%)

Diagnosed diabetes

Undiagnosed diabetes (fasting plasma

glucose ≥7.0 mmol/L)

Impaired fasting glucose (fasting plasma

glucose = 5.6 - 7.0 mmol/L)

0.0%

5.0%

10.0%

15.0%

20.0%

25.0%

Lavela - VA Prakash - VA Bauman - VA Imai -

Japanese

SCI DM Prevalence

Control DM Prevalence

Non-VA Control
35

Figure 7. Weighted mean differences in lipid levels (mg/dL): Spinal cord injured subjects vs. controls A. Total Cholesterol 

B. LDL Cholesterol C. HDL Cholesterol 
36

D. Triglycerides 
37 

Figure 8. Mean levels of total cholesterol, SCI studies 

Figure 9. Mean levels of LDL cholesterol, SCI studies 

1 300

Author (year)

Total Cholesterol

(95% CI)

Moussavi 195.9 (190.6, 201.2)

Baumann 99 190.0 (185.5, 194.5)

Baumann 98 191.6 (188.3, 194.9)

Zhong 188.0 (182.5, 193.5)

Baumann 92 189.5 (178.7, 200.3)

Krum 205.1 (200.4, 209.8)

Subtotal 193.9 (191.9, 195.8)

1 200

Author (year)

LDL Cholesterol

(95% CI)

Moussavi 120.2 (115.1, 125.3)

Baumann 99 126.0 (121.9, 130.1)

Baumann 98 125.3 (123.1, 127.5)

Zhong 124.0 (120.3, 127.7)

Baumann 92 126.0 (115.2, 136.8)

Subtotal 124.7 (122.9, 126.4)
38 

Figure 10. Mean levels of HDL cholesterol, SCI studies 

Figure 11. Mean levels of triglycerides, SCI studies 

1 60

Author (year)

HDL Cholesterol

(95% CI)

Moussavi 46.2 (44.4, 48.0)

Baumann 99 42.0 (40.4, 43.6)

Baumann 98 42.3 (41.5, 43.1)

Zhong 39.0 (37.8, 40.2)

Baumann 92 39.0 (37.0, 41.0)

Subtotal 42.0 (41.4, 42.6)

1 200

Author (year)

Triglycerides

(95% CI)

Moussavi 148.3 (133.6, 163.0)

Baumann 99 108.0 (101.9, 114.1)

Baumann 98 122.0 (119.8, 124.2)

Zhong 122.0 (118.5, 125.5)

Baumann 92 124.5 (102.0, 147.0)

Subtotal 122.4 (119.2, 125.5)

1 60

Author (year)

HDL Cholesterol

(95% CI)

Moussavi 46.2 (44.4, 48.0)

Baumann 99 42.0 (40.4, 43.6)

Baumann 98 42.3 (41.5, 43.1)

Zhong 39.0 (37.8, 40.2)

Baumann 92 39.0 (37.0, 41.0)

Subtotal 42.0 (41.4, 42.6)
39

Figure 12. Total cholesterol, LDL-C and triglyceride levels of able-bodied males by age (NHANES) 

Mean mg/dL and standard deviations 

300 250 200 150 100 

50 

▲

Ө ╬ ◊

▲ Ө ╬ ◊ ▲

Ө

Total cholesterol LDL-C Triglyce

Lipoprotein categories 

▲30-39 years

Ө 40-49 years

╬ 50-59 years◊ 60-74 years▲30-39 years

Ө 40-49 years

╬ 50-59 years◊ 60-74 years▲30-39 years

Ө 40-49 years

╬ 50-59 years◊ 60-74 years▲30-39 years

Ө 40-49 years

╬ 50-59 years◊ 60-74 years
40 

Figure 13. HDL cholesterol levels of able-bodied males by age (NHANES) 

25

30

35

40

45

50

55

60

65

70

30-39 years 40-49 years 50-59 years 60-69 years

Mean mg/dL and standard deviations
41

Figure 14. Mean BMI, SCI, and Control  Weaver Gupta Garshick Johnston Spungen Zhong Bauman Bauman 

15.020.0

25.0

30.035.0

SCI Mean BMI Control Mean BMI
42 

Figure 15. Prevalence of BMI levels by age group (NHANES 1999-2002)105

0

5

10

15

20

25

30

35

40

25-59 years 60-69 years

BMI levels by age group

Prevalence (%)

BMI <18.5

BMI 18.5 to <25

BMI 25 to <30

BMI 30 to <35

BMI ≥35
Appendixes cited in this report are available at http://www.ahrq.gov/clinic/tp/carbliptp.htm

43 

Question 2 

 Subject characteristics. The studies included more than 50,000 patients with SCI. Sample 

size ranged from 9646 to 28,239.49 Males (pooled prevalence 86 percent, 95 percent CI 80.4; 

90.9) and Caucasians comprised the majority of individuals; all studies identified patients at 

clinics or administrative health care databases (Table 1 and Appendix E Table 2). Among 

American studies, large cohorts2,49,50 (studies that analyzed nationally representative databases, 

including the Centers for Disease Control and Prevention and the national Behavioral Risk 

Factor Surveillance System Survey),37 were considered to have higher generalizability. 

Applicability of several large studies from the VA Spinal Cord Injury Services can be 

generalized to veterans seeking care in the VA clinics and, to a lesser extent, general veterans 

with SCI or the overall adult SCI population.3,34,37,48,51 Individuals differed by the level of injury, 

the time after injury, and functional status, but few studies included these factors in the analysis. 

Several studies reported prevalence of hypertension,3,30,32,34,37,39,48,51,53,55 but only a few examined 

other risk factors of cardiovascular diseases, including smoking and lipid levels.37,39,54

Furthermore, definitions of these comorbidities and methods to measure (and therefore, likely 

prevalence) varied across studies. The majority of the studies obtained events with ICD codes 

(the conceptual definition of outcomes is shown in Appendix F). However, the studies reported 

the prevalence of the outcomes obtained with different ICD codes. For example, one study53

defined CVDs with ICD codes 390-448 and 745-747 that included rheumatic and hypertensive 

diseases as well as congenital anomalies of the heart while another50 defined outcome as 

rehospitalization for diseases of the circulatory system, including heart disease, hypertension, 

pulmonary embolus, cerebrovascular diseases, and disease of the arteries and veins. Therefore, 

definitive comparisons of outcomes were not possible. The accuracy and reliability of the coding 

in different settings could not be estimated from the published articles. 

Cardiovascular prevalence in adults with chronic SCI. Crude prevalence estimates were 

reported in the majority of the studies and ranged from 0.05 percent for cerebrovascular disease53

to 58 percent for self reported cardiovascular symptoms56 and differed, depending on how events 

were defined and measured (self reported or identified with ICD codes) and on age and time after 

SCI. Therefore, an overall summary estimate was not provided. The prevalence of cardiovascular 

diseases was <1 percent in two studies32,50 and 2 to 3 percent in three studies52,53,55 (Table 2). 

One smaller study of 140 patients used the London School of Hygiene Questionnaire on Chest 

Pain and Intermittent Claudication and reported a higher prevalence of CVDs (13.4 percent).54

One study found an increase in prevalence in older patients to 19.3 percent after 60 years of age 

at time of injury and to 14.2 percent 30 or more years after injury (Table 3).52 The prevalence of 

congestive heart failure was 2.7 percent in one study,34 and the prevalence of other cardiac 

diseases 2 percent55 or <2 percent.53 The prevalence of cerebrovascular diseases varied from <1 

percent,53 to 1 percent39 or 2 percent.3

 The prevalence of coronary heart disease was 2 percent or 

less in three studies,32,39,53 6 percent among patients from the Vietnam Head and Spinal Cord 

Injury Study Registry,3

 and the highest was 12 percent among members of Paralyzed Veterans of 

America.37 The Stockholm Spinal Cord Injury Study56 examined self reported prevalence of 

“cardiovascular symptoms” and included ankle-leg edema, chest pain, and palpitations. More 

than half of the patients with SCI reported symptoms (55 percent of males and 69 percent of 

injured females). However, prevalence of diagnosed cardiac diseases was only 2 percent. 
Appendixes cited in this report are available at http://www.ahrq.gov/clinic/tp/carbliptp.htm

44 

Whether this represents under diagnosis of cardiovascular diseases or classification of 

nonspecific symptoms which did not reflect CVD is not known. Seventy-two percent of patients 

with complete cervical and thoracic injury reported having cardiovascular symptoms. The 

prevalence of arterial hypertension was <3 percent in three studies,30,32,53,55 5-10 percent in four 

studies,30,34,39,48 and more than 20 percent in four studies.3,37,48,51 The Vietnam Head and Spinal 

Cord Injury Study reported that 21 percent of the injured adults had hypertension3 and 25-49 

percent of the patients of the Spinal Cord Injury Service of VA medical centers were diagnosed 

with arterial hypertension.37,48,51 In addition, borderline hypertension was found in 33 percent of 

the injured veterans.51 The prevalence of myocardial infarction was <5 percent in three 

studies.3,39,53 

 SCI veterans had higher prevalence of myocardial infarction, 14 percent37 to 25 percent 

among those who were younger than 50 years at the time of injury and older than 50 years at the 

time of index admission to the Veterans hospital48 (Table 3). The highest prevalence of 33 

percent was reported among veterans who were older than 50 years at the time of injury 

representing the effect of age rather than injury 48 Patients with tetraplegia and ABC functional 

status had lower age adjusted rates of coronary heart diseases, including myocardial infarction, 

and higher rates of cerebrovascular diseases, dysrhythmia, and valvular disease (Table 4) by 

neurologic category among 834 patients.53 Prevalence of cardiovascular symptoms and arterial 

hypertension appeared to vary by the level of injury, though statistical differences in rates were 

not provided (Appendix E Table 3). 

Asymptomatic heart conditions in patients with SCI. Three studies reported cases of silent 

ischemia in asymptomatic adults with SCI.10,106,107 Tomographic thallium-201 myocardial 

perfusion imaging detected scintigraphic evidence of ischemia in 3 of 6 patients (50 percent) 

with tetraplegia and signs of infarction in one patient.106 A simple arm ergometry and 

radionuclide tomographic image test detected silent scintigraphic evidence of ischemia in 13 SCI 

patients with paraplegia from 20 tested having normal resting electrocardiograms (65 percent). 

Since five subjects had ECG evidence of ischemia on exercise testing, eight patients (62 percent) 

experienced undiagnosed coronary heart disease.107 Latent coronary artery was diagnosed in 12 

of 19 subjects with paraplegia (63 percent) using radionuclide myocardial perfusion imaging 

after upper body ergometry exercise.10 A recently published case control study108 of coronary 

scanning showed that 91 patients with chronic SCI had the higher mean calcium scores (75±218 

versus 28±104, p <0.001) compared to 273 age matched non-SCI controls. The prevalence of 

coronary artery calcification was greater in the SCI population than the control population (16 

percent versus 7 percent, p <0.01). 

 Pooled analysis detected a significant heterogeneity between studies in estimated prevalence 

of cardiovascular diseases (data not shown). Therefore, methodological heterogeneity made the 

pooled estimations not valid. Almost all variations in pooled prevalence of hypertension (14 

percent) and myocardial infarction (8 percent) were attributable to heterogeneity between 

studies. The fact that the summarized prevalence of all CVD events, including coronary heart 

and non ischemic heart diseases, was less than different forms of CVDs reported in the studies. 

Such discrepancy can reflect overlap and different definitions and methods to measure outcomes, 

and, probably, some proportion of undiagnosed cardiac pathology in SCI populations. Three 

studies reported prevalence in subgroups48,50,52 but not in the total sample. Conclusions and 

decisions based on pooled prevalence cannot be made.
45 

Cardiovascular mortality. Mortality from CVDs was more consistent than prevalence 

across five studies that reported this outcome (Table 5).1-3,49,52 Patients with SCI died from 

diseases of the arteries (ICD codes 440-448) in 0.849 to 1.52 per 1,000 injured according to two 

large studies of more than 29,000 patients.2,49 CVD (ICD codes 390-458) caused death in 1 

percent49 to 6.3 percent1

 to 10 percent52 of those injured. Men with SCI had higher CVD 

mortality (5.3 percent) compared to women (1 percent), with no formal statistical test of the 

effect modification reported.1

 Results were not controlled for potential differences in other CVD 

risk factors such as smoking status, diabetes, hypertension, and family history. Mortality 

increased with the age of the patients, being the highest after 75 years (10 percent).52 Less than 1 

percent of SCI patients died from cerebrovascular diseases1,2 and stroke.49 Cerebrovascular 

deaths were more common in men (0.7 percent) than women (0.2 percent) with unknown 

statistical significance of the differences.1

 Mortality from cerebrovascular diseases was 0.1 

percent2 among patients with complete tetraplegia and 0.2 percent after cervical or thoracic 

injury with no functional motor preservation.1

 Mortality from ischemic heart disease was <1 

percent in two studies.2,3 One European study that obtained post mortem records found that 2.5 

percent, including 2 percent men, died from ischemic heart disease.1

 One long-term followup 

study in U.S. veterans reported a two-fold increase in mortality from 5 years (0.4 percent) to 20 

years (0.9 percent) after injury, representing the association between age and mortality rather 

than SCI.3 Lung embolus caused death in 0.7 percent of patients with chronic SCI.1 Three studies 

reported that coronary heart disease was the primary cause of death in approximately 9 percent 

of patients with SCI (Figure 16). The proportion of deaths attributable to CVDs varied from 7.1 

percent for ischemic heart disease49 to 24 percent for any CVD1 (Table 6). CVDs are among the 

leading causes of death in patients with chronic SCI;1,49,52 however, the contribution of age 

cannot be estimated by analyzing the crude proportion of aging SCI patients who died from heart 

diseases. One study of 402 veterans with chronic SCI followed for 55.6 months36 showed that 

diabetes (relative risk 2.62, 95 percent CI 1.19; 5.77) and heart diseases (relative risk 3.66, 95 

percent CI 1.77; 7.78) were significant risk factors for death after adjustment for age. 

Cardiovascular prevalence and mortality in adults with chronic SCI compared to the 

general population according to age, race, and gender. Published evidence did not suggest that 

adults with chronic SCI experience CVDs more frequently than the general population. The 

Australian Risk Factor Prevalence Study of 327 patients with SCI and age and sex matched 

controls found that adults with SCI had a 50 percent reduction in arterial hypertension and no 

differences in odds of diabetes, myocardial infraction, angina pectoris, and cerebrovascular 

diseases (Table 7).39 Crude odds of arterial hypertension were lower by 84 percent34 in another 

study of 654 male veterans with SCI.34 The same study reported lower odds of congestive heart 

failure in injured compared to able-bodied veterans.34 The Stockholm Spinal Cord Injury Study 

showed that prevalence of circulatory diseases was lower by 75 percent in injured patients 

compared to healthy controls after adjustment for age, sex, socioeconomic status (odds ratio 0.25 

p value = 0.014),55 with no differences in rates of cardiac diseases, and use of cardiac 

medications. One larger study of 18,372 veterans with SCI, 6,433 able-bodied veterans, and 

221,650 in the general population, using 2003 Behavioral Risk Factor Surveillance System survey 

data,37 reported a three times higher rate of diabetes in injured veterans compared to the general 

population (20 percent versus 6.7 percent, odds ratio 3.32, 95 percent CI 1.34; 8.26),37 but similar 

odds compared to other veterans (21 percent, odds ratio 0.94, 95 percent CI 0.47; 1.87). SCI 

adults with diabetes had higher adjusted rates of coronary heart disease by 280 percent, 

myocardial infarction by 270 percent, arterial hypertension by 250 percent, and stroke by 230 
Appendixes cited in this report are available at http://www.ahrq.gov/clinic/epcindex.htm

46 

percent compared to SCI patients without diabetes (Figure 17).37 Diabetes is associated with an 

increased risk of heart disease, independent of SCI. The authors did not compare relative risk of 

heart diseases in diabetics with and without injury to estimate the effect of injury. 

 Odds ratios of cardiovascular outcomes were reported after adjustment for age. However, age 

may modify the association with injury and diabetes. For example, odds of diabetes were higher 

in injured veterans compared to the general population in all age groups but higher compared to 

able bodied veterans in those of 45-59, 55-59, and older than 70 years of age (Appendix E Table 

4). Despite no difference in management of diabetes, adults with SCI and diabetes had three to 

five times higher rates of foot sores compared with diabetics in the general population and ablebodied veterans with diabetes. Risk of diabetic retinopathy was 19 percent higher compared to 

diabetics in the general population (Table 8). 

 Evidence from one study suggested that neurological functional status may be associated 

with cardiovascular morbidity (Table 4). Patients with tetraplegia and no functional motor 

preservation had higher age adjusted odds ratio of cerebrovascular diseases, dysrhythmia, and 

valvular diseases and lower odds ratio of coronary heart disease compared to paraplegic patients 

(Figure 18). Adults with SCI and functional motor preservation had higher age adjusted odds of 

all CVDs, coronary atherosclerosis, dysrhythmia, and valvular disease compared to paraplegic 

and no functional motor preservation.53

 Morbidity can be estimated using surrogate outcomes. ECG is the most important single 

diagnostic indicator of cardiac arrhythmias and myocardial infarction.34 One large study of 

26,734 able-bodied male veterans and 654 patients with SCI found a decreased relative risk of 

ECG abnormalities in injured patients, only ST segment elevation in younger injured was 

observed more often in younger patients (Appendix E Table 5). Injured veterans with intact 

sympathetic innervation to the heart (injury level T6 and below) had lower risk of any ECG 

abnormalities compared to impaired sympathetic activity (injury level T5 and above) 

(Appendix E Table 6). Younger patients had lower risk of ECG abnormalities (Appendix E 

Table 7). Nearly all examined ECG abnormalities were associated with increased risk of death 

in able-bodied veterans, but only left bundle branch block (LBBB), left ventricular hypertrophy 

with strain, and atrial fibrillation accompanied the higher hazard ratio of death in patients with 

SCI (Table 9). Furthermore, these abnormalities were associated with a greater risk of dying in 

SCI compared to able-bodied adults. The rates of diagnosed hypertension (44 percent vs. 7 

percent), congestive heart failure (7 percent versus 1.7 percent), and coronary heart diseases (7 

percent versus 1.7 percent) were lower among SCI veterans compared to able-bodied (Figure 

19).34 The contribution of undiagnosed heart disease on death in SCI patients is not known and 

requires future research. 

 In addition to reported relative risk, three studies1,2,36 estimated age standardized mortality 

ratios from CVDs in SCI patients compared to the general population (Tables 10 and 11). Injured 

patients died from all cardiovascular diseases more often than age matched able-bodied adults 

(standardized mortality ratio 2.1, 95 percent CI 1.83; 2.37.1 However, the ratio was significant 

only for lung embolus (standardized mortality ratio11, 95 percent CI 4.19; 24.8) but not for other 

forms of CVD. SCI was associated with comparable increase in rates of cardiovascular death in 

men and women (Table 11). Cardiovascular mortality was lower in those injured after 1972 

(standardized mortality ratio 2.4, 95 percent CI 1.95; 3.01) compared to those injured from 1953-

1971 (standardized mortality ratio 7.1, 95 percent CI 2.31; 9.32) (Table 12).1

 Standardized
47 

mortality ratios in patients with cervical (standardized mortality ratio 1.1, 95 percent CI 0.72; 

1.53) or thoracic injuries (standardized mortality ratio 1, 95 percent CI 0.82; 1.84) did not 

differ from the general population in the European study of 888 injured adults followed up 

from 1953 to 1992.1

 

 The role of functional status was reported in one study. Patients with complete tetraplegia 

died from ischemic heart disease (ICD codes 410-414) (standardized mortality ratio 2.6, 95 

percent CI 1.3; 3.9), non ischemic heart diseases (standardized mortality ratio 23.4, 95 percent 

CI 16.5; 30.3), and cerebrovascular diseases (standardized mortality ratio 5.4, 95 percent CI 

1.8; 9) more often than would be expected from the same age able-bodied adults.2 

 Mortality from nonischemic heart diseases (standardized mortality ratio 5.6, 95 percent CI 

4.4; 6.8), artery diseases (standardized mortality ratio 4.5, 95 percent CI 2.1; 6.9), and lung 

emboli (standardized mortality ratio 11.4, 95 percent CI 4.2; 24.8) was higher in all injured 

adults compared to the general population.2

 Mortality from lung emboli contributed the most to 

the overall differences within the total population. The role of carbohydrate and lipid disorders 

(the focus of this review) in nonischemic heart disease and biologic plausibility for this finding 

is not well known. Therefore, it is possible that these are spurious findings based on multiple 

comparisons. 

 Three studies reported that coronary heart disease constitutes approximately 9 percent among 

primary causes of death in SCI patients.1-3 The proportion of deaths attributable to all CVDs 

varied from 18.8 percent for diseases of the heart49 to 24 percent for circulatory system 

disorders.1

 Cardiovascular diseases are among the leading causes of death in patients with 

chronic SCI.1,49,52 However, the contribution of age cannot be estimated analyzing crude 

proportion of aging SCI patients who died from heart diseases. One study of 402 veterans with 

chronic SCI followed by 55.6 months36 showed that diabetes (relative risk 2.62, 95 percent CI 

1.19; 5.77) and heart diseases (relative risk 3.66, 95 percent CI 1.77; 7.78) were significant risk 

factors for death after adjustment for age. 

 The role of lipid disorders to increase the risk of cardiovascular morbidity and mortality has 

not been evaluated in the published articles. The Australian Risk Factor Prevalence Study 

examined the overall cardiovascular risk in 102 injured patients and age matched control with 

scores from the MRFIT study (age, diastolic blood pressure, total cholesterol level, cigarettes per 

day, and sex).39 The injured patients had overall percentile position of risk <50 percent 

independent of age and years after injury. The authors concluded that increased blood pressure, 

elevated blood cholesterol, or smoking could not explain cardiovascular prevalence in SCI 

patients.39 Physical activity, BMI, cigarette use, and alcohol consumption were not associated 

with increased risk of cardiovascular diseases in the study of 97 injured adults.54 However, the 

size of this study was too small to rule out clinically meaningful associations. One study showed 

that diabetes in SCI patients was associated with an increased risk of coronary heart disease, 

myocardial infarction, arterial hypertension, high cholesterol, and stroke, the well known 

association in able-bodied adults.37 

Interpretation of findings. Published evidence suggested that for people with SCI, diabetes 

mellitus contributed to an increased risk of CVDs.37 The role of metabolic syndrome and lipid 

disorders had not yet been investigated. Increased rates of diabetes in SCI compared to ablebodied adults were reported in three articles30,32,37 with no differences in the other three.34,39,55

The degree of neurological impairment may be associated with cardiovascular mortality in SCI 

patients with no documented evidence of independent contribution of glucose and lipid 

disorders. Cardiovascular morbidity varied substantially among studies, being highest in injured 
48 

veterans. Many important confounders might explain such differences beyond the veteran status, 

since many veterans do not seek care from the VA.74 The studied veterans are more likely to be 

poor, without private insurance, have minority status, and/or have a service connected injury.74

Indirect comparisons of cardiovascular morbidity in injured patients with known incidence of 

CVD in the general population does not permit and accurately estimate the contribution of 

metabolic disorders in patients with SCI. 

Summary. Cardiovascular diseases are among the leading causes of death in patients with 

chronic SCI. However, when compared to able-bodied adults, cardiovascular prevalence in SCI 

patients did not show significant differences. 

a. Cardiovascular mortality in injured patients was compared to standardized by age 

mortality in the general population in three studies. Age adjusted mortality from 

nonischemic heart diseases (standardized mortality ratio 5.6, 95 percent CI 4.4; 6.8), 

artery diseases (standardized mortality ratio 4.5, 95 percent CI 2.1; 6.9), and lung emboli 

(standardized mortality ratio 11.4, 95 percent CI 4.2; 24.8) was higher in all injured 

adults compared to the general population. Cardiovascular mortality was lower in those 

injured after 1972 (standardized mortality ratio 2.4, 95 percent CI 1.95; 3.01) compared 

to those injured from 1953-1971 (standardized mortality ratio 7.1, 95 percent CI 2.31; 

9.32). 

Limited inconsistent evidence suggested higher risk of morbidity and mortality in 

adults who were older at time of injury. The role of functional status was examined in 

two studies reporting that patients with tetraplegia had higher odds of having and 

dying from cerebrovascular diseases. Inconsistent evidence suggested that patients 

with complete tetraplegia died from ischemic heart disease (standardized mortality 

ratio 2.6, 95 percent CI 1.3; 3.9) and nonischemic heart diseases (standardized 

mortality ratio 23.4, 95 percent CI 16.5; 30.3) more often than would be expected 

from the same age able-bodied adults. However, these findings may be based on 

chance due to the multiple comparisons and lack of significant associations with other 

cardiovascular outcomes. 

b. Diabetes contributed to higher risk of CVD in veterans with SCI compared to nondiabetic 

SCI veterans in one large study. No studies compared risk of CVD among diabetics with 

SCI to able-bodied diabetics. The role of lipid disorders to increase the risk of 

cardiovascular morbidity and mortality has not been evaluated in the published articles. 

One study concluded that increased blood pressure, elevated blood cholesterol, or 

smoking could not explain increased cardiovascular prevalence in SCI patients. 
49 

Table 1. Patient characteristics in studies that reported cardiovascular events in adults with SCI

Author Sample 

Country 

Patients 

Cardus, 199246 96 

USA 

Patients after traumatic SCI who resided in the county area and had to use 

assistive device for walking. Age: >18 years; Time after injury: >9 months. 

Controls: 96 nontrained able-bodied men matched by age. 

Krum, 199239 327 

Australia 

Patients with SCI and age and sex matched controls from the 1983 Australian 

Risk Factor Prevalence Study. Gender: 19% female; 25-64 years old; Time 

after injury: 34% more than 10 years after injury; Injury: 40% with cervical, 

35% with lower thoracic, 13% with upper thoracic, and 12% with lumbar levels 

of injury; ~41% with Frankel Grade A of completeness - complete motor and 

sensory deficit. 

Whiteneck, 

199252

834 

UK 

Patients with SCI, treated at the British spinal injury centers; Gender: 13% 

female; Age at time of injury was between 15 and 55 years—15-24 years 42%, 

25-34 years 27%, 35-44 years 18%, 45-55 years; median survival time 32 

years; Time after injury: >20 years; 412 survivors, Median survival time 32 

years; 85% survived at 10 years, 71% at 20 years, 53% at 30 years, and 35% 

at 40 years after injury. 

DeVivo, 19932 9,135 

USA 

Patients injured between 1973 and 1984 and treated at any of 13 regional SCI 

care systems. 

Imai, 199430 244 

Japan 

Males with SCI identified during the National Livelihood Basic Survey in Japan 

engaged in light work at special centers, who had medical examination for 

blood pressure and medical history. Mean age: 49.5 years; Time after injury: 

average 17.9 years; Injury: 19 patients injured at level C-T5, 24 at T6-T10, 139 

at T11-L1, and 13 at L2 or lower. 

Nam, 199447 1,027+2,007 

USA 

Patients admitted to medical centers with stroke and patients with traumatic 

SCI (paraplegia or quadriplegia). Population: average age 37.2±16.1 years. 

Levi, 199555 326 

Sweden 

Patients with traumatic SCI from the Stockholm Spinal Cord Injury Study, 

residents of the Greater Stockholm area. Control: participants in the Swedish 

Annual Level-of Living Survey (1,978 interviews). 

Levi, 199556 353 

Sweden 

Patients with traumatic SCI, participants in The Stockholm Spinal Cord Injury 

Study. Time after injury: 0-4 years after injury 23.97%; 5-17 years after injury 

48.76%; 18-44 years after injury 24.52%. 

McGlincheyBerroth, 199548 534 

USA 

VA settings 

Time: 1989-1992 

Patients with traumatic SCI admitted to the high quality Spinal Cord Injury 

Service of the VA Medical Center; mean age of 50 years (16-84 years), 23% 

were at least 65 years of age; Gender: 99% males; Time after injury: 16±13.1 

years, 12 hospital admissions since injury. 

Imai, 199632

(the same 

population as 

Imai, 1994)30

244, Japan Males with traumatic SCI at several rehabilitation centers; ages 22 to 69 years 

(mean 47.6); Time after injury: 17.3 years; Injury: C-T5 level 1%; T6-T10 12%; 

T11-Ll 69%; L2 8%. Control group (general population) National Livelihood 

Basic Survey conducted by the Ministry of Health and Welfare in 1989, on 

800,000 people in 240,000 households. 

Hartkopp,19971 888 

Denmark 

Patients (713 men and 175 women) who survived traumatic SCI and were 

rehabilitated at the Centre for Spinal Cord Injured in Hornbnk, Denmark. 

Population: median age at the time of injury 27.5 in 1953-1971 and 28.5 in 

1972-1990. 

Rish, 19973 230 

USA 

VA settings 

Time: 1967-1970 

to 1995 

Patients with traumatic SCI identified in the Vietnam Head and Spinal Cord 

Injury Study Registry who survived more then 72 hours, with significant 

myelopathy; mean age at injury 21.4 years, with previous excellent health 

(active duty military personnel) mean age at injury 21.4 years; median time 

after injury 25 years. 

DeVivo, 199949 28,239 

USA 

Patients admitted to the model system or to a Shriner's Hospital within 1 year 

of traumatic SCI who survived at least 24 hours after injury; Gender: 19% 

female; Race: 67.6% Caucasian, 20.7% African American, 8.1% Hispanic, 

3.6% Asian, Native American, or other; Time at injury: 54% of injuries occurred 

between the ages of 16 and 30 years, and 23% between 31 and 45 years; 

Injury: 53% cervical, C5-C8 34.5% and C1-C4 18.5% of the population; 53.8% 

neurologically complete, 27.2% motor functional, 19% sensory sparing or 

motor nonfunctional; 2.9% were ventilator-dependent. 
Table 1. Patient characteristics in studies that reported cardiovascular events in adults with SCI (continued)

50 

Author Sample 

Country 

Patients 

Groah, 200153 834 

UK 

Patients alive >20 years after SCI identified in 2 British spinal Injury centers; 

Mean age 57±10 years; Gender: 14% females; Time after injury: 29±6 years. 

Davies, 200254 97 

Canada 

Patients with segmental, nonprogressive traumatic SCI; mean age 47.5±4.5; 

Gender: 10% females; Age at injury: 31.67±16.4; Time after injury: 15.9±10.1 

years; Injury: Quadriplegic 42%; Paraplegic 57%; Undetermined 1%; 

Complete 33%; Incomplete 64%; Undetermined 3%; Traumatic 87%. 

Prakash, 200234 654 

USA 

VA settings 

Time: 1987-1999 

47,070 patients with at least one ECG obtained in the Palo Alto Veterans 

Affairs Health Care System; 26,734 able-bodied male veterans and 654 

patients with SCI. Mean age: 50±14 years. 

Cardenas, 

200450 8,668 

USA 

Patients with traumatic SCI identified in the Model System (hospitalized 

between acute hospitalization and comprehensive inpatient rehabilitation, 

admitted to a Model System within 365 days of injury) who reside in the 

geographic region in which the Model System facility is located; 3,904 patients 

with 11,047 followup interviews, Gender: 21.4% female; Race: 61.4% White 

Injury: C1-4 ASIA grades A, B, C: 4.6% 

 C1-4 ASIA grade D: 6.1% 

 C5-8 ASIA grades A, B, C: 19.1% 

 C5-8 ASIA grade D: 8.5% 

 T1-S5 ASIA grades A, B, C: 33.1% 

 T1-S5 ASIA grade D: 4.2%.

Lavela, 200637 5,690 

USA 

VA settings 

Time: 2003 

Veterans with SCI and disorders who use VA health services; Mean age 60 

years; Gender: 97% males; Race: White 81%; Time after injury: 24 years; 

Injury: 52% with paraplegic level injury. Control: 2003 Behavioral Risk Factor 

Surveillance System survey data for veteran and general population from the 

Centers for Disease Control and prevention. 6,433 general veteran group and 

221,650 general population group. 

Lee, 200651 168 

USA 

VA settings 

Patients with SCI identified in the Spinal Cord Injury Service of the Veterans 

Affairs Palo Alto Medical Center; Mean age 50.27±12.8 years; Gender: 11% 

female; Race: 62% White; Time after injury: 19.17±13 years; Injury: 73 (43%) 

had paraplegia and 95 (56%) tetraplegia. 

Garshick, 

200536 361 

USA 

VA settings 

Time: 1994-2000 

Males with chronic SCI, >20 years of age previously treated by the SCI 

Service at Veterans Affairs Boston Healthcare System, registered in the 

National Spinal Cord Injury Association database in Massachusetts, New 

Hampshire, Vermont, Maine, and Rhode Island (289 veterans and 72 

nonveterans); Mean age: 50.6±15.0 years (range 23-87), Race: 93% 

Caucasian, 5% African American, and 2% other races; Time after injury: 

17.5±12.8 years (range 1.0-56.5); Injury: 92% SCI was due to traumatic injury; 

37 deaths. 
51 

Table 2. Prevalence of CVD in adults with SCI 

Author Age, Years Outcomes Sample (n) Prevalence, % 

Garshick, 200536 Mean 50.6±15.0 Hypertension 361 24.4 

Groah,* 200153 Mean 57±10 Hypertension 834 0.58 

Krum, 199239 Hypertension 102 9 

Lavela, 200637 Mean 60 Hypertension 18,372 49 

Lee,* 200651 Mean 50.27±12.8 Hypertension 168 45.14 

Levi, 199555 Hypertension 326 0 

Prakash,* 200234 Mean 50±14 Hypertension 654 7 

Rish,* 19973 Mean at injury 21.4, 

median time after 

injury 25 

Hypertension 230 21 

Imai, 199632 Mean 47.6 Hypertension 244 16.39 

Imai, 199632 Mean 47.6 Hypotension 244 1.64 

Prehypertension 168 32.74 

Stage 1 hypertension 168 16.07 

Lee,* 200651 Mean 50.27±12.8 

Stage 2 hypertension 168 8.33 

Krum, 199239 Range 25-64 Cerebrovascular accident 102 1 

Rish,* 19973 Mean at injury 21.4, 

median time after 

injury 25 

Cerebrovascular accident 230 2 

Groah,* 2001 Cerebrovascular diseases 834 0.05 53 Mean 57±10 

Angina 834 0.07 

Krum, 199239 Range 25-64 Angina 102 2 

Prakash,* 200234 Mean 50±14 Coronary artery disease 654 1.7 

Rish,* 19973 Mean at injury 21.4, 

median time after 

injury 25 

Coronary artery disease 230 6 

Groah,* 200153 Mean 57±10 Coronary atherosclerosis 834 0.27 

Lavela, 200637 Mean 60 Coronary heart disease 18,372 12 

Groah,* 200153 Mean 57±10 Ischemic heart diseases 834 0.65 

Imai, 199632 Mean 47.6 Ischemic heart diseases 244 1.64 

Groah,* 200153 Mean 57±10 Myocardial infarction 834 0.28 

Krum, 199239 Range 25-64 Myocardial infarction 102 1.9 

Lavela, 200637 Mean 60 Myocardial infarction 18,372 14 

Rish,* 19973 Mean at injury 21.4, 

median time after 

injury 25 

Myocardial infarction 230 3 

Levi, 199555 Cardiac diseases 326 2 

Davies, 200254 Mean 47.5±4.5 Cardiovascular morbidity 140 13.4 

Groah,* 200153 Mean 57±10 Cardiovascular morbidity 834 2.72 

Imai, 199632 Mean 47.6 Circulatory diseases 244 0.82 

Levi, 199555 Circulatory diseases 326 2 

Prakash,* 200234 Mean 50 ± 14 Congestive heart failure 654 1.7 

Dysrhythmia 834 0.43 

Left bundle branch block 834 0.02 

Other CVD 834 0.81 

Groah,* 200153 Mean 57±10 

Valvular disease 834 0.2 

Levi, 199556 Cardiovascular 

symptoms: ankle-leg 

edema, chest pain, 

palpitations 

353 58 

* Outcomes events obtained with ICD codes 

† Hospitalizations with CVD diagnosis 
52 

Table 3. Prevalence of CVD in adults with SCI by age and years after injury 

Author Sample (n) Age at Injury Prevalence, % 

All CVD 

<30 years 2 

30-39 years 2.9 

40-49 years 5.2 

Whiteneck, 1992*52 834 

50-59 years 8.1 

 60+ years 19.3 

CVD symptoms 

Levi, 1995 21-40 years 57 56 162 

41-77 years 61 

Hypertension 

255 <50 years and <50 years at index 

submission 

5.09 

162 <50 years and >50 years at the time of 

index admission 

25.3 

McGlinchey-Berroth, 1995*†48

93 Age at injury and index hospital admission 

>50 years 

33.33 

Myocardial infarction 

255 <50 years and <5 years at index 

submission 

5.09 

162 <50 years of age and >50 years at the 

time of index admission 

25.3 

McGlinchey-Berroth, 1995†*48

93 >50 years of age 33.33 

 Years after Injury 

All CVD 

<10 years 2.9 

10-19 years 5.4 

20-29 years 10 

Whiteneck, 1992*52 834 

30+ years 14.2 

3,978 1 year 0.73 

1,714 10 years 0.41 

1,653 15 years 0.79 

1,251 20 years 0.4 

Cardenas, 2004*†50

2,451 5 years 0.53 

CVD symptoms 

87 0-4 years 48 

89 18-44 years 72 

Levi, 199556

177 5-17 years 55 

* Outcomes events obtained with ICD codes 

† Hospitalizations with CVD diagnosis 
53 

Table 4. Prevalence of CVD* according to SCI neurological category53

All SCI (N=834) Tetra ABC (N=99) Para ABC (N=285) All D (N=161) Neurological Category Number Rate Number Rate Number Rate Number Rate 

All CVD 458 27.2 64 35.2 279 29.9 115 21.2 

Coronary heart disease 109 6.5 5 2.1 63 6.6 41 7.4 

Myocardial infarction 47 2.8 1 0.3 31 3.2 15 2.6 

Angina 12 0.7 0 4 0.4 8 1.7 

Coronary atherosclerosis 46 2.7 3 1 25 2.7 18 3.1 

LBBB 4 0.2 1 0.3 3 0.3 0 

Hypertension 98 5.8 5 1.7 71 7.6 22 4.5 

Cerebrovascular disease 8 0.5 4 1.5 3 0.3 1 0.2 

Dysrhythmia 73 4.3 20 13.1 42 3.3 11 1.3 

Valvular disease 34 2 10 5 14 1.5 10 1.7 

Other CVD 136 8.1 20 9.2 86 1.4 30 1.5 

* Age adjusted rates per 1,000 SCI person years by neurological category 
54 

Table 5. Mortality from CVD in adults with SCI 

Author Sample Patient Characteristics Mortality, % Among 

all SCI Patients 

Arterial diseases 

DeVivo, 199949

Time: 1973-1998 

28,239 All SCI 0.08 

All SCI 0.15 

Ages 25-54 years 0.04 

Age >54 years 0.10 

Incomplete paraplegia 0.03 

Complete paraplegia 0.03 

Incomplete quadriplegia 0.04 

Complete quadriplegia 0.04 

Survival 1-5 years 0.09 

DeVivo, 19932

Time: 1973-1985 

9,135 

Survival >5 years 0.01 

Cardiovascular diseases 

Garshick, 200536

Time: 1994-2000 

Mean age: 50.6±15 

361 All SCI 2.2 

DeVivo, 199949

Time: 1973-1998 

28,239 All SCI 1.03 

All SCI 6.31 

Thoracic-lumbar injury/Frankel A-C 1.58 

Frankel D 3.04 

Frankel E 0.68 

Cervical lesion 0.00 

Thoracic/lumbar lesion 0.00 

Men 5.29 

Hartkopp, 19971

Time: 1954-1992 

Median age at time of 

injury: 27.5 from 1953-

1971 and 28.5 from 

1972-1990 

888 

Women 1.01 

All patients 10.07 

Paraplegia, ABC 5.76 

Quadriplegia, ABC 0.96 

All D and E 3.36 

15-24 0.08 

25-34 0.07 

35-44 0.24 

45-54 0.44 

55-64 1.33 

65-74 2.12 

Whiteneck, 199252

Time: 1943-1970 

Age at time of injury 15-

55, 42% 15-24 years, 

27% 25-34 years, 18% 

35-44 years, 13% 45-55 

years; Median survival 

time 32 years 

834 

75-84 10.20 

Cerebrovascular diseases 

All patients 0.90 

Thoracic-lumbar injury/Frankel A-C 0.23 

Frankel D 0.45 

Frankel E 0.00 

Men 0.68 

Hartkopp, 19971

Time: 1954-1992 

Median age at the time 

of injury 27.5 in 1953-

1971 and 28.5 in 1972-

1990 

888 

Women 0.23 

All patients 0.24 

Ages 25-54 years 0.15 

Age >54 years 0.04 

Incomplete paraplegia 0.03 

Complete paraplegia 0.02 

Incomplete quadriplegia 0.09 

Complete quadriplegia 0.10 

Survival 1-5 years 0.12 

DeVivo, 19932

Time:1973-1985 

9,135 

Survival >5 years 0.07 
Table 5. Mortality from cardiovascular diseases in patients with SCI (continued) 

55 

Author Sample Patient Characteristics Mortality, % Among 

all SCI Patients 

Ischemic heart disease 

All patients 2.48 

Thoracic-lumbar injury/Frankel A-C 0.56 

Frankel D 1.13 

Frankel E 0.56 

Men 2.14 

Hartkopp, 19971

Time: 1954-1992 

Median age at time of 

injury: 27.5 from 1953-

1971 and 28.5 from 

1972-1990 

888 

Women 0.34 

All patients 0.67 

Ages 25-54 years 0.19 

Age >54 years 0.44 

Incomplete paraplegia 0.14 

Complete paraplegia 0.12 

Incomplete quadriplegia 0.23 

Complete quadriplegia 0.18 

Survival 1-5 years 0.27 

DeVivo, 19932

Time: 1973-1985 

9,135 

Survival >5 years 0.12 

All patients 0.02 

Survival 5 years 0.43 

Survival 20 years 0.87 

Rish, 19973

Time: 1954-1992 

Mean age at injury 21.4 

years, Median time after 

injury 25 years 

230 

Survival >20 years 0.87 

Lung embolus 

All patients 0.68 

Thoracic-lumbar injury/Frankel A-C 0.11 

Frankel D 0.34 

Frankel E 0.11 

Men 0.68 

Hartkopp, 19971

Time: 1954-1992 

Median age at time of 

injury 27.5 from 1953-

1971 and 28.5 from 

1972-1990 

888 

Women 0.00 

Non ischemic heart disease 

All patients 0.92 

Ages 25-54 years 0.31 

Age >54 years 0.47 

Incomplete paraplegia 0.04 

Complete paraplegia 0.11 

Incomplete quadriplegia 0.28 

Complete quadriplegia 0.48 

Survival 1-5 years 0.32 

DeVivo, 19932

Time: 1973-1985 

9,135 

Survival >5 years 0.18 

Stroke 

DeVivo, 199949

Time: 1973-1998 

28,239 All patients 0.19 
56 

Figure 16. Percent of all deaths due to coronary heart disease among adults with SCI 

Table 6. Percent of all deaths from CVD among adults with SCI 

Author Disease (ICD Codes) % of all SCI Deaths 

Hartkopp, 1997 CVD (390-458) 24.0 1

Ischemic heart disease (410-414) 9.0 

DeVivo, 199949 Heart 18.8 

DeVivo, 19932

 Ischemic heart disease (410-414) 7.1 

Garshick, 2005 Circulatory system disorder (390-459) 21.6 36

Circulatory system disorder (390-459) as 

contributing cause of death 

18.9 

Rish, 19973

 Myocardial infarction 8.8 

Whiteneck, 199252 CVD 23.2 

0.0

1.0

2.0

3.0

4.0

5.0

6.0

7.0

8.0

9.0

Hartkopp, 19971

Ages 27.5-28.5

DeVivo, 19932 Rish, 19973

Age 46.4
57 

Table 7. Odds ratios of diabetes or CVD in adults with SCI compared to able bodied 

Odds Ratio (95% CI) 

Conditions Lavela, 200637

VA Settings 

%; Mean Age 60 Years 

Prakash, 200234

VA Settings 

Age 50±14 

Krum, 199239

Ages 25-64 

Coronary heart disease 0.24 (0.13; 0.43) 

Myocardial infarction 1.00 (0.14; 7.24)† 

Arterial hypertension 0.16 (0.12; 0.21) 0.40 (0.17; 0.92) † 

High cholesterol 

Stroke 

Diabetes 3.3 (1.3; 8.3)* 1.1 (0.88; 1.37) 3.13 (0.62; 15.89) † 

Congestive heart failure 0.24 (0.13; 0.43) 

Angina 0.67 (0.11; 4.1) † 

Cerebrovascular diseases 1.00 (0.06; 16.21) † 

* Adjusted for age, race, marital status, duration of injury, employments status, and educational level 

† Adjustment for age, matching by gender 

Bold - significant association at 95% confidence level 

Figure 17. Odds ratios* of cardiovascular outcomes in VA users with SCI and diabetes vs. SCI but no 

diabetes37

* Adjusted for age, race, marital status, duration of injury, employments status, and educational level 

Odds ratio 

 1 5

Odds ratio 

(95% CI) 

Coronary heart disease (12) 2.80 (2.20, 3.60) 

Myocardial infarction (14) 2.70 (2.10, 3.40) 

Arterial hypertension (49) 2.50 (2.10, 3.00) 

High cholesterol (48) 2.50 (2.10, 3.00) 

Stroke (8) 2.30 (1.70, 3.00) 

Outcome 

(Rate in SCI with diabetes) 

Odds ratio 

 1 5

Odds ratio 

(95% CI) 

Coronary heart disease (12) 2.80 (2.20, 3.60) 

Myocardial infarction (14) 2.70 (2.10, 3.40) 

Arterial hypertension (49) 2.50 (2.10, 3.00) 

High cholesterol (48) 2.50 (2.10, 3.00) 

Stroke (8) 2.30 (1.70, 3.00) 

Outcome 

(Rate in SCI with diabetes) 

Odds ratio 

 1 5

Odds ratio 

(95% CI) 

Coronary heart disease (12) 2.80 (2.20, 3.60) 

Myocardial infarction (14) 2.70 (2.10, 3.40) 

Arterial hypertension (49) 2.50 (2.10, 3.00) 

High cholesterol (48) 2.50 (2.10, 3.00) 

Stroke (8) 2.30 (1.70, 3.00) 

Outcome 

(Rate in SCI with diabetes) 

 1 5

Odds ratio 

(95% CI) 

Coronary heart disease (12) 2.80 (2.20, 3.60) 

Myocardial infarction (14) 2.70 (2.10, 3.40) 

Arterial hypertension (49) 2.50 (2.10, 3.00) 

High cholesterol (48) 2.50 (2.10, 3.00) 

Stroke (8) 2.30 (1.70, 3.00) 

Outcome 

(Rate in SCI with diabetes) 

Odds ratio 
58 

Table 8. Diabetes management and diabetes complications in VA users with SCI, in VA users without SCI, 

and non-VA user general population without SCI37

Diabetes 

Management or 

Complications 

Prevalence 

in VA SCI 

(%) 

Prevalence 

in VA Non 

SCI 

(%) 

Odds Ratio in VA 

SCI Compared to 

the VA Non SCI 

Population 

(95% CI) 

Prevalence in 

Non VA 

General 

Population 

(%) 

Odds Ratio in VA 

SCI Compared to 

Non VA General 

Population 

(95% CI) 

Duration of diabetes 

(>25 years) 

13.55 10.94 1.27 (0.97; 1.66) 9.75 1.44 (1.16; 1.79) 

Insulin therapy 26.03 28.51 0.88 (0.72; 1.08) 25.9 1.01 (0.85; 1.19) 

Oral agent 62.97 69.54 0.75 (0.62; 0.90) 66.35 0.86 (0.74; 1.01) 

Insulin + oral agent 11.25 12.82 0.86 (0.65; 1.13) 11.17 1.00 (0.79; 1.27) 

Foot sores with >4 

weeks to heal 

41.37 17.85 3.25 (2.65; 3.98) 13.12 4.68 (4.02; 5.46) 

Retinopathy 25.31 24.24 1.06 (0.86; 1.31) 22.27 1.19 (1.00; 1.41) 

Diabetes education 63.04 60.16 1.13 (0.94; 1.36) 49.84 1.72 (1.47; 2.00) 

Bold – significant association at 95% confidence level 

Figure 18. Adjusted odds ratio of CVD in patients with SCI: Tetraplegia with no functional motor preservation 

compared to paraplegia and no functional motor preservation 53

 Higher in Tetraplegia Odds ratio Higher in Paraplegia

0.1 1 21.2

Disease

Odds ratio

(95% CI)

All CVD 1.16 (0.93, 1.46)

Coronary heart disease 0.30 (0.13, 0.70)

Myocardial infarction 0.11 (0.10, 0.74)

Coronary atherosclerosis 0.49 (0.17, 1.39)

Hypertension 0.22 (0.09, 0.54)

Cerebrovascular disease 5.06 (1.21, 21.15)

Dysrhythmia 3.94 (2.45, 6.35)

Valvular disease 3.25 (1.57, 6.73)
59 

Table 9. Hazard ratio of dying having ECG abnormality vs. normal ECG among patients with SCI and ablebodied veterans 34

ECG Abnormalities Spinal Cord Injury 

Hazard Ratio 95% CI 

Able-bodied 

Hazard Ratio 95% CI 

Right bundle branch block 1.23 (0.4; 4) 2.21 (1.97; 2.47) 

Left bundle branch block 4.24 (1.5; 12) 1.98 (1.62; 2.42) 

Intraventricular conduction delay 1.15 (0.3; 5) 1.13 (0.99; 1.3) 

LVH with strain 3.28 (1.2; 9) 1.31 (1.14; 1.52) 

Left atrial abnormality 0.59 (0.2; 1.9) 1.55 (1.39; 1.74) 

Anterior Q wave 1.44 (0.5; 4.6) 2 (1.76; 2.28) 

Inferior Q wave 0.78 (0.3; 1.8) 1.32 (1.21; 1.43) 

Atrial fibrillation 3.54 (1.2; 11) 2.02 (1.79; 2.27) 

Premature ventricular contraction 0.33 (0.05; 2.5) 1.51 (1.36; 1.67) 

Abnormal ST depression 1 (0.5; 1.9) 1.9 (1.77; 2.04) 

Abnormal QT interval 0.27 (0.1; 18) 1.91 (1.77; 2.06) 

Bold – significant association at 95% confidence level 

Figure 19. Hazard ratio of dying based on ECG abnormality vs. normal ECG among VA users with SCI and 

able-bodied VA users34

1 12

Study

Hazard ratio

(95% CI)

Atrial fibrillation

SCI 3.54 (1.20, 11.00)

Able-bodied 2.02 (1.79, 2.27)

LBBB

SCI 4.24 (1.50, 12.00)

Able-bodied 1.98 (1.62, 2.42)

LVH with strain

SCI 3.28 (1.20, 9.00)

Able-bodied 1.31 (1.14, 1.52)
60 

Table 10. Age standardized mortality ratios in adults with chronic SCI compared to the general population 

(no adjustment for other confounding factors)2

 

Risk Factors Death (N) Standardized Mortality Ratio 

(95% CI) 

Ischemic heart disease (ICD codes 410-414) 

Age 25-54 years 17 1.4 (0.8; 2.0) 

Age >54 years 40 1.1 (0.8; 1.4) 

Incomplete paraplegia 13 1.4 (0.7; 2.1) 

Complete paraplegia 11 1 (0.4; 1.6) 

Incomplete quadriplegia 21 1 (0.6; 1.4) 

Complete quadriplegia 16 2.6 (1.3; 3.9) 

Survival 1-5 years 25 1.1 (0.7; 1.5) 

Survival >5 years 11 0.6 (0.2; 1.0) 

Non ischemic heart disease (ICD codes 420-429) 

Age 25-54 years 28 6.5 (4.1; 10.8) 

Age >54 years 43 4.2 (3; 5.4) 

Incomplete paraplegia 4 1.4 (0.4; 2.4) 

Complete paraplegia 10 2.8 (1.1; 4.5) 

Incomplete quadriplegia 26 4 (2.5; 5.5) 

Complete quadriplegia 44 23.4 (16.5; 30.3) 

Survival 1-5 years 29 4.1 (2.6; 5.6) 

Survival >5 years 16 3 (1.5; 4.5) 

Cerebrovascular diseases (ICD codes 430-438) 

Age 25-54 years 14 4.6 (2.2; 7.0) 

Age >54 years 4 0.4 (0; 0.8) 

Incomplete paraplegia 3 1.3 (0; 2.8) 

Complete paraplegia 2 0.8 (0; 1.9) 

Incomplete quadriplegia 8 1.4 (0.4; 2.4) 

Complete quadriplegia 9 5.4 (1.8; 9.0) 

Survival 1-5 years 11 2 (0.8; 3.2) 

Survival >5years 6 1.3 (0.2; 2.4) 

Diseases of arteries (ICD codes 440-448) 

Age 25-54 years 4 8.2 (0.2; 16.2) 

Age >54 years 9 1.2 (0; 3.5) 

Incomplete paraplegia 3 5.4 (0; 11.5) 

Complete paraplegia 3 5 (0; 10.6) 

Incomplete quadriplegia 4 2.7 (0.1; 5.3) 

Complete quadriplegia 4 9.4 (0.2; 18.6) 

Survival 1-5 years 8 5.8 (1.8; 9.8) 

Survival >5 years 1 0.9 (0; 2.7) 

 Bold - significant association at 95% confidence level 
61 

Table 11. Age standardized mortality ratios for cardiovascular death by gender compared to able bodied1

Standardized Mortality Ratio (95% CI) Cause of Death Men Women Both Genders 

Period of injury 1953-1990 (end of followup: December 31, 1992) 

CVD 1.2 (0.85; 1.53) 1 (0.52; 2.14) 1.2 (0.87; 1.49) 

Ischemic heart disease 0.7 (0.41; 1.06) 1 (0.14; 1.96) 0.7 (0.42; 1.02) 

Cerebrovascular disease 1 (0.35; 2.07) 1 (0.13; 3.98) 1 (0.43; 1.94) 

Lung embolus 14 (5.25; 31.1) 11 (4.19; 24.8) 

Total 2.1 (1.79; 2.38) 2 (1.53; 2.94) 2.1 (1.83; 2.37) 

Period of injury 1953-1971 (end of followup: December 31, 1973) 

CVD 3.2 (1.38; 6.29) 4 (0.09; 19.5) 3.2 (1.47; 6.12) 

Ischemic heart disease 1.1 (0.13; 3.91) 

Cerebrovascular disease 

Lung embolus 131 (27.1; 384) 107 (22.1; 313) 

Total 6.5 (4.66; 8.74) 12 (5.81; 22.3) 7.1 (5.31; 9.32) 

Period of injury 1972-1990 (end of followup: December 31, 1992) 

CVD 1.3 (0.71; 2.09) 3 (0.86; 6.16) 1.5 (0.89; 2.25) 

Ischemic heart disease 1.2 (0.58; 2.24) 1.2 (0.59; 2.13) 

Cerebrovascular disease 4 (0.53; 15.9) 1.4 (0.28; 3.96) 

Total 2.3 (1.79; 2.90) 3 (1.91; 5.09) 2.4 (1.95; 3.01) 

 Bold – significant association at 95% confidence level 
62 

Table 12. Age standardized mortality ratios from CVD in adults with SCI compared to the general population 

Author 

Sample Patient Characteristics Mortality/1,000 SCI Standardized Mortality 

Ratios (95% CI) 

Artery diseases 

Survival >5 years 0.11 0.9 (0; 2.7) 

Age >54 years 0.99 1.2 (0; 3.5) 

Incomplete quadriplegia 0.44 2.7 (0.1; 5.3) 

All patients 1.53 4.5 (2.1; 6.9) 

Complete paraplegia 0.33 5 (0; 10.6) 

Incomplete paraplegia 0.33 5.4 (0; 11.5) 

Survival 1-5 years 0.88 5.8 (1.8; 9.8) 

Age 25-54 years 0.44 8.2 (0.2; 16.2) 

DeVivo, 19932

N = 9,135 

(standardization by 

age, sex, and race) 

Complete quadriplegia 0.44 9.4 (0.2; 18.6) 

Garshick, 200536

N = 361 

All patients 1.15 (0.13-4.15) 

Cerebrovascular diseases 

Age >54 years 0.44 0.4 (0; 0.8) 

Complete paraplegia 0.22 0.8 (0; 1.9) 

Incomplete paraplegia 0.33 1.3 (0; 2.8) 

Survival >5 years 0.66 1.3 (0.2; 2.4) 

Incomplete quadriplegia 0.88 1.4 (0.4; 2.4) 

All patients 2.41 1.8 (1; 2.6) 

Survival 1-5 years 1.20 2 (0.8; 3.2) 

Age 25-54 years 1.53 4.6 (2.2; 7) 

DeVivo, 19932

N = 9,135 

(standardization by 

age, sex, and race) 

Complete quadriplegia 0.99 5.4 (1.8; 9) 

Men 6.76 0.95 (0.35; 2.07) 

All patients 9.01 0.99 (0.43; 1.94) 

Hartkopp, 19971

N = 888 

Women 2.25 1.1 (0.13; 3.98) 

Cardiovascular diseases 

Cervical lesion 1.07 (0.72; 1.53) 

Women 10.14 1.13 (0.52; 2.14) 

Men 52.93 1.15 (0.85; 1.53) 

All patients 63.06 1.15 (0.87; 1.49) 

Hartkopp, 19971

N = 888 

Thoracic/lumbar lesion 1.26 (0.82; 1.84) 

Ischemic heart disease 

DeVivo, 19932

N = 9,135 

(standardization by 

age, sex, and race) 

Survival >5 years 1.20 0.6 (0.2; 1) 

Women 3.38 0.67 (0.14; 1.96) 

Men 21.40 0.68 (0.41; 1.06) 

Hartkopp, 19971

N = 888 

All patients 24.77 0.68 (0.42; 1.02) 

Complete paraplegia 1.20 1 (0.4; 1.6) 

Incomplete quadriplegia 2.30 1 (0.6; 1.4) 

Age >54 years 4.38 1.1 (0.8; 1.4) 

Survival 1-5 years 2.74 1.1 (0.7; 1.5) 

All patients 6.68 1.3 (1; 1.6) 

Age 25-54 years 1.86 1.4 (0.8; 2) 

Incomplete paraplegia 1.42 1.4 (0.7; 2.1) 

DeVivo, 19932

N = 9,135 

(standardization by 

age, sex, and race) 

Complete quadriplegia 1.75 2.6 (1.3; 3.9) 

Lung embolus 

Hartkopp, 1997 All patients 6.76 11.4 (4.19; 24.8) 1

N = 888 Men 6.76 14.3 (5.25; 31.1) 
Table 12. Age standardized mortality ratios from CVDs in adults with SCI compared to the general population 

(continued) 

63 

Author 

Sample Patient Characteristics Mortality/1,000 SCI Standardized Mortality 

Ratios (95% CI) 

Nonischemic heart disease 

Incomplete paraplegia 0.44 1.4 (0.4; 2.4) 

Complete paraplegia 1.09 2.8 (1.1; 4.5) 

Survival >5 years 1.75 3 (1.5; 4.5) 

Incomplete quadriplegia 2.85 4 (2.5; 5.5) 

Survival 1-5 years 3.17 4.1 (2.6; 5.6) 

Age >54 years 4.71 4.2 (3; 5.4) 

All SCI 9.20 5.6 (4.4; 6.8) 

Age 25-54 years 3.07 6.5 (4.1; 10.8) 

DeVivo, 19932

N = 9,135 

Complete quadriplegia 4.82 23.4 (16.5; 30.3) 

Diseases of the heart 

Garshick, 200536

N = 361 

All patients 0.59 (0.19;1.38) 

Other diseases of the circulatory system 

Garshick, 200536

N = 361 

All patients 1.49 (0.31;4.36) 

Bold - significant association at 95% confidence level 
64 

Question 3 

 Exercise in adults with SCI. Of the 19 peer reviewed original articles, there were none 

reporting results of RCTs. The majority consisted of small, uncontrolled intervention trials (case 

series) or cross-sectional surveys using measures of self-reported physical activity. Variation in 

study design, intervention, and reported outcomes precluded quantitative pooling of results. A 

summary of findings from individual studies according to intervention type and outcomes was 

conducted. To facilitate review, these studies were separated by outcomes of interest: 

Carbohydrate-related outcomes (n=10) (Table 13) and lipid-related outcomes (n=13) (Table 14). 

These were then further organized by type of reported exercise, as follows: 

A. Active Exercise (AE): n=six studies of 57 individuals (40 males, five females, 12 

unreported; 36 paraplegic, three tetraplegic, nine unclassified and nine other) (8-24 weeks 

exercise duration).57-63

B. Functional Electrical Stimulation Exercise (FES): n=five studies of 32 individuals (27 

males, five females; eight paraplegic, 14 tetraplegic and ten unclassified) (8-52 weeks 

exercise duration)64-68

C. Passive Exercise (PE): n=0 studies 

D. Self-Reported Physical Activity: n=six studies of 215 individuals (205 males, 14 females; 

125 paraplegic, 93 tetraplegic, one unclassified) (no report of duration)13,14,54,69-71

E. Other: n=one study (nine males, seven females) (no report of duration)72 

Description of exercise intervention studies with carbohydrate related outcomes (Table 13) 

(n=10 studies of 101 individuals).13,14,58,60,62,64-68 The overall quality, quantity, and consistency of 

evidence for exercise as an intervention for carbohydrate disorders is poor. Study characteristics 

ranged from a case series using pre-post assessment of outcomes for six individuals randomly 

assigned to eight weeks of high- versus low-intensity arm crank exercise58 to a cross-sectional 

survey of 22 individuals who provided self-assessed physical activity levels and metabolic 

variables.13 The intervention type, frequency, intensity, and duration varied considerably across 

studies. Most involved several sessions of supervised exercise per week with a study duration 

ranging from eight weeks to one year. SCI level and severity, and duration since injury, varied 

across studies. More than 90 percent of subjects were men. One study was a survey of selfreported exercise or physical activity and assessed the impact of the respondent’s activity on 

major cardiovascular endpoints.54 Three studies examined the effects of active exercise 

(AE),58,60,62 while five examined the effects of FES exercise,64-68 on carbohydrate related 

measures. Two survey studies assessed the association between self-reported physical activity 

and these measures.13,14 The most commonly assessed measures were fasting plasma glucose and 

oral glucose tolerance tests, measuring post-oral load levels of glucose and insulin. None 

assessed glycosylated hemoglobin. 

Impact of exercise programs on carbohydrate related measures. There is mixed, low-quality 

evidence that a program of exercise improves carbohydrate-related measures. Of the five studies 

that measured fasting plasma glucose only one showed a statistically significant difference. Two 

(one AE; one FES) found no differences before and after intervention,60,65 while one FES study 

found a nonstatistically significant trend for reduction.67 Two surveys identified inverse 

correlations (r = -.53 and -.40 respectively) between self-reported physical activity and plasma 

glucose; one was statistically significant13 while the other was not.14 Measures of two-hour postload glucose were mixed. One FES study found a significant (p = .014), 13 percent post-training 

reduction in glucose levels, averaged across participants,66 while another FES study showed no 
65 

change.68 Both survey studies of self-reported physical activity identified inverse correlations (r 

= -.59 and -.34 respectively) with two-hour post-load glucose; the prior was statistically 

significant (p <0.01)14 while the latter was not.13 Impaired glucose tolerance and clearing were 

also reported. One AE study showed a statistically significant post-training 15 percent average 

reduction in area under the curve after glucose load,62 and one FES study found a significant 33 

percent average increase in glucose disposal.65 

 Measures of insulin levels were no more uniform than for glucose. Some studies assessed 

fasting insulin levels, while others assessed insulin levels after a standard glucose load or insulin 

area under the curve. One possible consistency in these studies is the lack of change in fasting 

plasma insulin levels after training. Two FES studies found no difference in fasting plasma 

insulin,65,67 while one identified decreased levels that were not significant.64 One survey study 

showed no correlation between self-reported physical activity and insulin;14 the other survey 

study did identify an inverse correlation (r = -.40), but it was not statistically significant (p 

>0.05).13 Plasma insulin concentrations after oral glucose load were also inconsistent. One FES 

study identified a nonsignificant 26 percent average reduction in two-hour post-load levels,66

while another FES study found no change.68 Similarly, one survey study identified a statistically 

significant inverse correlation (r = -.79. p <0.01) between self-reported physical activity and 

post-load insulin,14 while the other found no correlation.13 One AE study identified a significant 

33 percent average reduction in area under the curve for plasma insulin concentrations after 

glucose load.62 To further complicate any possible conclusions, the AE study comparing two 

programs of exercise (low intensity vs. high intensity)58 found insulin sensitivity to be decreased 

by an average of 33 percent for those assigned the low intensity intervention, but increased an 

average of 56 percent for those in the high intensity intervention. 

Description of exercise intervention studies with lipid or cardiovascular related outcomes 

(Table 14) (n=13 studies of 292 individuals).13,14,54,57-61,63,69-72 The quality, quantity, and 

consistency of evidence for studies reporting lipid related measures is also poor. Study designs 

were primarily reports of case series and cross-sectional surveys, with intervention type, 

frequency, intensity, and duration varied across studies. Nearly 90 percent of subjects were men, 

thus limiting extrapolation of findings in women. Six studies examined the effects of AE on lipid 

related measures.57-61,63 No eligible studies examined FES exercise. There were six survey 

studies that assessed the association between self-reported physical activity and lipid 

measures.13,14,54,69-71 One of these examined the association between physical activity and 

cardiovascular morbidity.54 One study, categorized as “other,” examined the effects of a weight 

management training program, including curriculum on exercise, on lipid outcomes.72 The most 

common lipid related measures were TC, HDL-C, LDL-C, the ratio of TC to HDL-C (TC/HDLC), and TG. 

Impact of exercise programs on lipid or cardiovascular related measures. Evidence may 

point to improved levels of TC after a training intervention, or with self-reported physical 

activity. Among the studies examining effects of AE interventions, two identified statistically 

significant reductions in TC levels (on average, 8 percent and 10 percent less than pretraining);60,63 these involved training programs with a body-weight supported treadmill63 or a 

wheelchair aerobic fitness trainer.60 One study found a nonsignificant 9 percent average 

decrease,61 while two showed no changes;58,59 all three of these studies involved arm crank 

exercise. Three survey studies examined self-reported exercise and TC levels.69-71 While one 

found no difference in TC levels between those who were physically active and those who were 

sedentary,69 two others identified significant inverse correlations (r = -.35 and -.33, p = 0.008 and 
66 

p <0.05, respectively). The study examining the weight management training program also 

identified a nonsignificant decrease in TC.72 

 Six AE studies reported outcomes for HDL-C.57-61,63 While three reported no changes,57,58,60

one reported a statistically significant increase59 and two reported very small, nonsignificant 

increases (10 percent and 8 percent).61,63 Four survey studies reported on HDL-C, with one 

identifying a significantly significant 14 percent decrease (p <0.05) for individuals who were 

physically active compared to those who were sedentary.69 Two others identified significant 

positive correlations (r = .46 and .63, p <0.05),13,14 while another reported no correlation.71

Oddly, the weight management study reported a significant decrease in HDL-C.72 Measures for 

TC/HDL-C were similarly inconclusive. Of five AE studies, two reported no changes,57,60 while 

three reported statistically significant reductions in values ranging from 18 percent to 23 

percent.58,61,63 Two survey studies identified significant inverse correlations between physical 

activity and TC/HDL-C (r = -.49, p <0.05 for both),14,70 one identified a significant reduction (p 

<0.05) among those who were physically active compared to sedentary,69 and one showed no 

correlation.71

 In two of four AE studies reporting LDL-C measures, levels were significantly decreased by 

15 percent and 25 percent (p = .05 for both);61,63 no changes were observed in the others.57,58

However, two of three survey studies identified significant inverse correlations between selfreported physical activity and LDL-C levels (r = -.28 and -.40, p = 0.003 and p <0.01 

respectively).70,71 The third survey study found no difference between groups.69 The weight 

management program was associated with a nonsignificant decrease.72

 While one study identified a statistically significant 31 percent average decrease in TG 

among those assigned a high intensity AE training protocol,58 two others showed decreases that 

were nonsignificant,61,63 and still two others found no change.59,60 Among the four self-report 

surveys, one identified a nonsignificant 32 percent decrease among those who were physically 

active compared to sedentary.69 Three others identified no correlation between physical activity 

and TG levels.13,70,71

 The study by Davies and McColl54 identified no association between physical activity levels 

and overall cardiovascular morbidity. 

Summary. Evidence on effects of exercise on lipid and carbohydrate metabolism disorders is 

inconclusive. Studies to date have been short in duration, involved few subjects, and relied on 

study designs highly susceptible to error. Future collaborative research is needed to study both 

efficacy and effectiveness of such interventions in the population of individuals with SCI. 

 Dietary and pharmacologic intervention studies with carbohydrate or lipid related 

outcomes in adults with SCI. 

Carbohydrate outcomes. There were no prospective studies that evaluated dietary and/or 

lifestyle interventions on carbohydrate related outcomes. 

Lipid related outcomes (Table 15.). Only two prospective studies that evaluated dietary 

and/or lifestyle interventions to reduce lipid levels were identified and met inclusion criteria.20,72

No studies assessing pharmacologic interventions were identified. The two dietary/lifestyle case 

series studies included 238 subjects, overwhelmingly male (87 percent). Quality of the two 

studies was poor. 

 One controlled clinical trial compared the effect of a dietary intervention referral compared 

to no dietary referral over a mean of 16 months.20 Overall, mean age was 38.5 years and 89 

percent were male. All subjects must have had an SCI of at least two years in duration. Group 1 

(n=86) received a dietary intervention referral based on the recommendations of the American 
67 

Heart Association and American Dietetic Association Guidelines. These subjects had a total 

cholesterol level greater than 200 mg/dL. Group 2 (n=136) received no dietary intervention 

referral. All subjects had a total cholesterol level ≤200 mg/dL. Group 1 subjects were 

significantly older (mean 42.8 versus 35.7, p <0.0001) and had a longer post-injury duration 

(15.6 versus 11.1 years, p <0.0001) compared to Group 2 subjects. Dietary intervention was 

effective in reducing some lipid parameters. There were significant reductions in total and low 

density lipoprotein cholesterol levels from baseline in Group 1, 234 to 224 (p <0.001) and 159 to 

151 (p = 0.004), respectively. Levels increased slightly but not significantly in Group 2. In 

Group 1, 67 percent had decreases in LDL-C compared to 47 percent in Group 2 (p = 0.007). 

Secondary analysis found 15 percent had reductions ranging from 30 to 69 mg/dL and the LDLC values declined from greater than 135 mg/dL to <135 mg/dL in 21 percent. There were no 

significant effects on high density lipoprotein cholesterol or triglyceride levels in either group. 

 The second uncontrolled pilot study evaluated a weight management program consisting of 

12 classes for 12 weeks, primarily led by a registered dietician.72 Classes covered nutrition, 

exercise, and behavior modification. The dietary approach utilized a time-calorie displacement 

diet. The study followed 16 overweight subjects (BMI ≥25), up to 24 weeks. Subjects were on 

average 44 years of age, nine were men, 13 were White, and three were African American. There 

were no significant changes in total and LDL cholesterol levels from baseline at weeks 12 and 

24. At week 12, TCl was reduced by 5.8 mg/dL (p = 0.28) and LDL cholesterol by 1.8 mg/dL (p 

= 0.76). By week 24, the mean changes were 0.3 mg/dL (p = 0.96) and -4.2 mg/dL (p = 0.42), 

respectively. HDL cholesterol was reduced significantly by 3.2 mg/dL from a baseline value of 

43.1 mg/dL (p = 0.03) at week 12 and -0.9 mg/dL (p = 0.59) by week 24. 
68

Table 13. Description of exercise intervention studies with carbohydrate related outcomes in people with SCI 

Reference Study Design; Sample Size Intervention Type Frequency; Intensity; Duration Subject Characteristics Outcomes of Interest 

A. Active exercise de Groot, 200358 Case series 

n=6 Random assignment to high vs. low intensity 

Arm crank exercise 

3 sessions/week; 60 minutes/session; High-intensity (HI; 70-80% heart rate reserve (HRR)) vs. low-intensity (LI; 40-50% HRR) 8 weeks of training 

4 males, 2 females; Age range 19-54 years; Mean duration since injury 116±77 days; 6 paraplegic (C5-L1) 

Insulin sensitivity (post-test/pre-test) 

Midha, 199960 Case series 

n=12 (Includes 2 nonSCI subjects) 

Wheelchair aerobic fitness trainer (WAFT) training program 

2-3 sessions/week; 20-30 minutes, until target heart rate of 90% age-predicted maximum reached; mean intensity 177 watts 10 weeks of training 

11 males, 1 female; Age range 22-58; Duration since injury range 4-29 years; 3 quadriplegic; 7 paraplegic; 1 stroke; 1 amputee 

Fasting serum glucose (mg/dL) 

Phillips, 200462 Case series 

n=9 

Body-weight supported treadmill training program 

68 sessions (2.8±0.2 sessions/week); Velocity and % weight supported varied for each participant; 6.0±0.3 months of training 

8 males, 1 female; Mean age 31±3 years; Mean duration since injury 8.1 years; 9 incomplete (C4-T12) 

A. Glucose toleranc(area under glucose time curve) B. Blood insulin concentration (area under insulin x time curve) 

B. Functional electrical stimulation exercise Chilibeck, 199964 Case series 

n=5 

Electrically stimulated leg cycling program 

3 sessions/week; 30 minutes/session; Power 6.0 watts, increased as possible each session; 50 revolutions/minute; 

4 males, 1 female; Age range 31-50 years; Duration since injury range 3-25 years; 5 complete (C5-T8) 

A. Glucose toleranc(area under glucose time curve) B. Fasting serum insulin (area under insulin x time curve) C. Insulin sensitivity 
Table 13. Description of exercise intervention studies with carbohydrate related outcomes in people with SCI (continued) 

69

Reference Study Design; Sample Size Intervention Type Frequency; Intensity; Duration Subject Characteristics Outcomes of Interest 

8 weeks of training index 

Hjeltnes, 199865 Case series 

n=5 

Electrically stimulated leg cycling program 

7 sessions/week; 30 minutes/session or until fatigued; Power 6.0 watts, increased by 6.1 watts each session; 50 revolutions/minute; 8 weeks of training 

5 males, 0 females; Mean age 35±3 years; Mean duration since injury 10.2±3.4 years; 5 tetraplegic; 5 complete (C5-C7) 

A. Insulin-mediated glucose disposal (uM/kg/minute) B. Mean steady-stainsulin (uU/mL) C. Mean steady-staglucose (mM) 

Jeon, 200266 Case series 

n=7 

Electrically stimulated leg cycling program 

3 sessions/week; 30 minutes/session; 50-60% VO2 maximum; 8 weeks of training 

5 males, 2 females; Age range 30-53 years;Duration since injury range 3-40 years; 3 tetraplegic 4 paraplegic 7 complete (C5-T10) 

A. 2-hour postload glucose (mg/dL); B. 2-hour postload insulin (uU/mL) 

Mahoney, 200567 Case series 

n=5 

Resistance exercise training program 

2 sessions/week; 4 sets of 10 unilateral, dynamic knee extensions; 12 weeks of training 

5 males, 0 females; Mean age 35.6±4.9 years; Mean duration since injury 13.4±6.5 years; 5 complete (C5-T9) 

A. Plasma glucose levels (mg/dL) B. Insulin concentration 

Mohr, 200168 Case series 

n=10 

Exercise program with functional electrical stimulation cycling ergometer 

3 sessions/week; 30 minutes/session; 50 revolutions/minute; 1 year of training 

8 males, 2 females; Mean age 35±2 years; Mean duration since injury 12±2; 6 tetraplegic (C6); 4 paraplegic (T4) 

A. 2-hour postload insulin (uU/mL) B. 2-hour postload glucose (mM/L) C. Insulin-stimulated glucose uptake rate(mg/min/kg) 
Table 13. Description of exercise intervention studies with carbohydrate related outcomes in people with SCI (continued) 

70

Reference Study Design; Sample Size Intervention Type Frequency; Intensity; Duration Subject Characteristics Outcomes of Interest 

C. Passive exercise No eligible studies D. Self-reported physical activity Jones, 200414 Cross-sectional 

case-control survey n=20 

NA Assessed physical activity levels (minutes/week) and metabolic variables 

NA 20 males, 0 females; 

Age range 16-52 years; Mean duration since injury 10.3±1.8 years; 11 tetraplegic (C4-C7); 9 paraplegic (T5-L5) 

A. Fasting plasma glucose (mM/L) B. Log 2-hour postload glucose (mM/L) C. Log fasting plasma insulin (uU/mL) D. Log 2-hour postload insulin (uU/mL) 

Manns, 200513 Cross-sectional 

survey n=22 

NA Assessed physical activity levels and metabolic variables 

NA 22 males, 0 females; 

Mean age 39±-9 years; Mean duration since injury 17±9 years; 22 paraplegic (T2-L2); 22 complete 

A. Fasting plasma glucose (mM/L) B. 2-hour postload glucose (mM/L) C. Fasting plasma insulin (uM/ml) D. 2-hour postlload insulin (uM/ml) 

E. Other No eligible studies 
71

Table 14. Description of exercise intervention studies with lipid or cardiovascular related outcomes in people with SCI 

Reference Study Design; Sample Size Intervention Type Frequency; Intensity; Duration Subject Characteristics Outcomes of Interest 

A. Active exercise Durán, 200157 Case series 

n=13 

Training program including mobility, strength, coordination, aerobic resistance, and relaxation activities 

3 sessions/week; 120 minutes/session; Target HR 40%-80% of maximal HR; 16 weeks of training 

12 males, 1 female; Mean age 26.3±8.3 years; Duration since injury range 2-120 months; 13 paraplegic 4 T6 or higher; 9 T6 or lower 

A. HDL (mg/dL) B. LDL (mg/dL) C. TC/HDL 

de Groot, 200358 Case series 

n=6 Random assignment to high vs. low intensity 

Arm crank exercise program 

3 sessions/week; 60 minutes/session; High intensity (HI; 70-80% heart rate reserve) vs. low intensity (LI; 40-50% HRR); 8 weeks of training 

4 males, 2 females; Age range 19-54 years; Mean duration since injury 116±77 days; 6 paraplegic (C5-L1) 

A. TC (post-test/pretest) B. HDL (post-test/ pre-test) C. LDL (post-test/ptest) D. TC/HDL-C (posttest/pre-test) F. TG (post-test/pretest) 

El-Sayed, 200559 Controlled case 

series n=12 

Arm crank exercise program 

3 sessions/week; 30 minutes/session; 60-65% VO2 peak; 12 weeks of training 

5 paraplegic (SCI); 7 able-bodied (AB); Mean age 32±1.6 years for AB; Mean age 31±2.9 years for SCI 

A. TC (mM/L) B. HDL-C (mM/L) C. TG (mM/L) 
Table 14. Description of exercise intervention studies with lipid or cardiovascular related outcomes in people with SCI (continu

72

Reference Study Design; Sample Size Intervention Type Frequency; Intensity; Duration Subject Characteristics Outcomes of Interest 

Midha, 199960 Case series 

n=12 (includes 2 non-SCI subjects) 

WAFT training program 

2-3 sessions/week; 20-30 minutes, until target heart rate of 90% age-predicted maximum reached; Mean intensity 177 watts; 10 weeks of training 

11 males, 1 female; Age range 22-58; Duration since injury range 4-29 years; 3 tetraplegic; 7 paraplegic; 1 stroke; 1 amputee 

A. TC (mg/dL) B. TG (mg/dL) C. HDL-C (mg/dL) D. TC/HDL-C 

Nash, 200161 Case series 

n=5 

Arm crank exercise program, with focus on resistance and endurance 

3 sessions/week; 45 minutes/session; Power output 400 kpm + 100 kpm every 3 minutes until peak VO2 maximum; 3 months of training 

5 males, 0 females; Age range 34-43 years; Mean duration since injury 4.8±1.4 years; 6 paraplegic; 5 complete (T6-L1) 

A. TC (mg/dL) B. HDL (mg/dL) C. LDL (mg/dL) D. TC/HDL-C E. TG (mg/dL) 
Table 14. Description of exercise intervention studies with lipid or cardiovascular related outcomes in people with SCI (continu

73

Reference Study Design; Sample Size Intervention Type Frequency; Intensity; Duration Subject Characteristics Outcomes of Interest 

Stewart, 200463 Case series 

n=9 

Body-weight supported treadmill training program 

68 sessions (2.8±0.2 sessions/week); Velocity and % weight support varied for each participant; 6.0±0.3 months of 

training 

8 males, 1 female; Mean age 31±3 years; Mean duration since injury 8.1 years; 9 incomplete (C4-T12) 

A. TC (mM) B. HDL-C (mM) C. LDL-C (mM) D. TC/HDL-C (mME. TG (mM) 

B. Functional electrical stimulation exercise No eligible studies C. Passive exercise No eligible studies 

D. Self-reported physical activity 
Table 14. Description of exercise intervention studies with lipid or cardiovascular related outcomes in people with SCI (continu

74

Reference Study Design; Sample Size Intervention Type Frequency; Intensity; Duration Subject Characteristics Outcomes of Interest 

Dallmeijer, 199970 Case-series 

survey n=19 

NA Assessed risk profiles and sport activity (hours/week) at t1 (during rehab) and t2 (1 year postdischarge) 

NA 15 males, 4 females; 

Mean age 40.7±14.7 years; Mean duration since injury 760±169 days; 9 tetraplegic; 10 paraplegic 

A. Difference TC (mM/L) B. Difference LDL-(mM/L) C. Difference TC/HDL-C (mML) D. TG (mM/L) 

Dallmeijer, 199769 Cross-sectional 

survey n=24 

NA Compared lipid levels between physically active (1.5-6.0 hours/week) and sedentary SCI patients 

NA 24 males, 0 females 

11 physically active 13 sedentary 24 tetraplegic 4 incomplete 20 complete 

A. TC (mM/L) B. HDL (mM/L) C. LDL-C (mM/L) D. TC/HDL-C E. TG 
Table 14. Description of exercise intervention studies with lipid or cardiovascular related outcomes in people with SCI (continu

75

Reference Study Design; Sample Size Intervention Type Frequency; Intensity; Duration Subject Characteristics Outcomes of Interest 

Davies, 200254 Cross-sectional 

survey n=97 

NA Assessed physical activity as determinant of cardiovascular morbidity (both measurements made with valid and reliable scale) 

NA 87 males, 10 females; 

Mean age 47.5±4.5 years; Mean duration since injury 15.9±10.1 years; 41 tetraplegic 55 paraplegic 1 undetermined 32 complete 62 incomplete 3 undetermined 

Cardiovascular morbidity 

Janssen, 199771 Cross-sectional 

survey n=37 

NA Assessed sport activity (hours/week) as determinant of lipid profiles 

NA 37 males, 0 females; 

Age range 19-71 years; Duration since injury range 4-33 years; 8 tetraplegic 29 paraplegic 23 complete 

A. TC (mM/L) B. HDL (mM/L) C. LDL-C (mM/L) E. TC/HDL-C F. TG 
Table 14. Description of exercise intervention studies with lipid or cardiovascular related outcomes in people with SCI (continu

76

Reference Study Design; Sample Size Intervention Type Frequency; Intensity; Duration Subject Characteristics Outcomes of Interest 

Jones, 200414 Cross-sectional 

case-control survey n=20 

NA Assessed physical activity levels (minutes/week) and metabolic variables 

NA 20 males, 0 females; 

Age range 16-52 years; Mean duration since injury 10.3±1.8 years; 11 tetraplegic (C4-C7) 9 paraplegic (T5-L5) 

A. TC/HDL (mM/L) B. Log HDL (mM/L

Manns, 200513 Cross-sectional 

survey n=22 

NA Assessed physical activity levels and metabolic variables 

NA 22 males, 0 females; 

Age range 39±9 years; Mean duration since injury 17±9 years; 22 paraplegic (T2-L2); 22 complete 

A. HDL-C (mM/L) B. TG (mM/L) 

E. Other Chen, 200672 Case series 

n=16 

NA Participation in weight management program where exercise behavior was taught 

Followup testing at 12 weeks and 24 weeks 

9 males, 7 females; Age range 21-66 years; Mean duration since injury 17.5 years 15 SCI 1 spinal cord illness 

A. TC (mg/dL) B. HDL-C (mg/dL) C. LDL-C (mg/dL) 
77

Table 15. Diet and pharmacologic therapy studies for prevention and/or treatment of carbohydrate and lipid metabolism disordcord injury and disease 

Reference 

Study Design Intervention Type Subject Characteristics; Duration Outcomes of Interest 

A. Diet therapy Szlachcic, 200120

Clinical controlled trial 

Group 1 (subjects had total cholesterol >200mg/dl): Dietary intervention referral (Seen ≥2 times/week, followed recommendations of American Heart Association and American Dietetic Association Guidelines) (n=86) Group 2 (subjects had total cholesterol <200mg/dl): Not referred for dietary intervention (n=136) 

222 subjects with SCI ≥2 years. Male 89% (n=198), females 11% (n=24). Mean age 38.5±11 years White: 22% (n=49) African American: 21% (n=47) Hispanic: 54% (n=120) Asian: 2% (n=4) Mean duration since injury Group 1 subjects significantly older (42.8 vs. 35.7, p <0.0001) and had longer post-injury duration (15.6 vs. 11.1, p <0.0001). Paraplegia, complete: 38% Paraplegia, incomplete: 12% Tetraplegia, complete: 38% Tetraplegia, incomplete: 16% Study duration: 16 months (mean) 

A. TC B. LDL C. TG D. HDL 

ComfolloA. TGrop <0Grop = B. LGrop = Grop noC. TGro162Grop noD. HNo s

Chen, 200672

Single group uncontrolled trial 

Weight management program consisting of 12 classes for 12 weeks, primarily led by registered dietician. Classes covered nutrition, exercise, and behavior modification. Dietary approach utilized a timecalorie displacement diet. 

16 overweight (BMI ≥25) subjects, 

Male 56% (n=9), female 44% (n=7) Mean age 44: (range 21-66) White: 81% (n=13) African American: 19% (n=3) Mean duration since injury: 17.5 Years since injury (15) or illness (1) Study duration: 12 weeks and 24 weeks 

A. TG B. LDL C. HDL 

Mea

duri

(wee

A. T201B. L136C. H43.1Mea
Table 15. Diet and pharmacologic therapy studies for prevention and/or treatment of carbohydrate and lipid metabolism disord

cord injury and disease (continued) 

78

Reference 

Study Design Intervention Type Subject Characteristics; Duration Outcomes of Interest 

durifolloA. TB. LC. H

B. Pharmacologic therapy No studies reporting 
79 

Chapter 4. Discussion 

Prevalence and Risk Estimates 

 The present systematic review evaluated published evidence regarding the prevalence of lipid 

and carbohydrate disorders, CVDs, and mortality in adults with chronic posttraumatic SCI. We 

attempted to assess the contribution of risk of these disorders to CVD morbidity and mortality 

and whether they vary according to SCI status or compared to able-bodied individuals. The 

potential efficacy and harms of interventions to improve carbohydrate and lipid disorders in this 

population was also examined. This information was synthesized to determine if compared to 

able-bodied adults individuals with SCI: 

1. have a different prevalence of carbohydrate disorders; 

2. have increased risk of CVD morbidity and mortality, 

3. have CVD and/or carbohydrate/lipid benefits from specific interventions; 

4. should have thresholds/methods for detection or treatment modified. 

 The level of evidence addressing these issues is low. Most studies were retrospective, small, 

lacked adequate controls, and did not assess or adjust for confounding factors. Outcome measure 

definitions varied widely. However, limited low quality data suggest that adults with SCI are not 

at markedly higher risk of carbohydrate and lipid disorders or CVD than appropriately matched 

able-bodied individuals. Except for assessment of body composition/obesity, evidence does not 

support that diagnostic and treatment thresholds or methods for carbohydrate and lipid disorders 

should differ in SCI compared to able-bodied individuals. Assessment of insulin resistance and 

impaired glucose tolerance are not routinely performed in able-bodied individuals. The 

effectiveness of screening to improve clinical outcomes by detection of pre-diabetes (impaired 

fasting glucose or impaired glucose tolerance), insulin resistance, and diabetes in asymptomatic 

adults has not been demonstrated.73 Use of these tests is limited due to their inconvenience, 

complexity of testing requirements, costs, and current lack of accuracy. The OGTT is 

inconvenient and not ordered by most physicians to diagnose diabetes, even among those at risk. 

Additionally, about one-half with IGT or OGTT would have normal tests if repeated. Similar 

concerns exist with the criteria used to define impaired fasting glucose. Because the glucose 

concentration distribution is unimodal, the choice of cutpoints used to designate abnormalities of 

carbohydrate metabolism is arbitrary. Very little high quality data exist on the independent role 

of gender, race, disease severity, level, or duration. Any observed differences in prevalence or 

risk is relatively small in magnitude, inconsistent in direction according to study or risk 

characteristic, and/or could be confounded by differences in other known risk factors: age, 

smoking, exercise status, family history, etc.). 

 Assessment of obesity using BMI, is likely to be inaccurate and underestimate body fat 

assessment in adults with SCI. For other measures of carbohydrate and lipid abnormalities there 

is no high quality evidence to indicate that different thresholds (or biomarkers) should exist for 

SCI individuals compared to able-bodied adults to identify patient risk level, define disease 

status, or initiate treatment. Little data exist on the effects of interventions to improve 

carbohydrate and lipid abnormalities, including the effect of exercise. 

 Several previous reports and reviews have suggested that the prevalence of carbohydrate and 

lipid disorders, as well as cardiovascular morbidity and mortality, is much higher in adults with 

SCI compared to able-bodied individuals. However, the prevalence of insulin resistance, 

metabolic syndrome, diabetes mellitus, impaired glucose tolerance, dyslipidemia, and obesity in 
80 

a population is highly dependent upon demographics of the population, including most 

importantly the age distribution, but also socioeconomic status and race/ethnicity. The 

dependence of these conditions on population characteristics makes it difficult to make between 

study comparisons, since the population characteristics vary greatly both between and within 

studies. These factors may explain the wide variation in study prevalence estimates as well as the 

relative risk compared to different able-bodied control populations. Additionally, definitions of 

disease or condition may also alter prevalence estimates. In the one included study assessing 

metabolic syndrome, the definitions used by the authors for hypertension, obesity, diabetes, and 

lipid disorders are not widely accepted or utilized in studies in able-bodied adults. Their 

definitions increase the estimated prevalence of disease in their population and relative to studies 

of able-bodied individuals that use established definitions. 

 Our findings of cardiovascular disease prevalence and mortality were lower than frequently 

reported. Previous reviews often incorporated a broad definition of CVD.76 Definitions included 

in these reports were hypertension, as well as self-reported signs and symptoms of leg swelling 

or palpitations.56 The clinical significance and the relation to CVD of leg swelling and 

palpitations are not clear. Accurate assessment of blood pressure in SCI individuals is 

problematic. No validated definitions or thresholds for hypertension interventions exist in SCI 

patients due to blood pressure measurement issues related to autonomic dysreflexia, muscle 

spasticity or hypotonicity, use of arms for wheelchair transportation, and, most importantly, the 

lack of long-term data correlating blood pressure and treatment with morbidity and mortality in 

SCI individuals. These highly prevalent conditions are much more common and inflate 

prevalence estimates of cardiovascular disease in SCI individuals but result in less morbidity 

than myocardial infarction or stroke. Use of self-reported disease classification or death 

certificates for cause of death may also result in biased estimates of disease prevalence or 

mortality. Several factors may contribute to the increased prevalence of undiagnosed CVD in 

SCI individuals, including access and quality of care, asymptomatic angina in patients with 

diabetes or upper level injury,77,78 and metabolic syndrome, unstable blood pressure, and cardiac 

rhythm.79,80 Screening to detect asymptomatic heart diseases, including coronary heart disease, 

arrhythmias, and autonomic dysreflexia, may result in higher prevalence of CVD in this 

population. 

 Prevalence of CVD in aging SCI individuals can be attributable to age rather than injury. 

Patients differed by the prevalence of risk factors prior to injury and by age at the time of injury, 

both could modify the association between SCI and CVD. Indeed, recently published 

retrospective analysis found that presence of cardiovascular disease prior to injury was 

associated with a 280 percent increase in risk of death (relative risk 2.8, 95 percent CI 1.22; 

6.40).81 For each additional year of age at injury, the relative risk of dying was increased by 8 

percent (RR 1.08, 95 percent CI 1.06; 1.09).81 

 Whether the reported increased risk of all CVD in tetraplegic compared to paraplegic 

individuals can be interpreted as an evidence of higher morbidity53,76 requires additional studies. 

Limited evidence suggests that CVD may contribute to approximately 20 percent of all deaths in 

SCI patients1,36,49,52 and coronary heart disease in 91-3 to 1381 percent of all deaths.1-3,81 There is 

insufficient evidence to determine whether percentage of deaths due to CVD differs in SCI adults 

compared to appropriately matched able-bodied individuals. One study suggested that presence 

of heart diseases was associated with an increased risk of death by 3.7 fold in SCI patients 

independent of age and other risk factors.52 Limited evidence suggests that the contribution of 
81 

different forms of heart disease (e.g., ischemic versus nonischemic coronary heart disease) to 

overall CVD mortality in SCI patients may differ from the general population. 

 CVD morbidity and mortality in SCI patients showed inconsistent differences compared to 

the general population. Survival rates in aging injured patients can depend on severity of CVD 

and quality of care. Whether the incidence of CVD was not well documented in the studies or the 

prognosis of CVD is worse in the SCI than in the able-bodied population is unclear. Case fatality 

from CVD in SCI patients compared to the general populations is not well established. However, 

some evidence suggested that case fatality rate for pneumonia was higher in injured than in the 

general population.109

 The independent contribution of diabetes and impaired glucose tolerance on CVD prevalence 

in adults with versus without SCI has not been reported. The association between metabolic 

control and CVD in adults with SCI remains unclear. Vascular complications were not different 

in SCI users of the VA health care system who were diabetic compared to diabetic able-bodied 

veterans.37 The role of lipid disorders on CVD in SCI individuals is not well documented and 

needs future investigation. 

 Some potentially eligible studies that may be cited as evidence of altered risk were excluded 

due to small sample size that limited generalizability (n=45, number of SCI individuals in each 

study ranged from 1-77). These studies were also of low quality and relevance because they were 

from a single center, not from the United States, lacked controls, and/or did not assess clinically 

relevant carbohydrate and lipid disorders. The impact of these studies on our overall findings 

regarding carbohydrate, lipid and body composition disorder prevalence, and subsequent clinical 

decision making is likely to be small. Only 17 excluded studies had control groups. The largest 

study reporting glucose intolerance and insulin resistance in the United States lacked controls, 

was comprised of 57 adults from a single center, and was published in 1983. The largest 

excluded controlled study of lipid disorders was a single center report comprised of 60 young 

SCI adults (mean age = 28 years) and 28 age and gender matched healthy able-bodied controls. 

Serum LDL cholesterol was higher (109 mg/dL vs. 91 mg/dL; p = 0.04) and HDL cholesterol 

lower (33 mg/dL vs. 44 mg/dL; p = 0.004) in SCI adults versus controls. The authors concluded 

that “serum lipoprotein levels should not be ignored for the followup of the patients with spinal 

cord injury.”75 We agree with their conclusion. Other excluded studies were of even lower 

quality and relevance to health care in the United States because they were smaller, from a single 

center, not from the United States, lacked controls, and/or did not assess clinically relevant 

carbohydrate and lipid disorders. 

Role of Exercise, Diet, and Pharmacologic Interventions 

 The evidence that exercise programs alter carbohydrate and lipid outcomes is of poor quality 

and inconclusive. There were relatively few consistent findings pertaining to plasma glucose, 

two-hour post-load glucose, fasting insulin, or two-hour post-load insulin. Similarly, little 

consistency was reported between studies for HDL-C, TC/HDL, and TG. Results may have 

indicated some overall post-training benefits for outcomes of TC and LDL-C. While many 

reported findings appear to be encouraging and are suggested as such in the primary papers as 

well as past reviews,85,110 caution is warranted when interpreting these studies. There was a 

general lack of quantity, quality, and consistency in methods and outcomes across studies. 

Overall, reports were based on short-term exercise protocols, often involved carefully recruited 

hospital- and/or clinic-based patients, and failed to consider implementation or sustainability of 
82 

exercise interventions in community-based populations. Only one study examined the effects of 

exercise on coronary heart disease outcomes.54 

 The exercise described in these papers varied considerably from one study to the next. In the 

cross-sectional surveys,13,14,54,69-71 parameters of physical activity were rarely reported. 

Generally, questions pertaining to amount of physical activity per week were asked.14,69-71 In 

exercise intervention studies, little consistency in duration, mode, frequency, or intensity of the 

exercise programs existed. The length of the exercise protocols ranged from 8 to 52 weeks; most 

were only 8 to 16 weeks in duration.57-61,64-67 These studies may not have been long enough to 

impart measurable physiological benefits to study participants. Further, the types of exercise, 

frequency of sessions, and intensity of exertion were also varied, making results about preferred 

forms of exercise inconclusive. 

 Patient populations and outcome measures were also highly inconsistent. Study designs 

consisted only of case series, involving small numbers of subjects in hospital or clinical settings, 

or the cross-sectional surveys. The total number of subjects participating was low (n=101 for 

carbohydrate studies and n=292 for lipid studies) and, for the most part, subjects were not 

randomly selected from broader patient or community populations. These methods are 

considered highly susceptible to bias. Subjects that participated in the case series studies were 

likely a highly-motivated group of individuals, nonrepresentative of the broader population of 

those with SCI. Little information was presented on those asked to participate but who chose to 

abstain. Further, the measures of self-reported exercise or physical activity utilized in the crosssectional surveys likely led to misclassification through recall error and social desirability issues. 

Even if measurement of physical activity was accurate, the cross-sectional nature of these 

surveys leaves results highly questionable due to possible confounding. For example, those who 

did not exercise may have had underlying carbohydrate and/or lipid metabolism disorders. This 

would make physical activity positively correlated, but not necessarily causally associated, with 

better carbohydrate and lipid measures. 

 None of the intervention studies used improvement in glycated hemoglobin (A1C) as an 

outcome. The effect of exercise on blood glucose often is delayed for several hours. A1C reflects 

the integrated effect on blood glucose throughout the day and A1C is easy to measure. Therefore, 

it would likely be preferable for future studies to track A1C changes rather than transient and 

more difficult to measure insulin or glucose levels or areas under the insulin and glucose curves 

for a few hours. 

 Even if consistent, convincing data were generated from these types of studies, there is no 

evidence for subsequent, successful translation of exercise interventions to a lesser motivated or 

community-based SCI population. Effectiveness of exercise interventions has yet to be studied in 

a population of individuals with SCI. Implementation and sustainability of exercise in this 

population is likely to be more challenging than in an able-bodied population, given the 

environmental barriers and physical risks, such as exercise-induced autonomic dysfunction and 

musculoskeletal injury.8,26 The risk of further, unperceived health problems, such as silent 

ischemia, in denervated subjects should be carefully considered prior to implementing exerciserelated recommendations or policies. 

 Exercise and dietary programs among able-bodied individuals have demonstrated a modest 

improvement in carbohydrate and lipid parameters among selected highly motivated individuals. 

Translation of these findings to community settings of SCI adults has not been demonstrated, and 

even the effectiveness in the general able-bodied population is unclear. For example, a recent 

randomized trial evaluated the effects of 22 weeks of aerobic training, resistance training, or both 
83 

(three times per week) on glycemic control in 251 able-bodied adults with Type 2 diabetes.86

Combined training resulted in a 1 percent absolute reduction in glycated hemoglobin values 

versus sedentary controls. Reductions due to either resistance or aerobic training alone were 

about one-half that seen with combination therapy. Their was no difference in lipid values, blood 

pressure, lean body mass, fat mass, or percent body fat of any of the exercise programs versus 

controls. Adverse events were more common in the exercise group, and 14 percent of those 

randomized to exercise dropped out. 

 Ultimately, higher-quality studies examining effects of exercise on the health of subjects with 

SCI need to be conducted. While carbohydrate and lipid metabolism measurements are 

important, intermediate measures, extending such studies into longer term outcomes such as 

diabetes mellitus, coronary heart disease, and survival are important. In addition, clinical and 

research questions pertaining to obesity in individuals with SCI remain to be answered. The most 

appropriate measurements and definition of obesity for those with SCI have not been identified 

at this time. To continue the use of BMI as a measurement of obesity, it must be assessed 

whether current BMI cutpoints for the general population can be extrapolated to those with SCI, 

or whether cutpoints need to be specific to this population, considering both SCI type and level. 

 Little information exists regarding the impact of dietary or pharmacologic interventions on 

adults with SCI. Recommendations currently exist for disease definitions for diabetes and lipid 

abnormalities in able-bodied adults. Several large RCTs have established the effectiveness of 

statins used for primary prevention in able-bodied adults with mean baseline LDL cholesterol of 

approximately 150 mg/dL. Many of these individuals had other competing risks such as 

hypertension and cigarette use. Use of statins in able-bodied adults with diabetes have been 

demonstrated to be effective even if baseline LDL-C is less than 130 mg/dL. The mean baseline 

LDL-C in populations of SCI individuals included in this review was 125 mg/dl. Effectiveness 

and harms associated with statins may differ in SCI individuals compared to able-bodied adults. 

However, unless contrary data exist, it seems reasonable to extrapolate these findings and 

recommendations for similar pharmacologic intervention thresholds for treatment of lipid 

abnormalities in SCI individuals as used in able-bodied adults. There have been no primary 

prevention studies among individuals with low HDL-C. Recent studies of treatments to raise 

HDL-C have been stopped due to harm. Existing recommendations to assess cardiovascular risk 

for able-bodied individuals suggest that all adults should have a complete lipid profile, including 

HDL and LDL cholesterol levels, as well as family history, smoking status, and gender. The 

treatment recommendations should be based on that comprehensive risk assessment. Future 

studies are needed to determine if SCI should be included as an independent risk factor. 

 With regard to interventions to prevent and treat diabetes, currently no large scale 

randomized trials have demonstrated that aggressive control of Type 2 diabetes reduces 

cardiovascular complications. A recent systematic review assessed the comparative effectiveness 

and safety of oral medications for Type 2 diabetes mellitus. The authors reported that there was 

no definitive evidence about the comparative effectiveness of oral diabetes agents on all-cause 

mortality, cardiovascular mortality or morbidity, peripheral arterial disease, neuropathy, 

retinopathy, or nephropathy.82 Two more recent meta-analyses of thiazolidinediones have been 

conducted. Among able-bodied patients with impaired glucose tolerance or Type 2 diabetes 

(n=14,291), rosiglitazone use for at least 12 months was associated with an increased risk of 

myocardial infarction and heart failure. There was no difference in increase risk in 

cardiovascular mortality.83 A review of pioglitazone (n=16,390) showed a significantly lower 

risk of death myocardial infarction or stroke among patients with Type 2 diabetes and 
84 

inadequately glycemic control. Serious heart failure was increased.84 Unless future RCTs 

demonstrate evidence to the contrary, a reasonable policy would be to implement existing 

diabetes detection and management guidelines used for able-bodied adults. 

Conclusions and Policy Implications 

 Available evidence regarding the prevalence, impact, and outcomes of carbohydrate and lipid 

disorders in adults with chronic SCI is weak. Evidence is limited by relatively few studies, small 

sample size, lack of appropriate control groups, failure to adjust for known confounding 

variables, and variation in reported outcomes. However, the existing evidence does not indicate 

that adults with SCI are at markedly greater risk for carbohydrate and lipid disorders or 

subsequent cardiovascular sequelae than able-bodied adults. Cardiovascular diseases are among 

the leading causes of death in aging patients with chronic SCI. Therefore, patients with SCI 

should be assessed and treated according to existing guidelines for able-bodied individuals to 

reduce cardiac morbidity and mortality in this population associated with carbohydrate and lipid 

disorders. 

 BMI to assess obesity and body composition is likely inaccurate and underestimates fat mass 

in adults with SCI. Available evidence does not support establishing different thresholds to 

define and treat abnormal traditional lipid and carbohydrate measures or to utilize other markers 

(e.g., insulin sensitivity or impaired glucose tolerance) for SCI individuals compared to ablebodied adults. Because evidence is weak, it is not possible to conclude that an increased risk of 

these disorders and their subsequent cardiovascular sequelae do not exist or that use of 

alternative measures of abnormality may not someday be found beneficial. 

 Individuals with SCI may have unique physiologic differences compared to able-bodied 

individuals. Therefore, caution is advised in attempting to extrapolate findings from studies 

conducted in able-bodied adults evaluating efficacy and harms of interventions to improve 

carbohydrate, lipid disorders and subsequent coronary vascular disease. 

 If clinical uncertainty regarding carbohydrate and lipid disorder risks in adults with SCI and 

determining the most appropriate interventions remain high priority areas, then future high 

quality research is needed. Until that time, a reasonable policy would be to use similar criteria to 

identify and treat carbohydrate and lipid disorders (outside of body composition assessment) in 

adults with SCI as currently recommended for able-bodied adults. The role of exercise in SCI 

individuals also represents a unique challenge and requires further exploration into the benefits, 

risks, and potential implications of broader based exercise programs. This systematic review did 

not assess the diagnosis and treatment of hypertension in SCI individuals or the other potential 

benefits of diagnosis and management of SCI individuals, such as improved wound healing. 

Additional clinical and research activities are needed to address these issues. 

Future Research

 A major gap in the evidence is the lack of high-quality prospective epidemiologic studies 

assessing the prevalence and impact of lipid and carbohydrate abnormalities and corresponding 

CVD complications in SCI individuals, especially compared to appropriately matched ablebodied controls. Future research could include a large prospective multicenter cohort study of 

adults with SCI. Risk assessment should be started at the time of injury and continued during 

long-term followup. Prevalence and incidence assessment needs to be objective rather than self 
85 

reported. Inclusion of baseline and followup physiologic and serologic values (e.g., body 

composition measures, actual lipid and carbohydrate laboratory values) and standardized 

outcomes are made according to well-recognized diagnostic criteria of heart diseases. Expansion 

of existing cohort studies in the VA, a large non-VA cohort study, and future RCTs that aim to 

test whether more aggressive screening or treatment within SCI populations actually reduces 

disease prevalence, morbidity, and mortality could be initiated. Additional information on 

women is needed. 

 To a large extent, research within the VHA patient population has provided an important 

foundation to the current knowledge, particularly within the United States, regarding the 

prevalence of carbohydrate and lipid disorders and relevant considerations in persons with SCI. 

If there is continued concern that adults with chronic SCI have a different prevalence than adults 

without SCI, then future research would benefit from an expansion of the existing cohort studies 

in the VA, a large non-VA cohort study, and future RCTs that aim to test whether more 

aggressive screening or treatment within SCI populations actually reduces disease prevalence, 

morbidity, and mortality. 

 The VA administrative and clinical datasets and data from other large health care systems 

provide researchers with a wealth of information regarding the epidemiology of carbohydrate 

and lipid disorders with SCI patients. These datasets allow for rapid estimation of the magnitude 

of disease burden from carbohydrate and lipid disorders and can help to develop hypotheses 

about the role SCI may play in the development of disease. However, administrative datasets 

often suffer from selection bias in terms of the persons included and the measurements obtained. 

Therefore, such datasets need to be enriched with prospective cohort style data collection. This 

can be accomplished by designing a registry of adults with SCI and collecting a baseline battery 

of key measurements on all persons. This comprehensive set of baseline measurements can then 

be combined with standard outcomes data collected in these healthcare settings to provide a 

detailed description of the natural history and etiology of various diseases. 

 While in many ways the VHA provides an ideal U.S. setting to obtain important information 

on persons with SCI, it must be accompanied by complementary research on representative SCI 

persons from health systems outside of the VA. This is particularly important, since women are 

currently underrepresented in VHA datasets, and veterans have often been found to have more 

competing comorbidities than nonveteran populations,37 which can make generalizations difficult 

without complementary non-VA data. Additionally, current reports indicate that approximately 

90 percent of SCI subjects were men. It is not known if this is representative of the U.S. SCI 

population or only those reporting this information. 

 RCTs will be needed to further extend the information obtained from future prospective 

observational studies. Regardless of whether or not future trials indicate that individuals with 

SCI are at an increased risk of carbohydrate and/or lipid disorders, it is clear that, like the general 

population, a significant number of SCI individuals do have carbohydrate and lipid disorders and 

techniques for treating these disorders may need to be modified to meet the specific needs of 

those with SCI to ensure that they are being most appropriately treated. RCTs will therefore be 

needed to compare the effectiveness of any such modifications in treatment technique and 

intensity, including the same pharmacological agents recommended for the general population 

and specific for SCI patients’ treatment options that would target impaired glucose tolerance and 

insulin sensitivity. 

 If prospective cohort studies identify an increased risk in adults with SCI, RCTs will be 

needed to further extend the information. Techniques for identifying and treating these 
86 

carbohydrate and lipid disorders and CVDs may need to be modified to meet the specific needs 

of those with SCI. In addition, continued clinical and research questions pertaining to obesity in 

individuals with SCI remain to be answered. These include identification of the most appropriate 

measurements and definition of obesity for those with SCI, and whether current BMI cutpoints 

for the general population can be validly extrapolated to those with SCI. 

 RCTs evaluating the potential effectiveness and harms of interventions to alter CVD risk 

factors and reduce CVD incidence, morbidity, and mortality are needed. The level of injury, 

neurological impairment, and other known or potential confounders including smoking status, 

hypertension, family history, race, age, diabetes, infections including, socioeconomic status, and 

quality of health care should be analyzed as possible effect modifiers of the association between 

well-known risk factors and cardiovascular morbidity and mortality. 

 Given the variation in design across studies, the lack of consistent findings in this review was 

not surprising. While improved studies will be challenging due to limited resources, complicated 

study questions, a relatively small subject population, and invasive intervention, policy 

recommendations cannot be generated until higher quality evidence is available. Consistent, 

higher quality research on exercise and metabolic and cardiovascular health in SCI patients is 

needed. Studies examining efficacy as well as effectiveness of exercise interventions are needed. 

 Continued research should be conducted to gain a better idea of the important barriers to 

exercise experienced by individuals with SCI and to develop novel methods to overcome these 

barriers. Preliminary studies may also assess which patients are most in need of intervention, the 

best types of exercise programs and equipment, and how to modify them based on characteristics 

of the injury. For example, telemedicine approaches to home-based exercise programs could 

potentially help overcome barriers to accessing traditional facilities or equipment. Whether 

qualitative or quantitative, this preliminary work would not only inform the development of 

exercise programs but also the research used to evaluate efficacy and effectiveness. 

 Accomplishing the level of research needed will likely require a collaboration of researchers 

across sites. Convening a consortium of experts is a practical first step. Cooperative research 

groups could determine the most appropriate and pragmatic study parameters, including 

intervention type and outcome measures, and could propose the most feasible quality studies. 

RCTs and prospective epidemiologic studies for individuals with SCI could both contribute 

enhanced knowledge to the current evidence base. While such studies are resource intensive, 

these accomplishments could perhaps be better achieved through the pooling of resources, either 

by funding agencies, or by researchers through multiple site collaborations. The VA medical 

system, the SCI model systems sites, or the National SCI Statistical Center at the University of 

Alabama Birmingham may be poised to lead such multi-site collaboration and studies. 

 Short-term, intermediate outcomes of exercise, as were typically reported in the current 

studies, may not be ideal or definitive measurements for this type of research. Studies ideally 

would focus on long-term clinically relevant outcomes such as prevention of diabetes mellitus, 

coronary heart disease, and mortality. 

 An RCT would provide the best evidence for or against the use of exercise to prevent or 

control carbohydrate and lipid disorders among those with SCI, though conducting adequately 

sized studies would be difficult and would require cooperative group participation. Studies on 

exercise and metabolic and cardiovascular outcomes in the SCI population will be more 

definitive if important demographic and injury parameters are considered. Key variables that 

should be included in future studies are patient age, race, and gender; comorbid conditions; 

baseline lipid and carbohydrate related measures; duration, level, and completeness of SCI; 
87 

functional status; baseline physical activity; exercise program type, frequency, intensity, and 

duration; and life satisfaction and other important psychosocial variables. RCTs and prospective 

epidemiologic studies with adequate numbers of participants should provide the least 

confounded evidence for or against exercise programs if the intervention and control groups are 

appropriately balanced and/or stratified by these variables. 

 Further research will be needed to translate any findings of exercise efficacy into effective 

community-based interventions. Even if efficacy is promising, it will remain to be seen if these 

interventions are feasible in a community setting, and if the interventions, as well as health 

outcomes, are sustainable over time. Further evidence on how best to motivate individuals to 

sustain exercise, while preventing and identifying potential harms, will be needed. 

 RCTs evaluating the potential effectiveness and harms of pharmacologic and dietary 

interventions to alter CVD risk factors (diabetes, lipid abnormalities, and/or obesity) and reduce 

CVD incidence, morbidity, and mortality may be needed if there is continued concern that results 

may differ in SCI populations compared to able-bodied adults. 

89 

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95 

List of Acronyms/Abbreviations 

AB Able bodied 

AE Active exercise 

AHRQ Agency for Healthcare Research and Quality 

BMI Body mass index 

C Cholesterol 

CDC Centers for Disease Control 

CI Confidence interval 

CVD Cardiovascular disease 

DXA Dual energy x-ray absorptiometry 

ECG Electrocardiogram 

EPC Evidence-based Practice Center 

FES Functional electrical stimulation 

HDL High-density lipoprotein 

HI High intensity 

HRR Heart rate reserve 

ICD International classification of diseases 

IGT Impaired glucose tolerance 

LBBB Left bundle branch blocks 

LDL Low-density lipoprotein 

LI Low intensity 

LVH Left ventricular hypertrophy 

MET Metabolic equivalents 

N Number 

NA Not applicable 

OGTT Oral glucose tolerance test 

OR Odds ratio 

PE Passive exercise 

RCT Randomized controlled trial 

SCI Spinal cord injury 

TC Total cholesterol 

TEP Technical expert panel 

TG Triglycerides 

VA Veterans Affairs 

VHA Veterans Health Administration 

WAFT Wheelchair aerobic fitness trainer 

WMD Weighted mean difference 
Appendixes 
A-1 

Appendix A: Technical Expert Panel Members and Affiliation 

TEP Member Affiliation 

Yuying Chen, MD, PhD Physical Medicine and Rehabilitation 

University of Alabama at Birmingham 

David R. Gater, Jr, PhD, MD Department of Veterans Affairs 

Hunter Holmes McGuire Medical Center 

Leonard Pogach, MD Department of Veterans Affairs 

New Jersey Health Care System 

Suparna Rajan, PhD, RD Department of Veterans Affairs 

Puget Sound Health Care System 

B-1 

Appendix B. Exact Search Strings 

Medical Subject Headings Terms and Key Words Number of Retrieved References

"Spinal Cord Injuries" [MeSH] AND ("Cardiovascular Diseases" [MeSH] OR 

"Cardiology" [MeSH]) NOT review NOT letter NOT editorial NOT Case 

Reports 

 Limits: All Adult: 19+ years, Entrez Date from 1990/01/01 to 2007/07/01, 

English, Humans 233

"Spinal Cord Injuries" [MeSH] AND Cardiovascular Diseases 

 Limits: English, Humans 1,467

"Spinal Cord Injuries" [MeSH] AND Cardiovascular Diseases 

 Limits: English, Randomized Controlled Trial, Humans 20

"Spinal Cord Injuries" [MeSH] AND Cardiovascular Diseases 

 Limits: English, Clinical Trial, Humans 55

"Spinal Cord Injuries" [MeSH] AND "Cardiovascular Diseases" [MeSH] 

 Limits: English, Clinical Trial, Humans 55

"Spinal Cord Injuries" [MeSH] AND "Cardiovascular Diseases" [MeSH] 

 Limits: English, Randomized Controlled Trial, Humans 20

"Spinal Cord Injuries" [MeSH] AND "Cardiovascular Diseases" [MeSH] 

 Limits: English, Meta-Analysis, Humans 1

"Spinal Cord Injuries" [MeSH] AND "Cardiovascular Diseases" [MeSH] 

 Limits: English, Humans 1,464

"Spinal Cord Injuries" [MeSH] AND "Cardiovascular Diseases" [MeSH] AND 

"Insulin Resistance" [MeSH] 

 Limits: English, Humans 2

"Cardiovascular Diseases" [MeSH] Limits: English, Humans 780,975

 ("Cardiovascular Diseases" [MeSH] OR "Cardiology" [MeSH]) NOT review 

NOT letter NOT editorial 

 Limits: Adult: 19-44 years, Middle Aged: 45-64 years, Middle Aged + Aged: 

45+ years, Aged: 65+ years, 80 and over: 80+ years, English, Humans 402,080

 ("Cardiovascular Diseases" [MeSH] OR "Cardiology" [MeSH]) 

 Limits: Adult: 19-44 years, Middle Aged: 45-64 years, Middle Aged + Aged: 

45+ years, Aged: 65+ years, 80 and over: 80+ years, English, Humans 456,995

 “Spinal Cord Injuries” [MeSH] NOT review NOT Letter NOT editorial AND 

"Diabetes Complications" [MeSH] NOT review NOT letter NOT editorial 

 Limits: Adult: 19-44 years, Middle Aged: 45-64 years, Middle Aged + Aged: 

45+ years, Aged: 65+ years, 80 and over: 80+ years, English, Humans 19

 "Trauma, Nervous System" [MeSH] AND ("Spinal Cord" [MeSH] OR "Spinal 

Cord Injuries" [MeSH] OR "Spinal Cord Diseases" [MeSH]) NOT review 

NOT letter NOT editorial AND ("Cardiovascular Diseases" [MeSH] OR 

"Cardiology" [MeSH]) 

 Limits: Adult: 19-44 years, Middle Aged: 45-64 years, Middle Aged + Aged: 

45+ years, Aged: 65+ years, 80 and over: 80+ years, English, Humans 669
B-2 

 "Autonomic Dysreflexia" [MeSH] AND ("Cardiovascular Diseases" [MeSH]) 

NOT review NOT letter NOT editorial 

 Limits: Adult: 19-44 years, Middle Aged: 45-64 years, Middle Aged + Aged: 

45+ years, Aged: 65+ years, 80 and over: 80+ years, English, Humans 17

 "Autonomic Dysreflexia" [MeSH] AND ("Cardiovascular Diseases" [MeSH]) 

 Limits: Adult: 19-44 years, Middle Aged: 45-64 years, Middle Aged + Aged: 

45+ years, Aged: 65+ years, 80 and over: 80+ years, English, Humans 23

 "Brown-Sequard Syndrome" [MeSH] AND ("Cardiology" [MeSH]) 

 Limits: Adult: 19-44 years, Middle Aged: 45-64 years, Middle Aged + Aged: 

45+ years, Aged: 65+ years, 80 and over: 80+ years, English, Humans 0

 "Brown-Sequard Syndrome" [MeSH] AND ("Cardiovascular Diseases" [MeSH]) 

 Limits: Adult: 19-44 years, Middle Aged: 45-64 years, Middle Aged + Aged: 

45+ years, Aged: 65+ years, 80 and over: 80+ years, English, Humans 8

 "Quadriplegia" [MeSH] NOT review NOT letter NOT editorial AND 

("Cardiovascular Diseases" [MeSH] OR "Cardiology" [MeSH]) 

 Limits: Adult: 19-44 years, Middle Aged: 45-64 years, Middle Aged + Aged: 

45+ years, Aged: 65+ years, 80 and over: 80+ years, English, Humans 299

 "Paraplegia" [MeSH] NOT review NOT letter NOT editorial AND 

("Cardiovascular Diseases" [MeSH] OR "Cardiology" [MeSH]) 

 Limits: Adult: 19-44 years, Middle Aged: 45-64 years, Middle Aged + Aged: 

45+ years, Aged: 65+ years, 80 and over: 80+ years, English, Humans 587

 "Spinal cord injury" AND ("Cardiovascular Diseases/epidemiology" [MeSH] 

OR "Cardiovascular Diseases/etiology" [MeSH] OR "Cardiovascular 

Diseases/prevention and control" [MeSH]) NOT review Not letter Not 

editorial 

 Limits: Adult: 19-44 years, Middle Aged: 45-64 years, Middle Aged + Aged: 

45+ years, Aged: 65+ years, 80 and over: 80+ years, English, Humans 259

Related Articles for PubMed (Select 16823238) 302

Select 3 document(s) 3

Search "Cardiovascular Diseases" [MeSH] AND "Spinal Cord Diseases" [MeSH] 

NOT review NOT case report NOT letter NOT editorial 

 Limits: All Adult: 19+ years, English, published in the last 10 years, Humans 288

Search "Cardiovascular Diseases" [MeSH] AND "Spinal Cord Diseases" [MeSH] 

NOT review NOT case report NOT letter NOT editorial 

 Limits: All Adult: 19+ years, English, Humans 888

Search "Cardiovascular Diseases" [MeSH] AND "Spinal Cord Diseases" [MeSH] 

NOT review NOT case report NOT letter NOT editorial 

 Limits: All Adult: 19+ years, Humans 1,320

Search "Cardiovascular Diseases" [MeSH] AND "Spinal Cord Diseases" [MeSH] 

 Limits: All Adult: 19+ years, Humans 3,040

Search "Cardiovascular Diseases" [MeSH] AND "Spinal Cord Diseases" [MeSH] 5,414

Search "Cardiovascular Diseases" [MeSH] 1,366,747

Search "Spinal Cord Diseases" [MeSH] 71,345
C-1 

Appendix C: Data Abstraction Form 

- ID of the study from PubMed or Cochrane ____________ 

- Number of the study _______________ 

- First author _____________ 

- Year of the publication____________ 

- Design of the study: 

- Observational prospective 

- Observational retrospective 

- Case-control 

Level of evidence: 

Description of the target population ______________________ 

Description and clear definition of primary outcomes_________________ 

Description and clear definition of secondary outcomes__________________ 

Validation of the measurements of the exposure_________________ 

Validation of the measurements of the outcomes___________________ 

Process of the subject selection_______________ 

Adequacy of the sampling (random selection or not)_______________ 

Assessment of selection bias____________________ 

Loss of followup_________________________ 

Length of followup (when applicable) in months_______________ 

Validity of the measurements of confounding factors_________________ 

Appropriateness matching________________________ 

Appropriateness of adjustment____________________ 

Appropriateness of standardization_____________________ 

Measurement of possible effect measure modification________________ 

External validity of the study____________________ 

Years of observation, interval______________________ 

Number of patients selected_________________________ 

Number of patients analyzed________________________ 

Data used in the analysis____________________ 

Adjustment for age of the patients, years________________ 

Adjustment for race of the patients_______________________ 

Adjustment for functional status, level of injury____________________ 

Adjustment for socioeconomic status of the patients_________________ 

Adjustment for comorbidities of the patients_________________ 

Patient age____________________ 

Patient race, % of blacks________________________ 

Patient gender, % of females_____________________ 

Time after injury in years_____________________ 

Diagnosis of insulin resistance and diagnostic criteria of insulin resistance________ 

Diagnosis of metabolic syndrome__________________ 

Diagnosis of diabetes mellitus ______________________ 

Diagnosis of impaired glucose tolerance____________________ 

% with insulin resistance__________________ 

% with metabolic syndrome__________________ 
C-2 

% with diabetes mellitus_______________________ 

% with glucose tolerance______________________ 

% with elevated cholesterol_______________________ 

% with elevated LDL_______________________ 

% with elevated TG_____________________ 

% with decreased HDL____________________ 

% with dyslipidemia_________________________ 

% with obesity___________________________ 

% with abdominal obesity_________________ 

Diagnosis of hypertension___________________ 

Proportion of fat in total body mass__________________ 

Proportion of abdominal fat in total body fat_____________ 

Waist-hip ratio________________ 

% of subjects with I class of obesity_________________ 

% of subjects with II class of obesity___________________ 

% of subjects with III class of obesity_________________________ 

Proportion of patients in the sample with upper cervical SCI______________ 

Proportion of patients in the sample with low cervical SCI_______________ 

Proportion of patients in the sample with upper thoracic SCI_____________ 

Proportion of patients in the sample with lower thoracic SCI_________________ 

Proportion of patients in the sample with lumbar SCI______________________ 

Proportion of patients in the sample with sacral SCI____________________ 

Proportion of patients in the sample with coccygeal SCI________________ 

Proportion of patients in the sample with tetraplegia _________________ 

Proportion of patients in the sample with paraplegia __________________ 

Functional status of the patients (definition and level)___________________ 

Incidence of arrhythmia, events/year in 1,000 patients with SCI___________ 

% of patients with SCI with arrhythmia_____________________ 

Incidence of heart arrest, events/year in 1,000 patients with SCI____________ 

% of patients with SCI with heart arrest___________________________ 

Incidence of congestive heart failure, events/year in 1,000 patients with SCI_______ 

% of patients with SCI with congestive heart failure_____________________ 

Incidence of coronary disease, events/year in 1,000 patients with SCI___________ 

% of patients with SCI with coronary disease______________________ 

Incidence of stroke, events/year in 1,000 patients with SCI________________ 

% of patients with SCI with stroke_____________________ 

Incidence of hypertension, events/year in 1,000 patients with SCI___________ 

% of patients with SCI with hypertension________________________ 

Incidence of chronic renal failure, events/year in 1,000 patients with SCI________ 

% of patients with SCI with chronic renal failure_____________________ 

Mean of glomerular filtration rate in ml per min_______________________ 

Mortality, all causes, events/year in 1,000 patients with SCI______________ 

% of patients with SCI who died within year of followup_______________ 

Cardiovascular mortality, events/year in 1,000 patients with SCI_________ 

% of patients with SCI who died from CVD events within year of followup_______ 

Relative risk of arrhythmia, 95% CI__________________ 
C-3 

Relative risk of arrest, 95% CI_____________________ 

Relative risk of CHF, 95% CI_______________________ 

Relative risk of coronary heart disease, 95% CI_________________ 

Relative risk of stroke, 95% CI______________________ 

Relative risk of hypertension, 95% CI___________________ 

Relative risk of CFR, 95% CI_________________________ 

Relative risk of all cause mortality, 95% CI____________________ 

Relative risk of CVD mortality, 95% CI______________________ 

Number of patients with arrhythmia ________________________ 

Number of patients with cardiac arrest________________________ 

Number of patients with congestive heart failure__________________ 

Number of patients with coronary heart disease_____________________ 

Number of patients with stroke___________________________ 

Number of patients with hypertension_______________________ 

Number of patients who died from CVD______________________ 

D-1 

Appendix D: List of Excluded Studies 

1. Case records of the Massachusetts General Hospital. 

Weekly clinicopathological exercises. Case 23-1998. 

Tachypnea, changed mental status, and pancytopenia 

in an elderly man with treated lymphoma. N Engl J 

Med 1998;339(4):254-61. No relevant outcomes 

2. Case records of the Massachusetts General Hospital. 

Weekly clinicopathological exercises. Case 8-2001. 

A 61-year-old man with transient quadriplegia and 

apnea. N Engl J Med 2001;344(11):832-9. No 

relevant outcomes 

3. Prevention of venous thromboembolism in the acute 

treatment phase after spinal cord injury: a 

randomized, multicenter trial comparing low-dose 

heparin plus intermittent pneumatic compression with 

enoxaparin. J Trauma 2003 Jun;54(6):1116-24; 

discussion 25-6. Not eligible target population 

4. Prevention of venous thromboembolism in the 

rehabilitation phase after spinal cord injury: 

prophylaxis with low-dose heparin or enoxaparin. J 

Trauma 2003 Jun;54(6):1111-5. Not eligible target 

population 

5. Abel R, Schablowski M, Rupp R, Gerner HJ. Gait 

analysis on the treadmill - monitoring exercise in the 

treatment of paraplegia. Spinal Cord 2002;40(1):17-

22. No relevant outcomes 

6. Abel T, Schneider S, Platen P, Struder HK. 

Performance diagnostics in handbiking during 

competition. Spinal Cord 2006;44(4):211-6. No 

relevant outcomes 

7. Adams MM, Ditor DS, Tarnopolsky MA, Phillips 

SM, McCartney N, Hicks AL. The effect of body 

weight-supported treadmill training on muscle 

morphology in an individual with chronic, motorcomplete spinal cord injury: A case study. J Spinal 

Cord Med 2006;29(2):167-71. No relevant outcomes 

8. Adkins VK, Mathewson C, Ayllon T, Jones ML. The 

ethics of using contingency management to reduce 

pressure ulcers: data from an exploratory study. 

Ostomy Wound Management 1999;45(3):56-8. No 

relevant data 

9. Agarwal S, Kobetic R, Nandurkar S, Marsolais EB. 

Functional electrical stimulation for walking in 

paraplegia: 17-year follow-up of 2 cases. J Spinal 

Cord Med 2003;26(1):86-91. No relevant outcomes 

10. Agarwal S, Triolo RJ, Kobetic R, Miller M, Bieri C, 

Kukke S, et al. Long-term user perceptions of an 

implanted neuroprosthesis for exercise, standing, and 

transfers after spinal cord injury. J Rehabil Res Dev 

2003;40(3):241-52. No relevant outcomes 

11. Alaedeen DI, Jasper J. Gastric bypass surgery in a 

paraplegic morbidly obese patient. Obesity Surgery 

2006;16(8):1107-8. Less than 100 patients in study 

12. Algood SD, Cooper RA, Fitzgerald SG, Cooper R, 

Boninger ML. Impact of a pushrim-activated powerassisted wheelchair on the metabolic demands, stroke 

frequency, and range of motion among subjects with 

tetraplegia. Arch Phys Med Rehabil 

2004;85(11):1865-71. No relevant outcomes 

13. al-Mahroos S, Malik AK, Sangam K, Burashid K. 

Progressive neurological symptoms in a diabetic 

patient. Postgraduate Medical Journal 

1998;74(877):699-700. Not adult spinal cord injury 

patients 

14. Ampil FL, Chin HW. Radiotherapy alone for 

extradural compression by spinal myeloma. Radiat 

Med 1995 May-Jun;13(3):129-31. Not eligible target 

population 

15. Andersen JL, Mohr T, Biering-Sorensen F, Galbo H, 

Kjaer M. Myosin heavy chain isoform transformation 

in single fibres from m. vastus lateralis in spinal cord 

injured individuals: effects of long-term functional 

electrical stimulation (FES). Pflugers Arch 

1996;431(4):513-8. No relevant outcomes 

16. Andersen JT, Bradley WE. Neuro-urological 

investigation in urinary bladder dysfunction. 

International Urology & Nephrology 1977;9(2):133-

43. No relevant data 

17. Anonymous. Spinal cord injury and obesity. 

Nephrology News & Issues 2005;19(3):23. No 

relevant data 

18. Apstein MD, George BC. Serum lipids during the 

first year following acute spinal cord injury. 

Metabolism: clinical and experimental 

1998;47(4):367-70. Not adult chronic SCI patients 

19. Attal N, Gaude V, Brasseur L, Dupuy M, Guirimand 

F, Parker F, et al. Intravenous lidocaine in central 

pain: a double-blind, placebo-controlled, 

psychophysical study. Neurology 2000 Feb 

8;54(3):564-74. Not eligible outcomes 

20. Averill A, Cotter AC, Nayak S, Matheis RJ, Shiflett 

SC. Blood pressure response to acupuncture in a 

population at risk for autonomic dysreflexia. Arch 

Phys Med Rehabil 2000 Nov;81(11):1494-7. Not 

eligible exposure 

21. Ayas NT, Epstein LJ, Lieberman SL, Tun CG, Larkin 

EK, Brown R, et al. Predictors of loud snoring in 

persons with spinal cord injury. Journal of Spinal 

Cord Medicine 2001;24(1):30-4. No relevant data 

22. Ayas NT, Garshick E, Lieberman SL, Wien MF, Tun 

C, Brown R. Breathlessness in spinal cord injury 

depends on injury level. Journal of Spinal Cord 

Medicine 1999;22(2):97-101. No relevant data 

23. Badami JP, Hinck VC. Symptomatic deposition of 

epidural fat in a morbidly obese woman. Ajnr: 

American Journal of Neuroradiology 1982;3(6):664-

5. Not adult spinal cord injury patients 

24. Bailes JE, Miele VJ. The science of sports medicine. 

Clinical Neurosurgery 2004;51:91-101. No relevant 

data 

25. Baker HW. Reproductive effects of nontesticular 

illness. Endocrinology & Metabolism Clinics of 

North America 1998;27(4):831-50. Not adult spinal 

cord injury patients 
D-2 

26. Baliga RR, Catz AB, Watson LD, Short DJ, Frankel 

HL, Mathias CJ. Cardiovascular and hormonal 

responses to food ingestion in humans with spinal 

cord transection. Clin Auton Res 1997 Jun;7(3):137-

41. Not eligible outcomes 

27. Ball R. Effect of severity, time to recompression with 

oxygen, and re-treatment on outcome in forty-nine 

cases of spinal cord decompression sickness. 

Undersea Hyperb Med 1993 Jun;20(2):133-45. Caseseries 

28. Barlascini CO, Schmitt JK, Adler RA. Insulin pump 

treatment of type I diabetes mellitus in a patient with 

C6 quadriplegia. Archives of Physical Medicine & 

Rehabilitation 1989;70(1):58-60. Less than 100 

patients in study 

29. Barstow TJ, Scremin AM, Mutton DL, Kunkel CF, 

Cagle TG, Whipp BJ. Changes in gas exchange 

kinetics with training in patients with spinal cord 

injury. Med Sci Sports Exerc 1996;28(10):1221-8. 

No relevant outcomes 

30. Barstow TJ, Scremin AM, Mutton DL, Kunkel CF, 

Cagle TG, Whipp BJ. Peak and kinetic 

cardiorespiratory responses during arm and leg 

exercise in patients with spinal cord injury. Spinal 

Cord 2000;38(6):340-5. No relevant outcomes 

31. Bauman WA, Adkins RH, Spungen AM, Waters RL, 

Kemp B, Herbert V. Levels of plasma homocysteine 

in persons with spinal cord injury. J Spinal Cord Med 

2001 Summer;24(2):81-6. Not eligible outcomes 

32. Bauman WA, Raza M, Chayes Z, Machac J. 

Tomographic thallium-201 myocardial perfusion 

imaging after intravenous dipyridamole in 

asymptomatic subjects with quadriplegia. Archives of 

physical medicine and rehabilitation 1993;74(7):740-

4. Case-series 

33. Bauman WA, Raza M, Spungen AM, Machac J. 

Cardiac stress testing with thallium-201 imaging 

reveals silent ischemia in individuals with paraplegia. 

Archives of Physical Medicine & Rehabilitation 

1994;75(9):946-50. Less than 100 patients in study 

34. Bauman WA, Spungen AM. Metabolic changes in 

persons after spinal cord injury. Physical Medicine & 

Rehabilitation Clinics of North America 

2000;11(1):109-40. Review 

35. Bauman WA, Spungen AM, Adkins RH, Kemp BJ. 

Metabolic and endocrine changes in persons aging 

with spinal cord injury. Assistive Technology 

1999;11(2):88-96. Review 

36. Bauman WA, Spungen AM, Raza M, Rothstein J, 

Zhang RL, Zhong YG, et al. Coronary artery disease: 

metabolic risk factors and latent disease in 

individuals with paraplegia. Mount Sinai Journal of 

Medicine 1992;59(2):163-8. Less than 100 patients in 

study 

37. Bauman WA, Spungen AM, Zhong YG, Mobbs CV. 

Plasma leptin is directly related to body adiposity in 

subjects with spinal cord injury. Hormone & 

Metabolic Research 1996;28(12):732-6. Less than 

100 patients in study 

38. Beaujeux R, Dietemann JL, Allal R, Wolfram-Gabel 

R. Posterior epidural adipose tissue and the narrow 

lumbar canal: replacement tissue or cause of 

impingement? Journal of Neuroradiology 

1995;22(2):63-70. Not english language 

39. Beck LA. Morbid obesity and spinal cord injury: a 

case study. Sci Nursing 1998;15(1):3-5. Less than 

100 patients in study 

40. Beck LA, Lovlien CA, Twedell DM. Care of 

morbidly obese people with spinal cord injury. 

[Review] [24 refs]. Journal of Trauma Nursing 

1996;3(4):98-107; quiz 8-9. No relevant data 

41. Bednar MM, Gross CE, Howard DB, Lynn M. 

Neutrophil activation in acute human central nervous 

system injury. Neurol Res 1997 Dec;19(6):588-92. 

Not eligible target population 

42. Beekman CE, Miller-Porter L, Schoneberger M. 

Energy cost of propulsion in standard and ultralight 

wheelchairs in people with spinal cord injuries. Phys 

Ther 1999;79(2):146-58. No relevant outcomes 

43. Begley S. IV. Genes, cells, drugs. Cures for the 

future. Fountains of youth. Newsweek 

2001;138(11A):84-6. No relevant data 

44. Begley S, Glick D. Eying the fetal future. In the 

shadows, a controversial search for cures. Newsweek 

1998;132(24):54-5. No relevant data 

45. Berenson JR, Lichtenstein A, Porter L, Dimopoulos 

MA, Bordoni R, George S, et al. Efficacy of 

pamidronate in reducing skeletal events in patients 

with advanced multiple myeloma. Myeloma Aredia 

Study Group. N Engl J Med 1996 Feb 22;334(8):488-

93. Not eligible target population 

46. Beres-Jones JA, Harkema SJ. The human spinal cord 

interprets velocity-dependent afferent input during 

stepping. Brain 2004;127:2232-46. No relevant 

outcomes 

47. Bernard PL, Mercier J, Varray A, Prefaut C. 

Influence of lesion level on the cardioventilatory 

adaptations in paraplegic wheelchair athletes during 

muscular exercise. Spinal Cord 2000;38(1):16-25. No 

relevant outcomes 

48. Betz R, Boden B, Triolo R, Mesgarzadeh M, Gardner 

E, Fife R. Effects of functional electrical stimulation 

on the joints of adolescents with spinal cord injury. 

Paraplegia 1996;34(3):127-36. No relevant outcomes 

49. Bhambhani Y, Tuchak C, Burnham R, Jeon J, 

Maikala R. Quadriceps muscle deoxygenation during 

functional electrical stimulation in adults with spinal 

cord injury. Spinal Cord 2000;38(10):630-8. No 

relevant outcomes 

50. Bhardwaj A, Long DM, Ducker TB, Toung TJ. 

Neurologic deficits after cervical laminectomy in the 

prone position. Journal of Neurosurgical 

Anesthesiology 2001;13(4):314-9. Not adult spinal 

cord injury patients 

51. Biering-Sorensen F, Schroder AK, Wilhelmsen M, 

Lomberg B, Nielsen H, Hoiby N. Bacterial 

contamination of bath-water from spinal cord 

lesioned patients with pressure ulcers exercising in 

the water. Spinal Cord 2000;38(2):100-5. No relevant 

outcomes 
D-3 

52. Biering-Sorensen M, Norup PW, Jacobsen E, 

Biering-Sorensen F. Treatment of sleep apnoea in 

spinal cord injured patients. Paraplegia 

1995;33(5):271-3. No relevant data 

53. Biesek D, Ksiazkiewicz B, Wanat-Slupska E. Conus 

medullaris and cauda equina infarct in the course of 

thrombosis of deep veins of lower extremities. Polski 

Merkuriusz Lekarski 2004;17(99):273-4. Not english 

language 

54. Bizzarini E, Saccavini M, Lipanje F, Magrin P, 

Malisan C, Zampa A. Exercise prescription in 

subjects with spinal cord injuries. Arch Phys Med 

Rehabil 2005;86(6):1170-5. No relevant outcomes 

55. Bjerkefors A, Jansson A, Thorstensson A. Shoulder 

muscle strength in paraplegics before and after kayak 

ergometer training. Eur J Appl Physiol 

2006;97(5):613-8. No relevant outcomes 

56. Bjerkefors A, Thorstensson A. Effects of kayak 

ergometer training on motor performance in 

paraplegics. Int J Sports Med 2006;27(10):824-9. No 

relevant outcomes 

57. Blackmer J, Marshall S. Obesity and spinal cord 

injury: an observational study. Spinal Cord 

1997;35(4):245-7. Less than 100 patients in study 

58. Blankenship LD, Strommen JA. 27-year-old man 

with a swollen leg. Mayo Clin Proc 2000;75(9):977-

80. No relevant outcomes 

59. Bloomfield SA, Mysiw WJ, Jackson RD. Bone mass 

and endocrine adaptations to training in spinal cord 

injured individuals. Bone 1996;19(1):61-8. No 

relevant outcomes 

60. Bode RK, Heinemann AW. Course of functional 

improvement after stroke, spinal cord injury, and 

traumatic brain injury. Arch Phys Med Rehabil 2002 

Jan;83(1):100-6. Not eligible target population 

61. Bodley R, Jamous A, Short D. Ultrasound in the 

early diagnosis of heterotopic ossification in patients 

with spinal injuries. Paraplegia 1993 Aug;31(8):500-

6. Not eligible outcomes 

62. Boot CR, Binkhorst RA, Hopman MT. Body 

temperature responses in spinal cord injured 

individuals during exercise in the cold and heat. Int J 

Sports Med 2006;27(8):599-604. No relevant 

outcomes 

63. Bostom AG, Toner MM, McArdle WD, Montelione 

T, Brown CD, Stein RA. Lipid and lipoprotein 

profiles relate to peak aerobic power in spinal cord 

injured men. Medicine & Science in Sports & 

Exercise 1991;23(4):409-14. Less than 100 patients 

in study 

64. Boudaoud L, Roussi J, Lortat-Jacob S, Bussel B, 

Dizien O, Drouet L. Endothelial fibrinolytic 

reactivity and the risk of deep venous thrombosis 

after spinal cord injury. Spinal Cord 1997 

Mar;35(3):151-7. Not eligible outcomes 

65. Bougenot MP, Tordi N, Betik AC, Martin X, Le Foll 

D, Parratte B, et al. Effects of a wheelchair ergometer 

training programme on spinal cord-injured persons. 

Spinal Cord 2003;41(8):451-6. No relevant outcomes 

66. Bowsher D. Central pain: clinical and physiological 

characteristics. J Neurol Neurosurg Psychiatry 1996 

Jul;61(1):62-9. Not eligible target population 

67. Brandt RA. Chronic spinal subdural haematoma. 

Surgical Neurology 1980;13(2):121-3. Not adult 

spinal cord injury patients 

68. Brenes G, Dearwater S, Shapera R, LaPorte RE, 

Collins E. High density lipoprotein cholesterol 

concentrations in physically active and sedentary 

spinal cord injured patients. Archives of Physical 

Medicine & Rehabilitation 1986;67(7):445-50. No 

relevant data 

69. Britt LD, Zolfaghari D, Kennedy E, Pagel KJ, 

Minghini A. Incidence and prophylaxis of deep vein 

thrombosis in a high risk trauma population. Am J 

Surg 1996 Jul;172(1):13-4. Not eligible target 

population 

70. Brock MV, Redmond JM, Ishiwa S, Johnston MV, 

Baumgartner WA, Laschinger JC, et al. Clinical 

markers in CSF for determining neurologic deficits 

after thoracoabdominal aortic aneurysm repairs. Ann 

Thorac Surg 1997 Oct;64(4):999-1003. Not eligible 

target population 

71. Bronner G. Female sexual function and chronic 

disease. Harefuah 2006;145(2):114-6. Not english 

language 

72. Buchholz AC, Bugaresti JM. A review of body mass 

index and waist circumference as markers of obesity 

and coronary heart disease risk in persons with 

chronic spinal cord injury. Spinal Cord 

2005;43(9):513-8. Review 

73. Buchholz AC, McGillivray CF, Pencharz PB. 

Physical activity levels are low in free-living adults 

with chronic paraplegia. Obes Res 2003;11(4):563-

70. No relevant outcomes 

74. Buchholz AC, Pencharz PB. Energy expenditure in 

chronic spinal cord injury. Current Opinion in 

Clinical Nutrition & Metabolic Care 2004;7(6):635-

9. Review 

75. Burns SP, Kapur V, Yin KS, Buhrer R. Factors 

associated with sleep apnea in men with spinal cord 

injury: a population-based case-control study. Spinal 

Cord 2001;39(1):15-22. No relevant data 

76. Burns SP, Nelson AL, Bosshart HT, Goetz LL, 

Harrow JJ, Gerhart KD, et al. Implementation of 

clinical practice guidelines for prevention of 

thromboembolism in spinal cord injury. J Spinal 

Cord Med 2005;28(1):33-42. Not eligible outcomes 

77. Burstein R, Zeilig G, Royburt M, Epstein Y, Ohry A. 

Insulin resistance in paraplegics--effect of one bout 

of acute exercise. International Journal of Sports 

Medicine 1996;17(4):272-6. Less than 100 patients in 

study 

78. Buss A, Brook GA, Kakulas B, Martin D, Franzen R, 

Schoenen J, et al. Gradual loss of myelin and 

formation of an astrocytic scar during Wallerian 

degeneration in the human spinal cord. Brain 2004 

Jan;127(Pt 1):34-44. Not eligible target population 

79. Buss A, Pech K, Merkler D, Kakulas BA, Martin D, 

Schoenen J, et al. Sequential loss of myelin proteins 

during Wallerian degeneration in the human spinal 

cord. Brain 2005 Feb;128(Pt 2):356-64. Not eligible 

target population 
D-4 

80. Butler JE, Ribot-Ciscar E, Zijdewind I, Thomas CK. 

Increased blood pressure can reduce fatigue of thenar 

muscles paralyzed after spinal cord injury. Muscle 

Nerve 2004;29(4):575-84. No relevant outcomes 

81. Cambria RP, Davison JK, Zannetti S, L'Italien G, 

Atamian S. Thoracoabdominal aneurysm repair: 

perspectives over a decade with the clamp-and-sew 

technique. Ann Surg 1997 Sep;226(3):294-303; 

discussion -5. Not eligible target population 

82. Cameron T, Broton JG, Needham-Shropshire B, 

Klose KJ. An upper body exercise system 

incorporating resistive exercise and neuromuscular 

electrical stimulation (NMS). J Spinal Cord Med 

1998;21(1):1-6. No relevant outcomes 

83. Canto M, Casas A, Sanchez MJ, Lorenzo A, Bataller 

L. Thoracic epidurals in heart valve surgery: 

neurologic risk evaluation. J Cardiothorac Vasc 

Anesth 2002 Dec;16(6):723-6. Not eligible target 

population 

84. Capodaglio P, Bazzini G. Predicting endurance limits 

in arm cranking exercise with a subjectively based 

method. Ergonomics 1996;39(7):924-32. No relevant 

outcomes 

85. Cardol M, de Jong BA, van den Bos GA, Beelem A, 

de Groot IJ, de Haan RJ. Beyond disability: 

perceived participation in people with a chronic 

disabling condition. Clin Rehabil 2002 Feb;16(1):27-

35. Not eligible outcomes 

86. Carhart MR, He J, Herman R, D'Luzansky S, Willis 

WT. Epidural spinal-cord stimulation facilitates 

recovery of functional walking following incomplete 

spinal-cord injury. IEEE Trans Neural Syst Rehabil 

Eng 2004;12(1):32-42. No relevant outcomes 

87. Cariga P, Ahmed S, Mathias CJ, Gardner BP. The 

prevalence and association of neck (coat-hanger) pain 

and orthostatic (postural) hypotension in human 

spinal cord injury. Spinal Cord 2002;40(2):77-82. No 

relevant outcomes 

88. Carlson AP, Yonas HM, Turner PT. Disorders of 

tumoral calcification of the spine: illustrative case 

study and review of the literature. Journal of Spinal 

Disorders & Techniques 2007;20(1):97-103. Not 

adult spinal cord injury patients 

89. Carvalho DC, de Cassia Zanchetta M, Sereni JM, 

Cliquet A. Metabolic and cardiorespiratory responses 

of tetraplegic subjects during treadmill walking using 

neuromuscular electrical stimulation and partial body 

weight support. Spinal Cord 2005;43(7):400-5. No 

relevant outcomes 

90. Carver RT, Boysel LC, Marciniak CM, Nussbaum 

SB. Myotonic dystrophy presenting as new-onset 

hand weakness and recurrent pneumonia in a patient 

with paraplegia: a case report. Archives of Physical 

Medicine & Rehabilitation 2004;85(11):1896-8. Less 

than 100 patients in study 

91. Catz A, Thaleisnik M, Fishel B, Ronen J, Spasser R, 

Fredman B, et al. Survival following spinal cord 

injury in Israel. Spinal Cord 2002 Nov;40(11):595-8. 

Not eligible outcomes 

92. Chalmers D, Morrison L. Epidemiology of nonsubmersion injuries in aquatic sporting and 

recreational activities. [Review] [114 refs]. Sports 

Medicine 2003;33(10):745-70. Not adult spinal cord 

injury patients 

93. Chao CY, Cheing GL. The effects of lower-extremity 

functional electric stimulation on the orthostatic 

responses of people with tetraplegia. Arch Phys Med 

Rehabil 2005 Jul;86(7):1427-33. Not eligible target 

population 

94. Chen CJ, Fang W, Chen CM, Wan YL. Spontaneous 

spinal epidural haematomas with repeated remission 

and relapse. Neuroradiology 1997 Oct;39(10):737-

40. Case report 

95. Chen CJ, Hsu WC. Imaging findings of spontaneous 

spinal epidural hematoma. J Formos Med Assoc 1997 

Apr;96(4):283-7. Not eligible target population 

96. Chen JT, Chen CC, Kao KP, Wu ZA, Liao KK. 

Conditioning effect on the long latency potentials in 

the lower limb to transcranial magnetic stimulation. 

Acta Neurol Scand 1998 Dec;98(6):412-21. Not 

eligible outcomes 

97. Chen SC, Lai CH, Chan WP, Huang MH, Tsai HW, 

Chen JJ. Increases in bone mineral density after 

functional electrical stimulation cycling exercises in 

spinal cord injured patients. Disabil Rehabil 

2005;27(22):1337-41. No relevant outcomes 

98. Chen Y, Devivo MJ, Jackson AB. Pressure ulcer 

prevalence in people with spinal cord injury: ageperiod-duration effects. Arch Phys Med Rehabil 2005 

Jun;86(6):1208-13. Not eligible outcomes 

99. Chen Y, Henson S, Jackson AB, Richards JS. 

Obesity intervention in persons with spinal cord 

injury. Spinal Cord 2006;44(2):82-91. Less than 100 

patients in study 

100. Chilibeck PD, Jeon J, Weiss C, Bell G, Burnham R. 

Histochemical changes in muscle of individuals with 

spinal cord injury following functional electrical 

stimulated exercise training. Spinal Cord 

1999;37(4):264-8. No relevant outcomes 

101. Chiou-Tan FY, Garza H, Chan KT, Parsons KC, 

Donovan WH, Robertson CS, et al. Comparison of 

dalteparin and enoxaparin for deep venous 

thrombosis prophylaxis in patients with spinal cord 

injury. Am J Phys Med Rehabil 2003 Sep;82(9):678-

85. Not eligible target population 

102. Chistyakov AV, Soustiel JF, Hafner H, Kaplan B, 

Feinsod M. The value of motor and somatosensory 

evoked potentials in evaluation of cervical 

myelopathy in the presence of peripheral neuropathy. 

Spine 2004;29(12):E239-47. Not adult spinal cord 

injury patients 

103. Chuang TY, Robinson LR, Nelson MR, Moss F, 

Chiou-Tan FY. Effect of isometric contraction on 

threshold somatosensory evoked potentials. Am J 

Phys Med Rehabil 1999;78(1):2-6. Not adult chronic 

SCI patients 

104. Cikajlo I, Matjacic Z, Bajd T. Development of a gait 

re-education system in incomplete spinal cord injury. 

J Rehabil Med 2003;35(5):213-6. No relevant 

outcomes 
D-5 

105. Claydon VE, Elliott SL, Sheel AW, Krassioukov A. 

Cardiovascular responses to vibrostimulation for 

sperm retrieval in men with spinal cord injury. J 

Spinal Cord Med 2006;29(3):207-16. Case-series 

106. Claydon VE, Hol AT, Eng JJ, Krassioukov AV. 

Cardiovascular responses and postexercise 

hypotension after arm cycling exercise in subjects 

with spinal cord injury. Arch Phys Med Rehabil 

2006;87(8):1106-14. No relevant outcomes 

107. Claydon VE, Krassioukov AV. Orthostatic 

hypotension and autonomic pathways after spinal 

cord injury. J Neurotrauma 2006 Dec;23(12):1713-

25. Not eligible outcomes 

108. Clinchot DM, Colachis SC, 3rd. An unusual cause of 

traumatic spinal cord injury: case report. Spinal Cord 

1997;35(3):181-2. Not adult chronic SCI patients 

109. Cohen AT. Venous thromboembolic disease 

management of the nonsurgical moderate- and highrisk patient. Seminars in Hematology 2000;37(3 

Suppl 5):19-22. Not adult spinal cord injury patients 

110. Colachis SC, 3rd, Clinchot DM. The association 

between deep venous thrombosis and heterotopic 

ossification in patients with acute traumatic spinal 

cord injury. Paraplegia 1993 Aug;31(8):507-12. Not 

eligible target population 

111. Colgan R, Nicolle LE, McGlone A, Hooton TM. 

Asymptomatic bacteriuria in adults. American 

Family Physician 2006;74(6):985-90. Not adult 

spinal cord injury patients 

112. Collins HL, Rodenbaugh DW, DiCarlo SE. Spinal 

cord injury alters cardiac electrophysiology and 

increases the susceptibility to ventricular 

arrhythmias. Progress in Brain Research 

2006;152:275-88. No relevant data 

113. Conrad MF, Crawford RS, Davison JK, Cambria RP. 

Thoracoabdominal aneurysm repair: a 20-year 

perspective. Ann Thorac Surg 2007 Feb;83(2):S856-

61; discussion S90-2. Not eligible target population 

114. Cooper RA, Baldini FD, Boninger ML, Cooper R. 

Physiological responses to two wheelchair-racing 

exercise protocols. Neurorehabil Neural Repair 

2001;15(3):191-5. No relevant outcomes 

115. Corfman TA, Cooper RA, Boninger ML, Koontz 

AM, Fitzgerald SG. Range of motion and stroke 

frequency differences between manual wheelchair 

propulsion and pushrim-activated power-assisted 

wheelchair propulsion. J Spinal Cord Med 

2003;26(2):135-40. No relevant outcomes 

116. Cosman BC, Eastman DA, Perkash I, Stone JM. 

Hemorrhoidal bleeding in chronic spinal cord injury: 

results of multiple banding. Int J Colorectal Dis 

1994;9(4):174-6. Not eligible outcomes 

117. Cosman BC, Vu TT. Lidocaine anal block limits 

autonomic dysreflexia during anorectal procedures in 

spinal cord injury: a randomized, double-blind, 

placebo-controlled trial. Dis Colon Rectum 2005 

Aug;48(8):1556-61. Not eligible outcomes 

118. Courtois F, Geoffrion R, Landry E, Belanger M. Hreflex and physiologic measures of ejaculation in 

men with spinal cord injury. Arch Phys Med Rehabil 

2004 Jun;85(6):910-8. Case-series 

119. Croxford JL. Therapeutic potential of cannabinoids in 

CNS disease. [Review] [219 refs]. CNS Drugs 

2003;17(3):179-202. Not adult spinal cord injury 

patients 

120. Cruse JM, Lewis RE, Jr., Bishop GR, Kliesch WF, 

Gaitan E, Britt R. Decreased immune reactivity and 

neuroendocrine alterations related to chronic stress in 

spinal cord injury and stroke patients. Pathobiology 

1993;61(3-4):183-92. Not eligible target population 

121. Curtis KA, McClanahan S, Hall KM, Dillon D, 

Brown KF. Health, vocational, and functional status 

in spinal cord injured athletes and nonathletes. 

Archives of Physical Medicine & Rehabilitation 

1986;67(12):862-5. Less than 100 patients in study 

122. Curtis KA, Tyner TM, Zachary L, Lentell G, Brink 

D, Didyk T, et al. Effect of a standard exercise 

protocol on shoulder pain in long-term wheelchair 

users. Spinal Cord 1999;37(6):421-9. No relevant 

outcomes 

123. Dallmeijer AJ, Hopman MT, van As HH, van der 

Woude LH. Physical capacity and physical strain in 

persons with tetraplegia; the role of sport activity. 

Spinal Cord 1996;34(12):729-35. No relevant 

outcomes 

124. Dallmeijer AJ, van der Woude LH, Hollander AP, 

van As HH. Physical performance during 

rehabilitation in persons with spinal cord injuries. 

Med Sci Sports Exerc 1999;31(9):1330-5. No 

relevant outcomes 

125. Dallmeijer AJ, van der Woude LH, Hollander PA, 

Angenot EL. Physical performance in persons with 

spinal cord injuries after discharge from 

rehabilitation. Med Sci Sports Exerc 

1999;31(8):1111-7. No relevant outcomes 

126. Dallmeijer AJ, Zentgraaff ID, Zijp NI, van der 

Woude LH. Submaximal physical strain and peak 

performance in handcycling versus handrim 

wheelchair propulsion. Spinal Cord 2004;42(2):91-8. 

No relevant outcomes 

127. Daniel WW, Coogler CE. Statistical applications in 

physical medicine. part II. American Journal of 

Physical Medicine 1975;54(1):25-47. No relevant 

data 

128. Davis R, Patrick J, Barriskill A. Development of 

functional electrical stimulators utilizing cochlear 

implant technology. Med Eng Phys 2001;23(1):61-8. 

No exercise program or physical activity 

129. Davoodi R, Andrews BJ, Wheeler GD, Lederer R. 

Development of an indoor rowing machine with 

manual FES controller for total body exercise in 

paraplegia. IEEE Trans Neural Syst Rehabil Eng 

2002;10(3):197-203. No relevant outcomes 

130. de Carvalho DC, Cliquet A, Jr. Energy expenditure 

during rest and treadmill gait training in quadriplegic 

subjects. Spinal Cord 2005;43(11):658-63. No 

relevant outcomes 

131. de Groot PC, Poelkens F, Kooijman M, Hopman MT. 

Preserved flow-mediated dilation in the inactive legs 

of spinal cord-injured individuals. Am J Physiol 

Heart Circ Physiol 2004 Jul;287(1):H374-80. Not 

eligible outcomes 
D-6 

132. de Groot S, Dallmeijer AJ, Kilkens OJ, van Asbeck 

FW, Nene AV, Angenot EL, et al. Course of gross 

mechanical efficiency in handrim wheelchair 

propulsion during rehabilitation of people with spinal 

cord injury: a prospective cohort study. Arch Phys 

Med Rehabil 2005;86(7):1452-60. No relevant 

outcomes 

133. De Mello MT, Esteves AM, Tufik S. Comparison 

between dopaminergic agents and physical exercise 

as treatment for periodic limb movements in patients 

with spinal cord injury. Spinal Cord 2004;42(4):218-

21. No relevant outcomes 

134. de Mello MT, Lauro FA, Silva AC, Tufik S. 

Incidence of periodic leg movements and of the 

restless legs syndrome during sleep following acute 

physical activity in spinal cord injury subjects. Spinal 

Cord 1996;34(5):294-6. No relevant outcomes 

135. De Mello MT, Silva AC, Esteves AM, Tufik S. 

Reduction of periodic leg movement in individuals 

with paraplegia following aerobic physical exercise. 

Spinal Cord 2002;40(12):646-9. No relevant 

outcomes 

136. de Seze J, Delalande S, Fauchais AL, Hachulla E, 

Stojkovic T, Ferriby D, et al. Myelopathies secondary 

to Sjogren's syndrome: treatment with monthly 

intravenous cyclophosphamide associated with 

corticosteroids. J Rheumatol 2006;33(4):709-11. Not 

adult chronic SCI patients 

137. Dela F, Stallknecht B, Biering-Sorensen F. An intact 

central nervous system is not necessary for insulinmediated increases in leg blood flow in humans. 

Pflugers Archiv - European Journal of Physiology 

2000;441(2-3):241-50. Less than 100 patients in 

study 

138. Demirel S, Demirel G, Tukek T, Erk O, Yilmaz H. 

Risk factors for coronary heart disease in patients 

with spinal cord injury in Turkey. Spinal Cord 2001 

Mar;39(3):134-8. Not eligible outcomes 

139. DeVivo MJ, Rutt RD, Black KJ, Go BK, Stover SL. 

Trends in spinal cord injury demographics and 

treatment outcomes between 1973 and 1986. Arch 

Phys Med Rehabil 1992 May;73(5):424-30. Nto 

eligible outcomes 

140. DeVivo MJ, Shewchuk RM, Stover SL, Black KJ, 

Go BK. A cross-sectional study of the relationship 

between age and current health status for persons 

with spinal cord injuries. Paraplegia 1992 

Dec;30(12):820-7. Not eligible outcomes 

141. DeVivo MJ, Stover SL, Black KJ. Prognostic factors 

for 12-year survival after spinal cord injury. Arch 

Phys Med Rehabil 1992 Feb;73(2):156-62. Not 

eligible outcomes 

142. Diego MA, Field T, Hernandez-Reif M, Hart S, 

Brucker B, Field T, et al. Spinal cord patients benefit 

from massage therapy. Int J Neurosci 

2002;112(2):133-42. No relevant outcomes 

143. Dietz V, Colombo G, Muller R. Single joint 

perturbation during gait: neuronal control of 

movement trajectory. Exp Brain Res 

2004;158(3):308-16. Not adult chronic SCI patients 

144. Dihlmann SW, Mayer HM. Lumbar epidural 

lipomatosis. Zeitschrift fur Rheumatologie 

1995;54(6):417-23. Not english language 

145. Dimond B. Mental capacity requirements and a 

patient's right to die. Br J Nurs 2006 Nov 9-

22;15(20):1130-1. Legal Cases 

146. Dishman RK, Berthoud HR, Booth FW, Cotman CW, 

Edgerton VR, Fleshner MR, et al. Neurobiology of 

exercise. Obesity 2006;14(3):345-56. Not adult 

spinal cord injury patients 

147. Ditor DS, Kamath MV, MacDonald MJ, Bugaresti J, 

McCartney N, Hicks AL. Effects of body weightsupported treadmill training on heart rate variability 

and blood pressure variability in individuals with 

spinal cord injury. J Appl Physiol 2005;98(4):1519-

25. No relevant outcomes 

148. Ditor DS, Latimer AE, Ginis KA, Arbour KP, 

McCartney N, Hicks AL. Maintenance of exercise 

participation in individuals with spinal cord injury: 

effects on quality of life, stress and pain. Spinal Cord 

2003;41(8):446-50. No relevant outcomes 

149. Ditor DS, Macdonald MJ, Kamath MV, Bugaresti J, 

Adams M, McCartney N, et al. The effects of bodyweight supported treadmill training on cardiovascular 

regulation in individuals with motor-complete SCI. 

Spinal Cord 2005;43(11):664-73. No relevant 

outcomes 

150. Do Ouro S, Esteban S, Sibirceva U, Whittenberg B, 

Portenoy R, Cruciani RA. Safety and tolerability of 

high doses of intrathecal fentanyl for the treatment of 

chronic pain. Journal of Opioid Management 

2006;2(6):365-8. Less than 100 patients in study 

151. Dobkin B, Apple D, Barbeau H, Basso M, Behrman 

A, Deforge D, et al. Weight-supported treadmill vs 

over-ground training for walking after acute 

incomplete SCI. Neurology 2006;66(4):484-93. No 

relevant outcomes 

152. Doita M, Sakai H, Harada T, Nishida K, Miyamoto 

H, Kaneko T, et al. Evaluation of impairment of hand 

function in patients with cervical myelopathy. J 

Spinal Disord Tech 2006;19(4):276-80. Not adult 

chronic SCI patients 

153. Donato V, Bonfili P, Bulzonetti N, Santarelli M, Osti 

MF, Tombolini V, et al. Radiation therapy for 

oncological emergencies. Anticancer Res 2001 MayJun;21(3C):2219-24. Not eligible target population 

154. Douglas H, Swanson C, Gee T, Bellamy N. Outcome 

measurement in Australian rehabilitation 

environments. J Rehabil Med 2005 Sep;37(5):325-9. 

Not eligible target population 

155. Dubras P. Predictors of physical activity among 

individuals with spinal cord injuries. Ottawa: 

National Library of Canada = BibliothÃ ̈que 

nationale du Canada; 2002. 

156. Ducker TB. C6 cervical radiculopathy and 

assymptomatic large C3/4 central disc herniation. 

Journal of Spinal Disorders 1994;7(4):361-2; 

discussion 2-4. Not adult spinal cord injury patients 

157. Duckworth WC, Jallepalli P, Solomon SS. Glucose 

intolerance in spinal cord injury. Archives of 

Physical Medicine & Rehabilitation 1983;64(3):107-

10. Less than 100 patients in study 
D-7 

158. Duckworth WC, Solomon SS, Jallepalli P, 

Heckemeyer C, Finnern J, Powers A. Glucose 

intolerance due to insulin resistance in patients with 

spinal cord injuries. Diabetes 1980;29(11):906-10. 

Less than 100 patients in study 

159. Dudgeon BJ, Tyler EJ, Rhodes LA, Jensen MP. 

Managing usual and unexpected pain with physical 

disability: a qualitative analysis. Am J Occup Ther 

2006;60(1):92-103. No exercise program or physical 

activity 

160. Dudra J, Shiiya N, Matsui Y, Sakuma M, Ishii K, 

Asada M, et al. Operative results of 

thoracoabdominal repair for chronic type B aortic 

dissection. J Cardiovasc Surg (Torino) 1997 

Apr;38(2):147-51. Not eligible target population 

161. Dujardin L, Marcelli C, Herisson C, Simon L. 

Epidural lipomatosis: complication of long-term 

corticotherapy. Apropos of 2 cases. Revue de 

Medecine Interne 1996;17(7):563-7. Not english 

language 

162. Edwards CC, 2nd, Heller JG, Silcox DH, 3rd. T-Saw 

laminoplasty for the management of cervical 

spondylotic myelopathy: clinical and radiographic 

outcome. Spine 2000;25(14):1788-94. Not adult 

chronic SCI patients 

163. Effing TW, van Meeteren NL, van Asbeck FW, Prevo 

AJ. Body weight-supported treadmill training in 

chronic incomplete spinal cord injury: a pilot study 

evaluating functional health status and quality of life. 

Spinal Cord 2006;44(5):287-96. No relevant outcomes 

164. Elder CP, Apple DF, Bickel CS, Meyer RA, Dudley 

GA. Intramuscular fat and glucose tolerance after 

spinal cord injury--a cross-sectional study. Spinal 

Cord 2004;42(12):711-6. Less than 100 patients in 

study 

165. Elokda AS, Nielsen DH, Shields RK. Effect of 

functional neuromuscular stimulation on postural 

related orthostatic stress in individuals with acute 

spinal cord injury. J Rehabil Res Dev 2000 SepOct;37(5):535-42. Not eligible target population 

166. El-Sayed MS, Younesian A. Lipid profiles are 

influenced by arm cranking exercise and training in 

individuals with spinal cord injury. Spinal Cord 

2005;43(5):299-305. Less than 100 patients in study 

167. El-Sayed MS, Younesian A, Rahman K, Ismail FM, 

El-Sayed A. The effects of arm cranking exercise and 

training on platelet aggregation in male spinal cord 

individuals. Thromb Res 2004;113(2):129-36. No 

relevant outcomes 

168. El-Zaatari MM, Hulten K, Fares Y, Baassiri A, 

Balkis M, Almashhrawi A, et al. Successful treatment 

of Candida albicans osteomyelitis of the spine with 

fluconazole and surgical debridement: case report. 

Journal of Chemotherapy 2002;14(6):627-30. Not 

adult spinal cord injury patients 

169. Epstein N. Thoracic ossification of the posterior 

longitudinal ligament, ossification of the yellow 

ligament from T9-T12 with superimposed acute 

T10/T11 disc herniation: controversies in surgical 

management. Journal of Spinal Disorders 

1996;9(5):446-7; discussion 7-50. Not adult spinal 

cord injury patients 

170. Epstein SK, Singh N. Respiratory acidosis. 

Respiratory Care 2001;46(4):366-83. Not adult spinal 

cord injury patients 

171. Eser PC, Donaldson Nde N, Knecht H, Stussi E. 

Influence of different stimulation frequencies on 

power output and fatigue during FES-cycling in 

recently injured SCI people. IEEE Trans Neural Syst 

Rehabil Eng 2003;11(3):236-40. No relevant 

outcomes 

172. Esmail Z, Shalansky KF, Sunderji R, Anton H, 

Chambers K, Fish W. Evaluation of captopril for the 

management of hypertension in autonomic 

dysreflexia: a pilot study. Arch Phys Med Rehabil 

2002 May;83(5):604-8. Not eligible outcomes 

173. Excoffon SG, Wallace H. Chiropractic and 

rehabilitative management of a patient with 

progressive lumbar disk injury, spondylolisthesis, and 

spondyloptosis. J Manipulative Physiol Ther 

2006;29(1):66-71. Not adult chronic SCI patients 

174. Faghri PD, Yount J. Electrically induced and 

voluntary activation of physiologic muscle pump: a 

comparison between spinal cord-injured and ablebodied individuals. Clin Rehabil 2002 

Dec;16(8):878-85. Not eligible outcomes 

175. Faghri PD, Yount JP, Pesce WJ, Seetharama S, Votto 

JJ. Circulatory hypokinesis and functional electric 

stimulation during standing in persons with spinal 

cord injury. Arch Phys Med Rehabil 2001 

Nov;82(11):1587-95. Not eligible outcomes 

176. Faist M, Ertel M, Berger W, Dietz V. Impaired 

modulation of quadriceps tendon jerk reflex during 

spastic gait: differences between spinal and cerebral 

lesions. Brain 1999 Mar;122 ( Pt 3):567-79. Not 

eligible outcomes 

177. Fedoroff JP, Lipsey JR, Starkstein SE, Forrester A, 

Price TR, Robinson RG. Phenomenological 

comparisons of major depression following stroke, 

myocardial infarction or spinal cord lesions. J Affect 

Disord 1991 May-Jun;22(1-2):83-9. Not eligible 

target population 

178. Felici F, Bernardi M, Radio A, Marchettoni P, 

Castellano V, Macaluso A. Rehabilitation of walking 

for paraplegic patients by means of a treadmill. 

Spinal Cord 1997;35(6):383-5. No relevant outcomes 

179. Fiedler RC, Granger CV. Uniform data system for 

medical rehabilitation: report of first admissions for 

1996. Am J Phys Med Rehabil 1998 JanFeb;77(1):69-75. Not eliglble target population 

180. Field-Fote EC. Combined use of body weight 

support, functional electric stimulation, and treadmill 

training to improve walking ability in individuals 

with chronic incomplete spinal cord injury. Arch 

Phys Med Rehabil 2001;82(6):818-24. No relevant 

outcomes 

181. Field-Fote EC, Tepavac D. Improved intralimb 

coordination in people with incomplete spinal cord 

injury following training with body weight support 

and electrical stimulation. Phys Ther 2002;82(7):707-

15. No relevant outcomes 
D-8 

182. Fitzgerald SG, Cooper RA, Thorman T, Cooper R, 

Guo S, Boninger ML. The GAME(Cycle) exercise 

system: comparison with standard ergometry. J 

Spinal Cord Med 2004;27(5):453-9. No relevant 

outcomes 

183. Fletcher DJ, Taddonio RF, Byrne DW, Wexler LM, 

Cayten CG, Nealon SM, et al. Incidence of acute care 

complications in vertebral column fracture patients 

with and without spinal cord injury. Spine 1995 May 

15;20(10):1136-46. Not eligible target population 

184. Flores J, Kunihara T, Shiiya N, Yoshimoto K, 

Matsuzaki K, Yasuda K. Extensive deployment of the 

stented elephant trunk is associated with an increased 

risk of spinal cord injury. J Thorac Cardiovasc Surg 

2006 Feb;131(2):336-42. Not eligible target 

population 

185. Flores J, Shiiya N, Kunihara T, Matsuzaki K, Yasuda 

K. Risk of spinal cord injury after operations of 

recurrent aneurysms of the descending aorta. Ann 

Thorac Surg 2005 Apr;79(4):1245-9; discussion 9. 

Not eligible target population 

186. Fogel GR, Cunningham PY, 3rd, Esses SI. Spinal 

epidural lipomatosis: case reports, literature review 

and meta-analysis. Spine Journal: Official Journal of 

the North American Spine Society 2005;5(2):202-11. 

Not adult spinal cord injury patients 

187. Fornusek C, Davis GM. Maximizing muscle force via 

low-cadence functional electrical stimulation cycling. 

J Rehabil Med 2004;36(5):232-7. No relevant 

outcomes 

188. Franco JC, Perell KL, Gregor RJ, Scremin AM. Knee 

kinetics during functional electrical stimulation 

induced cycling in subjects with spinal cord injury: a 

preliminary study. J Rehabil Res Dev 

1999;36(3):207-16. No relevant outcomes 

189. Franga DL, Hawkins ML, Medeiros RS, Adewumi D. 

Recurrent asystole resulting from high cervical spinal 

cord injuries. Am Surg 2006 Jun;72(6):525-9. Caseseries 

190. Frank E. Endoscopic suction decompression of 

idiopathic epidural lipomatosis. Surgical Neurology 

1998;50(4):333-5; discussion 5. Not adult spinal cord 

injury patients 

191. Freedman G, Entero H, Brem H. Practical treatment 

of pain in patients with chronic wounds: 

pathogenesis-guided management. American Journal 

of Surgery 2004;188(1A Suppl):31-5. Not adult 

spinal cord injury patients 

192. Frey GC, McCubbin JA, Dunn JM, Mazzeo RS. 

Plasma catecholamine and lactate relationship during 

graded exercise in men with spinal cord injury. Med 

Sci Sports Exerc 1997;29(4):451-6. No relevant 

outcomes 

193. Friedman D, Flanders A, Thomas C, Millar W. 

Vertebral artery injury after acute cervical spine 

trauma: rate of occurrence as detected by MR 

angiography and assessment of clinical 

consequences. AJR Am J Roentgenol 1995 

Feb;164(2):443-7; discussion 8-9. Not eligible target 

population 

194. Frisbie JH. Microvascular instability in tetraplegic 

patients: preliminary observations. Spinal Cord 2004 

May;42(5):290-3. Not eligible outcomes 

195. Frisbie JH. Fibrinogen metabolism in patients with 

spinal cord injury. J Spinal Cord Med 

2006;29(5):507-10. Not eligible outcomes 

196. Frisbie JH, Sharma GV. Circadian rhythm of 

pulmonary embolism in patients with acute spinal 

cord injury. Am J Cardiol 1992 Sep 15;70(7):827-8. 

Not eligible target population 

197. Frisbie JH, Sharma GV. Pulmonary embolism 

manifesting as acute disturbances of behavior in 

patients with spinal cord injury. Paraplegia 1994 

Aug;32(8):570-2. Not eligible target population 

198. Fujii Y, Mammen EF, Farag A, Muz J, Salciccioli 

GG, Weingarden ST. Thrombosis in spinal cord 

injury. Thromb Res 1992 Dec 1;68(4-5):357-68. 

Case-series 

199. Fukui MB, Swarnkar AS, Williams RL. Acute 

spontaneous spinal epidural hematomas. AJNR Am J 

Neuroradiol 1999 Aug;20(7):1365-72. Not eligible 

target population 

200. Fukuoka Y, Endo M, Kagawa H, Itoh M, Nakanishi 

R. Kinetics and steady-state of VO2 responses to arm 

exercise in trained spinal cord injury humans. Spinal 

Cord 2002;40(12):631-8. No relevant outcomes 

201. Fuller DA, Mark A, Keenan MA. Excision of 

heterotopic ossification from the knee: a functional 

outcome study. Clin Orthop Relat Res 2005 

Sep;438:197-203. Case report 

202. Galea M, Tumminia J, Garback LM. 

Telerehabilitation in spinal cord injury persons: a 

novel approach. Telemedicine Journal & E-Health 

2006;12(2):160-2. No relevant data 

203. Galla JD, Ergin MA, Lansman SL, McCullough JN, 

Nguyen KH, Spielvogel D, et al. Use of 

somatosensory evoked potentials for thoracic and 

thoracoabdominal aortic resections. Ann Thorac Surg 

1999 Jun;67(6):1947-52; discussion 53-8. Not 

eligible target population 

204. Gandevia SC, Petersen N, Butler JE, Taylor JL. 

Impaired response of human motoneurones to 

corticospinal stimulation after voluntary exercise. J 

Physiol 1999;521 Pt 3:749-59. Not adult chronic SCI 

patients 

205. Gao CG, Ge JP, Chen LS. The situation of sildenafil 

in the treatment of men with erectile dysfunction. 

Zhong Hua Nan Ke Xue 2002;8(4):302-4. Not 

english language 

206. Gardner MB, Holden MK, Leikauskas JM, Richard 

RL. Partial body weight support with treadmill 

locomotion to improve gait after incomplete spinal 

cord injury: a single-subject experimental design. 

Phys Ther 1998;78(4):361-74. No relevant outcomes 

207. Garland DE, Adkins RH, Stewart CA, Ashford R, 

Vigil D. Regional osteoporosis in women who have a 

complete spinal cord injury. J Bone Joint Surg Am 

2001 Aug;83-A(8):1195-200. Not eligible outcomes 

208. Gass EM, Gass GC. Thermoregulatory responses to 

repeated warm water immersion in subjects who are 

paraplegic. Spinal Cord 2001;39(3):149-55. No 

relevant outcomes 
D-9 

209. Gass EM, Gass GC, Pitetti K. Thermoregulatory 

responses to exercise and warm water immersion in 

physically trained men with tetraplegia. Spinal Cord 

2002;40(9):474-80. No relevant outcomes 

210. Gates PE, Campbell IG, George KP. Absence of 

training-specific cardiac adaptation in paraplegic 

athletes. Med Sci Sports Exerc 2002;34(11):1699-

704. No relevant outcomes 

211. Gazzani F, Bernardi M, Macaluso A, Coratella D, 

Ditunno JF, Jr., Castellano V, et al. Ambulation 

training of neurological patients on the treadmill with 

a new Walking Assistance and Rehabilitation Device 

(WARD). Spinal Cord 1999;37(5):336-44. No 

relevant outcomes 

212. Geist RA. Onset of chronic illness in children and 

adolescents: psychotherapeutic and consultative 

intervention. American Journal of Orthopsychiatry 

1979;49(1):4-23. Not adult spinal cord injury 

patients 

213. Gerrits HL, de Haan A, Sargeant AJ, Dallmeijer A, 

Hopman MT. Altered contractile properties of the 

quadriceps muscle in people with spinal cord injury 

following functional electrical stimulated cycle 

training. Spinal Cord 2000;38(4):214-23. No relevant 

outcomes 

214. Gerrits HL, de Haan A, Sargeant AJ, van Langen H, 

Hopman MT. Peripheral vascular changes after 

electrically stimulated cycle training in people with 

spinal cord injury. Arch Phys Med Rehabil 

2001;82(6):832-9. No relevant outcomes 

215. Gerrits HL, Hopman MT, Offringa C, Engelen BG, 

Sargeant AJ, Jones DA, et al. Variability in fibre 

properties in paralysed human quadriceps muscles 

and effects of training. Pflugers Arch 

2003;445(6):734-40. No relevant outcomes 

216. Gerrits HL, Hopman MT, Sargeant AJ, Jones DA, De 

Haan A. Effects of training on contractile properties 

of paralyzed quadriceps muscle. Muscle Nerve 

2002;25(4):559-67. No relevant outcomes 

217. Gfohler M, Lugner P. Dynamic simulation of FEScycling: influence of individual parameters. IEEE 

Trans Neural Syst Rehabil Eng 2004;12(4):398-405. 

No relevant outcomes 

218. Giangregorio LM, Hicks AL, Webber CE, Phillips 

SM, Craven BC, Bugaresti JM, et al. Body weight 

supported treadmill training in acute spinal cord 

injury: impact on muscle and bone. Spinal Cord 

2005;43(11):649-57. No relevant outcomes 

219. Giangregorio LM, Webber CE, Phillips SM, Hicks 

AL, Craven BC, Bugaresti JM, et al. Can body 

weight supported treadmill training increase bone 

mass and reverse muscle atrophy in individuals with 

chronic incomplete spinal cord injury? Appl Physiol 

Nutr Metab 2006;31(3):283-91. No relevant 

outcomes 

220. Gibberd FB. The neurogenic bladder. Clinics in 

Obstetrics & Gynaecology 1981;8(1):149-60. Not 

adult spinal cord injury patients 

221. Ginis KA, Latimer AE, Hicks AL, Craven BC. 

Development and evaluation of an activity measure 

for people with spinal cord injury. Med Sci Sports 

Exerc 2005;37(7):1099-111. No relevant outcomes 

222. Godin LM. Physical self-perceptions and physical 

activity participation of adult males with acquired 

spinal cord injuries [Dissertation/Thesis]; 2002. 

223. Golden MA, Donaldson MC, Whittemore AD, 

Mannick JA. Evolving experience with 

thoracoabdominal aortic aneurysm repair at a single 

institution. J Vasc Surg 1991 Jun;13(6):792-6; 

discussion 6-7. Not eligible target population 

224. Goldstein I, Kim E, Steers WD, Pryor JL, Wilde DW, 

Natanegara F, et al. Efficacy and safety of tadalafil in 

men with erectile dysfunction with a high prevalence 

of comorbid conditions: results from MOMENTUS: 

multiple observations in men with erectile 

dysfunction in National Tadalafil Study in the US. 

Journal of Sexual Medicine 2007;4(1):166-75. No 

relevant data 

225. Gonzalez F, Chang JY, Banovac K, Messina D, 

Martinez-Arizala A, Kelley RE. Autoregulation of 

cerebral blood flow in patients with orthostatic 

hypotension after spinal cord injury. Paraplegia 1991 

Jan;29(1):1-7. Not eligible outcomes 

226. Gordon IL, Kohl CA, Arefi M, Complin RA, Vulpe 

M. Spinal cord injury increases the risk of abdominal 

aortic aneurysm. Am Surg 1996 Mar;62(3):249-52. 

Not eligible outcomes 

227. Grange CC, Bougenot MP, Groslambert A, Tordi N, 

Rouillon JD. Perceived exertion and rehabilitation 

with wheelchair ergometer: comparison between 

patients with spinal cord injury and healthy subjects. 

Spinal Cord 2002;40(10):513-8. No relevant 

outcomes 

228. Grasso R, Ivanenko YP, Zago M, Molinari M, 

Scivoletto G, Castellano V, et al. Distributed 

plasticity of locomotor pattern generators in spinal 

cord injured patients. Brain 2004;127:1019-34. No 

relevant outcomes 

229. Grasso R, Ivanenko YP, Zago M, Molinari M, 

Scivoletto G, Lacquaniti F. Recovery of forward 

stepping in spinal cord injured patients does not 

transfer to untrained backward stepping. Exp Brain 

Res 2004;157(3):377-82. No relevant outcomes 

230. Greco S, Auriti A, Fiume D, Gazzeri G, Gentilucci 

G, Antonini L, et al. Spinal cord stimulation for the 

treatment of refractory angina pectoris: a two-year 

follow-up. Pacing Clin Electrophysiol 1999;22(1):26-

32. Not adult chronic SCI patients 

231. Green D, Chen D, Chmiel JS, Olsen NK, Berkowitz 

M, Novick A, et al. Prevention of thromboembolism 

in spinal cord injury: role of low molecular weight 

heparin. Arch Phys Med Rehabil 1994 

Mar;75(3):290-2. Not eligible target population 

232. Green D, Lee MY, Lim AC, Chmiel JS, Vetter M, 

Pang T, et al. Prevention of thromboembolism after 

spinal cord injury using low-molecular-weight 

heparin. Ann Intern Med 1990 Oct 15;113(8):571-4. 

Not eligible target population 

233. Green D, Twardowski P, Wei R, Rademaker AW. 

Fatal pulmonary embolism in spinal cord injury. 

Chest 1994 Mar;105(3):853-5. Not eligible target 

population 
D-10 

234. Greydanus DE, Demarest DS, Sears JM. Sexual 

dysfunction in adolescents. Seminars in Adolescent 

Medicine 1985;1(3):177-87. Not adult spinal cord 

injury patients 

235. Griepp RB, Ergin MA, Galla JD, Lansman S, Khan 

N, Quintana C, et al. Looking for the artery of 

Adamkiewicz: a quest to minimize paraplegia after 

operations for aneurysms of the descending thoracic 

and thoracoabdominal aorta. J Thorac Cardiovasc 

Surg 1996 Nov;112(5):1202-13; discussion 13-5. Not 

eligible target population 

236. Grigorenko A, Bjerkefors A, Rosdahl H, Hultling C, 

Alm M, Thorstensson A. Sitting balance and effects 

of kayak training in paraplegics. J Rehabil Med 

2004;36(3):110-6. No relevant outcomes 

237. Grimm DR, Almenoff PL, Bauman WA, De 

Meersman RE. Baroreceptor sensitivity response to 

phase IV of the Valsalva maneuver in spinal cord 

injury. Clin Auton Res 1998 Apr;8(2):111-8. Not 

eligible outcomes 

238. Grossman S. How can nurses use limit setting to 

facilitate spinal cord patients' independence? SCI 

Nurs 1997;14(3):105-7. No exercise program or 

physical activity 

239. Grote EH. The CNS control of glucose metabolism. 

Acta Neurochirurgica - Supplementum 1981;31:1-

160. Review 

240. Guihan M, Simmons B, Nelson A, Bosshart HT, 

Burns SP. Spinal cord injury providers' perceptions 

of barriers to implementing selected clinical practice 

guideline recommendations. J Spinal Cord Med 2003 

Spring;26(1):48-58. Not eligible target population 

241. Gunduz S, Ogur E, Mohur H, Somuncu I, Acjksoz E, 

Ustunsoz B. Deep vein thrombosis in spinal cord 

injured patients. Paraplegia 1993 Sep;31(9):606-10. 

Not eligible target population 

242. Gurney AB, Robergs RA, Aisenbrey J, Cordova JC, 

McClanahan L. Detraining from total body exercise 

ergometry in individuals with spinal cord injury. 

Spinal Cord 1998;36(11):782-9. No relevant 

outcomes 

243. Gutterman P. Acute spinal subdural hematoma 

following lumbar puncture. Surgical Neurology 

1977;7(6):355-6. Not adult spinal cord injury patients 

244. Hagerman F, Jacobs P, Backus D, Dudley GA. 

Exercise responses and adaptations in rowers and 

spinal cord injury individuals. Med Sci Sports Exerc 

2006;38(5):958-62. No relevant outcomes 

245. Hagisawa S, Ferguson-Pell M, Cardi M, Miller SD. 

Assessment of skin blood content and oxygenation in 

spinal cord injured subjects during reactive 

hyperemia. J Rehabil Res Dev 1994;31(1):1-14. Not 

eligible outcomes 

246. Hagobian TA, Jacobs KA, Kiratli BJ, Friedlander 

AL. Foot cooling reduces exercise-induced 

hyperthermia in men with spinal cord injury. Med Sci 

Sports Exerc 2004;36(3):411-7. No relevant 

outcomes 

247. Haldeman S, Bradley WE, Bhatia N. Evoked 

responses from the pudendal nerve. Journal of 

Urology 1982;128(5):974-80. Not adult spinal cord 

injury patients 

248. Haldi PA. Double trouble: diabetes and SCI. Sci 

Nursing 2003;20(2):106-8. Less than 100 patients in 

study 

249. Halliday SE, Zavatsky AB, Hase K. Can functional 

electric stimulation-assisted rowing reproduce a racewinning rowing stroke? Arch Phys Med Rehabil 

2004;85(8):1265-72. No relevant outcomes 

250. Hansen NL, Conway BA, Halliday DM, Hansen S, 

Pyndt HS, Biering-Sorensen F, et al. Reduction of 

common synaptic drive to ankle dorsiflexor 

motoneurons during walking in patients with spinal 

cord lesion. J Neurophysiol 2005;94(2):934-42. No 

relevant outcomes 

251. Harris S, Chen D, Green D. Enoxaparin for 

thromboembolism prophylaxis in spinal injury: 

preliminary report on experience with 105 patients. 

Am J Phys Med Rehabil 1996 Sep-Oct;75(5):326-7. 

Not eligible target population 

252. Hart KA, Rintala DH, Fuhrer MJ. Educational 

interests of individuals with spinal cord injury living 

in the community: medical, sexuality, and wellness 

topics. Rehabil Nurs 1996;21(2):82-90. No exercise 

program or physical activity 

253. Hartkopp A, Harridge SD, Mizuno M, Ratkevicius A, 

Quistorff B, Kjaer M, et al. Effect of training on 

contractile and metabolic properties of wrist 

extensors in spinal cord-injured individuals. Muscle 

Nerve 2003;27(1):72-80. No relevant outcomes 

254. Harvey L, de Jong I, Goehl G, Mardwedel S. Twelve 

weeks of nightly stretch does not reduce thumb webspace contractures in people with a neurological 

condition: a randomised controlled trial. Aust J 

Physiother 2006;52(4):251-8. Not eligible outcomes 

255. Harvey LA, McQuade L, Hawthorne S, Byak A. 

Quantifying the magnitude of torque physiotherapists 

apply when stretching the hamstring muscles of 

people with spinal cord injury. Arch Phys Med 

Rehabil 2003;84(7):1072-5. No relevant outcomes 

256. Hashimoto H, Iida J, Shin Y, Hironaka Y, Sakaki T. 

Spinal dural arteriovenous fistula with 

perimesencephalic subarachnoid haemorrhage. J Clin 

Neurosci 2000;7(1):64-6. Not adult chronic SCI 

patients 

257. Hautvast RW, Blanksma PK, DeJongste MJ, Pruim J, 

van der Wall EE, Vaalburg W, et al. Effect of spinal 

cord stimulation on myocardial blood flow assessed 

by positron emission tomography in patients with 

refractory angina pectoris. Am J Cardiol 

1996;77(7):462-7. Not adult chronic SCI patients 

258. Hautvast RW, Brouwer J, DeJongste MJ, Lie KI. 

Effect of spinal cord stimulation on heart rate 

variability and myocardial ischemia in patients with 

chronic intractable angina pectoris--a prospective 

ambulatory electrocardiographic study. Clin Cardiol 

1998;21(1):33-8. Not adult chronic SCI patients 

259. Hautvast RW, DeJongste MJ, Staal MJ, van Gilst 

WH, Lie KI. Spinal cord stimulation in chronic 

intractable angina pectoris: a randomized, controlled 

efficacy study. Am Heart J 1998;136(6):1114-20. Not 

adult chronic SCI patients 
D-11 

260. He Q, Li J, Bettiol E, Jaconi ME. Embryonic stem 

cells: new possible therapy for degenerative diseases 

that affect elderly people. Journals of Gerontology 

Series A-Biological Sciences & Medical Sciences 

2003;58(3):279-87. No relevant data 

261. Healy ME, Hesselink JR, Ostrup RC, Alksne JF. 

Demonstration by magnetic resonance of 

symptomatic spinal epidural lipomatosis. 

Neurosurgery 1987;21(3):414-5. Not adult spinal 

cord injury patients 

262. Heilbrun MP, Davis DO. Spastic paraplegia 

secondary to cord constriction by the dura. Case 

report. Journal of Neurosurgery 1973;39(5):645-7. 

Not adult spinal cord injury patients 

263. Heimbach RD. Hyperbaric medicine--demonstration 

cases. Transactions of the Association of Life 

Insurance Medical Directors of America 67:126-34, 

1985 1985;67:126-34. No relevant data 

264. Henderson CE. Application of ventilatory strategies 

to enhance functional activities for an individual with 

spinal cord injury. J Neurol Phys Ther 

2005;29(2):107-11. No relevant outcomes 

265. Henriksen JD. Part V: secondary health problems: 

Specialized care of the spinal cord injured patient. 

Journal of Practical Nursing 1976;26(10):21. No 

relevant data 

266. Hicks AL, Adams MM, Martin Ginis K, 

Giangregorio L, Latimer A, Phillips SM, et al. Longterm body-weight-supported treadmill training and 

subsequent follow-up in persons with chronic SCI: 

effects on functional walking ability and measures of 

subjective well-being. Spinal Cord 2005;43(5):291-8. 

No relevant outcomes 

267. Hicks AL, Martin KA, Ditor DS, Latimer AE, 

Craven C, Bugaresti J, et al. Long-term exercise 

training in persons with spinal cord injury: effects on 

strength, arm ergometry performance and 

psychological well-being. Spinal Cord 

2003;41(1):34-43. No relevant outcomes 

268. Higuchi Y, Kitamura S, Kawashima N, Nakazawa K, 

Iwaya T, Yamasaki M. Cardiorespiratory responses 

during passive walking-like exercise in quadriplegics. 

Spinal Cord 2006;44(8):480-6. No relevant outcomes 

269. Hirsh EH, Brandenburg D, Hersh T, Brooks WS, Jr. 

Chronic intestinal pseudo-obstruction. Journal of 

Clinical Gastroenterology 1981;3(3):247-54. Not 

adult spinal cord injury patients 

270. Hjeltnes N, Aksnes AK, Birkeland KI, Johansen J, 

Lannem A, Wallberg-Henriksson H. Improved body 

composition after 8 wk of electrically stimulated leg 

cycling in tetraplegic patients. Am J Physiol 

1997;273(3):R1072-9. No relevant outcomes 

271. Hjeltnes N, Wallberg-Henriksson H. Improved work 

capacity but unchanged peak oxygen uptake during 

primary rehabilitation in tetraplegic patients. Spinal 

Cord 1998;36(10):691-8. No relevant outcomes 

272. Ho MH, Bhatia NN, Khorram O. Physiologic role of 

nitric oxide and nitric oxide synthase in female lower 

urinary tract. [Review] [42 refs]. Current Opinion in 

Obstetrics & Gynecology 2004;16(5):423-9. No 

relevant data 

273. Ho RM, Freed MM. Persistent hypertension in young 

spinal cord injured individuals resulting from aortic 

repair. Arch Phys Med Rehabil 1991 Sep;72(10):743-

6. Not eligible target population 

274. Hopman MT, Groothuis JT, Flendrie M, Gerrits KH, 

Houtman S. Increased vascular resistance in 

paralyzed legs after spinal cord injury is reversible by 

training. J Appl Physiol 2002;93(6):1966-72. No 

relevant outcomes 

275. Hopman MT, Houtman S, Groothuis JT, Folgering 

HT. The effect of varied fractional inspired oxygen 

on arm exercise performance in spinal cord injury 

and able-bodied persons. Arch Phys Med Rehabil 

2004;85(2):319-23. No relevant outcomes 

276. Hopman MT, Monroe M, Dueck C, Phillips WT, 

Skinner JS. Blood redistribution and circulatory 

responses to submaximal arm exercise in persons 

with spinal cord injury. Scand J Rehabil Med 

1998;30(3):167-74. No relevant outcomes 

277. Hopman MT, van der Woude LH, Dallmeijer AJ, 

Snoek G, Folgering HT. Respiratory muscle strength 

and endurance in individuals with tetraplegia. Spinal 

Cord 1997;35(2):104-8. No relevant outcomes 

278. Hornby TG, Zemon DH, Campbell D. Roboticassisted, body-weight-supported treadmill training in 

individuals following motor incomplete spinal cord 

injury. Phys Ther 2005;85(1):52-66. No relevant 

outcomes 

279. Houtman S, Colier WN, Oeseburg B, Hopman MT. 

Systemic circulation and cerebral oxygenation during 

head-up tilt in spinal cord injured individuals. Spinal 

Cord 2000 Mar;38(3):158-63. Not eligible outcomes 

280. Houtman S, Thielen JJ, Binkhorst RA, Hopman MT. 

Effect of a pulsating anti-gravity suit on peak 

exercise performance in individual with spinal cord 

injuries. Eur J Appl Physiol Occup Physiol 

1999;79(2):202-4. No relevant outcomes 

281. Hubault A. Nervous arthropathies. Revue 

Neurologique 1982;138(12):1009-17. Not english 

language 

282. Hunt KJ, Ferrario C, Grant S, Stone B, McLean AN, 

Fraser MH, et al. Comparison of stimulation patterns 

for FES-cycling using measures of oxygen cost and 

stimulation cost. Med Eng Phys 2006;28(7):710-8. 

No relevant outcomes 

283. Huntoon E, Sinaki M. Thoracic osteoporotic fracture 

without upper back pain. Am J Phys Med Rehabil 

2004;83(9):729. Not adult chronic SCI patients 

284. Hutzler Y, Ochana S, Bolotin R, Kalina E. Aerobic 

and anaerobic arm-cranking power outputs of males 

with lower limb impairments: relationship with sport 

participation intensity, age, impairment and 

functional classification. Spinal Cord 

1998;36(3):205-12. No relevant outcomes 

285. Hwang WS, Roh SI, Lee BC, Kang SK, Kwon DK, 

Kim S, et al. Patient-specific embryonic stem cells 

derived from human SCNT blastocysts. Science 

2005;308(5729):1777-83. No relevant data 

286. Ide M, Ogata H, Kobayashi M, Wada F. Muscle 

damage occurring in wheelchair sports people. Spinal 

Cord 1997;35(4):234-7. No relevant outcomes 
D-12 

287. Ide M, Tajima F, Furusawa K, Mizushima T, Ogata 

H. Wheelchair marathon racing causes striated 

muscle distress in individuals with spinal cord injury. 

Arch Phys Med Rehabil 1999 Mar;80(3):324-7. Not 

eligible outcomes 

288. Iida H, Tachibana S, Kitahara T, Horiike S, Ohwada 

T, Fujii K. Association of head trauma with cervical 

spine injury, spinal cord injury, or both. J Trauma 

1999 Mar;46(3):450-2. Not eligible outcomes 

289. Iles JF, Ali A, Pardoe J. Task-related changes of 

transmission in the pathway of heteronymous spinal 

recurrent inhibition from soleus to quadriceps motor 

neurones in man. Brain 2000;123 ( Pt 11):2264-72. 

Not adult chronic SCI patients 

290. Illman A, Stiller K, Williams M. The prevalence of 

orthostatic hypotension during physiotherapy 

treatment in patients with an acute spinal cord injury. 

Spinal Cord 2000 Dec;38(12):741-7. Not eligible 

target population 

291. Iseli E, Cavigelli A, Dietz V, Curt A. Prognosis and 

recovery in ischaemic and traumatic spinal cord 

injury: clinical and electrophysiological evaluation. J 

Neurol Neurosurg Psychiatry 1999 Nov;67(5):567-

71. Not eligible target population 

292. Israel JF, Campbell DD, Kahn JH, Hornby TG. 

Metabolic costs and muscle activity patterns during 

robotic- and therapist-assisted treadmill walking in 

individuals with incomplete spinal cord injury. Phys 

Ther 2006;86(11):1466-78. No relevant outcomes 

293. Iversen PO, Groot PD, Hjeltnes N, Andersen TO, 

Mowinckel MC, Sandset PM. Impaired circadian 

variations of haemostatic and fibrinolytic parameters 

in tetraplegia. Br J Haematol 2002 Dec;119(4):1011-

6. Not eligible outcomes 

294. Jacobs PL, Johnson B, Mahoney ET. Physiologic 

responses to electrically assisted and frame-supported 

standing in persons with paraplegia. J Spinal Cord 

Med 2003;26(4):384-9. No relevant outcomes 

295. Jacobs PL, Johnson B, Somarriba GA, Carter AB. 

Reliability of upper extremity anaerobic power 

assessment in persons with tetraplegia. J Spinal Cord 

Med 2005;28(2):109-13. No relevant outcomes 

296. Jacobs PL, Mahoney ET. Peak exercise capacity of 

electrically induced ambulation in persons with 

paraplegia. Med Sci Sports Exerc 2002;34(10):1551-

6. No relevant outcomes 

297. Jacobs PL, Mahoney ET, Johnson B. Reliability of 

arm Wingate Anaerobic Testing in persons with 

complete paraplegia. J Spinal Cord Med 

2003;26(2):141-4. No relevant outcomes 

298. Jacobs PL, Mahoney ET, Nash MS, Green BA. 

Circuit resistance training in persons with complete 

paraplegia. J Rehabil Res Dev 2002;39(1):21-8. No 

relevant outcomes 

299. Jacobs PL, Nash MS. Modes, benefits, and risks of 

voluntary an delectrically induced exercise in persons 

with spinal cord injury. Journal of Spinal Cord 

Medicine 2001;24(1):10-8. No relevant data 

300. Jacobs PL, Nash MS, Klose KJ, Guest RS, NeedhamShropshire BM, Green BA. Evaluation of a training 

program for persons with SCI paraplegia using the 

Parastep 1 ambulation system: part 2. Effects on 

physiological responses to peak arm ergometry. Arch 

Phys Med Rehabil 1997;78(8):794-8. No relevant 

outcomes 

301. Jaconi M. Embryonic stem cells: new possible 

therapy of degenerative diseases. Therapeutische 

Umschau 2002;59(11):588-95. Not english language 

302. Jaeger-Denavit O, Lacert P, Pannier S, Grossiord A. 

Study of cutaneous blood flow as a function of local 

skin temperature in paraplegia and guadraplegia due 

to spinal cord lesions. Revue Europeenne d Etudes 

Cliniques et Biologiques 1972;17(5):518-24. Not 

english language 

303. Jain NB, Brown R, Tun CG, Gagnon D, Garshick E. 

Determinants of forced expiratory volume in 1 

second (FEV1), forced vital capacity (FVC), and 

FEV1/FVC in chronic spinal cord injury. Archives of 

Physical Medicine & Rehabilitation 

2006;87(10):1327-33. No relevant data 

304. Jamieson WR, Janusz MT, Gudas VM, Burr LH, 

Fradet GJ, Henderson C. Traumatic rupture of the 

thoracic aorta: third decade of experience. Am J Surg 

2002 May;183(5):571-5. Not eligible target 

population 

305. Janosky VJ. Stem cells: potential cures or abortion 

lures? DePaul Journal of Health Care Law 

2002;6(1):111-57. No relevant data 

306. Janssen TW, Dallmeijer AJ, van der Woude LH. 

Physical capacity and race performance of handcycle 

users. J Rehabil Res Dev 2001;38(1):33-40. No 

relevant outcomes 

307. Janssen TW, Dallmeijer AJ, Veeger DJ, van der 

Woude LH. Normative values and determinants of 

physical capacity in individuals with spinal cord 

injury. J Rehabil Res Dev 2002;39(1):29-39. No 

relevant outcomes 

308. Janssen TW, van Oers CA, Rozendaal EP, Willemsen 

EM, Hollander AP, van der Woude LH. Changes in 

physical strain and physical capacity in men with 

spinal cord injuries. Med Sci Sports Exerc 

1996;28(5):551-9. No relevant outcomes 

309. Janssen TW, van Oers CA, van Kamp GJ, 

TenVoorde BJ, van der Woude LH, Hollander AP. 

Coronary heart disease risk indicators, aerobic power, 

and physical activity in men with spinal cord injuries. 

Arch Phys Med Rehabil 1997 Jul;78(7):697-705. 

Case-control with <50 cases 

310. Jaworski TM, Richards JS, Lloyd LK. Retrospective 

review of sexual and marital satisfaction of spinal 

cord injury and diabetic males post penile injection or 

implant. Urology 1992;40(2):127-31. No relevant 

data 

311. Jeon JY, Weiss CB, Steadward RD, Ryan E, 

Burnham RS, Bell G, et al. Improved glucose 

tolerance and insulin sensitivity after electrical 

stimulation-assisted cycling in people with spinal 

cord injury. Spinal Cord 2002;40(3):110-7. Less than 

100 patients in study 
D-13 

312. Jeremic B, Grujicic D, Cirovic V, Djuric L, Mijatovic 

L. Radiotherapy of metastatic spinal cord 

compression. Acta Oncol 1991;30(8):985-6. Not 

eligible target population 

313. Jesel M. Anomalies of conduction of the distal 

segment of nerve fibers in slowly developing neuritic 

and radiculo-neuritic diseases. Revue Neurologique 

1968;118(6):411-8. Not english language 

314. Jessurun GA, DeJongste MJ, Hautvast RW, Tio RA, 

Brouwer J, van Lelieveld S, et al. Clinical follow-up 

after cessation of chronic electrical neuromodulation 

in patients with severe coronary artery disease: a 

prospective randomized controlled study on putative 

involvement of sympathetic activity. Pacing Clin 

Electrophysiol 1999;22(10):1432-9. Not adult 

chronic SCI patients 

315. Jezernik S, Scharer R, Colombo G, Morari M. 

Adaptive robotic rehabilitation of locomotion: a 

clinical study in spinally injured individuals. Spinal 

Cord 2003;41(12):657-66. No relevant outcomes 

316. Johnson RH, Spaulding JM. Disorders of the 

autonomic nervous system. Chapter 10. Sweating. 

Contemporary Neurology Series 1974(11):179-98. 

No relevant data 

317. Jones EA, Manaster BJ, May DA, Disler DG. 

Neuropathic osteoarthropathy: diagnostic dilemmas 

and differential diagnosis. Radiographics 2000 2000 

Oct;20(Spec No):S279-93. No relevant data 

318. Jones LM, Legge M, Goulding A. Intensive exercise 

may preserve bone mass of the upper limbs in spinal 

cord injured males but does not retard 

demineralisation of the lower body. Spinal Cord 

2002;40(5):230-5. No relevant outcomes 

319. Jones LM, Legge M, Goulding A. Healthy body mass 

index values often underestimate body fat in men 

with spinal cord injury. Archives of Physical 

Medicine & Rehabilitation 2003;84(7):1068-71. Less 

than 100 patients in study 

320. Jones LM, Legge M, Goulding A. Factor analysis of 

the metabolic syndrome in spinal cord-injured men. 

Metabolism: Clinical & Experimental 

2004;53(10):1372-7. Less than 100 patients in study 

321. Jones T, Ugalde V, Franks P, Zhou H, White RH. 

Venous thromboembolism after spinal cord injury: 

incidence, time course, and associated risk factors in 

16,240 adults and children. Arch Phys Med Rehabil 

2005 Dec;86(12):2240-7. Not eligible target 

population 

322. Jonsson B, Annertz M, Sjoberg C, Stromqvist B. A 

prospective and consecutive study of surgically 

treated lumbar spinal stenosis. Part I: Clinical 

features related to radiographic findings. Spine 1997 

Dec 15;22(24):2932-7. Not eligible target population 

323. Jozsa L, Kannus P, Jarvinen TA, Balint J, Jarvinen 

M. Number and morphology of mechanoreceptors in 

the myotendinous junction of paralysed human 

muscle. J Pathol 1996 Feb;178(2):195-200. Not 

eligible target population 

324. Kabalin JN, Lennon S, Gill HS, Wolfe V, Perkash I. 

Incidence and management of autonomic dysreflexia 

and other intraoperative problems encountered in 

spinal cord injury patients undergoing extracorporeal 

shock wave lithotripsy without anesthesia on a 

second generation lithotriptor. J Urol 1993 

May;149(5):1064-7. Not eligible outcomes 

325. Kadyan V, Clinchot DM, Mitchell GL, Colachis SC. 

Surveillance with duplex ultrasound in traumatic 

spinal cord injury on initial admission to 

rehabilitation. J Spinal Cord Med 2003 

Fall;26(3):231-5. Not eligible target population 

326. Kahn NN. Platelet-stimulated thrombin and PDGF 

are normalized by insulin and Ca2+ channel blockers. 

Am J Physiol 1999 May;276(5 Pt 1):E856-62. Not 

eligible outcomes 

327. Kahn NN, Bauman WA, Sinha AK. Demonstration 

of a novel circulating anti-prostacyclin receptor 

antibody. Proc Natl Acad Sci U S A 1997 Aug 

5;94(16):8779-82. Not eligible outcomes 

328. Kahn NN, Bauman WA, Sinha AK. Circulating 

heavy chain IgG, a pathological mediator for 

coronary artery disease, recognizes platelet surface 

receptors of both prostacyclin and insulin. Platelets 

2003 Jun;14(4):203-10. Not eligible outcomes 

329. Kahn NN, Bauman WA, Sinha AK. Appearance of a 

novel prostacyclin receptor antibody and duration of 

spinal cord injury. J Spinal Cord Med 2005;28(2):97-

102. Not eligible outcomes 

330. Kameyama J, Handa Y, Hoshimiya N, Sakurai M. 

Restoration of shoulder movement in quadriplegic 

and hemiplegic patients by functional electrical 

stimulation using percutaneous multiple electrodes. 

Tohoku J Exp Med 1999 Apr;187(4):329-37. Not 

eligible outcomes 

331. Kapidzic-Durakovic S, Zonic-Imamovic M, 

Mulaosmanovic A. Family participation in 

determination of FIM and Barthel indices. Bosn J 

Basic Med Sci 2006 May;6(2):51-3. Not eligible 

outcomes 

332. Karlsson AK. Insulin resistance and sympathetic 

function in high spinal cord injury. Spinal Cord 

1999;37(7):494-500. Less than 100 patients in study 

333. Karlsson AK, Attvall S, Jansson PA, Sullivan L, 

Lonnroth P. Influence of the sympathetic nervous 

system on insulin sensitivity and adipose tissue 

metabolism: a study in spinal cord-injured subjects. 

Metabolism: Clinical & Experimental 1995;44(1):52-

8. Less than 100 patients in study 

334. Karlsson AK, Elam M, Friberg P, Biering-Sorensen 

F, Sullivan L, Lonnroth P. Regulation of lipolysis by 

the sympathetic nervous system: a microdialysis 

study in normal and spinal cord-injured subjects. 

Metabolism: Clinical & Experimental 

1997;46(4):388-94. Less than 100 patients in study 

335. Katz PG, Greenstein A. Urinary incontinence 

associated with neurologic disorders. [Review] [29 

refs]. Seminars in Urology 1989;7(2):133-8. No 

relevant data 
D-14 

336. Kawashima N, Nakazawa K, Ishii N, Akai M, Yano 

H. Potential impact of orthotic gait exercise on 

natural killer cell activities in thoracic level of spinal 

cord-injured patients. Spinal Cord 2004;42(7):420-4. 

No relevant outcomes 

337. Kawashima N, Sone Y, Nakazawa K, Akai M, Yano 

H. Energy expenditure during walking with weightbearing control (WBC) orthosis in thoracic level of 

paraplegic patients. Spinal Cord 2003;41(9):506-10. 

No relevant outcomes 

338. Kerslake RW, Jaspan T, Worthington BS. Magnetic 

resonance imaging of spinal trauma. Br J Radiol 1991 

May;64(761):386-402. Not eligible outcomes 

339. Kerstin W, Gabriele B, Richard L. What promotes 

physical activity after spinal cord injury? An 

interview study from a patient perspective. Disabil 

Rehabil 2006;28(8):481-8. No relevant outcomes 

340. Kesiktas N, Paker N, Erdogan N, Gulsen G, Bicki D, 

Yilmaz H. The use of hydrotherapy for the 

management of spasticity. Neurorehabil Neural 

Repair 2004;18(4):268-73. No relevant outcomes 

341. Ketover SR, Ansel HJ, Goldish G, Roche B, Gebhard 

RL. Gallstones in chronic spinal cord injury: is 

impaired gallbladder emptying a risk factor? 

Archives of Physical Medicine & Rehabilitation 

1996;77(11):1136-8. No relevant data 

342. Keyser RE, Rasch EK, Finley M, Rodgers MM. 

Improved upper-body endurance following a 12-

week home exercise program for manual wheelchair 

users. J Rehabil Res Dev 2003;40(6):501-10. No 

relevant outcomes 

343. Khan SH, Hattingh S, Griebel RW. Spinal epidural 

abscess. Canadian Journal of Neurological Sciences 

2001;28(3):254-5. Not adult spinal cord injury 

patients 

344. Khoynezhad A, Donayre CE, Bui H, Kopchok GE, 

Walot I, White RA. Risk factors of neurologic deficit 

after thoracic aortic endografting. Ann Thorac Surg 

2007 Feb;83(2):S882-9; discussion S90-2. Not 

eligible target population 

345. Kilkens OJ, Dallmeijer AJ, De Witte LP, Van Der 

Woude LH, Post MW. The Wheelchair Circuit: 

Construct validity and responsiveness of a test to 

assess manual wheelchair mobility in persons with 

spinal cord injury. Arch Phys Med Rehabil 

2004;85(3):424-31. No relevant outcomes 

346. Kim V, Spandorfer J. Epidemiology of venous 

thromboembolic disease. Emergency Medicine 

Clinics of North America 2001;19(4):839-59. Not 

adult spinal cord injury patients 

347. King ML, Lichtman SW, Pellicone JT, Close RJ, 

Lisanti P. Exertional hypotension in spinal cord 

injury. Chest 1994 Oct;106(4):1166-71. Not eligible 

outcomes 

348. Kishi Y, Robinson RG, Kosier JT. Suicidal ideation 

among patients with acute life-threatening physical 

illness: patients with stroke, traumatic brain injury, 

myocardial infarction, and spinal cord injury. 

Psychosomatics 2001 Sep-Oct;42(5):382-90. Not 

eligible target population 

349. Kishi Y, Robinson RG, Kosier JT. Suicidal ideation 

among patients during the rehabilitation period after 

life-threatening physical illness. J Nerv Ment Dis 

2001 Sep;189(9):623-8. Not eligible outcomes 

350. Kjaer M, Dela F, Sorensen FB, Secher NH, Bangsbo 

J, Mohr T, et al. Fatty acid kinetics and carbohydrate 

metabolism during electrical exercise in spinal cordinjured humans. Am J Physiol Regul Integr Comp 

Physiol 2001;281(5):R1492-8. No relevant outcomes 

351. Kjaer M, Mohr T, Biering-Sorensen F, Bangsbo J. 

Muscle enzyme adaptation to training and taperingoff in spinal-cord-injured humans. Eur J Appl Physiol 

2001;84(5):482-6. No relevant outcomes 

352. Kjaer M, Pollack SF, Mohr T, Weiss H, Gleim GW, 

Bach FW, et al. Regulation of glucose turnover and 

hormonal responses during electrical cycling in 

tetraplegic humans. Am J Physiol 1996;271(1):R191-

9. No relevant outcomes 

353. Kjaer M, Pott F, Mohr T, Linkis P, Tornoe P, Secher 

NH. Heart rate during exercise with leg vascular 

occlusion in spinal cord-injured humans. J Appl 

Physiol 1999;86(3):806-11. No relevant outcomes 

354. Klokker M, Mohr T, Kjaer M, Galbo H, Pedersen 

BK. The natural killer cell response to exercise in 

spinal cord injured individuals. Eur J Appl Physiol 

Occup Physiol 1998;79(1):106-9. No relevant 

outcomes 

355. Knechtle B, Hardegger K, Muller G, Odermatt P, 

Eser P, Knecht H. Evaluation of sprint exercise 

testing protocols in wheelchair athletes. Spinal Cord 

2003;41(3):182-6. No relevant outcomes 

356. Knechtle B, Kopfli W. Treadmill exercise testing 

with increasing inclination as exercise protocol for 

wheelchair athletes. Spinal Cord 2001;39(12):633-6. 

No relevant outcomes 

357. Knechtle B, Muller G, Knecht H. Optimal exercise 

intensities for fat metabolism in handbike cycling and 

cycling. Spinal Cord 2004;42(10):564-72. No 

exercise program or physical activity 

358. Knechtle B, Muller G, Willmann F, Eser P, Knecht 

H. Comparison of fat oxidation in arm cranking in 

spinal cord-injured people versus ergometry in 

cyclists. Eur J Appl Physiol 2003;90(5):614-9. No 

relevant outcomes 

359. Knoller N, Auerbach G, Fulga V, Zelig G, Attias J, 

Bakimer R, et al. Clinical experience using incubated 

autologous macrophages as a treatment for complete 

spinal cord injury: phase I study results. J Neurosurg 

Spine 2005 Sep;3(3):173-81. Not eligible target 

population 

360. Kocina P. Body composition of spinal cord injured 

adults. Sports Medicine 1997;23(1):48-60. Review 

361. Kondo T, Saito K, Nishigami J, Ohshima T. Fatal 

injuries of the brain stem and/or upper cervical spinal 

cord in traffic accidents: nine autopsy cases. Sci 

Justice 1995 Jul-Sep;35(3):197-201. Not eligible 

target population 

362. Konz KR, Chia JK, Kurup VP, Resnick A, Kelly KJ, 

Fink JN. Comparison of latex hypersensitivity among 

patients with neurologic defects. J Allergy Clin 

Immunol 1995 May;95(5 Pt 1):950-4. Not eligible 

outcomes 
D-15 

363. Kooijman M, Rongen GA, Smits P, Hopman MT. 

Preserved alpha-adrenergic tone in the leg vascular 

bed of spinal cord-injured individuals. Circulation 

2003 Nov 11;108(19):2361-7. Not eligible outcomes 

364. Krassioukov AV, Furlan JC, Fehlings MG. 

Autonomic dysreflexia in acute spinal cord injury: an 

under-recognized clinical entity. J Neurotrauma 2003 

Aug;20(8):707-16. Not eligible target population 

365. Krause JS, Broderick L. Patterns of recurrent 

pressure ulcers after spinal cord injury: identification 

of risk and protective factors 5 or more years after 

onset. Arch Phys Med Rehabil 2004;85(8):1257-64. 

No exercise program or physical activity 

366. Kucukdeveci AA, Yavuzer G, Tennant A, Suldur N, 

Sonel B, Arasil T. Adaptation of the modified Barthel 

Index for use in physical medicine and rehabilitation 

in Turkey. Scand J Rehabil Med 2000 Jun;32(2):87-

92. Not eligible outcomes 

367. Kunihara T, Matsuzaki K, Shiiya N, Saijo Y, Yasuda 

K. Naloxone lowers cerebrospinal fluid levels of 

excitatory amino acids after thoracoabdominal aortic 

surgery. J Vasc Surg 2004 Oct;40(4):681-90. Not 

eligible target population 

368. Kuo HC. Therapeutic effects of suburothelial 

injection of botulinum a toxin for neurogenic detrusor 

overactivity due to chronic cerebrovascular accident 

and spinal cord lesions. Urology 2006 Feb;67(2):232-

6. Not eligible outcomes 

369. Lagerquist O, Zehr EP, Docherty D. Increased spinal 

reflex excitability is not associated with neural 

plasticity underlying the cross-education effect. J 

Appl Physiol 2006;100(1):83-90. Not adult chronic 

SCI patients 

370. Langmayr JJ, Ortler M, Dessl A, Twerdy K, Aichner 

F, Felber S. Management of spontaneous 

extramedullary spinal haematomas: results in eight 

patients after MRI diagnosis and surgical 

decompression. J Neurol Neurosurg Psychiatry 1995 

Oct;59(4):442-7. Not eligible target population 

371. Lanza GA, Sestito A, Sandric S, Cioni B, Tamburrini 

G, Barollo A, et al. Spinal cord stimulation in 

patients with refractory anginal pain and normal 

coronary arteries. Ital Heart J 2001;2(1):25-30. Not 

adult chronic SCI patients 

372. Lapides J, Diokno AC, Lowe BS, Kalish MD. 

Followup on unsterile intermittent selfcatheterization. Journal of Urology 1974;111(2):184-

7. No relevant data 

373. Lassau-Wray ER, Ward GR. Varying physiological 

response to arm-crank exercise in specific spinal 

injuries. J Physiol Anthropol Appl Human Sci 

2000;19(1):5-12. No relevant outcomes 

374. Lawton MT, Porter RW, Heiserman JE, Jacobowitz 

R, Sonntag VK, Dickman CA. Surgical management 

of spinal epidural hematoma: relationship between 

surgical timing and neurological outcome. J 

Neurosurg 1995 Jul;83(1):1-7. Not eligible target 

population 

375. Leaf DA, Bahl RA, Adkins RH. Risk of cardiac 

dysrhythmias in chronic spinal cord injury patients. 

Paraplegia 1993 Sep;31(9):571-5. Case-series 

376. Lecouvet F, Richard F, Vande Berg B, Malghem J, 

Maldague B, Jamart J, et al. Long-term effects of 

localized spinal radiation therapy on vertebral 

fractures and focal lesions appearance in patients 

with multiple myeloma. Br J Haematol 1997 

Mar;96(4):743-5. Not eligible target population 

377. Leduc BE, Dagher JH, Mayer P, Bellemare F, 

Lepage Y. Estimated prevalence of obstructive sleep 

apnea-hypopnea syndrome after cervical cord injury. 

Archives of Physical Medicine & Rehabilitation 

2007;88(3):333-7. No relevant data 

378. Lee CS, Lu YH, Lee ST, Lin CC, Ding HJ. 

Evaluating the prevalence of silent coronary artery 

disease in asymptomatic patients with spinal cord 

injury. Int Heart J 2006 May;47(3):325-30. Caseseries 

379. Lee MY, Myers J, Hayes A, Madan S, Froelicher VF, 

Perkash I, et al. C-reactive protein, metabolic 

syndrome, and insulin resistance in individuals with 

spinal cord injury. Journal of Spinal Cord Medicine 

2005;28(1):20-5. Less than 100 patients in study 

380. Leist M, Ghezzi P, Grasso G, Bianchi R, Villa P, 

Fratelli M, et al. Derivatives of erythropoietin that are 

tissue protective but not erythropoietic. Science 

2004;305(5681):239-42. Not adult spinal cord injury 

patients 

381. Leite CC, Escobar BE, Bazan C, 3rd, Jinkins JR. 

MRI of cervical facet dislocation. Neuroradiology 

1997 Aug;39(8):583-8. Not eligible outcomes 

382. Lena P, Teboul J, Mercier B, Bonnet F. Motor deficit 

of the lower limbs and urinary incontinence 

following peridural anesthesia. Annales Francaises d 

Anesthesie et de Reanimation 1998;17(9):1144-7. 

Not english language 

383. Leroux A, Fung J, Barbeau H. Postural adaptation to 

walking on inclined surfaces: II. Strategies following 

spinal cord injury. Clin Neurophysiol 

2006;117(6):1273-82. No relevant outcomes 

384. Levi L, Wolf A, Belzberg H. Hemodynamic 

parameters in patients with acute cervical cord 

trauma: description, intervention, and prediction of 

outcome. Neurosurgery 1993 Dec;33(6):1007-16; 

discussion 16-7. Not eligible target population 

385. Levi R, Hultling C, Nash MS, Seiger A. The 

Stockholm spinal cord injury study: 1. Medical 

problems in a regional SCI population. Paraplegia 

1995 Jun;33(6):308-15. Not eligible target 

population 

386. Linden D, Berlit P. Magnetic motor evoked potentials 

(MEP) in diseases of the spinal cord. Acta Neurol 

Scand 1994 Nov;90(5):348-53. Not eligible outcomes 

387. Lischke V, Westphal K, Behne M, Wilke HJ, 

Rosenthal D, Marquardt G, et al. Thoracoscopic 

microsurgical technique for vertebral surgery--

anesthetic considerations. Acta Anaesthesiol Scand 

1998;42(10):1199-204. No exercise program or 

physical activity 

388. Liu JE, Tahmoush AJ, Roos DB, Schwartzman RJ. 

Shoulder-arm pain from cervical bands and scalene 

muscle anomalies. J Neurol Sci 1995 

Feb;128(2):175-80. Not eligible outcome 
D-16 

389. Liusuwan A, Widman L, Abresch RT, McDonald 

CM. Altered body composition affects resting energy 

expenditure and interpretation of body mass index in 

children with spinal cord injury. Journal of Spinal 

Cord Medicine 27 Suppl 1:S24-8, 2004 

2004;27(Suppl 1):S24-8. Not adult spinal cord injury 

patients 

390. Logemann JA, Veis S, Colangelo L. A screening 

procedure for oropharyngeal dysphagia. Dysphagia 

1999 Winter;14(1):44-51. Not eligible outcomes 

391. LoPresti EF, Brienza DM. Adaptive software for 

head-operated computer controls. IEEE Trans Neural 

Syst Rehabil Eng 2004;12(1):102-11. No exercise 

program or physical activity 

392. Loudon JK, Cagle PE, Figoni SF, Nau KL, Klein 

RM. A submaximal all-extremity exercise test to 

predict maximal oxygen consumption. Med Sci 

Sports Exerc 1998;30(8):1299-303. Not adult chronic 

SCI patients 

393. Lu K, Lee TC, Liang CL, Chen HJ. Delayed apnea in 

patients with mid- to lower cervical spinal cord 

injury. Spine 2000 Jun 1;25(11):1332-8. Not eligible 

outcomes 

394. Luce JM, Culver BH. Respiratory muscle function in 

health and disease. Chest 1982;81(1):82-90. Not 

adult spinal cord injury patients 

395. Lundgren-Nilsson A, Tennant A, Grimby G, 

Sunnerhagen KS. Cross-diagnostic validity in a 

generic instrument: an example from the Functional 

Independence Measure in Scandinavia. Health Qual 

Life Outcomes 2006;4:55. Not eligible outcomes 

396. Lunney M. Critical thinking and accuracy of nurses' 

diagnoses. [Review] [26 refs]. International Journal 

of Nursing Terminologies & Classifications 

2003;14(3):96-107. Not adult spinal cord injury 

patients 

397. Luther SL, Nelson A, Powell-Cope G. Provider 

attitudes and beliefs about clinical practice 

guidelines. SCI Nurs 2004 Winter;21(4):206-12. Not 

eligible target population 

398. Maki KC, Briones ER, Langbein WE, Inman-Felton 

A, Nemchausky B, Welch M, et al. Associations 

between serum lipids and indicators of adiposity in 

men with spinal cord injury. Paraplegia 

1995;33(2):102-9. Less than 100 patients in study 

399. Manns PJ, Chad KE. Determining the relation 

between quality of life, handicap, fitness, and 

physical activity for persons with spinal cord injury. 

Arch Phys Med Rehabil 1999;80(12):1566-71. No 

relevant outcomes 

400. Manns PJ, McCubbin JA, Williams DP. Fitness, 

inflammation, and the metabolic syndrome in men 

with paraplegia. Archives of Physical Medicine & 

Rehabilitation 2005;86(6):1176-81. Less than 100 

patients in study 

401. Maranzano E, Latini P, Beneventi S, Perruci E, 

Panizza BM, Aristei C, et al. Radiotherapy without 

steroids in selected metastatic spinal cord 

compression patients. A phase II trial. American 

Journal of Clinical Oncology 1996;19(2):179-83. Not 

adult spinal cord injury patients 

402. Matthews JM. Succinylcholine-induced 

hyperkalemia and rhabdomyolysis in a patient with 

necrotizing pancreatitis. Anesthesia & Analgesia 

2000;91(6):1552-4. No relevant data 

403. Maurice-Williams RS. Spinal dural arteriovenous 

malformations--a treatable cause of progressive 

paraparesis in elderly people. Age Ageing 1992 

Nov;21(6):412-6. Not eligible target population 

404. Maxwell RA, Chavarria-Aguilar M, Cockerham WT, 

Lewis PL, Barker DE, Durham RM, et al. Routine 

prophylactic vena cava filtration is not indicated after 

acute spinal cord injury. J Trauma 2002 

May;52(5):902-6. Not eligible target population 

405. Mazzocchio R, Kitago T, Liuzzi G, Wolpaw JR, 

Cohen LG. Plastic changes in the human H-reflex 

pathway at rest following skillful cycling training. 

Clin Neurophysiol 2006;117(8):1682-91. Not adult 

chronic SCI patients 

406. McColl MA, Friedland J. The effects of age and 

disability on social support. Int J Rehabil Res 1995 

Dec;18(4):325-40. Not eligible outcomes 

407. McDermott S, Moran R, Platt T, Issac T, Wood H, 

Dasari S. Depression in adults with disabilities, in 

primary care. Disabil Rehabil 2005 Feb 4;27(3):117-

23. Not eligible outcomes 

408. McGirt MJ, Woodworth GF, Lynch JR, Laskowitz 

DT. Synthes Award for Resident Research in Spinal 

Cord & Spinal Column Injury: Statins for the 

treatment of neurological injury: a role beyond 

cholesterol lowering. Clinical Neurosurgery 

2004;51:320-8. No relevant data 

409. Meggiorin G, Onali A, Manduco G, Coraddu M. 

Continuous epidural anesthesia with a double 

catheter for sedation for surgery of the vertebral 

dorsolumbar column. Minerva Anestesiologica 

1999;65(9):653-8. Not english language 

410. Mello MT, Silva AC, Rueda AD, Poyares D, Tufik S. 

Correlation between K complex, periodic leg 

movements (PLM), and myoclonus during sleep in 

paraplegic adults before and after an acute physical 

activity. Spinal Cord 1997;35(4):248-52. No relevant 

outcomes 

411. Melman A. Pathophysiologic basis of erectile 

dysfunction. What can we learn from animal 

models?. [Review] [27 refs]. International Journal of 

Impotence Research 2001;13(3):140-2. Not adult 

spinal cord injury patients 

412. Menssen HD, Sakalova A, Fontana A, Herrmann Z, 

Boewer C, Facon T, et al. Effects of long-term 

intravenous ibandronate therapy on skeletal-related 

events, survival, and bone resorption markers in 

patients with advanced multiple myeloma. J Clin 

Oncol 2002 May 1;20(9):2353-9. Not eligible target 

population 

413. Merli GJ, Crabbe S, Doyle L, Ditunno JF, Herbision 

GJ. Mechanical plus pharmacological prophylaxis for 

deep vein thrombosis in acute spinal cord injury. 

Paraplegia 1992 Aug;30(8):558-62. Not eligible 

target population 
D-17 

414. Mersdorf A, Goldsmith PC, Diederichs W, Padula 

CA, Lue TF, Fishman IJ, et al. Ultrastructural 

changes in impotent penile tissue: a comparison of 65 

patients. Journal of Urology 1991;145(4):749-58. No 

relevant data 

415. Mirvis SE, Geisler FH. Intraoperative sonography of 

cervical spinal cord injury: results in 30 patients. AJR 

Am J Roentgenol 1990 Sep;155(3):603-9. Not 

eligible outcomes 

416. Miyakoshi N, Shimada Y, Suzuki T, Hongo M, Itoi 

E. Magnetic resonance imaging of spinal 

involvement by hematopoietic malignancies 

requiring surgical decompression. J Orthop Sci 

2003;8(2):207-12. Not eligible target population 

417. Mohr T, Andersen JL, Biering-Sorensen F, Galbo H, 

Bangsbo J, Wagner A, et al. Long-term adaptation to 

electrically induced cycle training in severe spinal 

cord injured individuals. Spinal Cord 1997;35(1):1-

16. No relevant outcomes 

418. Mohr T, Dela F, Handberg A, Biering-Sorensen F, 

Galbo H, Kjaer M. Insulin action and long-term 

electrically induced training in individuals with 

spinal cord injuries. Medicine & Science in Sports & 

Exercise 2001;33(8):1247-52. Less than 100 patients 

in study 

419. Mohr T, Podenphant J, Biering-Sorensen F, Galbo H, 

Thamsborg G, Kjaer M. Increased bone mineral 

density after prolonged electrically induced cycle 

training of paralyzed limbs in spinal cord injured 

man. Calcif Tissue Int 1997;61(1):22-5. No relevant 

outcomes 

420. Monroe MB, Tataranni PA, Pratley R, Manore MM, 

Skinner JS, Ravussin E. Lower daily energy 

expenditure as measured by a respiratory chamber in 

subjects with spinal cord injury compared with 

control subjects. Am J Clin Nutr 1998;68(6):1223-7. 

No exercise program or physical activity 

421. Morse JM, Mitcham C. The experience of agonizing 

pain and signals of disembodiment. J Psychosom Res 

1998 Jun;44(6):667-80. Not eligible outcomes 

422. Morton SM, Bastian AJ. Cerebellar contributions to 

locomotor adaptations during splitbelt treadmill 

walking. J Neurosci 2006;26(36):9107-16. Not adult 

chronic SCI patients 

423. Mostwin JL. Urinary incontinence.[comment]. 

Journal of Urology 1995;153(2):352-3. No relevant 

data 

424. Moynahan M, Mullin C, Cohn J, Burns CA, Halden 

EE, Triolo RJ, et al. Home use of a functional 

electrical stimulation system for standing and 

mobility in adolescents with spinal cord injury. Arch 

Phys Med Rehabil 1996;77(10):1005-13. Not adult 

chronic SCI patients 

425. Muller G, Odermatt P, Perret C. A new test to 

improve the training quality of wheelchair racing 

athletes. Spinal Cord 2004;42(10):585-90. No 

relevant outcomes 

426. Munakata M, Kameyama J, Kanazawa M, Nunokawa 

T, Moriai N, Yoshinaga K. Circadian blood pressure 

rhythm in patients with higher and lower spinal cord 

injury: simultaneous evaluation of autonomic nervous 

activity and physical activity. J Hypertens 

1997;15(12):1745-9. No relevant outcomes 

427. Muraki S, Yamasaki M, Ehara Y, Kikuchi K, Seki K. 

Cardiovascular and respiratory responses to passive 

leg cycle exercise in people with spinal cord injuries. 

Eur J Appl Physiol Occup Physiol 1996;74(1):23-8. 

No relevant outcomes 

428. Muraki S, Yamasaki M, Ehara Y, Kikuchi K, Seki K. 

Effect of maximal arm exercise on skin blood flux in 

the paralyzed lower limbs in persons with spinal cord 

injury. Eur J Appl Physiol Occup Physiol 

1996;74(5):481-3. No relevant outcomes 

429. Muraki S, Yamasaki M, Ishii K, Kikuchi K, Seki K. 

Relationship between core temperature and skin 

blood flux in lower limbs during prolonged arm 

exercise in persons with spinal cord injury. Eur J 

Appl Physiol Occup Physiol 1996;72(4):330-4. No 

relevant outcomes 

430. Murphy RJ, Hartkopp A, Gardiner PF, Kjaer M, 

Beliveau L. Salbutamol effect in spinal cord injured 

individuals undergoing functional electrical 

stimulation training. Arch Phys Med Rehabil 

1999;80(10):1264-7. No relevant outcomes 

431. Murray S, Collins PD, James MA. An investigation 

into the 'carry over' effect of neurostimulation in the 

treatment of angina pectoris. Int J Clin Pract 

2004;58(7):669-74. Not adult chronic SCI patients 

432. Mutton DL, Scremin AM, Barstow TJ, Scott MD, 

Kunkel CF, Cagle TG. Physiologic responses during 

functional electrical stimulation leg cycling and 

hybrid exercise in spinal cord injured subjects. Arch 

Phys Med Rehabil 1997;78(7):712-8. No relevant 

outcomes 

433. Myllynen P, Koivisto VA, Nikkila EA. Glucose 

intolerance and insulin resistance accompany 

immobilization. Acta Medica Scandinavica 

1987;222(1):75-81. Less than 100 patients in study 

434. Naaman SC, Stein RB, Thomas C. Minimizing 

discomfort with surface neuromuscular stimulation. 

Neurorehabil Neural Repair 2000;14(3):223-8. Not 

eligible outcomes 

435. Nash MS, DeGroot J, Martinez-Arizala A, Mendez 

AJ. Evidence for an exaggerated postprandial lipemia 

in chronic paraplegia. Journal of Spinal Cord 

Medicine 2005;28(4):320-5. Less than 100 patients in 

study 

436. Nash MS, Jacobs PL, Mendez AJ, Goldberg RB. 

Circuit resistance training improves the atherogenic 

lipid profiles of persons with chronic paraplegia. 

Journal of Spinal Cord Medicine 2001;24(1):2-9. 

Less than 100 patients in study 
D-18 

437. Nash MS, Jacobs PL, Montalvo BM, Klose KJ, Guest 

RS, Needham-Shropshire BM. Evaluation of a 

training program for persons with SCI paraplegia 

using the Parastep 1 ambulation system: part 5. 

Lower extremity blood flow and hyperemic 

responses to occlusion are augmented by ambulation 

training. Arch Phys Med Rehabil 1997;78(8):808-14. 

No relevant outcomes 

438. Nash MS, Johnson BM, Jacobs PL. Combined 

hyperlipidemia in a single subject with tetraplegia: 

ineffective risk reduction after atorvastatin 

monotherapy. Journal of Spinal Cord Medicine 

2004;27(5):484-7. Less than 100 patients in study 

439. Nash MS, Montalvo BM, Applegate B. Lower 

extremity blood flow and responses to occlusion 

ischemia differ in exercise-trained and sedentary 

tetraplegic persons. Arch Phys Med Rehabil 

1996;77(12):1260-5. No relevant outcomes 

440. Nehra A, Moreland RB. Neurologic erectile 

dysfunction. [Review] [202 refs]. Urologic Clinics of 

North America 2001;28(2):289-308. No relevant data 

441. New PW, Rawicki HB, Bailey MJ. Nontraumatic 

spinal cord injury: demographic characteristics and 

complications. Archives of Physical Medicine & 

Rehabilitation 2002;83(7):996-1001. No relevant 

data 

442. Nicolle LE. Asymptomatic bacteriuria: when to 

screen and when to treat. Infectious Disease Clinics 

of North America 2003;17(2):367-94. No relevant 

data 

443. Nieshoff EC, Birk TJ, Birk CA, Hinderer SR, 

Yavuzer G. Double-blinded, placebo-controlled trial 

of midodrine for exercise performance enhancement 

in tetraplegia: a pilot study. J Spinal Cord Med 

2004;27(3):219-25. No relevant outcomes 

444. Noel P. Study of afferent conduction in the external 

saphenous nerve using the method of evoked cerebral 

potentials. Revue Neurologique 1975;131(3):193-

210. Not english language 

445. Nomura K, Takei Y, Yanagida Y. Comparison of 

cardio-locomotor synchronization during running and 

cycling. Eur J Appl Physiol 2003;89(3):221-9. Not 

adult chronic SCI patients 

446. Norman KE, Pepin A, Barbeau H. Effects of drugs on 

walking after spinal cord injury. Spinal Cord 

1998;36(10):699-715. No relevant outcomes 

447. Norton JA, Gorassini MA. Changes in cortically 

related intermuscular coherence accompanying 

improvements in locomotor skills in incomplete 

spinal cord injury. J Neurophysiol 2006;95(4):2580-

9. No relevant outcomes 

448. O'Connor RJ, Cano SJ, Thompson AJ, Hobart JC. 

Exploring rating scale responsiveness: does the total 

score reflect the sum of its parts? Neurology 2004 

May 25;62(10):1842-4. Not eligible target population 

449. O'Connor TJ, Cooper RA, Fitzgerald SG, Dvorznak 

MJ, Boninger ML, VanSickle DP, et al. Evaluation of 

a manual wheelchair interface to computer games. 

Neurorehabil Neural Repair 2000;14(1):21-31. No 

relevant outcomes 

450. O'Connor TJ, Fitzgerald SG, Cooper RA, Thorman 

TA, Boninger ML. Does computer game play aid in 

motivation of exercise and increase metabolic 

activity during wheelchair ergometry? Med Eng Phys 

2001;23(4):267-73. No relevant outcomes 

451. Oester YT, Zalis AW, Rodriquez AA. Possible 

diagnostic applications of sensory evoked potentials. 

Archives of Physical Medicine & Rehabilitation 

1972;53(1):21-7. Not adult spinal cord injury 

patients 

452. Ogino H, Sasaki H, Minatoya K, Matsuda H, 

Yamada N, Kitamura S. Combined use of 

adamkiewicz artery demonstration and motor-evoked 

potentials in descending and thoracoabdominal 

repair. Ann Thorac Surg 2006 Aug;82(2):592-6. Not 

eligible target population 

453. Ohta Y, Hayashi T, Sasaki C, Shiote M, Manabe Y, 

Shoji M, et al. Cauda equina syndrome caused by 

idiopathic sacral epidural lipomatosis. Intern Med 

2002;41(7):593-4. Not adult chronic SCI patients 

454. Okawa H, Tajima F, Makino K, Kawazu T, 

Mizushima T, Monji K, et al. Kinetic factors 

determining wheelchair propulsion in marathon 

racers with paraplegia. Spinal Cord 1999;37(8):542-

7. No relevant outcomes 

455. Okita Y, Takamoto S, Ando M, Morota T, Yamaki F, 

Matsukawa R, et al. Repair for aneurysms of the 

entire descending thoracic aorta or thoracoabdominal 

aorta using a deep hypothermia. Eur J Cardiothorac 

Surg 1997 Jul;12(1):120-6. Not eligible target 

population 

456. Oku Y, Kurusu M, Hara Y, Sugita M, Muro S, Chin 

K, et al. Ventilatory responses and subjective 

sensations during arm exercise and hypercapnia in 

patients with lower-cervical and upper-thoracic spinal 

cord injuries. Intern Med 1997;36(11):776-80. No 

relevant outcomes 

457. Olive JL, McCully KK, Dudley GA. Blood flow 

response in individuals with incomplete spinal cord 

injuries. Spinal Cord 2002;40(12):639-45. No 

exercise program or physical activity 

458. Olive JL, Slade JM, Bickel CS, Dudley GA, McCully 

KK. Increasing blood flow before exercise in spinal 

cord-injured individuals does not alter muscle 

fatigue. J Appl Physiol 2004;96(2):477-82. No 

relevant outcomes 

459. Olive JL, Slade JM, Dudley GA, McCully KK. Blood 

flow and muscle fatigue in SCI individuals during 

electrical stimulation. J Appl Physiol 

2003;94(2):701-8. No relevant outcomes 

460. Orlandi G, Fanucchi S, Strata G, Pataleo L, Landucci 

Pellegrini L, Prontera C, et al. Transient autonomic 

nervous system dysfunction during hyperacute 

stroke. Acta Neurol Scand 2000 Nov;102(5):317-21. 

Not eligible target population 

461. Osaka T, Endo M, Yamakawa M, Inoue S. Energy 

expenditure by intravenous administration of 

glucagon-like peptide-1 mediated by the lower 

brainstem and sympathoadrenal system. Peptides 

2005;26(9):1623-31. Not human subjects 
D-19 

462. Ozgurtas T, Alaca R, Gulec M, Kutluay T. Do spinal 

cord injuries adversely affect serum lipoprotein 

profiles? Military Medicine 2003;168(7):545-7. Less 

than 100 patients in study 

463. Pacher P, Batkai S, Kunos G. The endocannabinoid 

system as an emerging target of pharmacotherapy. 

Pharmacological Reviews 2006;58(3):389-462. Not 

adult spinal cord injury patients 

464. Pahl MV, Vaziri ND, Gonzales E. Coagulation 

profile in persons with long-standing spinal cord 

injury. J Am Paraplegia Soc 1994 Jul;17(3):133-5. 

Case-series 

465. Papadopoulos A, Wright S, Ensor J. Evaluation and 

attributional analysis of an aromatherapy service for 

older adults with physical health problems and carers 

using the service. Complement Ther Med 1999 

Dec;7(4):239-44. Not eligible target population 

466. Parke WW, Whalen JL, Bunger PC, Settles HE. 

Intimal musculature of the lower anterior spinal 

artery. Spine 1995 Oct 1;20(19):2073-9. Not eligible 

target population 

467. Peng CT, Ger J, Yang CC, Tsai WJ, Deng JF, Bullard 

MJ. Prolonged severe withdrawal symptoms after 

acute-on-chronic baclofen overdose. J Toxicol Clin 

Toxicol 1998;36(4):359-63. Not adult chronic SCI 

patients 

468. Pepin A, Ladouceur M, Barbeau H. Treadmill 

walking in incomplete spinal-cord-injured subjects: 

2. Factors limiting the maximal speed. Spinal Cord 

2003;41(5):271-9. No relevant outcomes 

469. Pepin A, Norman KE, Barbeau H. Treadmill walking 

in incomplete spinal-cord-injured subjects: 1. 

Adaptation to changes in speed. Spinal Cord 

2003;41(5):257-70. No relevant outcomes 

470. Perell K, Scremin A, Scremin O, Kunkel C. 

Quantifying muscle tone in spinal cord injury patients 

using isokinetic dynamometric techniques. Paraplegia 

1996;34(1):46-53. No relevant outcomes 

471. Perkash A, Sullivan G, Toth L, Bradleigh LH, Linder 

SH, Perkash I. Persistent hypercoagulation associated 

with heterotopic ossification in patients with spinal 

cord injury long after injury has occurred. Paraplegia 

1993 Oct;31(10):653-9. Case-series 

472. Perkins TA, de NDN, Hatcher NA, Swain ID, Wood 

DE. Control of leg-powered paraplegic cycling using 

stimulation of the lumbo-sacral anterior spinal nerve 

roots. IEEE Trans Neural Syst Rehabil Eng 

2002;10(3):158-64. No relevant outcomes 

473. Peterson C. The use of electrical stimulation and 

taping to address shoulder subluxation for a patient 

with central cord syndrome. Phys Ther 

2004;84(7):634-43. No relevant outcomes 

474. Petrofsky JS, Laymon M. Blood pressure and heart 

rate responses during a fatiguing isometric exercise in 

paraplegic men with hypertension. Eur J Appl 

Physiol 2000;83(4):274-82. No relevant outcomes 

475. Petrofsky JS, Stacy R, Laymon M. The relationship 

between exercise work intervals and duration of 

exercise on lower extremity training induced by 

electrical stimulation in humans with spinal cord 

injuries. Eur J Appl Physiol 2000;82(5):504-9. No 

relevant outcomes 

476. Phillips SM, Stewart BG, Mahoney DJ, Hicks AL, 

McCartney N, Tang JE, et al. Body-weight-support 

treadmill training improves blood glucose regulation 

in persons with incomplete spinal cord injury. Journal 

of Applied Physiology 2004;97(2):716-24. Less than 

100 patients in study 

477. Phillips WT, Burkett LN. Augmented upper body 

contribution to oxygen uptake during upper body 

exercise with concurrent leg functional electrical 

stimulation in persons with spinal cord injury. Spinal 

Cord 1998;36(11):750-5. No relevant outcomes 

478. Piatt JH, Jr. Detected and overlooked cervical spine 

injury among comatose trauma patients: from the 

Pennsylvania Trauma Outcomes Study. Neurosurg 

Focus 2005 Oct 15;19(4):E6. Not eligible outcomes 

479. Pongratz G, Zietz B, Gluck T, Scholmerich J, Straub 

RH. Corticotropin-releasing factor modulates 

cardiovascular and pupillary autonomic reflexes in 

man: is there a link to inflammation-induced 

autonomic nervous hyperreflexia? Ann N Y Acad Sci 

2002 Jun;966:373-83. Not eligible target population 

480. Popovic MR, Keller T, Pappas IP, Dietz V, Morari 

M. Surface-stimulation technology for grasping and 

walking neuroprosthesis. IEEE Eng Med Biol Mag 

2001 Jan-Feb;20(1):82-93. Not eligible target 

population 

481. Popovic MR, Thrasher TA, Adams ME, Takes V, 

Zivanovic V, Tonack MI. Functional electrical 

therapy: retraining grasping in spinal cord injury. 

Spinal Cord 2006;44(3):143-51. No relevant 

outcomes 

482. Post MJ, Becerra JL, Madsen PW, Puckett W, 

Quencer RM, Bunge RP, et al. Acute spinal subdural 

hematoma: MR and CT findings with pathologic 

correlates. AJNR Am J Neuroradiol 1994 

Nov;15(10):1895-905. Not eligible target population 

483. Powell M, Kirshblum S, O'Connor KC. Duplex 

ultrasound screening for deep vein thrombosis in 

spinal cord injured patients at rehabilitation 

admission. Arch Phys Med Rehabil 1999 

Sep;80(9):1044-6. Not eligible target population 

484. Price MJ, Campbell IG. Thermoregulatory responses 

of spinal cord injured and able-bodied athletes to 

prolonged upper body exercise and recovery. Spinal 

Cord 1999;37(11):772-9. No relevant outcomes 

485. Price MJ, Campbell IG. Thermoregulatory responses 

during prolonged upper-body exercise in cool and 

warm conditions. J Sports Sci 2002;20(7):519-27. No 

relevant outcomes 

486. Price MJ, Campbell IG. Effects of spinal cord lesion 

level upon thermoregulation during exercise in the 

heat. Med Sci Sports Exerc 2003;35(7):1100-7. No 

relevant outcomes 

487. Price R, Lehmann JF, Boswell-Bessette S, Burleigh 

A, deLateur BJ. Influence of cryotherapy on 

spasticity at the human ankle. Arch Phys Med 

Rehabil 1993 Mar;74(3):300-4. Not eligible outcomes 

488. Prophet S. Summary of ICD-9-CM Coordination and 

Maintenance Committee meeting. Journal of Ahima 

1999;70(2):64-70; quiz 5-6. No relevant data 
D-20 

489. Protas EJ, Holmes SA, Qureshy H, Johnson A, Lee 

D, Sherwood AM. Supported treadmill ambulation 

training after spinal cord injury: a pilot study. Arch 

Phys Med Rehabil 2001;82(6):825-31. No relevant 

outcomes 

490. Quirke TE, Ritota PC, Swan KG. Inferior vena caval 

filter use in U.S. trauma centers: a practitioner 

survey. Journal of Trauma-Injury Infection & Critical 

Care 1997;43(2):333-7. No relevant data 

491. Rades D, Hoskin PJ, Stalpers LJ, Schulte R, 

Poortmans P, Veninga T, et al. Short-course 

radiotherapy is not optimal for spinal cord 

compression due to myeloma. Int J Radiat Oncol Biol 

Phys 2006 Apr 1;64(5):1452-7. Not eligible target 

population 

492. Raymond J, Davis GM, Clarke J, Bryant G. 

Cardiovascular responses during arm exercise and 

orthostatic challenge in individuals with paraplegia. 

Eur J Appl Physiol 2001;85(1):89-95. No relevant 

outcomes 

493. Raymond J, Davis GM, Climstein M, Sutton JR. 

Cardiorespiratory responses to arm cranking and 

electrical stimulation leg cycling in people with 

paraplegia. Med Sci Sports Exerc 1999;31(6):822-8. 

No relevant outcomes 

494. Raymond J, Davis GM, Fahey A, Climstein M, 

Sutton JR. Oxygen uptake and heart rate responses 

during arm vs combined arm/electrically stimulated 

leg exercise in people with paraplegia. Spinal Cord 

1997;35(10):680-5. No relevant outcomes 

495. Raymond J, Davis GM, van der Plas M. 

Cardiovascular responses during submaximal 

electrical stimulation-induced leg cycling in 

individuals with paraplegia. Clin Physiol Funct 

Imaging 2002;22(2):92-8. No relevant outcomes 

496. Raymond J, Schoneveld K, Van Kemenade CH, 

Davis GM. Onset of electrical stimulation leg cycling 

in individuals with paraplegia. Med Sci Sports Exerc 

2002;34(10):1557-62. No relevant outcomes 

497. Razdan S, Kaul RL, Motta A, Kaul S, Bhatt RK. 

Prevalence and pattern of major neurological 

disorders in rural Kashmir (India) in 1986. 

Neuroepidemiology 1994;13(3):113-9. Not eligible 

outcomes 

498. Rena F, Moshe S, Abraham O. Couples' adjustment 

to one partner's disability: the relationship between 

sense of coherence and adjustment. Soc Sci Med 

1996 Jul;43(2):163-71. Not eligible outcomes 

499. Rendeli C, Castorina M, Ausili E, Girardi E, Fundaro 

C, Caldarelli M, et al. Risk factors for atherogenesis 

in children with spina bifida. Childs Nervous System 

2004;20(6):392-6. Not adult spinal cord injury 

patients 

500. Rieder HP, Peyer C. Sex differences in the serum 

lipoprotein relations of normal persons and multiple 

sclerosis patients. Clinica Chimica Acta 

1970;30(2):305-10. Not adult spinal cord injury 

patients 

501. Rittenberg JD, Burns SP, Little JW. Worsening 

myelopathy masked by peripheral nerve disorders. 

Journal of Spinal Cord Medicine 2004;27(1):72-7. 

Less than 100 patients in study 

502. Rodgers MM, Keyser RE, Gardner ER, Russell PJ, 

Gorman PH. Influence of trunk flexion on 

biomechanics of wheelchair propulsion. J Rehabil 

Res Dev 2000;37(3):283-95. No relevant outcomes 

503. Rodgers MM, Keyser RE, Rasch EK, Gorman PH, 

Russell PJ. Influence of training on biomechanics of 

wheelchair propulsion. J Rehabil Res Dev 

2001;38(5):505-11. No relevant outcomes 

504. Rohde V, Kuker W, Reinges MH, Gilsbach JM. 

Microsurgical treatment of spontaneous and nonspontaneous spinal epidural haematomas: 

neurological outcome in relation to aetiology. Acta 

Neurochir (Wien) 2000;142(7):787-92; discussion 

92-3. Not eligible target population 

505. Roig RL, Worsowicz GM, Stewart DG, Cifu DX. 

Geriatric rehabilitation. 3. Physical medicine and 

rehabilitation interventions for common disabling 

disorders. Archives of Physical Medicine & 

Rehabilitation 2004;85(7 Suppl 3):S12-7; quiz S27-

30. No relevant data 

506. Rosche J, Paulus C, Maisch U, Kaspar A, Mauch E, 

Kornhuber HH. The effects of therapy on spasticity 

utilizing a motorized exercise-cycle. Spinal Cord 

1997;35(3):176-8. No relevant outcomes 

507. Rotter KP, Larrain CG. Gallstones in spinal cord 

injury (SCI): a late medical complication? Spinal 

Cord 2003;41(2):105-8. No relevant data 

508. Rousseau MC, Guillotel B. Risk factors for deep 

venous thrombosis in tetraparesic mentally retarded 

patients. Brain Inj 2001 Dec;15(12):1041-4. Not 

eligible target population 

509. Roussi J, Bentolila S, Boudaoud L, Casadevall N, 

Vallee C, Carlier R, et al. Contribution of D-Dimer 

determination in the exclusion of deep venous 

thrombosis in spinal cord injury patients. Spinal Cord 

1999 Aug;37(8):548-52. Not eligible outcomes 

510. Rubenstein JN, Schaeffer AJ. Managing complicated 

urinary tract infections: the urologic view. Infectious 

Disease Clinics of North America 2003;17(2):333-

51. No relevant data 

511. Rutchik A, Weissman AR, Almenoff PL, Spungen 

AM, Bauman WA, Grimm DR. Resistive inspiratory 

muscle training in subjects with chronic cervical 

spinal cord injury. Arch Phys Med Rehabil 

1998;79(3):293-7. No relevant outcomes 

512. Sabatier MJ, Stoner L, Mahoney ET, Black C, Elder 

C, Dudley GA, et al. Electrically stimulated 

resistance training in SCI individuals increases 

muscle fatigue resistance but not femoral artery size 

or blood flow. Spinal Cord 2006;44(4):227-33. No 

relevant outcomes 

513. Sabick MB, Kotajarvi BR, An KN. A new method to 

quantify demand on the upper extremity during 

manual wheelchair propulsion. Arch Phys Med 

Rehabil 2004 Jul;85(7):1151-9. Not eligible outcomes 

514. Saenz de Tejada I, Goldstein I. Diabetic penile 

neuropathy. Urologic Clinics of North America 

1988;15(1):17-22. Not adult spinal cord injury 

patients 
D-21 

515. Sae-Sia W, Wipke-Tevis DD, Williams DA. Elevated 

sacral skin temperature (T(s)): a risk factor for 

pressure ulcer development in hospitalized 

neurologically impaired Thai patients. Appl Nurs Res 

2005 Feb;18(1):29-35. Not eligible outcomes 

516. Safi HJ, Miller CC, 3rd. Spinal cord protection in 

descending thoracic and thoracoabdominal aortic 

repair. Ann Thorac Surg 1999 Jun;67(6):1937-9; 

discussion 53-8. Not eligible target population 

517. Sairyo K, Katoh S, Sakai T, Mishiro T, Ikata T. 

Characteristics of velocity-controlled knee movement 

in patients with cervical compression myelopathy: 

what is the optimal rehabilitation exercise for spastic 

gait? Spine 2001;26(23):E535-8. Not adult chronic 

SCI patients 

518. Saltzstein RJ, Hardin S, Hastings J. Osteoporosis in 

spinal cord injury: using an index of mobility and its 

relationship to bone density. J Am Paraplegia Soc 

1992 Oct;15(4):232-4. Not eligible outcomes 

519. Salvador de la Barrera S, Barca-Buyo A, MontotoMarques A, Ferreiro-Velasco ME, Cidoncha-Dans 

M, Rodriguez-Sotillo A. Spinal cord infarction: 

prognosis and recovery in a series of 36 patients. 

Spinal Cord 2001 Oct;39(10):520-5. Not eligible 

target population 

520. Sampson EE, Burnham RS, Andrews BJ. Functional 

electrical stimulation effect on orthostatic 

hypotension after spinal cord injury. Arch Phys Med 

Rehabil 2000 Feb;81(2):139-43. Not eligible 

outcomes 

521. Sankale M, Diop B, Quenum C, Ancelle JP, Frament 

V. 4 atypical cases of primary carcinoma of the liver. 

Semaine des Hopitaux 1969;45(5):301-8. Not english 

language 

522. Scalzitti DA. Because of the risk of developing 

heterotopic ossification, are passive range of motion 

exercises contraindicated following traumatic 

injuries? Phys Ther 2003;83(7):659-7. No relevant 

outcomes 

523. Scelsi R, Scelsi L, Bocchi R, Lotta S. Morphological 

changes in the skin microlymphatics in recently 

injured paraplegic patients with ilio-femoral venous 

thrombosis. Paraplegia 1995 Aug;33(8):472-5. Not 

eligible target population 

524. Scelza WM, Kalpakjian CZ, Zemper ED, Tate DG. 

Perceived barriers to exercise in people with spinal 

cord injury. Am J Phys Med Rehabil 2005;84(8):576-

83. No relevant outcomes 

525. Schalow G. Partial cure of spinal cord injury 

achieved by 6 to 13 months of coordination dynamic 

therapy. Electromyogr Clin Neurophysiol 

2003;43(5):281-92. No relevant outcomes 

526. Schalow G, Blanc Y, Jeltsch W, Zach GA. 

Electromyographic identification of spinal oscillator 

patterns and recouplings in a patient with incomplete 

spinal cord lesion: oscillator formation training as a 

method to improve motor activities. Gen Physiol 

Biophys 1996;15 Suppl 1:121-220. No relevant 

outcomes 

527. Schalow G, Paasuke M. Low-load coordination 

dynamics in athletes, physiotherapists, gymnasts, 

musicians and patients with spinal cord injury, after 

stroke, traumatic brain lesion and with cerebral palsy. 

Electromyogr Clin Neurophysiol 2003;43(4):195-

201. No relevant outcomes 

528. Schalow G, Paasuke M, Kolts I. High-load 

coordination dynamics in athletes, physiotherapists, 

gymnasts, musicians and patients with CNS injury. 

Electromyogr Clin Neurophysiol 2003;43(6):353-65. 

No relevant outcomes 

529. Schizas C, Ballesteros C, Roy P. Cauda equina 

compression after trauma: an unusual presentation of 

spinal epidural lipoma. Spine 2003;28(8):E148-51. 

Less than 100 patients in study 

530. Schmid A, Halle M, Stutzle C, Konig D, Baumstark 

MW, Storch MJ, et al. Lipoproteins and free plasma 

catecholamines in spinal cord injured men with 

different injury levels. Clin Physiol 2000 

Jul;20(4):304-10. Not eligible outcomes 

531. Schmid A, Huonker M, Barturen JM, Stahl F, 

Schmidt-Trucksass A, Konig D, et al. 

Catecholamines, heart rate, and oxygen uptake during 

exercise in persons with spinal cord injury. J Appl 

Physiol 1998;85(2):635-41. No relevant outcomes 

532. Schmid A, Huonker M, Stahl F, Barturen JM, Konig 

D, Heim M, et al. Free plasma catecholamines in 

spinal cord injured persons with different injury 

levels at rest and during exercise. J Auton Nerv Syst 

1998;68(1):96-100. No relevant outcomes 

533. Schmid A, Huonker M, Stober P, Barturen JM, 

Schmidt-Trucksass A, Durr H, et al. Physical 

performance and cardiovascular and metabolic 

adaptation of elite female wheelchair basketball 

players in wheelchair ergometry and in competition. 

Am J Phys Med Rehabil 1998;77(6):527-33. No 

relevant outcomes 

534. Schmid A, Schmidt-Trucksass A, Huonker M, Konig 

D, Eisenbarth I, Sauerwein H, et al. Catecholamines 

response of high performance wheelchair athletes at 

rest and during exercise with autonomic dysreflexia. 

Int J Sports Med 2001;22(1):2-7. No relevant 

outcomes 

535. Schmitt AB, Buss A, Breuer S, Brook GA, Pech K, 

Martin D, et al. Major histocompatibility complex 

class II expression by activated microglia caudal to 

lesions of descending tracts in the human spinal cord 

is not associated with a T cell response. Acta 

Neuropathol (Berl) 2000 Nov;100(5):528-36. Not 

eligible target population 

536. Schneider DA, Sedlock DA, Gass E, Gass G. 

VO2peak and the gas-exchange anaerobic threshold 

during incremental arm cranking in able-bodied and 

paraplegic men. Eur J Appl Physiol Occup Physiol 

1999;80(4):292-7. No relevant outcomes 

537. Schubert V, Fagrell B. Postocclusive reactive 

hyperemia and thermal response in the skin 

microcirculation of subjects with spinal cord injury. 

Scand J Rehabil Med 1991;23(1):33-40. Not eligible 

outcomes 
D-22 

538. Scott CI, Jr. Medical and social adaptation in 

dwarfing conditions. Birth Defects: Original Article 

Series 1977;13(3C):29-43. Not adult spinal cord 

injury patients 

539. Scott D, Papa MZ, Sareli M, Velano A, Ben-Ari GY, 

Koller M. Management of hemorrhoidal disease in 

patients with chronic spinal cord injury. Tech 

Coloproctol 2002 Apr;6(1):19-22. Not eligible 

outcomes 

540. Scremin AM, Kurta L, Gentili A, Wiseman B, Perell 

K, Kunkel C, et al. Increasing muscle mass in spinal 

cord injured persons with a functional electrical 

stimulation exercise program. Arch Phys Med 

Rehabil 1999;80(12):1531-6. No relevant outcomes 

541. Sedlock DA, Schneider DA, Gass E, Gass G. Excess 

post-exercise oxygen consumption in spinal cordinjured men. Eur J Appl Physiol 2004;93(1):231-6. 

No relevant outcomes 

542. Seelen HA, Potten YJ, Drukker J, Reulen JP, Pons C. 

Development of new muscle synergies in postural 

control in spinal cord injured subjects. J 

Electromyogr Kinesiol 1998;8(1):23-34. No relevant 

outcomes 

543. Selmi F, Davies KG, Sharma RR, Redfern RM. 

Idiopathic spinal extradural lipomatosis in a nonobese otherwise healthy man. British Journal of 

Neurosurgery 1994;8(3):355-8. Not adult spinal cord 

injury patients 

544. Sencer W. THE CEREBROSPINAL FLUID IN 

MYELORADICULOPATHIES ASSOCIATED 

WITH DIABETES MELLITUS. Journal of the 

Mount Sinai Hospital, New York 1964 MayJun;31:202-11. Not adult spinal cord injury patients 

545. Seymour RJ, Lacefield WE. Wheelchair cushion 

effect on pressure and skin temperature. Archives of 

Physical Medicine & Rehabilitation 1985;66(2):103-

8. No relevant data 

546. Shaffer EA. Gallstone disease: Epidemiology of 

gallbladder stone disease. Best Practice & Research 

in Clinical Gastroenterology 2006;20(6):981-96. Not 

adult spinal cord injury patients 

547. Shetty KR, Sutton CH, Rudman IW, Rudman D. 

Lipid and lipoprotein abnormalities in young 

quadriplegic men. American Journal of the Medical 

Sciences 1992;303(4):213-6. Less than 100 patients 

in study 

548. Shiiya N, Kunihara T, Matsuzaki K, Yasuda K. 

Evolving strategy and results of spinal cord 

protection in type I and II thoracoabdominal aortic 

aneurysm repair. Ann Thorac Cardiovasc Surg 2005 

Jun;11(3):178-85. Not eligible target population 

549. Shimizu T, Shimada H, Shirakura K. Scapulohumeral 

reflex (Shimizu). Its clinical significance and testing 

maneuver. Spine 1993 Nov;18(15):2182-90. Not 

eligible outcomes 

550. Shiraishi N, Matsumura G. Prevention of vascular 

injury to the spinal cord incidence of a great posterior 

radicular artery. Okajimas Folia Anat Jpn 2005 

Mar;81(6):143-6. Not eligible target population 

551. Sidman JM. Sexual functioning and the physically 

disabled adult. American Journal of Occupational 

Therapy 1977;31(2):81-5. No relevant data 

552. Silva AC, Neder JA, Chiurciu MV, Pasqualin DC, da 

Silva RC, Fernandez AC, et al. Effect of aerobic 

training on ventilatory muscle endurance of spinal 

cord injured men. Spinal Cord 1998;36(4):240-5. No 

relevant outcomes 

553. Silver JR, Noori Z. Pulmonary embolism following 

anticoagulation therapy. International Disability 

Studies 1991;13(1):16-9. Less than 100 patients in 

study 

554. Sinderby C, Weinberg J, Sullivan L, Borg J, 

Lindstrom L, Grassino A. Diaphragm function in 

patients with cervical cord injury or prior 

poliomyelitis infection. Spinal Cord 1996;34(4):204-

13. No relevant outcomes 

555. Sinderby C, Weinberg J, Sullivan L, Lindstrom L, 

Grassino A. Electromyographical evidence for 

exercise-induced diaphragm fatigue in patients with 

chronic cervical cord injury or prior poliomyelitis 

infection. Spinal Cord 1996;34(10):594-601. No 

relevant outcomes 

556. Singh A, Crockard HA. Quantitative assessment of 

cervical spondylotic myelopathy by a simple walking 

test. Lancet 1999;354(9176):370-3. Not adult chronic 

SCI patients 

557. Slade JM, Bickel CS, Dudley GA. The effect of a 

repeat bout of exercise on muscle injury in persons 

with spinal cord injury. Eur J Appl Physiol 

2004;92(3):363-6. No relevant outcomes 

558. Sliwa JA, Mason K, Yarkony G, Press J, Lovell L. 

The value of routine chest roentgenograms on 

admission for rehabilitation after traumatic spinal 

cord injury. Am J Phys Med Rehabil 1994 

Apr;73(2):84-8. Not eligible target population 

559. Smals AG. Impotence: organic causes. Nederlands 

Tijdschrift voor Geneeskunde 1986;130(15):675-80. 

Not english language 

560. Smith HC, Davey NJ, Savic G, Maskill DW, Ellaway 

PH, Frankel HL. Motor unit discharge characteristics 

during voluntary contraction in patients with 

incomplete spinal cord injury. Exp Physiol 1999 

Nov;84(6):1151-60. Not eligible outcomes 

561. Smith J, Caldwell E, Sugrue M. Difference in trauma 

team activation criteria between hospitals within the 

same region. Emerg Med Australas 2005 OctDec;17(5-6):480-7. Not eligible target population 

562. Stanghelle JK, Festvag LV. Postpolio syndrome: a 5 

year follow-up. Spinal Cord 1997;35(8):503-8. Not 

adult chronic SCI patients 

563. Steers WD. Rat: overview and innervation. [Review] 

[112 refs]. Neurourology & Urodynamics 

1994;13(2):97-118. Not human subjects 

564. Stein RB, Chong SL, James KB, Bell GJ. Improved 

efficiency with a wheelchair propelled by the legs 

using voluntary activity or electric stimulation. Arch 

Phys Med Rehabil 2001;82(9):1198-203. No exercise 

program or physical activity 

565. Stein RB, Zehr EP, Lebiedowska MK, Popovic DB, 

Scheiner A, Chizeck HJ. Estimating mechanical 

parameters of leg segments in individuals with and 

without physical disabilities. IEEE Trans Rehabil 

Eng 1996 Sep;4(3):201-11. Not eligible outcomes 
D-23 

566. Steinberg LL, Lauro FA, Sposito MM, Tufik S, 

Mello MT, Naffah-Mazzacoratti MG, et al. 

Catecholamine response to exercise in individuals 

with different levels of paraplegia. Braz J Med Biol 

Res 2000;33(8):913-8. No relevant outcomes 

567. Steinberg LL, Sposito MM, Lauro FA, Tufik S, 

Mello MT, Naffah-Mazzacoratti MG, et al. Serum 

level of serotonin during rest and during exercise in 

paraplegic patients. Spinal Cord 1998;36(1):18-20. 

No relevant outcomes 

568. Sterbis JR, Lewis VL, Bushman W. Urologic and 

plastic surgical collaboration for continent diversion 

when urine leakage is complicated by pressure ulcers 

or obesity. Journal of Spinal Cord Medicine 

2003;26(2):124-8. No relevant data 

569. Stoner L, Sabatier M, VanhHiel L, Groves D, Ripley 

D, Palardy G, et al. Upper vs lower extremity arterial 

function after spinal cord injury. J Spinal Cord Med 

2006;29(2):138-46. Not eligible outcomes 

570. Strachan RK, Cook J, Wilkie W, Kennedy NS. An 

evaluation of pneumatic orthoses in thoracic 

paraplegia. Paraplegia 1985;23(5):295-305. Less than 

100 patients in study 

571. Stroman PW, Nance PW, Ryner LN. BOLD MRI of 

the human cervical spinal cord at 3 tesla. Magn 

Reson Med 1999;42(3):571-6. Not adult chronic SCI 

patients 

572. Subbotin AV, Kovalenko VN, Apasova NA. The 

clinical picture and differential diagnosis of spinal 

strokes. Zhurnal Nevropatologii i Psikhiatrii Imeni S 

- S - Korsakova 1970;70(6):824-8. Not english 

language 

573. Sugiyama T, Fugelso P, Avon M. Extracorporeal 

shock wave lithotripsy in neurologically impaired 

patients. Semin Urol 1992 May;10(2):109-11. Not 

eligible outcomes 

574. Sutbeyaz ST, Koseoglu BF, Gokkaya NK. The 

combined effects of controlled breathing techniques 

and ventilatory and upper extremity muscle exercise 

on cardiopulmonary responses in patients with spinal 

cord injury. Int J Rehabil Res 2005;28(3):273-6. No 

relevant outcomes 

575. Swarczinski C, Dijkers M. The value of serial leg 

measurements for monitoring deep vein thrombosis 

in spinal cord injury. J Neurosci Nurs 1991 

Oct;23(5):306-14. Not eligible target population 

576. Sytin LV, Slepushkin VD, Zoloev GK, Argintaev ES, 

Lasukova TV. Disorders of metabolism and their 

pathogenesis in patients with spinal cord injuries. 

Ortopediia Travmatologiia i Protezirovanie 

1989(5):16-8. Not english language 

577. Szlachcic Y, Adkins RH, Adal T, Yee F, Bauman W, 

Waters RL. The effect of dietary intervention on lipid 

profiles in individuals with spinal cord injury. J 

Spinal Cord Med 2001 Spring;24(1):26-9. Not 

eligible exposure 

578. Szlachcic Y, Adkins RH, Waters RL, Govindarajan 

S, Wang J, Yee F, et al. Incidence and clinical 

correlates of increased serum creatine kinase levels in 

persons with spinal cord injury. J Spinal Cord Med 

2002;25(3):156-60. No exercise program or physical 

activity 

579. Taira T, Kawamura H, Tanikawa T, Iseki H, 

Kawabatake H, Takakura K. A new approach to 

control central deafferentation pain: spinal intrathecal 

baclofen. Stereotact Funct Neurosurg 1995;65(1-

4):101-5. Not eligible outcomes 

580. Taira T, Kawamura H, Tanikawa T, Kawabatake H, 

Iseki H, Ueda A, et al. A new approach to the control 

of central deafferentation pain--spinal intrathecal 

baclofen. Acta Neurochir Suppl 1995;64:136-8. Not 

eligible outcomes 

581. Takahashi M, Sakaguchi A, Matsukawa K, Komine 

H, Kawaguchi K, Onari K. Cardiovascular control 

during voluntary static exercise in humans with 

tetraplegia. J Appl Physiol 2004;97(6):2077-82. No 

relevant outcomes 

582. Tarabulcy E. Neurogenic diseases of the bladder in 

the geriatric population. Geriatrics 1974;29(9):123-8 

passim. No relevant data 

583. Tariq M, Morais C, Kishore PN, Biary N, Al Deeb S, 

Al Moutaery K. Neurological recovery in diabetic 

rats following spinal cord injury. Journal of 

Neurotrauma 1998;15(4):239-51. Not human subjects 

584. Tator CH, Koyanagi I. Vascular mechanisms in the 

pathophysiology of human spinal cord injury. J 

Neurosurg 1997 Mar;86(3):483-92. Not eligible 

target population 

585. Taylor PN, Burridge JH, Dunkerley AL, Wood DE, 

Norton JA, Singleton C, et al. Clinical use of the 

Odstock dropped foot stimulator: its effect on the 

speed and effort of walking. Arch Phys Med Rehabil 

1999 Dec;80(12):1577-83. Not eligible outcomes 

586. Teasell RW, Arnold JM. Alpha-1 adrenoceptor 

hyperresponsiveness in three neuropathic pain states: 

complex regional pain syndrome 1, diabetic 

peripheral neuropathic pain and central pain states 

following spinal cord injury. Pain Research & 

Management 2004;9(2):89-97. No relevant data 

587. Teixeira da Cunha-Filho I, Henson H, Qureshy H, 

Williams AL, Holmes SA, Protas EJ. Differential 

responses to measures of gait performance among 

healthy and neurologically impaired individuals. 

Arch Phys Med Rehabil 2003;84(12):1774-9. No 

relevant outcomes 

588. Telfeian AE, Reiter GT, Durham SR, Marcotte P. 

Spine surgery in morbidly obese patients. Journal of 

Neurosurgery 2002;97(1 Suppl):20-4. Less than 100 

patients in study 

589. Ter Woerds W, De Groot PC, van Kuppevelt DH, 

Hopman MT. Passive leg movements and passive 

cycling do not alter arterial leg blood flow in subjects 

with spinal cord injury. Phys Ther 2006;86(5):636-

45. No relevant outcomes 

590. Theisen D, Fornusek C, Raymond J, Davis GM. 

External power output changes during prolonged 

cycling with electrical stimulation. J Rehabil Med 

2002;34(4):171-5. No relevant outcomes 

591. Theisen D, Vanlandewijck Y, Sturbois X, Francaux 

M. Cutaneous vascular response and 

thermoregulation in individuals with paraplegia 

during sustained arm-cranking exercise. Int J Sports 

Med 2001;22(2):97-102. No relevant outcomes 
D-24 

592. Thijssen DH, Heesterbeek P, van Kuppevelt DJ, 

Duysens J, Hopman MT. Local vascular adaptations 

after hybrid training in spinal cord-injured subjects. 

Med Sci Sports Exerc 2005;37(7):1112-8. No 

relevant outcomes 

593. Thomas AJ, Jr. Ejaculatory dysfunction. Fertility & 

Sterility 1983;39(4):445-54. No relevant data 

594. Thomas SL, Gorassini MA. Increases in corticospinal 

tract function by treadmill training after incomplete 

spinal cord injury. J Neurophysiol 2005;94(4):2844-

55. No relevant outcomes 

595. Thorfinn J, Sjoberg F, Sjostrand L, Lidman D. 

Perfusion of the skin of the buttocks in paraplegic 

and tetraplegic patients, and in healthy subjects after 

a short and long load. Scand J Plast Reconstr Surg 

Hand Surg 2006;40(3):153-60. Not eligible outcomes 

596. Thrasher TA, Flett HM, Popovic MR. Gait training 

regimen for incomplete spinal cord injury using 

functional electrical stimulation. Spinal Cord 

2006;44(6):357-61. No relevant outcomes 

597. Thyberg M, Ertzgaard P, Gylling M, Granerus G. 

Blood pressure response to detrusor pressure 

elevation in patients with a reflex urinary bladder 

after a cervical or high thoracic spinal cord injury. 

Scand J Rehabil Med 1992 Dec;24(4):187-93. Not 

eligible outcomes 

598. Tomaio A, Kirshblum SC, O'Connor KC, Johnston 

M. Treatment of acute deep vein thrombosis in spinal 

cord injured patients with enoxaparin: a cost analysis. 

J Spinal Cord Med 1998 Jul;21(3):205-10. Not 

eligible target population 

599. Trimble MH, Kukulka CG, Behrman AL. The effect 

of treadmill gait training on low-frequency 

depression of the soleus H-reflex: comparison of a 

spinal cord injured man to normal subjects. Neurosci 

Lett 1998;246(3):186-8. No relevant outcomes 

600. Trumbower RD, Faghri PD. Kinematic analyses of 

semireclined leg cycling in able-bodied and spinal 

cord injured individuals. Spinal Cord 

2005;43(9):543-9. No relevant outcomes 

601. Truss MC, Djamilian MH, Tan HK, Hinrichs H, 

Feistner H, Stief CG, et al. Single potential analysis 

of cavernous electrical activity. Four years' 

experience in more than 500 patients with erectile 

dysfunction. European Urology 1993;24(3):358-65. 

No relevant data 

602. Tsuji M, Kurihara A, Uratsuji M, Shoda E. Cervical 

myelopathy with Prader-Willi syndrome in a 13-yearold boy. A case report. Spine 1991;16(11):1342-4. 

Not adult spinal cord injury patients 

603. Uijl SG, Houtman S, Folgering HT, Hopman MT. 

Training of the respiratory muscles in individuals 

with tetraplegia. Spinal Cord 1999;37(8):575-9. No 

relevant outcomes 

604. Unsal A, Yilmaz B, Turgut AT, Taskin F, Alaca R, 

Karaman CZ. Evaluation of varicocele frequency of 

patients with spinal cord injury by color Doppler 

ultrasonography: a new etiological factor for 

varicocele? Eur J Radiol 2006 Jan;57(1):154-7. Not 

eligible outcomes 

605. Vale FL, Oliver M, Cahill DW. Rigid 

occipitocervical fusion. J Neurosurg 1999 Oct;91(2 

Suppl):144-50. Not eligible outcomes 

606. van Dijk JM, Lubout CM, Brouwer PA. Cervical 

high-intensity intramedullary lesions without spinal 

cord compression in achondroplasia. J Neurosurg 

Spine 2007 Apr;6(4):304-8. Not eligible target 

population 

607. van Hedel HJ, Waldvogel D, Dietz V. Learning a 

high-precision locomotor task in patients with 

Parkinson's disease. Mov Disord 2006;21(3):406-11. 

Not adult chronic SCI patients 

608. van Hedel HJ, Wirth B, Dietz V. Limits of locomotor 

ability in subjects with a spinal cord injury. Spinal 

Cord 2005;43(10):593-603. No relevant outcomes 

609. Vaziri ND, Gordon S, Nikakhtar B. Lipid 

abnormalities in chronic renal failure associated with 

spinal cord injury. Paraplegia 1982;20(3):183-9. Less 

than 100 patients in study 

610. Vemireddi NK. Sexual counseling for chronically 

disabled patients. Geriatrics 1978;33(7):65-9. No 

relevant data 

611. Ventimiglia B, Patti F, Reggio E, Failla G, Morana 

C, Lopes M, et al. Disorders of micturition in 

neurological patients. A clinical study of 786 

patients. J Neurol 1998 Mar;245(3):173-7. Not 

eligible outcomes 

612. Verellen J, Theisen D, Vanlandewijck Y. Influence 

of crank rate in hand cycling. Med Sci Sports Exerc 

2004;36(10):1826-31. No relevant outcomes 

613. Veron JP, Escourolle R. Current data on orthostatic 

hypotension. Presse Medicale 1968;76(49):2343-6. 

Not english language 

614. Vestergaard P, Krogh K, Rejnmark L, Mosekilde L. 

Fracture rates and risk factors for fractures in patients 

with spinal cord injury. Spinal Cord 

1998;36(11):790-6. No exercise program or physical 

activity 

615. Vidal J, Javierre C, Curia FJ, Garrido E, Lizarraga 

MA, Segura R. Long-term evolution of blood lipid 

profiles and glycemic levels in patients after spinal 

cord injury. Spinal Cord 2003;41(3):178-81. No 

relevant data 

616. Vidal J, Javierre C, Segura R, Lizarraga A, Barbany 

JR, Perez A. Physiological adaptations to exercise in 

people with spinal cord injury. J Physiol Biochem 

2003;59(1):11-8. No relevant outcomes 

617. Vinet A, Bernard PL, Poulain M, Varray A, Le 

Gallais D, Micallef JP. Validation of an incremental 

field test for the direct assessment of peak oxygen 

uptake in wheelchair-dependent athletes. Spinal Cord 

1996;34(5):288-93. No relevant outcomes 

618. Vinet A, Le Gallais D, Bouges S, Bernard PL, 

Poulain M, Varray A, et al. Prediction of VO(2peak) 

in wheelchair-dependent athletes from the adapted 

Leger and Boucher test. Spinal Cord 

2002;40(10):507-12. No relevant outcomes 

619. Vitenzon AS, Mironov EM, Petrushanskaya KA. 

Functional electrostimulation of muscles as a method 

for restoring motor functions. Neurosci Behav 

Physiol 2005 Sep;35(7):709-14. Not eligible 

outcomes 
D-25 

620. Vogel G. Cell biology. Still waiting their turn. 

Science 2005;308(5728):1536-7. No relevant data 

621. Wade TP, Andrus CH. Cardiorespiratory effects of 

laparotomy in patients with spinal cord injury. Am 

Surg 1993 Oct;59(10):689-91. Not eligible exposure 

622. Wald A. Systemic diseases causing disorders of 

defecation and continence. Seminars in 

Gastrointestinal Disease 1995;6(4):194-202. No 

relevant data 

623. Walker WA, Evans BJ, Pate JW, Weiman DS, Riddle 

JC. Coronary operations in patients with spinal cord 

injury. Ann Thorac Surg 1996 Mar;61(3):789-94. 

Case-series 

624. Wall BM, Huch KM, Runyan KR, Williams HH, 

Gavras H, Cooke CR. Effects of vasopressin V1-

receptor blockade during acute and sustained 

hypovolemic hypotension. Am J Physiol 1996 

Feb;270(2 Pt 2):R356-64. Not eligible exposure 

625. Wallington M, Mendis S, Premawardhana U, Sanders 

P, Shahsavar-Haghighi K. Local control and survival 

in spinal cord compression from lymphoma and 

myeloma. Radiother Oncol 1997 Jan;42(1):43-7. Not 

eligible target population 

626. Walterbusch G, Fromke J, Sydow M. A simple 

method to reduce ischemic time of the spinal cord in 

extensive thoracoabdominal aneurysm operations. 

Thorac Cardiovasc Surg 2003 Feb;51(1):46-8. Not 

eligible target population 

627. Wang H, Hiatt WR, Barstow TJ, Brass EP. 

Relationships between muscle mitochondrial DNA 

content, mitochondrial enzyme activity and oxidative 

capacity in man: alterations with disease. Eur J Appl 

Physiol Occup Physiol 1999;80(1):22-7. No relevant 

outcomes 

628. Wang JS, Yang CF, Wong MK. Effect of strenuous 

arm crank exercise on platelet function in patients 

with spinal cord injury. Arch Phys Med Rehabil 

2002;83(2):210-6. No relevant outcomes 

629. Wang JS, Yang CF, Wong MK, Chow SE, Chen JK. 

Effect of strenuous arm exercise on oxidized-LDLpotentiated platelet activation in individuals with 

spinal cord injury. Thromb Haemost 2000;84(1):118-

23. No relevant outcomes 

630. Waring WP, Karunas RS. Acute spinal cord injuries 

and the incidence of clinically occurring 

thromboembolic disease. Paraplegia 1991 

Jan;29(1):8-16. Not eligible target population 

631. Warms CA, Belza BL, Whitney JD, Mitchell PH, 

Stiens SA. Lifestyle physical activity for individuals 

with spinal cord injury: a pilot study. Am J Health 

Promot 2004;18(4):288-91. No relevant outcomes 

632. Washburn RA, Zhu W, McAuley E, Frogley M, 

Figoni SF. The physical activity scale for individuals 

with physical disabilities: development and 

evaluation. Arch Phys Med Rehabil 2002;83(2):193-

200. No exercise program or physical activity 

633. Waters JH, Watson TB, Ward MG. Conus medullaris 

injury following both tetracaine and lidocaine spinal 

anesthesia. Journal of Clinical Anesthesia 

1996;8(8):656-8. Not adult spinal cord injury 

patients 

634. Waters RL, Meyer PR, Jr., Adkins RH, Felton D. 

Emergency, acute, and surgical management of spine 

trauma. Arch Phys Med Rehabil 1999 

Nov;80(11):1383-90. Not eligible target population 

635. Webborn N, Price MJ, Castle PC, Goosey-Tolfrey 

VL. Effects of two cooling strategies on 

thermoregulatory responses of tetraplegic athletes 

during repeated intermittent exercise in the heat. J 

Appl Physiol 2005;98(6):2101-7. No relevant 

outcomes 

636. Weck M, Pause M, Pinzer T. Spinal meningioma as 

differential diagnosis of diabetic polyneuropathy. 

Deutsche Medizinische Wochenschrift 

2001;126(20):590-2. Not english language 

637. Weigang E, Hartert M, von Samson P, Pechstein U, 

Genstorfer J, Pitzer K, et al. Improved spinal cord 

perfusion during thoracoabdominal aortic repair. 

Thorac Cardiovasc Surg 2005 Apr;53(2):69-73. Not 

eligible target population 

638. Weiss HD. Mechanism of erection. Medical Aspects 

of Human Sexuality 1973;7(2):28. No relevant data 

639. Wekre LL, Stanghelle JK, Lobben B, Oyhaugen S. 

The Norwegian Polio Study 1994: a nation-wide 

survey of problems in long-standing poliomyelitis. 

Spinal Cord 1998;36(4):280-4. Not adult chronic SCI 

patients 

640. Wernig A, Nanassy A, Muller S. Maintenance of 

locomotor abilities following Laufband (treadmill) 

therapy in para- and tetraplegic persons: follow-up 

studies. Spinal Cord 1998;36(11):744-9. No relevant 

outcomes 

641. Wernig A, Nanassy A, Muller S. Laufband 

(treadmill) therapy in incomplete paraplegia and 

tetraplegia. J Neurotrauma 1999;16(8):719-26. No 

relevant outcomes 

642. Wheeler GD, Andrews B, Lederer R, Davoodi R, 

Natho K, Weiss C, et al. Functional electric 

stimulation-assisted rowing: Increasing 

cardiovascular fitness through functional electric 

stimulation rowing training in persons with spinal 

cord injury. Arch Phys Med Rehabil 

2002;83(8):1093-9. No relevant outcomes 

643. Wheeler GD, Ashley EA, Harber V, Laskin JJ, 

Olenik LM, Sloley D, et al. Hormonal responses to 

graded-resistance, FES-assisted strength training in 

spinal cord-injured. Spinal Cord 1996;34(5):264-7. 

No relevant outcomes 

644. Whitehouse FW. Two minutes with diabetes. 

Medical Times 1967;95(3):354-5. Not adult spinal 

cord injury patients 

645. Widerstrom-Noga EG, Felipe-Cuervo E, Yezierski 

RP. Chronic pain after spinal injury: interference 

with sleep and daily activities. Arch Phys Med 

Rehabil 2001;82(11):1571-7. No exercise program or 

physical activity 

646. Wieler M, Stein RB, Ladouceur M, Whittaker M, 

Smith AW, Naaman S, et al. Multicenter evaluation 

of electrical stimulation systems for walking. Arch 

Phys Med Rehabil 1999 May;80(5):495-500. Not 

eligible outcomes 
D-26 

647. Wien MF, Garshick E, Tun CG, Lieberman SL, 

Kelley A, Brown R. Breathlessness and exercise in 

spinal cord injury. J Spinal Cord Med 

1999;22(4):297-302. No relevant outcomes 

648. Williams RC, Jr., Sugiura K, Tan EM. Antibodies to 

microtubule-associated protein 2 in patients with 

neuropsychiatric systemic lupus erythematosus. 

Arthritis Rheum 2004 Apr;50(4):1239-47. Not 

eligible taret population 

649. Willis BK, Greiner F, Orrison WW, Benzel EC. The 

incidence of vertebral artery injury after midcervical 

spine fracture or subluxation. Neurosurgery 1994 

Mar;34(3):435-41; discussion 41-2. Not eligible 

outcomes 

650. Willoughby DS, Priest JW, Jennings RA. Myosin 

heavy chain isoform and ubiquitin protease mRNA 

expression after passive leg cycling in persons with 

spinal cord injury. Arch Phys Med Rehabil 

2000;81(2):157-63. No relevant outcomes 

651. Willoughby DS, Priest JW, Nelson M. Expression of 

the stress proteins, ubiquitin, heat shock protein 72, 

and myofibrillar protein content after 12 weeks of leg 

cycling in persons with spinal cord injury. Arch Phys 

Med Rehabil 2002;83(5):649-54. No relevant 

outcomes 

652. Winchester PK, Williamson JW, Mitchell JH. 

Cardiovascular responses to static exercise in patients 

with Brown-Sequard syndrome. J Physiol 2000;527 

Pt 1:193-202. Not adult chronic SCI patients 

653. Winemiller MH, Stolp-Smith KA, Silverstein MD, 

Therneau TM. Prevention of venous 

thromboembolism in patients with spinal cord injury: 

effects of sequential pneumatic compression and 

heparin. J Spinal Cord Med 1999 Fall;22(3):182-91. 

Not eligible target population 

654. Winther K, Gleerup G, Snorrason K, BieringSorensen F. Platelet function and fibrinolytic activity 

in cervical spinal cord injured patients. Thromb Res 

1992 Feb 1;65(3):469-74. Not eligible outcomes 

655. Witt MA, Grantmyre JE. Ejaculatory failure. World 

Journal of Urology 1993;11(2):89-95. No relevant 

data 

656. Woertler K, Lindner N, Gosheger G, Brinkschmidt C, 

Heindel W. Osteochondroma: MR imaging of tumorrelated complications. Eur Radiol 2000;10(5):832-40. 

Not eligible target population 

657. Wohlgemuth WA, Stoehr M. Percutaneous arterial 

interventional treatment of exercise-induced 

neurogenic intermittent claudication due to ischaemia 

of the lumbosacral plexus. J Neurol 2002;249(8):988-

92. Not adult chronic SCI patients 

658. Wong PY, Wang YC, Chu NK, Tang FT, Wong MK. 

Body weight, serum uric acid and lipid profile one 

year after spinal cord injury. Chang Gung Medical 

Journal 2001;24(9):569-75. Less than 100 patients in 

study 

659. Yaggie JA, Niemi TJ, Buono MJ. Adaptive sweat 

gland response after spinal cord injury. Arch Phys 

Med Rehabil 2002;83(6):802-5. No exercise program 

or physical activity 

660. Yamamoto M, Tajima F, Okawa H, Mizushima T, 

Umezu Y, Ogata H. Static exercise-induced increase 

in blood pressure in individuals with cervical spinal 

cord injury. Arch Phys Med Rehabil 1999;80(3):288-

93. No relevant outcomes 

661. Yamamoto Y, Noto Y, Saito M, Ichizen H, Kida H. 

Spinal cord compression by heterotopic ossification 

associated with pseudohypoparathyroidism. Journal 

of International Medical Research 1997;25(6):364-8. 

Not adult spinal cord injury patients 

662. Yamasaki M, Kim KT, Choi SW, Muraki S, 

Shiokawa M, Kurokawa T. Characteristics of body 

heat balance of paraplegics during exercise in a hot 

environment. J Physiol Anthropol Appl Human Sci 

2001;20(4):227-32. No relevant outcomes 

663. Yamasaki M, Komura T, Tahara Y, Katsuno K, 

Fukuyama Y, Michimuko R, et al. Peak oxygen 

uptake and respiratory function in persons with spinal 

cord injury. Appl Human Sci 1996;15(1):14-7. No 

relevant outcomes 

664. Yamasaki M, Komura T, Tahara Y, Muraki S, 

Tsunawake N, Ehara Y, et al. Relationship between 

physical characteristics and physiological responses 

during maximal arm cranking in paraplegics. Spinal 

Cord 1998;36(8):579-83. No relevant outcomes 

665. Yekutiel M, Brooks ME, Ohry A, Yarom J, Carel R. 

The prevalence of hypertension, ischaemic heart 

disease and diabetes in traumatic spinal cord injured 

patients and amputees. Paraplegia 1989 

Feb;27(1):58-62. Case-series 

666. Yen HL, Cheng CH, Lin JW. Cervical myelopathy 

due to gouty tophi in the intervertebral disc space. 

Acta Neurochirurgica 2002;144(2):205-7. Not adult 

spinal cord injury patients 

667. Yeung JJ, Kim HJ, Abbruzzese TA, VignonClementel IE, Draney-Blomme MT, Yeung KK, et al. 

Aortoiliac hemodynamic and morphologic adaptation 

to chronic spinal cord injury. J Vasc Surg 2006 

Dec;44(6):1254-65. Not eligible outcomes 

668. Yokoyama O, Ishiura Y, Nakamura Y, Kunimi K, 

Mita E, Namiki M. Urodynamic effects of 

intravesical instillation of lidocaine in patients with 

overactive detrusor. J Urol 1997 May;157(5):1826-

30. Not eligible outcomes 

669. Yokoyama O, Sakuma F, Itoh R, Sashika H. 

Paraplegia after aortic aneurysm repair versus 

traumatic spinal cord injury: functional outcome, 

complications, and therapy intensity of inpatient 

rehabilitation. Arch Phys Med Rehabil 2006 

Sep;87(9):1189-94. Not eligible target population 

670. Yoshimatsu H, Nagata K, Goto H, Sonoda K, Ando 

N, Imoto H, et al. Conservative treatment for cervical 

spondylotic myelopathy. prediction of treatment 

effects by multivariate analysis. Spine J 

2001;1(4):269-73. Not adult chronic SCI patients 

671. Yoshimura O, Takayanagi K, Kobayashi R, Hosoda 

M, Minematsu A, Sasaki H, et al. Possibility of 

independence in ADL (Activities of Daily Living) for 

patients with cervical spinal cord injuries--an 

evaluation based on the Zancolli Classification of 

Residual Arm Functions. Hiroshima Journal of 

Medical Sciences 1998;47(2):57-62. No relevant data 
D-27 

672. Young WF, Tuma R, O'Grady T. Intraoperative 

measurement of spinal cord blood flow in 

syringomyelia. Clin Neurol Neurosurg 2000 

Sep;102(3):119-23. Not eligible target population 

673. Zafonte R, Millis S, Mann N, Black K, Watanabe T, 

DeSantis N, et al. Functional independence measure 

prediction: an initial evaluation of residents' skills. 

Am J Phys Med Rehabil 2000 May-Jun;79(3):278-

82. Not eligible target population 

674. Zamparo P, Pagliaro P. The energy cost of level 

walking before and after hydro-kinesi therapy in 

patients with spastic paresis. Scand J Med Sci Sports 

1998;8(4):222-8. Not adult chronic SCI patients 

675. Zhou S. Chronic neural adaptations to unilateral 

exercise: mechanisms of cross education. Exerc Sport 

Sci Rev 2000;28(4):177-84. Not adult chronic SCI 

patients 

676. Zhu GY, Shen Y. Application of pudendal evoked 

potentials in diagnosis of erectile dysfunction. Asian 

Journal of Andrology 1999;1(3):145-50. Not adult 

spinal cord injury patients 

677. Zlotolow SP, Levy E, Bauman WA. The serum 

lipoprotein profile in veterans with paraplegia: the 

relationship to nutritional factors and body mass 

index. Journal of the American Paraplegia Society 

1992;15(3):158-62. Less than 100 patients in study 

E-1

Appendix E: Evidence Tables Appendix E Table 1. Prevalence of metabolic syndromes, diabetes, glucose, lipid abnormalities, and BMI in adults with chronic 

Reference Study Design Subject Characteristics Prevalence

Prevalence of metabolic syndrome and insulin resistance in people with SCI and disease Lee, 20051 Convenience sample of 

93 SCI patients from a Veterans Affairs hospital and local community. All were diagnosed for lipid panel, insulin, and glucose values. 

USA 

Male: 86.0% (n=80) Female: 14.0% (n=13) Paraplegia: 58.1% (n=54) Tetraplegia: 41.9% (n=39) 

Metabolic syndrome and insulin resist

22.6% (21 of 93 subjects) 

Bauman, 19992 Cross-sectional study 

including a convenience sample of 201 SCI patients from a single clinical center who had oral glucose tolerance tests. Patients were subgrouped by level of injury. USA 

Mean age (years): 39 Male: 84% (n=169) Female: 16% (n=32) White: 27% (n=54) Latino: 57% (n=114) African American: 14% (n=28) BMI: 25 Injury: Mean duration of SCI (years): 13 Mean age at injury: 25 Tetra complete: 28% (n=56) Tetra incomplete: 12% (n=25) Para complete: 42% (n=84) Para incomplete: 18% (n=36) 

Hyperinsulinemia Tetraplegia group 53% (n=43) Paraplegia group 37% (n=44) P <0.05 

Prevalence of diabetes in people with SCI and disease Bauman, 19992 Cross-sectional study 

including a convenience sample of 201 SCI patients from a single clinical center who had oral glucose tolerance tests. Patients were subgrouped by level of injury. USA 

Mean age (years): 39 Male: 84% (n=169) Female: 16% (n=32) White: 27% (n=54) Latino: 57% (n=114) African American: 14% (n=28) BMI: 25 Injury: Mean duration of SCI (years): 13 Mean age at injury: 25 Tetra complete: 28% (n=56) Tetra incomplete: 12% (n=25) Para complete: 42% (n=84) Para incomplete: 18% (n=36). 

Diabetes: 13.4% (n=27) 

Results from fasting glucose testing: 

Overall diabetes: 3% (n=7) Tetraplegia complete: 4% (n=2) Tetraplegia incomplete: 0% (n=0) Paraplegia complete: 1% (n=1) Paraplegia incomplete: 11% (n=4) Results from 2 hour glucose challeng

Overall diabetes: 13% (n=27) Tetraplegia complete: 23% (n=13) Tetraplegia incomplete: 16% (n=4) Paraplegia complete: 6% (n=5) Paraplegia incomplete: 11% (n=4) 
Appendix E Table 1. Prevalence of metabolic syndromes, diabetes, glucose, lipid abnormalities, and BMI in adults with chronic 

(continued) 

E-2

Reference Study Design Subject Characteristics Prevalence

Lavela, 20063 National cross-sectional 

survey of 3,737 Veterans Affairs SCI subjects. 

USA 

Veterans with SCI subgroups 1. Veterans with spinal disease (VSD) A. With diabetes (n=741) Mean age (years): 64.1* Male: 98.2% (n=728) White: 76.6% (n=568) Nonwhite: 23.4% (n=173)* Mean duration of SCI (years): 23.9 Paraplegia: 67.3% (n=499)* Tetraplegia: 32.7% (n=242) Mean age at injury: 40.0* B. Without diabetes (n=2,967) Mean age (years): 59.2 Male: 96.8% (n=2,872) White: 82.7% (n=2,454) Nonwhite: 17.3% (n=513) Mean duration of SCI (years): 23.8 Paraplegia: 61.6% (n=1,828) Tetraplegia: 38.4% (n=1,139) Mean age at injury: 35.4 * p=0.000, A vs. B 2. GVP = General Veteran Population (n=6,413) 3. GP = General Population, from Centers for Disease Control Behavioral Risk Factor Surveillance System 2003 survey data (n=221,650) 

Diabetes prevalence

VSD 20.0%; GVP 21.0%; GP 7.6%* *p <0.0001, VSD vs. GP Diabetes prevalence by comparison g

Age (years) <40: VSD 4.6%; GVP 3.9%; GP 1.9% 40-44: VSD 6.7%; GVP 13.7%; GP 5.45-49: VSD 10.2%; GVP 8.0%; GP 6.50-54: VSD 17.5%; GVP 16.2%; GP 955-59: VSD 20.2%; GVP 18.7%; GP 60-64: VSD 23.1%; GVP 35.2%; GP 65-69: VSD 24.9%; GVP 28.6%; GP 70+: VSD 26.2%; GVP 24.0%; GP 15Duration of diabetes: comparison of g

VSD n=741; GVP n=1,342; GP n=16,Mean duration (years): VSD 25.5; GVDuration >25 years: VSD 13.6%*; GV*p ≤0.01, VSD vs. GP Risk for clinical conditions, SCI veteracompared to SCI veterans without dia

A. Coronary Heart Disease (n=3,177) Percent in SCI/D group: 12%; OR 2.8 B. Myocardial infarction (n=3,230) Percent in SCI/D group: 14%; OR 2.9 C. High cholesterol (n=3,415) Percent in SCI/D group: 48%; OR 2.5 D. Stroke (n=3,170) Percent in SCI/D group: 8%; OR 2.3 [E. Hypertension (n=3,438) Percent in SCI/D group: 49%; OR 2.5 

Frisbie, 20054 Chart review of 166 

Veterans Affairs patients admitted for SCI rehabilitation within 108 days of paralysis using discharge diagnosis. 

Patients ≥40 years at time 

of injury (n=87) were followed for five years. 

USA 

Veterans with SCI subgroups A. Age <40 years at time of injury (n=79) Mean age (years): 27 Male: 94.9% (n=75) SCI, cervical: 56% (n=44) Complete motor: 72% (n=56) A. Age ≥40 years at time of injury (n=87) Mean age (years): 60 Male: 97.7% (n=85) SCI, cervical: 67% (n=58) Complete motor: 43% (n=37) B subgroups 

Diabetes prevalence by comparison g

acute SCI 

Age (years) 16-39: 0% (n=79) ≥40: 21% (18 of 87 subjects) Diabetes prevalence at 5-year followu

time of SCI

20% (13 of 64* subjects) *excludes subjects lost to death and fnon-diabetic subgroup developed dia5-year mortality in patients ≥40 years

Diabetic subgroup (n=17, one lost to fmortality rate 41%* Non-diabetic subgroup (n=64, 5 lost t
Appendix E Table 1. Prevalence of metabolic syndromes, diabetes, glucose, lipid abnormalities, and BMI in adults with chronic 

(continued) 

E-3

Reference Study Design Subject Characteristics Prevalence

B1. Diabetic subgroup n=18 (21%) (all males) Mean age: 66 SCI, cervical: 72% (n=13) Complete motor: 33% (n=6) B2. Non-diabetic subgroup n=69 (79%) Mean age: 59 SCI, cervical: 65% (n=45) Complete motor: 45% (n=31) Inclusion: treatment for DM; 2 fasting blood glucose levels >140mg%, a single random glucose of >200mg%, or a single hemoglobin A1C >7mg% Exclusion: DM was rejected if related to administration of corticosteroids 

mortality rate 16%. p=0.04 between groups 

Garshick, 20055 A prospective mortality 

study of 361 SCI males injured ≥1 year 

A. Survivors (n=324) Mean age (years): 48.9 White: 93.2% (n=302) Nonwhite: 6.8% (n=22) BMI: 26.3 Age at SCI: 32.2 Mean duration of SCI (years): 16.7 Level of Injury Complete cervical: 21.3% (n=69) T1-T4: 14.8% (n=48) T5-T12: 12.4% (n=40) Others: 10.8% (n=35) Incomplete Cervical ASIA C: 10.8% (n=35) Cervical ASIA D: 12.4% (n=40) Other ASIA C: 7.7% (n=25) Other ASIA D: 9.9% (n=32) B. Deceased (n=37) Mean age (years): 65.0 White: 94.6% (n=35) Nonwhite: 5.4% (n=2) BMI: 26.0 Age at SCI: 40.8 Mean duration of SCI (years): 24.2

Level of Injury Complete cervical: 16.2% (n=6) T1-T4: 10.8% (n=4) T5-T12: 18.9% (n=7) 

Diabetes prevalence 10.0%

A. Survivors (n=324) 8.3% (n=27) B. Deceased subjects (n=37) 24.3% (Observed/expected deaths 2.0/0.53 

Standardized mortality ratio 3.74 [95%
Appendix E Table 1. Prevalence of metabolic syndromes, diabetes, glucose, lipid abnormalities, and BMI in adults with chronic 

(continued) 

E-4

Reference Study Design Subject Characteristics Prevalence

Others: 8.1% (n=3) Incomplete Cervical ASIA C: 16.2% (n=6) Cervical ASIA D: 5.4% (n=2) Other ASIA C: 16.2% (n=6) Other ASIA D: 8.1% (n=3) 

Lee, 20051 Convenience sample of 

93 SCI patients from a Veterans Affairs hospital and local community. All were diagnosed for lipid panel, insulin, and glucose values. 

USA 

Male: 86.0% (n=80) Female: 14.0% (n=13) Paraplegia: 58.1% (n=54) Tetraplegia: 41.9% (n=39) 

Diabetes prevalence

21.3% (20 of 93 subjects) 

Prakash, 20026 Population:26,734 ablebodied male veterans and 

654 patients with spinal cord injuries 47,070 patients with at least one ECG obtained in the Palo Alto Veterans Affairs Health Care System. Retrospective cohort to examine prevalence of ECG abnormalities in individuals with spinal cord injuries. 

A. SCI (n=654) Mean age: 50 Annual mortality: 2.6% Duration of followup: 8 years Hypertension: 7% (p<0.001 vs. B) Congestive heart failure: 1.7% (p<0.001 vs. B)Coronary artery disease: 1.7% (p<0.001 vs. B)Pulmonary disease: 4.8% (p=0.01 vs. B) B. Able-bodied controls (n=26,734) Mean age: 56 Annual mortality: 3.0% Duration of followup: 8 years Hypertension: 44.0% Congestive heart failure: 7.0% Coronary artery disease: 7.0% Pulmonary disease: 5.5% Exclusion criteria: inpatient setting or emergency room at the time of ECG. 

Diabetes prevalence

A. SCI: 11.0% (72 of 654 subjects) B. Able-bodied controls: 10.0% (2,673 

Imai, 19967 Questionnaire of 244 

male SCI patients at 8 rehabilitation centers compared to general population. 

Japan Likely same cohort as Imai 1994)8

Mean age: 47.6 (range: 22-69) Mean duration of SCI: 17.3 Site of injury subgroups: A. Cervical (C) Thoracic (T) 5: 11.0% (n=23) B. T6-T10: 12.0% (n=30) C. T11-Lumbar (L) 1: 69.0% (n=173) D. L2-or below: 8.0% (n=18) 

Incomplete motor: 4.1% (n=10, 5 cervical and 5 thoracolumbar) 

Comparison of diabetes prevalence b

the general population, Outpatient rat

SCI: 61.5 General population: 12.2 Comparison of diabetes prevalence b

subgroup, Outpatient rate per 1,000 p

A. C-T5: 0.0 B. T6-T10: 28 (extracted from graph) C. T11-L1: 62D. E. L2-or below: 165
Appendix E Table 1. Prevalence of metabolic syndromes, diabetes, glucose, lipid abnormalities, and BMI in adults with chronic 

(continued) 

E-5

Reference Study Design Subject Characteristics Prevalence

McGlincheyBerroth, 19959 Cross-sectional analysis of hospitalizations among 

534 patients with SCI admitted to the high quality Spinal Cord Injury Service of the VA medical center (part of the Aging with a Long-Term Disability Research Program database). 

510 discharged from the hospitals were included in the analysis. 

Mean age: 50 (range 16-84) Mean duration of SCI: 16 Male: 99.0%. Group 1 (N=225) persons <50 years of age at the time of injury and <5 years at index submission. Group 2 (N=162) <50 years of age at the time of injury but >50 years at the time of index admission. Group 3 (N=93) persons >50 years of age at the time of injury. Exclusion criteria: not available discharge summary; current hospitalization, transfer to the long term care facility. 

Diabetes prevalence 9.8% (47 of 480 

A. Group 1 (N=225) 3.9% B. Group 2 (N=162) 12.3% C. Group 3 (N=93) 22.6% 

Zhong, 199510 SCI men (Veterans Affairs 

patients) studied during annual physical exam. 

USA 

197 men with chronic SCI, 103 paraplegia and 94 tetraplegia Mean age: 50 (21-77) Mean duration of SCI: 18 (1-49) Mean BMI: 25 (15.8-47.8) Exclusion criteria: No prior history of diabetes or gout 

Diabetes prevalence

Diabetes: 18.3% (n=36) 

Bauman, 199411 Veteran SCI patients, 

matched for age and BMI were compared to veteran controls. 

USA 

SCI (n=100) A. Paraplegia 50.0% (n=50) Mean age: 51.2 Mean BMI: 25.7 Mean duration of SCI: 19 B. Tetraplegia 50.0% (n=50) Mean age: 47.2 Mean BMI: 24.6 Mean duration of SCI: 17 Controls n=50 Mean age: 51 years Mean BMI: 26.9 

Diabetes prevalence

SCI: 22.0% (n=22) Control: 6.0% (n=3) 

Comparison of mean fasting plasma ggroups 

A. Paraplegia: Normal 91; IGT 97; DiaB. Tetraplegia: Normal 87; IGT 90; DiC. Control: Normal 97; IGT 104; Diab*p<0.05 versus Normal, † p<0.05 vers

Imai, 19948 Survey of 195 SCI male 

patients in Japan 

Mean age: 49.5 Mean duration of SCI: 17.9 Site of injury subgroups: C-T5: 9.7% (n=19) T6-T10: 12.3% (n=24) T11-L1: 71.3% (n=139) L2-or below: 6.7% (n=13) 

Prevalence of diabetes by level of inju

All subjects: 5.6% C-T10: 0.0% (32 subjects) T11-L2: 6.5% (9 of 139 subjects) L2-or below: 15.4 (2 of 13 subjects) Outpatient rate per 1,000 population

T11-L2: 65 L2-or below: 154 
Appendix E Table 1. Prevalence of metabolic syndromes, diabetes, glucose, lipid abnormalities, and BMI in adults with chronic 

(continued) 

E-6

Reference Study Design Subject Characteristics Prevalence

Standard outpatient morbidity ratio (g

T11-L2: 326* L2-or below: 945* *p<0.01 versus general population 

Charlifue, 199912 A longitudinal, crosssectional study of 315 SCI 

patients 

Mean age: 37.1 Male: 80.3% (n=253) Mean duration of SCI: 9.3 

Subgroups A. Paraplegia ABC*: 46.7% (n=147) Mean age: 37.2 Male: 76.4% (n=112) Mean duration of SCI: 9.3 B. Tetraplegia ABC*: 42.2% (n=133) Mean age: 35.9 Male: 84.2 (n=112) Mean duration of SCI: 9.5 C. All D*: 11.1% (n=35) Mean age: 40.6 Male: 82.9 (n=29) Mean duration of SCI: 8.9 ASIA Impairment Scale: A = complete, no function; B = incomplete, sensory only; C = incomplete, some sensory and motor function; and D = incomplete, useful motor function. 

Prevalence of diabetes (baseline)

Overall: 2.5% (8 of 315 subjects) Paraplegia ABC: 3.4% (5 of 147 subjeTetraplegia ABC: 1.5% (2 of 133 subjAll D: 2.9% (1 of 35 subjects) Prevalence of diabetes (at 5 years)

Overall: 3.8% (12 of 315 subjects) Paraplegia ABC: 4.8% (7 of 147 subjeTetraplegia ABC: 3.0% (4 of 133 subjAll D: 2.9% (1 of 35 subjects) Diagnosis of DM by age group (basel

<30 years: 0.0% (n=82) 30-50 years: 2.1% (4 of 190 subjects) 50+ years: 9.3% (4 of 43 subjects) Diagnosis of DM by age group (at 5 y

<30 years: 0.0% (n=82) 30-50 years: 4.1% (8 of 190 subjects) 50 + years: 11.6% (5 of 43 subjects) 

Rish, 199713 230 Vietnam vets with 

SCI were reviewed for a 25 year followup USA 

Mean age: 21.4 years with previous excellent health at baseline Site of injury: C2-T1: 21.0% (n=48) T2-T10: 31.0% (N=71) T11-L1: 23.0% (n=52) L2-sacrum: 14% (n=32) No vertebral injury noted: 11.0% (n=27) Paraplegia, complete: 47.0% (n=109) Paraplegia, incomplete: 28.0% (n=64) Tetraplegia, complete: 14.0% (n=31) Tetraplegia, incomplete: 9.0% (n=21) Not delineated: 2.0% (n=5) 

Prevalence of diabetes: 29/230 (13%) 
Appendix E Table 1. Prevalence of metabolic syndromes, diabetes, glucose, lipid abnormalities, and BMI in adults with chronic 

(continued) 

E-7

Reference Study Design Subject Characteristics Prevalence

Prevalence of glucose intolerance in people with SCI and disease Zhong, 199510 SCI men (Veterans Affairs 

patients) studied during annual physical exam. 

USA 

197 men with chronic SCI, 103 paraplegia and 94 tetraplegia Mean age: 50 years (21-77) Mean duration of SCI: 18 (1-49) Mean BMI: 25 (15.8-47.8) Exclusion criteria: No prior history of diabetes or gout 

Impaired glucose tolerance prevalenc

Impaired Glucose Tolerance: 29.4% (

Bauman, 199411 Veteran SCI patients, 

matched for age and BMI were compared to veteran controls. 

USA 

SCI (n=100) A. Paraplegia 50.0% (n=50) Mean age: 51.2 Mean BMI: 25.7 Mean duration of SCI: 19 B. Tetraplegia 50.0% (n=50) Mean age: 47.2 Mean BMI: 24.6 Mean duration of SCI: 17 Controls n=50 Mean age: 51 years Mean BMI: 26.9 

Impaired glucose tolerance prevalenc

SCI: 34.0% (n=34) Controls: 12.0% (n=6) Comparison of mean fasting plasma g

groups 

A. Paraplegia: Normal 91; IGT 97; DiaB. Tetraplegia: Normal 87; IGT 90; DiC. Control: Normal 97; IGT 104; Diab*p<0.05 versus Normal, † p<0.05 vers

Bauman, 19992 Cross-sectional study 

including a convenience sample of 201 SCI patients from a single clinical center who had oral glucose tolerance tests. Patients were subgrouped by level of injury. USA 

Mean age (years): 39 Male: 84% (n=169) Female: 16% (n=32) White: 27% (n=54) Latino: 57% (n=114) African American: 14% (n=28) BMI: 25 Injury: Mean duration of SCI (years): 13 Mean age at injury: 25 Tetra complete: 28% (n=56) Tetra incomplete: 12% (n=25) Para complete: 42% (n=84) Para incomplete: 18% (n=36). 

Impaired glucose tolerance: 27.9% (n

Comparison of mean fasting serum gpeak serum glucose (Pk Glu) in mg/d(FP Ins) in microU/ml, peak plasma inamong groups (p-value for 3 df F-stat

Tetra complete 

FS Glu=97 

PK Glu=193 

Tetra incomplete 

FS Glu=102 

Pk Glu=178 

Para complete 

FS Glu=97 

Pk Glu=158 

Para incomplete 

FS Glu=106; 

Pk Glu=158 

P-value by groups 

p <0.0001 p <0.0001 

Mean lipid values in subjects with SCI and disease Moussavi, 200114 A cross-sectional study of 

189 community-dwelling SCI patients 

USA 

Mean age (years): 43.1 (range 19.2-81.9) Men: 76.7% (n=145) Women: 23.3% (n=44) White: 59.3% (n=112) African American: 22.2% (n=42) Hispanic: 17.5% (n=33) 

Mean serum lipid values

Total cholesterol (TC): 195.9 Low Density Lipoprotein (LDL): 120.2 High Density Lipoprotein (HDL): 46.2 Triglyceride (TG): 148.3 Mean lipids values by gender

Male (n=138): TC 193.9; LDL 120.8; H
Appendix E Table 1. Prevalence of metabolic syndromes, diabetes, glucose, lipid abnormalities, and BMI in adults with chronic 

(continued) 

E-8

Reference Study Design Subject Characteristics Prevalence

Other: 1.1% (n=2) Mean duration of SCI (years): 12.5 (0.5-47.0 Tetraplegia (A,B,C*): 41.3% Paraplegia (A,B,C*): 39.2% Tetraplegia or paraplegia, level D*: 19.6% *Based on American Spinal Injury Association Impairment Scale. (A) no function, (B) sensory only, (C) some sensory and motor preservation, (D) useful motor function, and (E) normal. 

Female (n=41): TC 202.4; LDL 118.1

Mean lipids values by race 

White (n=104): TC 194.9; LDL 117.9; African American (n=41): TC 190.9; L106.8 Hispanic American (n=32): TC 203.4; 177.4 

Bauman, 199915 Cohort of outpatient SCI 

patients (n=320) seen for annual exam vs. ablebodied controls (n=303) matched by age and ethnicity 

USA 

SCI subjects (n=320) Mean age: 41 (20-77) Male: 73% (n=234) Female: 27% (n=86) White: 47% (n=150) African American: 28% (n=90) Hispanic: 26% (n=83) Mean BMI: 25 (13.8-54.8) Body fat: 36% (21.1-72.3) BMI ≥27.8: 28% Mean duration of SCI: 15 (1-57) Motor complete: 65.6% Motor incomplete: 34.4% Sedentary able-bodied controls (n=303) Mean age: 42 (21-75) Male: 81.0% (n=245) Female: 16.0% (n=48) White: 56.0% (n=170) African American: 29% (n=88) Hispanic: 16.0% (n=48) Mean BMI: 29.9 (19.7-49.9) (p<0.0001 vs. SCI) Body fat: 31.0% (10.2-72.5) (p<0.0001 vs. SCI) BMI ≥27.8: 64.0% (p<0.0001 vs. SCI) 

Comparison of mean lipid values betw

TC: SCI 190; Control 207* LDL: SCI 126; Control 137* HDL: SCI 42; Control 47** TG: SCI 108; Control 118† * p<0.0001 (between groups), ** p<0.Comparison of mean lipid values betw

A. Males: SCI n=233; Control n=244 TC: SCI 191; Control 209* LDL: SCI 129; Control 139** HDL: SCI 39; Control 45* TG: SCI 114; Control 126† * p<0.0001, ** p<0.01, † p<0.0005 B. Females: SCI n=87; Control n=59 TC: SCI 188; Control 199 LDL: SCI 118; Control 129 HDL: SCI 51; Control 54 TG: SCI 94; Control 82 Comparison of mean lipid values amo

A. White: SCI n=149; Control n=169 TC: SCI 187; Control 209* LDL: SCI 125; Control 138** HDL: SCI 41; Control 46* TG: SCI 105; Control 119† * p<0.0001, ** p<0.005, † p<0.01 B. African American: SCI n=88; ContrTC: SCI 195; Control 204 LDL: SCI 128; Control 133 HDL: SCI 49; Control 51 TG: SCI 91; Control 101 C. Hispanic: SCI n=83; Control n=43 TC: SCI 190; Control 209* 
Appendix E Table 1. Prevalence of metabolic syndromes, diabetes, glucose, lipid abnormalities, and BMI in adults with chronic 

(continued) 

E-9

Reference Study Design Subject Characteristics Prevalence

LDL: SCI 126; Control 138** HDL: SCI 49; Control 51 TG: SCI 91; Control 101 * p<0.01, ** p<0.05 

Bauman, 1998a16 A cohort of 600 SCI 

patients was investigated for lipid profiles and by ethnicity subgroups in a SCI clinic over 24 months. 

USA 

Mean age: 37.6 BMI: 25.0 White race: 26.5% (n=159) Hispanic: 47.0% (n=282) African American: 26.5% (n=159) Mean duration of SCI: 12.4 Tetraplegia, complete: 30.8% (n=185) Tetraplegia, incomplete: 18.7% (n=112) Paraplegia, complete: 32.8% (n=197) Paraplegia, incomplete: 17.7% (n=106) A. White (n=159) Mean age: 41.4 BMI: 24.9 Mean duration of SCI: 17.4 A. White (n=159) Mean age: 41.4 BMI: 24.9 Mean duration of SCI: 17.4 B. Hispanic (n=282) Mean age: 36.0 BMI: 25.3 Mean duration of SCI: 10.6 C. African American (n=159) Mean age: 36.6 BMI: 24.5 Mean duration of SCI: 10.6 

Overall Mean lipid values 

TC: 190 LDL: 124 HDL: 42 TG: 122 Mean lipid values between groups

TC: White 190; Hispanic 190: African LDL: White 125; Hispanic 124: AA 12HDL: White 40; Hispanic 39: AA 47* TG: White 121; Hispanic 137: AA 96* * p<0.05 for African American versus Categorical Groupings by Ethnic Grou

1. LDL (mg/mL) <100: White 24.0%; Hispanic 27.0%: 100-130: White 38.0%; Hispanic 34.0131-160: White 24.0%; Hispanic 22.0≥161: White 14.0%; Hispanic 17.0%: 2. HDL (mg/mL) <30: White 19.0%; Hispanic 21.0%: A30-34: White 17.0%; Hispanic 15.0%: 35-40: White 18.0%; Hispanic 24.0%: >40: White 46.0%; Hispanic 40.0%: A* p<0.05 for African American versus 

Bauman, 1998b17

Same cohort as Bauman 1998a16

A cohort of 541 SCI patients were investigated for lipid profiles and by neurological deficit subgroups over a period of 2 years in a SCI clinic in CA 

USA 

A. Tetraplegia (n=247) Mean age: 38 Male: 90.0% (n=222) Female: 10.0% (n=25) White race: 35.0% (n=86) African American: 20.0% (n=49) Hispanic: 45.0% (n=111) Mean duration of SCI: 13 Motor complete: 63.2% Motor incomplete: 36.8% 

Comparison of mean lipid profiles betsubgroupsA. Tetraplegia (n=247) TC: 184; Complete 181; Incomplete 1LDL: 121; Complete 122; Incomplete HDL: 39; Complete 38; Incomplete 40 TG: 122; Complete 118; Incomplete 1B. Paraplegia (n=294) TC: 198; Complete 205; Incomplete 1LDL: 122; Complete 129; Incomplete HDL: 45; Complete 47; Incomplete 4
Appendix E Table 1. Prevalence of metabolic syndromes, diabetes, glucose, lipid abnormalities, and BMI in adults with chronic 

(continued) 

E-10

Reference Study Design Subject Characteristics Prevalence

B. Paraplegia (n=294) Mean age: 37 Male: 84% (n=247) Female: 16.0% (n=47) White race: 17.0% (n=50)* African American: 28.0% (n=82) Hispanic: 55.0% (n=162) Mean duration of SCI: 12 Motor complete: 70.1% Motor incomplete: 29.9% * p<0.01 between groups 

TG: 129; Complete 132; Incomplete 1

Zhong, 199510 SCI men (Veterans 

Affairs patients) studied during annual physical exam USA 

197 men with chronic SCI, 103 paraplegia and 94 tetraplegia Mean age: 50 (21-77) Mean duration of SCI: 18 (1-49) Mean BMI: 25 (15.8-47.8) Exclusion criteria: No prior history of diabetes or gout 

Mean lipid values in the study groups 

A. All SCI subjects TC: 188 LDL: 124 HDL: 39 TG: 122 B. Paraplegia (n=103) vs. Tetraplegia TC: Paraplegia 191; Tetraplegia 185 LDL: Paraplegia 125; Tetraplegia 123 HDL: Paraplegia 38; Tetraplegia 39 TG: Paraplegia 130; Tetraplegia 114 

Mean lipid values between subgroups insulin levels A. Normal insulin levels (n=119) LDL: 123 HDL: 39 TG: 109 B. Hyperinsulinemia (n=78)* LDL: 126 HDL: 37 TG: 143 (p=0.004 vs. normal insulin g*Defined as peak plasma insulin >150

tolerance test (75g) 

Bauman, 199218 Veteran SCI patients, 

matched for age and BMI, were compared to veteran controls 

USA 

A. Paraplegia: n=50 Mean age (years): 49.5 Mean BMI: 26.0 Mean duration of SCI: 17.6 B. Tetraplegia: n=50 Mean age: 46.2 Mean BMI: 24.0 

Mean lipid values in the study groups 

A. Paraplegia (n=50) TC: 191* LDL: 124 HDL: 37** TG: 148 B. Tetraplegia (n=50) 
Appendix E Table 1. Prevalence of metabolic syndromes, diabetes, glucose, lipid abnormalities, and BMI in adults with chronic 

(continued) 

E-11

Reference Study Design Subject Characteristics Prevalence

Mean duration of SCI: 15.0 C. Controls: n=50 Mean age: 48.8 Mean BMI: 26.8 

TC: 188* LDL: 128 HDL: 40** TG: 101† 

Controls (n=50) TC: 210 LDL: 136 HDL: 48 TG: 134 * p<0.01, ** p<0.0001, † p<0.05 acrosHDL cholesterol levels by SCI and su

A. All SCI subjects (n=100) <30: 13.0% (n=13) 30-34: 24% (n=24) ≥35: 63.0% (n=63) B. Paraplegia (n=50) <30: 18.0% (n=9) 30-34: 22% (n=11) ≥35: 60.0% (n=30) B. Paraplegia (n=50) <30: 8.0% (n=4) 30-34: 26% (n=13) ≥35: 66.0% (n=33) 

Krum, 199219 Risk factors for 

cardiovascular disease in 327 consecutive SCI patients, matched for age and sex, were compared to controls from the Australian population 

Age range: 25-64 Male: 84.0% (n=275) Female:16.0% (n=52) Duration of SCI: 34% had SCI for more than 10 years 

Control subjects (n not reported) 

Total cholesterol levels by age in mal

All ages: SCI 208; Control 217(estimaAge 25-29: SCI 185; Control 198Age 30-34: SCI 197; Control 204Age 35-39: SCI 216; Control 217 Age 40-44: SCI 206; Control 214Age 45-49: SCI 216; Control 226Age 50-54: SCI 216 ; Control 227Age 55-59: SCI 209 ; Control 229Age 60-64: SCI 206; Control 232 Total cholesterol levels, female gende

Female: SCI 190; Control 217 SCI, >10 years: SCI 192Total cholesterol levels by level of spi

Cervical: 188Low thoracic: 182

High thoracic: 199Lumbar: 205
Appendix E Table 1. Prevalence of metabolic syndromes, diabetes, glucose, lipid abnormalities, and BMI in adults with chronic 

(continued) 

E-12

Reference Study Design Subject Characteristics Prevalence

Prevalence of obesity and mean BMI categories in people with SCI and disease Weaver, 200720 Observational, retrospective 

review of clinical and administrative data of 7,959 veterans with SCI/D (5% had injuries <1 year) USA 

Mean age (years): 58.2 Age ≥65 years: 35.0% (n=2,786) Age 50-64 years: 38.0% (n=3,024) Age <50 years: 27.0% (n=2,149) Male: 98% (n=7,800) White race: 75.0% (n=5,969) African American: 20.0% (n=1,592) Hispanic and other race: 6.0% (n=478) Mean duration of SCI (years): 20 Complete: 37.0% Incomplete: 28.0% Paraplegia: 56.0% 

Mean BMI and categories

Mean BMI: 25.8 BMI <25: 47% (n=3,741) BMI 25-29.9: 33% (n=2,650) BMI ≥30: 20% (n=1,592) 

BMI categories by level of injury 

Paraplegia (n=4,457) <25 (normal weight): 45.0% 25-29.9 (overweight): 33.0% ≥30 (obese): 23%Tetraiplegia (n=3,50<25 (normal weight): 50.0% 25-29.9 (overweight): 35.0% ≥30 (obese): 17.0% *P<0.0001, paraplegia vs. tetraplegia 

OR for BMI in Veterans. Reference ca(normal weight) 

N=7,959 Overweight* OR (C

Age <50 1.0 (reference) Age 50-64 †1.4 (1.2-1.5) Age 65+ †1.3 (1.2-1.5) White 1.0 (reference) Black ‡0.8 (0.8-0.9) Hispanic 1.1 (0.9-1.3) Tetraplegia 1.0 (reference) Paraplegia †1.2 (1.1-1.3) 

*BMI 25-29.9. **BMI ≥30. †P <0.001. ‡

Gupta, 200621 Retrospective chart review of 

408 (387 analyzed) Veterans Affairs patients USA 

Mean age: 55.8 (median 56 years; (range 21-85) Males: 98.3% (n=401) Females: 1.7% (n=7) Mean duration of SCI: 19 (range 2 months-60 years) Paraplegia: 52.2% (n=213) Tetraplegia: 47.7% (n=195) 

Mean BMI

Paraplegia (n=213): 28.36 Tetraplegia (n=195): 27.29 Prevalence by BMI cut points 

BMI <18.5 (underweight): 3.6% (n=14) 

BMI 18.5-25 (normal weight): 27.9% (n

BMI ≥25 (overweight): 68.8% (n=255) 

obese (BMI ≥30; n=76) Mean BMI and duration of injury

0-5 years: 28.11 (n=60) 5-10 years: 28.86 (n=46) 10-15 years: 27.49 (n=39) 15-20 years: 28.76 (n=49) 20-25 years: 26.28 (n=52) >25 years: 27.55 (n=133) 
Appendix E Table 1. Prevalence of metabolic syndromes, diabetes, glucose, lipid abnormalities, and BMI in adults with chronic 

(continued) 

E-13

Reference Study Design Subject Characteristics Prevalence

Prevalence of those overweight and o

Age, years 20-39: BMI ≥25 33.3% (n=11); BMI ≥3

40-59: BMI ≥25 65.0% (n=147); BMI ≥

60-74: BMI ≥25 70.1% (n=68); BMI ≥3

>75: BMI ≥25 61.3% (n=19); BMI ≥30 

Garshick, 20055 A prospective mortality study 

of 361 SCI males injured ≥1 year 

A. Survivors (n=324) Mean age (years): 48.9 White: 93.2% (n=302) Nonwhite: 6.8% (n=22) Age at SCI: 32.2 Mean duration of SCI (years): 16.7 Level of Injury Complete cervical: 21.3% (n=69) T1-T4: 14.8% (n=48) T5-T12: 12.4% (n=40) Others: 10.8% (n=35) Incomplete Cervical ASIA C: 10.8% (n=35) Cervical ASIA D: 12.4% (n=40) Other ASIA C: 7.7% (n=25) Other ASIA D: 9.9% (n=32) 

B. Deceased (n=37) Mean age (years): 65.0 White: 94.6% (n=35) Nonwhite: 5.4% (n=2) Age at SCI: 40.8 Mean duration of SCI (years): 24.2 Level of Injury Complete cervical: 16.2% (n=6) T1-T4: 10.8% (n=4) T5-T12: 18.9% (n=7) Others: 8.1% (n=3) Incomplete Cervical ASIA C: 16.2% (n=6) Cervical ASIA D: 5.4% (n=2) Other ASIA C: 16.2% (n=6) Other ASIA D: 8.1% (n=3) 

Mean BMI: 

A. Survivors (n=324): 26.3 B. Deceased (n=37): 26.0 
Appendix E Table 1. Prevalence of metabolic syndromes, diabetes, glucose, lipid abnormalities, and BMI in adults with chronic 

(continued) 

E-14

Reference Study Design Subject Characteristics Prevalence

Johnston, 200522 Cross-sectional survey of 

SCI (n=199) patients in New Jersey (patients from database & community were recruited) compared to national population (n=246,025) 

USA 

SCI subjects (n=199) Mean age: 39.6 Male: 74.9% (n=149) Female: 25.1% (n=50) White race: 74.4% (n=148) African American: 20.1% (n=40) Asian: 1.5% (n=3) Other race: SCI 4.0% (n=8) Mean weight: 168.2 Mean duration of SCI: 8.11 Paraplegia incomplete: 27% Paraplegia complete: 71% Paraplegia minimal: 3% Tetraplegia incomplete: 53% Tetraplegia complete: 42% Tetraplegia minimal: 2% Control (n=246,025) Mean age: 45.1 Male: 48.3% (n=115,632) Female: 53% (n=130,393) White race: 46.2% (n=113,664) African American: 16.4% (n=40,348) Asian: 11.1% (n=27,309) Other race: 26.3% (n=64,705) Mean weight: 171.9 Inclusion: >18 years old; traumatic SCI; >1 year post injury Exclusion: normal neurological exam; non-traumatic injury; inability to understand English without translator. 

Mean BMI

SCI subjects (n=199): 24.5 Control (n=246,025): 26.1 BMI Categories

A. <18.5 (underweight): SCI 7.1%; Control 4.0% B. 18.5-24.9 (normal weight) SCI 48.9% Control 39.3% C. 25-25.9 (overweight) SCI 31.3% Control 35.2% ≥30 (obese) SCI 12.6% Control 20.9% Use physical activity or exercise to los

overweight/obese: 

SCI 50.0% Control 69.8% 

Spungen, 200323 In a cross-sectional study, 

133 male SCI patients were compared to 100 controls matched to age, ethnicity and height 

USA 

Tetraplegia (n=66) Mean age: 40 White race: 31.8% (n=21) African American: 7.6% (n=5) Hispanic: 60.6% (n=40) Mean duration of SCI: 14 Motor complete: 68.2% Motor Incomplete: 31.8% Paraplegia (n=67) Mean age: 37 (p<0.0005 vs. control) White race: 16.4% (n=11) 

Mean BMI

Tetraplegia (n=66): 25.4 Paraplegia (n=67): 25.8 Control (n=100): 27.3 Comparisons among groups of total b

A. Mean total body fat (kg) Tetraplegia: 24.1* Paraplegia: 23.9† Control: 18.7 *p <0.005, tetraplegia vs. control. †p <B. Mean total body fat (kg) by age amTetraplegia: <40 (years) 20.3; ≥40 29
Appendix E Table 1. Prevalence of metabolic syndromes, diabetes, glucose, lipid abnormalities, and BMI in adults with chronic 

(continued) 

E-15

Reference Study Design Subject Characteristics Prevalence

African American: 9.0% (n=6) Hispanic: 74.6% (n=50) Mean duration of SCI: 12 Motor complete: 73.1% Motor Incomplete: 26.9% Complete (n=94) Incomplete (n=39) Control (n=100) Mean age: 44 White race: 19% (n=19) African American: 6% (n=6) Hispanic: 75% (n=75) 

Paraplegia: <40 22.7; ≥40 26.2 Control: <40 18.7; ≥40 18.8 C. Mean percent of body fat by age amTetraplegia: <40 31%; ≥40 39%, p<0.

Paraplegia: <40 30%; ≥40 36%, p<0.

Control: <40 21%; ≥40 23% 

D. Mean total body fat (kg), motor-commean total body fat (kg) Tetraplegia: Complete 23.3; IncompleParaplegia: Complete 24.7; IncompleE. Mean percent of body fat, motor-coTetraplegia: Complete 34%; IncompleParaplegia: Complete 33%; Incomplet

Bauman, 199915 Cohort of outpatient SCI 

patients (n=320) seen for annual exam vs. able-bodied controls (n=303) matched by age and ethnicity 

USA 

SCI subjects (n=320) Mean age: 41 (20-77) Male: 73.0% (n=234) Female: 27.0% (n=86) White: 47.0% (n=150) African American: 28.0% (n=90) Hispanic: 26.0% (n=83) Mean duration of SCI: 15 (1-57) Motor complete: 65.6% Motor incomplete: 34.4% Sedentary able-bodied controls (n=303) Mean age: 42 (21-75) Male: 81.0% (n=245) Female: 16.0% (n=48) White: 56.0% (n=170) African American: 29.0% (n=88) Hispanic: 16.0% (n=48) 

Mean BMI and Body Fat

A. SCI subjects (n=320) Mean BMI: 25 (13.8-54.8) Estimated body fat: 36.0% (21.1-72.3) BMI ≥27.8: 28.0% 

B. Sedentary able-bodied controls (n=Mean BMI: 29.9 (19.7-49.9) (p<0.0001 Estimated body fat: 31.0% (10.2-72.5) BMI ≥27.8: 64.0% (p<0.0001 vs. SCI) 

Bauman, 19992 Cross-sectional study 

including a convenience sample of 201 SCI patients from a single clinical center who had oral glucose tolerance tests. Patients were subgrouped by level of injury. 

USA 

Mean age (years): 39 Male: 84% (n=169) Female: 16% (n=32) White: 27% (n=54) Latino: 57% (n=114) African American: 14% (n=28) BMI: 25 Injury: Mean duration of SCI (years): 13 Mean age at injury: 25 Tetra complete: 28% (n=56) Tetra incomplete: 12% (n=25) 

Mean BMI (kg/m2):Overall: 25 Tetra complete: 23 Tetra incomplete: 26 Para complete: 25 Para incomplete: 25 Total body fat (%): Overall: 34 Tetra complete: 34 Tetra incomplete: 35 Para complete: 34 
Appendix E Table 1. Prevalence of metabolic syndromes, diabetes, glucose, lipid abnormalities, and BMI in adults with chronic 

(continued) 

E-16

Reference Study Design Subject Characteristics Prevalence

Para complete: 42% (n=84) Para incomplete: 18% (n=36) 

Para incomplete: 31 

Anson, 199624 Data from 348 post-acute 

SCI patients were collected during routine followup in Georgia 

USA 

Mean age: 36.6 (median 33 years; range 32.4-44.2) Male: 81.9% (n=285) Female: 18.1% (n=63) White 80.2% (n=279) Non-white 19.5% (n=69) Time since injury

1-2 years 25.9% (n=90) 3.5 years 25.3% (n=88) 6-10 years 29.3% (n=102) 11-15 years 11.8% (n=41) >15 years 7.8% (n=27) 

Weight status

Underweight 22.3% (n=69); Ideal weigOverweight 26.9% (n=83); Obese 12.9

Weight status by years since injury Time since injury A. 1-2 years Underweight 21.6% (n=19); Ideal weigOverweight 29.5% (n=26); Obese 9.1% B. 3-5 years Underweight 20.3% (n=16); Ideal weigOverweight 24.1% (n=19; Obese 13.9C. 6-10 years Underweight 25.6% (n=21); Ideal weigOverweight 24.4% (n=20); Obese 12.2D. 11-15 years Underweight 27.0% (n=10); Ideal weigOverweight 27.0% (n=10); Obese 21.6E. >15 years Underweight 13.0% (n=3); Ideal weighOverweight 34.8% (n=8); Obese 13.0% *Weight categories not defined 

Zhong, 199510 SCI men studied during 

annual physical exam. 

Veterans Affairs patients, USA 

197 men with chronic SCI, 103 paraplegia and 94 tetraplegia Mean age: 50 (21-77) Mean duration of SCI: 18 (1-49) Exclusion criteria: No prior history of diabetes or gout 

Mean BMI

25 (15.8-47.8) BMI >27.8 (n=48) There was a positive correlation betwe(r=0.59, p<0.001) By linear regression analysis, there wabetween BMI (r=0.20, p<0.01) and LDwith age, date of injury, peak plasma glipoprotein value. 

Bauman, 199218 Veteran SCI patients, 

matched for age and BMI, were compared to veteran controls 

USA 

Paraplegia: n=50 Mean age (years): 49.5 Mean duration of SCI: 17.6 Tetraplegia: n=50 Mean age: 46.2 Mean duration of SCI: 15.0 Control: n=50 Mean age: 48.8 

Mean BMI

Paraplegia: n=50: 26.0 Tetraplegia: n=50: 24.0 Control: n=50: 26.8 
E-17

Appendix E Table 2. Cardiovascular events in adults with chronic traumatic SCI 

Study Sample Risk factors 

Cardus, 199225

Case-control study to compare probability of cardiovascular diseases in patients with SCI compared to the able-bodied persons. Adjustment not reported. Matching by age. 

640 patients over 18 year of age, more than 9 months after traumatic SCI who resided in the county area and had to use assistive device for walking. 96 eligible. Controls: 96 non trained able bodied men matched by age. 

Risk factors of cardiovascular disease; age, blood pressure, blood cholesterol, fasting glucose, ECG abnormalities, self reported smoking. Age at injury and the time after injury. 

Risk of cardiovascular dcalculation with cut off fohealthy 50 year old mennormal ECG, systolic blblood cholesterol less th

Age 

Time Aft

Injury 

(Months

21±3.2 65±27 

19.1±3.5 252±96 

44.7±12 57±21 

37.4±6.6 232±122 

Krum, 199219

Cross sectional analysis of cardiovascular morbidity in association with risk factor scores among Australian adults with spinal cord injury. Time: 1983 Adjustment: age Matching by gender and age 

327 patients with SCI and age and sex matched controls from the 1983 Australian Risk Factor Prevalence Study. Exclusion criteria not reported but only 102 patients who completed questionnaire were analyzed. Population: 102 patients, 19% female, 25-64 years old; 34% more than 10 years after injury; 40% with cervical, 35% with lower thoracic, 13% with upper thoracic, and 12% with lumbar levels of injury; ~41% with Frankel Grade A of completeness complete motor and sensory deficit 

Cardiovascular risk factor score (RFS) 

derived from the MRFIT study (age, diastolic blood pressure (DBP), total cholesterol (TC) level, cigarettes/day, sex): =0.1091*Age+0.288*DBP+0.008*Total cholesterol+0.227*cigarettes/day. 

Prevalence of arterial hyinfarction, cerebrovascuadjusted percentile posithe general population. 

Prevalence 

Hypertension Angina MI Cerebrovascular accident Diabetes Hypertension Angina MI Cerebrovascular diseases Diabetes 

Cardiac risk factor score 

Age 

Mean of 

Compa

Subject

F

25-29 30-34 35-39 40-44 
Appendix E Table 2. Cardiovascular events in adults with chronic traumatic SCI (continued) 

E-18

Study Sample Risk factors 

45-49 50-54 55-59 60-69 all ages >10 years after injury 

Whiteneck, 199226

Retrospective analysis to examine morbidity and mortality in SCI patients compared to the general population. Time: 1943-1970 Adjustment age, gender, level of injury, time after injury 

834 individuals with 20 or more years after SCI treated at the British spinal injury centers Exclusion criteria: childhood injuries, injuries in older adults (>55 years), not willing to complete interview. Population: 13% female, 412 survivors, 282 (68%) completed the interview, Age at time of injury was between 15 and 55 years—15-24 years 42%, 25-34 years 27%, 35-44 years 18%, 45-55 years 13%; median survival time 32 years; 85% survived at 10 years, 71% at 20 years, 53% at 30 years, and 35% at 40 years after injury. 

Level and completeness of injury and age at injury. Paraplegia with Frankel grades A, B, or C – no functional motor preservation; Quadriplegia with Frankel grades A, B, or C – no functional motor preservation; Para- or quadriplegia with Frankel grades D or E – functional motor preservation 

Disease-specific mortali(23.2%), 38 patients die31 from other disease odiseases, 5 from other c

CVD Mortality 

All cases Para ABC Quadriplegia ABC All D and E Annual CVD mortality matched Age 15-24 25-34 35-44 45-54 55-64 65-74 75-84 

CVD Incidence by age Age at Episode 

<30 30-39 40-49 50-59 60+ Years After Injury <10 10-19y 20-29y 30+ 
Appendix E Table 2. Cardiovascular events in adults with chronic traumatic SCI (continued) 

E-19

Study Sample Risk factors 

DeVivo, 199327

Retrospective analysis to compare age, sex, race, and causespecific mortality rates in patients with SCI 12 years after injury vs. the general population. Time: 1973-December 21, 1985 Adjustment: standardization by age, sex, and race 

9,135 persons injured between 1973 and 1984 and treated at any of 13 regional spinal cord injury care systems Exclusion criteria: not reported. Population: 854 SCI patients who died during followup time. 

Age, neurological level, and extent of spinal cord lesion 

Standardized mortality r(ratio of 1 = no increase Ischemic heart disease Non ischemic heart diseCerebrovascular diseasDiseases of arteries (ICMortality in SCI patients

Cause 

Ischemic heart disease (ICD codes 410-414) Non ischemic heart dis(ICD codes 420-429) Cerebrovascular disea(ICD codes 430-438) Diseases of arteries (ICcodes 440-448) 

Imai, 19948

Cross-sectional analysis of morbidity rates and standardized morbidity ratios according to the site of injury compared to the general population. Time: 1990 Adjustment: age 

307 (244 responded) men with SCI identified during the National Livelihood Basic Survey in Japan engaged in light work at special centers, who had medical examination for blood pressure and medical history. Exclusion criteria: 195 were analyzed among 228 eligible for not reported reasons. Population: mean age was 49.5 years old; the average post-injury period 17.9 years; 19 patients injured at level C-T5, 24 at T6-T10, 139 at T11-L1, and 13 at L2 or lower. 

Level of injury: C-T5; T6-T10; T11-L2; L2 ; Age: 40th, 50th, 60th Outpatient rate of hyper

diabetes = (number of o1,000 Standardized morbidity expected number of outObesity. Self reported trmedications. 

Level of Injury N 

C-T5 Renal diseases 2 T6-T10 Renal diseases 6 Hypertension 5 T11-L2 Hypertension 21 Renal diseases 18 Diabetes mellitus 9 Hypotension 3 L2 Hypertension 5 Renal diseases 4 Diabetes mellitus 2 
Appendix E Table 2. Cardiovascular events in adults with chronic traumatic SCI (continued) 

E-20

Study Sample Risk factors 

Prevalence of obesity: 

Age Obesity 

40th 6.8 50th 2.5 

60th 1 

Treatment with Antih

Age SCI 

30th 9.1 

40th 15.6 

50th 21.8 60th 45.5 

Nam, 199428

Retrospective medical chart review to test the hypothesis that the SCI population has an increased incidence of stroke, and to identify stroke risk factors unique to SCI patients. Time: 1980-1990. Adjustment not reported 

1,027 patients admitted to medical centers with stroke and 2,007 patients with SCI (paraplegia or quadriplegia) including 13 patients with stroke. Exclusion criteria: non traumatic SCI, stroke before SCI. Population: 2 patients with traumatic SCI followed by stroke. Population: average age 37.2±16.1years 

Traumatic SCI Prevalence of stroke aft

cases/2,007 SCI patient

Levi,199529

Cross-sectional Stockholm Spinal Cord Injury Study. Time: 1988-89. Adjustment: age, sex, socioeconomic status 

326 patients with SCI from the Stockholm Spinal Cord Injury Study, residents of the Greater Stockholm area. Control participants in the Swedish Annual Level of Living Survey (1,978 interviews) Exclusion criteria: residents of Gotland Population: 80% males 

Spinal cord injury Prevalence of diabetes, 

problems and self repor

Disorder SCI 

 % 

Diabetes mellitus 

1 

Circulatory 2 

Hypertension 0 Cardiac 2 Use of cardiac medication 

2 
Appendix E Table 2. Cardiovascular events in adults with chronic traumatic SCI (continued) 

E-21

Study Sample Risk factors 

Levi, 199530

Cross-sectional analysis of the associations between patient characteristics and prevalence of internal diseases and symptoms. Adjustment: age, gender, duration of injury, functional status 

353 subjects with traumatic SCI, participants in The Stockholm Spinal Cord Injury Study. Exclusion criteria- not reported. Population: 19% female 

0-4 years after injury 23.97% 5-17 years after injury 48.76% 18-44 years after injury 24.52% 

ASIA/IMSOP Impairment Scale Grade level of injury as cervical complete, thoracic incomplete, lumbo-sacral complete, lumbo-sacral incomplete; age at injury as continuous variable; duration of injury as shorter (0-4 years), intermediate (5-17 years), longer (18-44 years) 

Prevalence of cardiovaschest pain, palpitations. 

Risk Factors 

Total Males Females Age at injury 21-40 Age at injury 41-77 Duration of injury 0-4 yeDuration of injury 5-17 Duration of injury 18-44 Cervical injury, completCervical injury, incompThoracic injury, compleThoracic injury, incompLumbosacral injury, comLumbosacral injury, inc

McGlinchey-Berroth, 19959

Cross-sectional analysis of hospitalizations among patients surviving late life injury. Time: 1989-1992. Adjustment not reported. 

534 patients with SCI admitted to the high quality Spinal Cord Injury Service of the VA medical center (part of the Aging with a Long-Term Disability Research Program database). Exclusion criteria: not available discharge summary; current hospitalization, transfer to the long term care facility. Population: 510 discharged from hospitals were included in the analysis; mean age of 50 years (16-84 years); 23% were at least 65 years of age; 16±13.1 years after injury, 12±12 hospital admissions since injury; 99% male. 

Group 1 (N=225) persons <50 years of age at the time of injury and <5 years at index submission. Group 2 (N=162) <50 years of age at the time of injury but >50 years at the time of index admission. Group 3 (N=93) persons >50 years of age at the time of injury. 

Hospitalization due to m401.9), diabetes (ICD 25(ICD 401.0 to 401.9). Prevalence of CVD in S

Outcomes Group 

N 255 Myocardial infarction 5.09 Diabetes 3.92 Hypertension 5.09 Stroke 0 

Imai, 19967

Cross-sectional analysis of morbidity in SCI patients compared to the general Japanese population. Time: 1989. Adjustment not reported, 

244 males with SCI at several Rehabilitation Centers (Workman's Accident Compensation Rehabilitation Workshops). Exclusion criteria: 20% did not respond to the questionnaire. Population: Age 22 to 69 years (mean 47.6); mean postinjury periods 17.3 years; C-T5 level -1%; T6-T10 12%; 

Level of injury: C-T5; T6-T10; T11-L2; L2- Age: 40th, 50th, 60th Outpatient rate = (numb

studied) * 1,000 Standardized morbidity outpatients/expected nu. . . . . 
Appendix E Table 2. Cardiovascular events in adults with chronic traumatic SCI (continued) 

E-22

Study Sample Risk factors 

standardization by age with general population 

T11-Ll 69%; L2 -8%. Control group (general population). National Livelihood Basic Survey conducted by the Ministry of Health and Welfare in 1989, on 800,000 people in 240,000 households. 

S

M

All CVD 53Hypertension 16Hypotension 16Ischemic heart diseases 16Other diseases of circulatory system 8Diabetes mellitus 6

Hartkopp,199731

Retrospective cohort to examine mortality among SCI compared to the general population. Time: SCIs that occurred between January 1, 1953, and December 31, 1990; deaths before December 31, 1992. Adjustment standardization by age 

888 individuals (713 men and 175 women) who survived SCI and were rehabilitated at the Centre for Spinal Cord Injured in Hornbnk, Denmark. Exclusion criteria: permanent respiratory support, severe SCI with 

specialized treatment Population: median age at the time of injury 27.5 in 1953-1971 and 28.5 from 1972-1990 

Neurological level of last preserved segment at time of injury, functional level according to Frankel scale at last followup: functionally complete tetraplegia (cervical cord lesions and Frankel class AC), functionally complete paraplegia (thoracic and lumbar cord lesions and Frankel class A-C), Frankel class D, and Frankel class E. Years of injury: 1953-1971 and 1972-1990 

Mortality from cardiovasRegistry of Causes of Dof vital statistics Denma

certificates, and post mo

Death (ICD codes) Cardiovascular disease (390-458) Ischemic heart disease (410-414) Cerebrovascular disease (430-438) Lung embolus (450) Total 

Tetrap

C 

Frankel A-C 

N 

Cardiovascular disease 

9 

Ischemic heart disease 

2 

Cerebrovascular disease 

2 

Lung embolus 1 Total 67 

Standardized mortality rexpected number of dea
Appendix E Table 2. Cardiovascular events in adults with chronic traumatic SCI (continued) 

E-23

Study Sample Risk factors 

Rish, 199713Retrospective review of the charts to analyze incidence and causes of deaths among Vietnam veterans over 25 periods after SCI. Time: 1967-1970 to 1995. Adjustment not reported. 

230 patients with SCI identified in the Vietnam Head and Spinal Cord Injury Study Registry who survived more than 72 hours, with significant myelopathy; and with available medical records. Exclusion criteria not reported. Population: mean age at injury 21.4 years, with previous excellent health (active duty military personnel); median time after injury 25 years 

Level of injury; Myelopathy (quadriplegic, paraplegic, complete, incomplete); Mechanism of injury (penetrating wounds, closed injuries) 

The initial diagnosis of hcoronary artery diseasevascular accidents. DeaPrevalence of diabetes 

Diagnosis 

Hypertension Obesity Diabetes Coronary artery diseasMyocardial infarction Cerebrovascular accid

Mortality from Myocardipatients) 

Year After Injury D

5 

20 

>20 

DeVivo, 199932

Retrospective cohort to examine trends in mortality and causes of death among patients with SCI. Time: 1973-1998 Adjustment: age at injury, sex, race, etiology of injury, number of days from injury, neurological level of injury, Frankel grade or, American Spinal Injury Association (ASIA) Impairment Scale, ventilator dependency, sponsor of care, autopsy. 

28,239 consecutive patients admitted to the model system or to a Shriner's Hospital within 1 year of traumatic SCI who survived at least 24 hours after injury. Exclusion criteria not reported. Population: 19% females; 67.6% Caucasian, 20.7% African American, 8.1% Hispanic, 3.6% Asian, Native American, or other; 54% of injuries occurred between the ages of 16 and 30 years, and 23% between 31 and 45 years; 53% cervical, C5-C8 34.5% and C1-C4 18.5% of the population; 53.8% neurologically complete, 27.2% motor functional, 19% sensory sparing or motor nonfunctional; 2.9% were ventilator-dependent. 

Age at injury, neurological level of injury (C1-C4, C5-C8, T1-S5), Frankel grade or ASIA Impairment Scale (each grade separately), injury year (1973-1977, 1978-1982, 1983-1987, 1988-1992, 1993-1998). 

Length of survival confirIndex and cause of deaInjury Statistical Center, death certificates, and aStandardized mortality rdeaths for each neurolo

from each of three startanniversary of injury, anfollowup termination. Thwere then applied to 19rates (the most recent aexpectancies. CVD mortality after 1 ye

Year of 

Death 

N of 

Deaths 

1973-77 74 1978-82 278 1983-87 370 1988-92 340 1993-98 481 Total 1,543 

. . . 
Appendix E Table 2. Cardiovascular events in adults with chronic traumatic SCI (continued) 

E-24

Study Sample Risk factors 

Adjusted Odds Ratios foFirst Post-injury Year Re

 He

1978-82 1983-87 1988-92 1993-1998 

Groah, 200133Prospective observation to examine incidence of cardiovascular disease in people with longterm SCI. Time: 1970-1993 Followup after injury: 20 years Adjustment: age 

834 patients alive >20 years after spinal cord injury identified in 2 British Spinal Injuries Centers Eligible 545, 15-55 years old at the time of injury, initially admitted to one of the 2 British SCI centers within 1 year of injury, residence in a 13-county catchment area at the time of injury. Exclusion criteria: death during 20 years after injury, congenital cardiovascular diseases, subclinical disease. Population: mean age 57±10 years, duration of SCI 29±6 years, females 14% 

Level of injury and Frankel/ASIA grade: 1. Tetraplegia Frankel/ ASIA Impairment grade A, B, or C (Tetra ABC) 2. Paraplegia Frankel/ ASIA Impairment grade A, B, or C (Para ABC) 3. All Frankel/ASIA Impairment grade Ds (All D) (37% between C4 and C7 and 40% between T11 and L4) 

Incidence of cardiovascthe number of new CVD time for each neurologicdisease outcomes defin745-747 and obtained thCVD, coronary heart discerebrovascular diseasedysrhythmia, “other cardcongestive heart failuredeep venous thrombosi

Davies, 200234Cross-sectional analysis to assess the risk of cardiovascular morbidity in adults with SCI relative to lifestyle risk factors. Time: 1972-1992 Adjustment: age, duration of cigarette use 

140 patients with segmental, nonprogressive traumatic SCI, benign tumors, transverse myelitis, vascular infarcts, and congenital defects. Exclusion criteria: death (20), refusal to participate (10), poor health (1) Loss of followup: 12.3% Population: 97 patients, mean age 47.5±4.5; 10% female; age at injury 31.67±16.4; duration of disability 15.9±10.1 years. Quadriplegia 42% Paraplegic 57% Undetermined 1% Complete 33% Incomplete 64% Undetermined 3% Traumatic 87% Nontraumatic 13% 

Self reported current lifestyle risks using selected sections of Lyndhurst Computerized Health Risk Assessment (LCHRA): Physical activity, BMI, cigarette use and alcohol consumption. Variation in lifestyle since SCI. Internal consistency reliabilities for the subscales used in this study ranged from a low a = 0.56 for bladder management to a high a = 0.82 for physical activity. 

Cardiovascular morbiditSchool of Hygiene QuesIntermittent Claudication physician diagnosis in gspecificity 48-98% and sunivariate analyses (corcardiovascular morbidity level with duration of cigconsumption, bladder sealcohol use, BMI, and a 

Age Duration of cigarette uCardiovascular morbid
Appendix E Table 2. Cardiovascular events in adults with chronic traumatic SCI (continued) 

E-25

Study Sample Risk factors 

Prakash, 20026Retrospective cohort to examine prevalence of ECG abnormalities in individuals with spinal cord injuries. Time: 1987-1999 Followup: 5.6 years Adjustment not reported 

47,070 patients with at least one ECG obtained in the Palo Alto Veterans Affairs Health Care System Exclusion criteria: inpatient setting or emergency room at the time of ECG Population: 26,734 able-bodied male veterans and 654 patients with SCI (age 50 ± 14) 

Level of injury by the effect on sympathetic innervation of heart: intact injury Level T6 and below or impaired injury level T5 and above. Age below and above 65 years 

Clinical events: Diabetedisease, congestive heaStandardized computerhypertrophy: R wave >1>24mm in lead V1, an R SV1 + RV5 or V6 >35mof one of: right or left buconduction delay, right vabnormal ST depressiothan 450 msec. Abnorm>0.5mm in any one of leas LVH voltage criteria wMortality obtained from 

Cardenas, 200435

Cross-sectional analysis at several time points to examine the reasons for rehospitalization in persons with acute traumatic spinal cord injury. Time: 1995-2002; 20 years of followup. Adjustment: age, gender, education, ethnicity, marital and vocational status.

Patients with traumatic SCI identified in the Model System (hospitalized between acute hospitalization and comprehensive inpatient rehabilitation, admitted to a Model System within 365 days of injury) who reside in the geographic region in which the Model System facility is located. 5,180 patients analyzed, 4,251 (82.1%) had year-1 followup interviews; 3,904 (91.8%) were matched by the Model System data. Exclusion criteria: no followup interviews with system identification code and unique patient identifier in the Model Systems Form II at first year anniversary; refusal to participate (1 site); small sample size of patients at sites. Loss of followup: 17.9 %. Population: 3,904 patients with 11,047 followup interviews, 21.4% female, 61.4% White; C1-4 ASIA grades A, B, C: 4.6% C1-4 ASIA grade D: 6.1% C5-8 ASIA grades A, B, C: 19.1% C5-8 ASIA grade D: 8.5% T1-S5 ASIA grades A, B, C: 33.1% T1-S5 ASIA grade D: 4.2%

Residence at discharge; payer, length of 

stay at time of initial rehabilitation; level of injury and functional status at discharge from initial rehabilitation.

A rehospitalization is an1-night hospitalization foan emergency departmeinterview and not by doccardiovascular disease rehospitalization reporte

Year of Followup 

1 5 

10 15 20 

Total 
Appendix E Table 2. Cardiovascular events in adults with chronic traumatic SCI (continued) 

E-26

Study Sample Risk factors 

Garshick, 20055Prospective cohort study to examine the association between comorbid medical conditions and other health related factors and mortality in patients with chronic SCI. Time: 1994-2000 Followup: 55.6 months (interquartile range 42.0-67.5 months; range 0.33-74.4 months); 1,544 person-years. Adjustment age 

402 subjects with chronic SCI, >20 years of age previously treated by the SCI Service at Veterans Affairs Boston Healthcare System, registered in the National Spinal Cord Injury Association database in Massachusetts, New Hampshire, Vermont, Maine, and Rhode Island Exclusion criteria: other neurological diseases (polio, stroke, or multiple sclerosis), mechanical ventilation or tracheotomy. Population: 361 males (289 veterans and 72 nonveterans), mean age: 50.6 ± 15.0 years (range 23-87), mean years since injury 17.5 ± 12.8 years (range 1.0-56.5); 93% Caucasian, 5% African American, and 2% other races, 92%, SCI was due to traumatic injury. 37 deaths. 

Hypertension and diabetes diagnosed by a doctor, heart disease as treatment for 'heart trouble' reported in the 10 years prior to study entry using the respiratory health questionnaire based on the ATS DLD-78 adult respiratory questionnaire. Medical records were reviewed for subjects who reported diabetes, hypertension, or heart disease for doctorconfirmed diagnosis in a discharge summary, problem list, or in a progress note. 

Date of death and causeDecember 2000 using tStandardized mortality rAnalysis System (LTASof Safety and Health. Causes of death using IDiseases of the heart (3429); Other diseases of 405, 415-417, 430-438, veins, and pulmonary ci

 Ali

Heart Disease 1Hypertension 7Diabetes 2

U

Circulatory system disorder 390-59 8 Diabetes Diseases of the heart Other diseases of the circulatory system Diseases of the arterieveins, and pulmonary circulation 

Age Adjusted relative ris

Hypertension Heart disease Diabetes 

Multivariate relative risk 

Diabetes 2.6Heart disease 3.6
Appendix E Table 2. Cardiovascular events in adults with chronic traumatic SCI (continued) 

E-27

Study Sample Risk factors 

Lavela, 20063

A national crosssectional survey of veterans with spinal cord injuries to analyze prevalence of diabetes and its complications compared to the general population. Time: 2003 Adjustment: age, race, marital status, duration of injury, employment, and education. 

18,372 veterans with SCI and disorders who use VA health services. Exclusion criteria: veterans who used non VA care, gestational diabetes, multiple sclerosis. Control: 2003 Behavioral Risk Factor Surveillance System survey data for veteran and general population from the Centers for Disease Control and prevention. Population: 5,690 responders (rate 31%), 3,737 eligible. 6,433 general veteran group and 221,650 general population group. Males 97%; Whites 81%; mean age 60 years; 52% with paraplegic level injury; mean years after injury 24 years. 

Presence of spinal cord injury; race; mean duration of injury; level of injury, age at injury; behavioral risk factors: smoking and alcohol intake; diabetes mellitus. 

Self reported diabetes wDysfunction Health Care reported coronary heart arterial hypertension, sthepatitis, pressure sorecare indicators; quality o

Lee, 200636

Cross sectional analysis of the association between plasma homocysteine and arterial hypertension in patients with SCI. Time: not reported. Adjustment not reported 

168 patients with SCI identified in the Spinal Cord Injury Service of the Veterans Affairs Palo Alto Medical Center Exclusion criteria: not reported. Population: mean age 50.27±12.8 years; mean duration of injury of 19.17±13 years; 73 (43%) had paraplegia and 95 (56%) had tetraplegia; 11% female; 62% White. 

Functional status: paraplegia; tetraplegia Absolute rates of hypert

resistance, and the presobtained from medical revaluation date. Prevalence of hypertens

N=168 

Total Pre hypertension Stage 1 hypertension Stage 2 hypertension 

Bold - significant association at 95% confidence level; STD - standard deviation; SMR - standardized morbidity ratios 
E-28 

Appendix E Table 3. Prevalence of cardiovascular symptoms* and hypertension depending on level on injury 

Author Sample (n) Level of injury Prevalence, %

CVD symptoms 

53 Cervical injury, complete 72 

93 Cervical injury, incomplete 57 

8 Lumbosacral injury, complete 62 

47 Lumbosacral injury, incomplete 38 

78 Thoracic injury, complete 72 

Levi, 199530

48 Thoracic injury, incomplete 58 

Hypertension 

L2 level of injury 2.05 

T11-L2 level of injury 8.61 

Imai, 19948 244 

T6-T10 level of injury 2.05 

*Cardiovascular symptoms included ankle and leg edema, chest pain and/or palpitations 

Appendix E Table 4. Prevalence and odds of diabetes in adults with SCI, able bodied veterans, and the 

general population3

 

Age Prevalence 

in SCI, % 

Prevalence 

in Veterans, 

% 

Odds Ratio of 

Diabetes in SCI vs. 

Veterans 

Prevalence in 

Population, % 

Odds Ratio of Diabetes in 

SCI vs. General 

Population 

<40 4.6 3.9 1.19 0.97 1.45 1.9 2.48 2.12 2.91 

40-44 6.7 13.7 0.45 0.39 0.52 5 1.36 1.20 1.55 

45-59 10.2 8 1.31 1.14 1.50 6.7 1.58 1.42 1.42 

50-54 17.5 16.2 1.09 0.99 1.22 9.4 2.05 1.88 1.88 

55-59 20.2 18.7 1.1 0.99 1.22 13 1.69 1.56 1.56 

60-64 23.1 35.2 0.55 0.50 0.61 16 1.58 1.46 1.46 

65-69 24.9 28.6 0.83 0.75 0.91 15.7 1.78 1.65 1.65 

>70 26.2 24 1.12 1.02 1.23 15.6 1.92 1.78 1.78 

Appendix E Table 5. Relative risk of ECG abnormalities in adults with SCI compared to able-bodied controls6

Age <65 years Age >65 years Electrocardiogram Abnormalities Relative Risk (95% CI) Relative Risk (95% CI) 

Any ECG abnormalities 1.01 (0.87; 1.16) 0.81 (0.66; 0.99) 

Left ventricular hypertrophy with strain 0.47 (0.26; 0.88) 0.48 (0.16; 1.45) 

PVC 0.39 (0.18; 0.87) 0.70 (0.32; 1.53) 

Any Q wave 0.65 (0.47; 0.91) 1.10 (0.74; 1.64) 

Anterior Q wave 1.11 (0.62; 2.02) 1.11 (0.42; 2.92) 

Inferior Q wave 0.61 (0.41; 0.93) 1.09 (0.67; 1.78) 

Abnormal QTc 1.11 (0.85; 1.45) 0.69 (0.41; 1.14) 

Left atrial abnormality 1.51 (1.00; 2.27) 0.46 (0.12; 1.81) 

IVCD 0.47 (0.24; 0.94) 0.67 (0.17; 2.67) 

Atrial fibrillation 0.67 (0.25; 1.81) 0.72 (0.30; 1.69) 

ST elevation 1.20 (1.00; 1.44) 1.17 (0.73; 1.88) 

ST depression 1.06 (0.82; 1.36) 0.38 (0.22; 0.66) 

Bold – significant association at 95% confidence level
E-29 

Appendix E Table 6. Relative risk of electrocardiogram abnormalities in patients with SCI with intact sympathetic 

innervation to the heart (injury level T6 and below) compared to impaired sympathetic activity (injury level T5 

and above)6

ECG Abnormalities Relative Risk (95% CI) 

Any ECG abnormalities 0.49 (0.39; 0.62) 

LVH with strain 0.57 (0.19; 1.66) 

Inferior Q wave 1.04 (0.54; 1.99) 

Anterior Q wave 0.44 (0.16; 1.22) 

Any Q wave 0.69 (0.41; 1.15) 

Left atrial abnormality 0.13 (0.04; 0.36) 

IVCD 0.28 (0.07; 1.08) 

Abnormal QTc 0.60 (0.39; 0.94) 

Atrial fibrillation 0.19 (0.04; 0.90) 

ST depression 0.72 (0.46; 1.14) 

ST elevation 0.19 (0.12; 0.28) 

Bold – significant association at 95% confidence level

Appendix E Table 7. Relative risk of ECG abnormalities in patients with SCI younger vs. 

older than 65 years of age6

ECG Abnormalities Relative Risk (95% CI) 

Any ECG abnormalities 0.56 (0.44; 0.72) 

RBBB 0.17 (0.07; 0.43) 

LBBB 0.19 (0.04; 0.93) 

LVH with strain 0.64 (0.18; 2.27) 

Any Q wave 0.32 (0.19; 0.53) 

Anterior Q wave 0.53 (0.17; 1.62) 

Inferior Q wave 0.30 (0.16; 0.57) 

Abnormal QTc 0.75 (0.42; 1.33) 

Left atrial abnormality 2.20 (0.53; 9.17) 

IVCD 0.76 (0.16; 3.55) 

Atrial fibrillation 0.15 (0.04; 0.56) 

ST elevation 1.25 (0.76; 2.06) 

ST depression 0.97 (0.53; 1.79) 

Bold - significant association at 95% confidence level
E-30 

References for Appendix E 

(Note that reference numbers are different than those in the text of the report) 

1. Lee MY, Myers J, Hayes A, et al. C-reactive 

protein, metabolic syndrome, and insulin 

resistance in individuals with spinal cord injury. J 

Spinal Cord Med 2005; 28(1):20-5. 

2. Bauman WA, Adkins RH, Spungen AM, et al. The 

effect of residual neurological deficit on oral 

glucose tolerance in persons with chronic spinal 

cord injury. Spinal Cord 1999 Nov; 37(11):765-

71. 

3. Lavela SL, Weaver FM, Goldstein B, et al. 

Diabetes mellitus in individuals with spinal cord 

injury or disorder. J Spinal Cord Med 2006; 

29(4):387-95. 

4. Frisbie JH. Diabetes mellitus and preventable 

spinal cord injury. J Spinal Cord Med 2005; 

28(1):60-3. 

5. Garshick E, Kelley A, Cohen SA, et al. A 

prospective assessment of mortality in chronic 

spinal cord injury. Spinal Cord 2005 Jul; 

43(7):408-16. 

6. Prakash M, Raxwal V, Froelicher VF, et al. 

Electrocardiographic findings in patients with 

chronic spinal cord injury. Am J Phys Med 

Rehabil 2002 Aug; 81(8):601-8. 

7. Imai K, Kadowaki T, Aizawa Y, et al. Problems in 

the health management of persons with spinal cord 

injury. J Clin Epidemiol 1996 May; 49(5):505-10. 

8. Imai K, Kadowaki T, Aizawa Y, et al. Morbidity 

rates of complications in persons with spinal cord 

injury according to the site of injury and with 

special reference to hypertension. Paraplegia 1994 

Apr; 32(4):246-52. 

9. McGlinchey-Berroth R, Morrow L, Ahlquist M, et 

al. Late-life spinal cord injury and aging with a 

long term injury: characteristics of two emerging 

populations. J Spinal Cord Med 1995 Jul; 

18(3):183-93. 

10. Zhong YG, Levy E, Bauman WA. The 

relationships among serum uric acid, plasma 

insulin, and serum lipoprotein levels in subjects 

with spinal cord injury. Horm Metab Res 1995 

Jun; 27(6):283-6. 

11. Bauman WA, Spungen AM. Disorders of 

carbohydrate and lipid metabolism in veterans 

with paraplegia or quadriplegia: a model of 

premature aging. Metabolism 1994 Jun; 

43(6):749-56. 

12. Charlifue SW, Weitzenkamp DA, Whiteneck GG. 

Longitudinal outcomes in spinal cord injury: 

aging, secondary conditions, and well-being. Arch 

Phys Med Rehabil 1999 Nov; 80(11):1429-34. 

13. Rish BL, Dilustro JF, Salazar AM, et al. Spinal 

cord injury: a 25-year morbidity and mortality 

study. Mil Med 1997 Feb; 162(2):141-8. 

14. Moussavi RM, Ribas-Cardus F, Rintala DH, et al. 

Dietary and serum lipids in individuals with spinal 

cord injury living in the community. J Rehabil Res 

Dev 2001 Mar-Apr; 38(2):225-33. 

15. Bauman WA, Adkins RH, Spungen AM, et al. Is 

immobilization associated with an abnormal 

lipoprotein profile? Observations from a diverse 

cohort. Spinal Cord 1999 Jul; 37(7):485-93. 

16. Bauman WA, Adkins RH, Spungen AM, et al. 

Ethnicity effect on the serum lipid profile in 

persons with spinal cord injury. Arch Phys Med 

Rehabil 1998 Feb; 79(2):176-80. 

17. Bauman WA, Adkins RH, Spungen AM, et al. The 

effect of residual neurological deficit on serum 

lipoproteins in individuals with chronic spinal cord 

injury. Spinal Cord 1998 Jan; 36(1):13-7. 

18. Bauman WA, Spungen AM, Zhong YG, et al. 

Depressed serum high density lipoprotein 

cholesterol levels in veterans with spinal cord 

injury. Paraplegia 1992 Oct; 30(10):697-703. 

19. Krum H, Howes LG, Brown DJ, et al. Risk factors 

for cardiovascular disease in chronic spinal cord 

injury patients. Paraplegia 1992 Jun; 30(6):381-8. 

20. Weaver FM, Collins EG, Kurichi J, et al. 

Prevalence of obesity and high blood pressure in 

veterans with spinal cord injuries and disorders: a 

retrospective review. Am J Phys Med Rehabil 

2007 Jan; 86(1):22-9. 

21. Gupta N, White KT, Sandford PR. Body mass 

index in spinal cord injury -- a retrospective study. 

Spinal Cord 2006 Feb; 44(2):92-4. 

22. Johnston MV, Diab ME, Chu BC, et al. Preventive 

services and health behaviors among people with 

spinal cord injury. J Spinal Cord Med 2005; 

28(1):43-54. 

23. Spungen AM, Adkins RH, Stewart CA, et al. 

Factors influencing body composition in persons 

with spinal cord injury: a cross-sectional study. J 

Appl Physiol 2003 Dec; 95(6):2398-407. 

24. Anson CA, Shepherd C. Incidence of secondary 

complications in spinal cord injury. Int J Rehabil 

Res 1996 Mar; 19(1):55-66. 

25. Cardus D, Ribas-Cardus F, McTaggart WG. 

Coronary risk in spinal cord injury: assessment 

following a multivariate approach. Arch Phys Med 

Rehabil 1992 Oct; 73(10):930-3. 
E-31 

26. Whiteneck GG, Charlifue SW, Frankel HL, et al. 

Mortality, morbidity, and psychosocial outcomes 

of persons spinal cord injured more than 20 years 

ago. Paraplegia 1992 Sep; 30(9):617-30. 

27. DeVivo MJ, Black KJ, Stover SL. Causes of death 

during the first 12 years after spinal cord injury. 

Arch Phys Med Rehabil 1993 Mar; 74(3):248-54. 

28. Nam CC, Odderson IR. Stroke in the spinal cord 

injured. J Am Paraplegia Soc 1994 Jan; 17(1):36-

8. 

29. Levi R, Hultling C, Seiger A. The Stockholm 

Spinal Cord Injury Study. 3. Health-related issues 

of the Swedish annual level-of-living survey in 

SCI subjects and controls. Paraplegia 1995 Dec; 

33(12):726-30. 

30. Levi R, Hultling C, Seiger A. The Stockholm 

Spinal Cord Injury Study: 2. Associations between 

clinical patient characteristics and post-acute 

medical problems. Paraplegia 1995 Oct; 

33(10):585-94. 

31. Hartkopp A, Bronnum-Hansen H, Seidenschnur 

AM, et al. Survival and cause of death after 

traumatic spinal cord injury. A long-term 

epidemiological survey from Denmark. Spinal 

Cord 1997 Feb; 35(2):76-85. 

32. DeVivo MJ, Krause JS, Lammertse DP. Recent 

trends in mortality and causes of death among 

persons with spinal cord injury. Arch Phys Med 

Rehabil 1999 Nov; 80(11):1411-9. 

33. Groah SL, Weitzenkamp D, Sett P, et al. The 

relationship between neurological level of injury 

and symptomatic cardiovascular disease risk in the 

aging spinal injured. Spinal Cord 2001 Jun; 

39(6):310-7. 

34. Davies DS, McColl MA. Lifestyle risks for three 

disease outcomes in spinal cord injury. Clin 

Rehabil 2002 Feb; 16(1):96-108. 

35. Cardenas DD, Hoffman JM, Kirshblum S, et al. 

Etiology and incidence of rehospitalization after 

traumatic spinal cord injury: a multicenter 

analysis. Arch Phys Med Rehabil 2004 Nov; 

85(11):1757-63. 

36. Lee MY, Myers J, Abella J, et al. Homocysteine 

and hypertension in persons with spinal cord 

injury. Spinal cord: the official journal of the 

International Medical Society of Paraplegia 2006; 

44(8):474-9. 

F-1 

Appendix F: Conceptual Definition of Outcomes 

 Cardiovascular diseases1 (CVD). Pathological conditions involving the cardiovascular 

system including the heart; the blood vessels; or the pericardium. 

 Operational definition: Prevalence of CVD and diabetes and incidence rate of CVD events. 

Definitions of CVD events are presented below. 

Variable Definition

Arrhythmia Any variation from the normal rhythm or rate of the heartbeat 

Arrhythmia, sinus Irregularity of the heart rate related to functioning of the sinoatrial node

Atrial fibrillation Disorder of cardiac rhythm characterized by rapid, irregular atrial 

impulses and ineffective atrial contractions 

Atrial flutter Rapid, irregular atrial contractions due to an abnormality of atrial 

excitation 

Bradycardia Excessive slowness in the action of the heart, usually with a heart rate 

below 60 beats per minute 

Cardiac complexes, 

premature 

A premature contraction of the heart that is initiated somewhere other 

than the sinoatrial node 

Atrial premature 

complexes 

Premature contractions of the heart arising from an ectopic atrial focus 

Ventricular premature 

complexes 

Premature contractions of the ventricle, the most common of all 

arrhythmias 

Heart block Impairment of conduction in heart excitation. It is often applied 

specifically to atrioventricular heart block 

Long QT syndrome A syndrome characterized by history of syncopal episodes and a long 

QT interval, sometimes leading to sudden death due to paroxysmal 

ventricular arrhythmia 

Sick sinus syndrome Dysfunction of the sinoatrial node manifested by persistent sinus 

bradycardia, sinus arrest, sinoatrial exit block, chronic atrial 

fibrillation and inability of the heart to resume sinus rhythm 

following cardioversion for atrial fibrillation 

Tachycardia Excessive rapidity in the action of the heart, usually with a heart rate 

above 100 beats per minute 

Ventricular fibrillation Turbulent, disorganized electrical activity of the heart in such a way 

that the recorded electrocardiographic deflections continuously 

change in shape, magnitude, and direction 

Heart arrest Abrupt cessation of cardiac pump function which may be reversible by 

a prompt intervention but will lead to death in its absence

Cardiovascular collapse A sudden loss of effective blood flow due to cardiac and/or peripheral 

vascular factors which may reverse spontaneously (e.g., 

neurocardiogenic syncope; vasovagal syncope) or only with 

interventions (e.g., cardiac arrest)

Congestive heart failure Defective cardiac filling and/or impaired contraction and emptying, 

resulting in the heart's inability to pump a sufficient amount of blood 

to meet the needs of the body tissues or to be able to do so only with 

an elevated filling pressure 
F-2 

Coronary disease An imbalance between myocardial functional requirements and the 

capacity of the coronary vessels to supply sufficient blood flow 

Coronary artery abnormalities 

1. Chronic atherosclerotic lesions 

2. Acute (active) lesions (plaque fissuring, platelet aggregation, acute 

thrombosis) 

3. Anomalous coronary artery anatomy 

Myocardial infarction Gross necrosis of the myocardium, as a result of interruption of the 

blood supply to the area 

1. Healed 

2. Acute 

Pericarditis Inflammation of the pericardium 

Stroke Sudden, nonconvulsive loss of neurological function due to an ischemic 

or hemorrhagic intracranial vascular event. In general, 

cerebrovascular accidents are classified by anatomic location in the 

brain, vascular distribution, etiology, age of the affected individual, 

and hemorrhagic vs. nonhemorrhagic nature.

Hypertension Persistently high systemic arterial blood pressure. Based on multiple 

readings, hypertension is currently defined as when systolic blood 

pressure is consistently greater than 140 mm Hg or when diastolic 

pressure is consistently 90 mm Hg or more. 

Death Irreversible cessation of all biologic functions 

Cardiovascular mortality Death from cardiovascular diseases (considered as immediate and 

underlying cause of death) 

International Classification of Diseases Codes to Identify Outcomes2

404 Hypertensive heart and kidney disease 

 Includes: disease: cardiorenal; cardiovascular renal; any condition classifiable to 402 

with any condition classifiable to 403 

 Additional code to specify type of heart failure (428.0-428.43), if known 

 Additional code to identify the stage of chronic kidney disease (585.1-585.6), if known 

 The following fifth-digit sub-classification is for use with category 404: 

 0 without heart failure or chronic kidney disease 

 1 with heart failure 

 2 with chronic kidney disease 

 3 with heart failure and chronic kidney disease 

402 Hypertensive heart disease 

 Includes: hypertensive: cardiomegaly; cardiopathy; cardiovascular disease; heart 

(disease) (failure), any condition classifiable to 429.0-429.3, 429.8, 429.9 due to 

hypertension 

 Use additional code to specify type of heart failure (428.0-428.43), if known 

427 Cardiac dysrhythmias 

427.0 Paroxysmal supraventricular tachycardia 

 Paroxysmal tachycardia: atrial [PAT]; atrioventricular [AV]; junctional nodal 
F-3 

427.1 Paroxysmal ventricular tachycardia 

 Ventricular tachycardia (paroxysmal) 

427.2 Paroxysmal tachycardia, unspecified 

 Bouveret-Hoffmann syndrome 

 Paroxysmal tachycardia 

427.3 Atrial fibrillation and flutter 

427.31 Atrial fibrillation 

427.32 Atrial flutter 

427.5 Cardiac arrest 

 Cardiorespiratory arrest 

427.6 Premature beats 

427.60 Premature beats, unspecified 

 Ectopic beats 

 Extrasystoles 

 Extrasystolic arrhythmia 

 Premature contractions or systoles NOS 

427.8 Other specified cardiac dysrhythmias 

427.81 Sinoatrial node dysfunction 

 Sinus bradycardia: persistent severe 

 Syndrome: sick sinus; tachycardia-bradycardia 

427.9 Cardiac dysrhythmia, unspecified 

 Arrhythmia (cardiac) NOS 

428.0 Congestive heart failure, unspecified 

 Congestive heart disease 

 Right heart failure (secondary to left heart failure) 

428.1 Left heart failure 

 Acute edema of lung with heart disease NOS or heart failure 

 Acute pulmonary edema with heart disease NOS or heart failure 

 Cardiac asthma 

 Left ventricular failure 

428.9 Heart failure, unspecified 

 Cardiac failure NOS 

 Heart failure NOS 

 Myocardial failure NOS 

 Weak heart 

428 Heart failure 

 Code, if applicable, heart failure due to hypertension first (402.0-402.9, with fifth-digit 1 

or 404.0-404.9 with fifth-digit 1 or 3) 

429.2 Cardiovascular disease, unspecified 

 Arteriosclerotic cardiovascular disease [ASCVD] 

 Cardiovascular arteriosclerosis 

 Cardiovascular: degeneration (with mention of arteriosclerosis) disease (with mention of 

arteriosclerosis) 

 Sclerosis (with mention of arteriosclerosis) 

 Additional code to identify presence of arteriosclerosis 

794 Nonspecific abnormal results of function studies 
F-4 

250 Diabetes mellitus 

250.0 Diabetes mellitus without mention of complication 

 Diabetes mellitus without mention of complication or manifestation classifiable to 250.1-

250.9 

 Diabetes (mellitus) NOS 

250.6 Diabetes with neurological manifestations 

 Additional code to identify manifestation, as: 

 diabetic: 

 amyotrophy (358.1) 

 gastroparalysis (536.3) 

 gastroparesis (536.3) 

 mononeuropathy (354.0-355.9) 

 neurogenic arthropathy (713.5) 

 peripheral autonomic neuropathy (337.1) 

 polyneuropathy (357.2) 

250.7 Diabetes with peripheral circulatory disorders 

 Use additional code to identify manifestation, as: 

 diabetic: 

 gangrene (785.4) 

 peripheral angiopathy (443.81) 

250.8 Diabetes with other specified manifestations 

 Diabetic hypoglycemia 

 Hypoglycemic shock 

 Use additional code to identify manifestation, as: 

 any associated ulceration (707.10-707.9) 

 diabetic bone changes (731.8) 

International Classification of Diseases Codes to Identify Outcomes in Individual Studies: 

Groah, 2001:3 Cardiovascular disease outcomes defined by ICD/9 codes 390-448 and 745-747: 

DISEASES OF THE CIRCULATORY SYSTEM (390-459) 

ACUTE RHEUMATIC FEVER (390-392) 

CHRONIC RHEUMATIC HEART DISEASE (393-398) 

HYPERTENSIVE DISEASE (401-405) 

ISCHEMIC HEART DISEASE (410-414) 

Includes: that with mention of hypertension 

Additional code to identify presence of hypertension (401.0-405.9) 

DISEASES OF PULMONARY CIRCULATION (415-417) 

OTHER FORMS OF HEART DISEASE (420-429) 

CEREBROVASCULAR DISEASE (430-438) 

Includes: with mention of hypertension (conditions classifiable to 401-405) 

DISEASES OF ARTERIES, ARTERIOLES, AND CAPILLARIES (440-448) 

745 Bulbus cordis anomalies and anomalies of cardiac septal closure 

746 Other congenital anomalies of heart 

747 Other congenital anomalies of circulatory system 
F-5 

McGlinchey-Berroth, 19954

 Hospitalization due to myocardial infarction (ICD-9-CM 410.9), 

diabetes (ICD 250.00 to 250.9), and hypertension (ICD 401.0 to 401.9). 

410 Acute myocardial infarction 

Includes: cardiac infarction; coronary (artery):embolism; occlusion; rupture; thrombosis; 

infarction of heart, myocardium, or ventricle; rupture of heart, myocardium, or ventricle; 

ST elevation (STEMI) and non-ST elevation (NSTEMI) myocardial infarction; any condition 

classifiable to 414.1-414.9 specified as acute or with a stated duration of 8 weeks or less 

The following fifth-digit subclassification is for use with category 410: 

0 episode of care unspecified 

1 initial episode of care 

The fifth-digit 1 to designate the first episode of care (regardless of facility site) for a newly 

diagnosed myocardial infarction. The fifth-digit 1 is assigned regardless of the number of times a 

patient may be transferred during the initial episode of care. 

2 subsequent episode of care 

The fifth-digit 2 to designate an episode of care following the initial episode when the patient is 

admitted for further observation, evaluation or treatment for a myocardial infarction that has 

received initial treatment, but is still less than 8 weeks old. 

410.0 Of anterolateral wall 

ST elevation myocardial infarction (STEMI) of anterolateral wall 

410.1 Of other anterior wall 

Infarction: 

anterior (wall) NOS (with contiguous portion of intraventricular septum) 

anteroapical (with contiguous portion of intraventricular septum) 

anteroseptal (with contiguous portion of intraventricular septum) 

ST elevation myocardial infarction (STEMI) of other anterior wall 

410.2 Of inferolateral wall 

ST elevation myocardial infarction (STEMI) of inferolateral wall 

410.3 Of inferoposterior wall 

ST elevation myocardial infarction (STEMI) of inferoposterior wall 

410.4 Of other inferior wall 

Infarction: diaphragmatic wall NOS (with contiguous portion of intraventricular septum) 

inferior (wall) NOS (with contiguous portion of intraventricular septum) 

ST elevation myocardial infarction (STEMI) of other inferior wall 

410.5 Of other lateral wall 

Infarction: apical-lateral; basal-lateral; high lateral; posterolateral 

ST elevation myocardial infarction (STEMI) of other lateral wall 

410.6 True posterior wall infarction 

Infarction: posterobasal; strictly posterior 

ST elevation myocardial infarction (STEMI) of true posterior wall 

410.7 Subendocardial infarction 

Non-ST elevation myocardial infarction (NSTEMI) 

Nontransmural infarction 

410.8 Of other specified sites 

Infarction of: atrium; papillary muscle; septum alone 

ST elevation myocardial infarction (STEMI) of other specified sites 
F-6 

410.9 Unspecified site 

401 Essential hypertension 

Includes: high blood pressure ; hyperpiesia; hyperpiesis; hypertension (arterial) (essential) 

(primary) (systemic); hypertensive vascular: degeneration; disease 

DeVivo, 1993:5

 Ischemic heart disease (ICD codes 410-414); Non ischemic heart disease (ICD 

codes 420-429); Cerebrovascular diseases (ICD codes 430-438); Diseases of arteries (ICD codes 

440-448) 

ISCHEMIC HEART DISEASE (410-414) 

Includes: 

that with mention of hypertension 

Additional code to identify presence of hypertension (401.0-405.9) 

410 Acute myocardial infarction 

Includes: 

cardiac infarction 

coronary (artery): 

embolism 

occlusion 

rupture 

thrombosis 

infarction of heart, myocardium, or ventricle 

rupture of heart, myocardium, or ventricle 

ST elevation (STEMI) and non-ST elevation (NSTEMI) myocardial infarction 

any condition classifiable to 414.1-414.9 specified as acute or with a stated duration of 8 weeks 

or less 

The following fifth-digit subclassification is for use with category 410: 

0 episode of care unspecified 

Use when the source document does not contain sufficient information for the assignment of 

fifth-digit 1 or 2. 

1 initial episode of care 

Use fifth-digit 1 to designate the first episode of care (regardless of facility site) for a newly 

diagnosed myocardial infarction. The fifth-digit 1 is assigned regardless of the number of times a 

patient may be transferred during the initial episode of care. 

2 subsequent episode of care 

Use fifth-digit 2 to designate an episode of care following the initial episode when the patient is 

admitted for further observation, evaluation or treatment for a myocardial infarction that has 

received initial treatment, but is still less than 8 weeks old. 

411 Other acute and subacute forms of ischemic heart disease 

412 Old myocardial infarction ;Healed myocardial infarction 

Past myocardial infarction diagnosed on ECG [EKG] or other special investigation, but currently 

presenting no symptoms 

413 Angina pectoris 

414 Other forms of chronic ischemic heart disease 

Excludes: 

arteriosclerotic cardiovascular disease [ASCVD] (429.2) 

cardiovascular: 
F-7 

arteriosclerosis or sclerosis (429.2) 

degeneration or disease (429.2) 

OTHER FORMS OF HEART DISEASE (420-429) 

420 Acute pericarditis 

Includes: 

acute: 

mediastinopericarditis 

myopericarditis 

pericardial effusion 

pleuropericarditis 

pneumopericarditis 

Excludes: 

acute rheumatic pericarditis (391.0) 

postmyocardial infarction syndrome [Dressler's] (411.0) 

421 Acute and subacute endocarditis 

422 Acute myocarditis 

Excludes: 

acute rheumatic myocarditis (391.2) 

423 Other diseases of pericardium 

Excludes: 

that specified as rheumatic (393) 

424 Other diseases of endocardium 

Excludes: 

bacterial endocarditis (421.0-421.9) 

rheumatic endocarditis (391.1, 394.0-397.9) 

syphilitic endocarditis (093.20-093.24) 

425 Cardiomyopathy 

Includes: 

Myocardiopathy 

426 Conduction disorders 

427 Cardiac dysrhythmias 

428 Heart failure 

Code, if applicable, heart failure due to hypertension first (402.0-402.9, with fifth-digit 1 or 

404.0-404.9 with fifth-digit 1 or 3) 

CEREBROVASCULAR DISEASE (430-438) 

Includes: 

with mention of hypertension (conditions classifiable to 401-405) 

Use additional code to identify presence of hypertension 

430 Subarachnoid hemorrhage 

Meningeal hemorrhage 

Ruptured: 

berry aneurysm 

(congenital) cerebral aneurysm NOS 

432 Other and unspecified intracranial hemorrhage 

433 Occlusion and stenosis of precerebral arteries 

The following fifth-digit subclassification is for use with category 433: 
F-8 

0 without mention of cerebral infarction 

1 with cerebral infarction 

Includes: 

embolism of basilar, carotid, and vertebral arteries 

narrowing of basilar, carotid, and vertebral arteries 

obstruction of basilar, carotid, and vertebral arteries 

thrombosis of basilar, carotid, and vertebral arteries 

434 Occlusion of cerebral arteries 

The following fifth-digit subclassification is for use with category 434: 

0 without mention of cerebral infarction 

1 with cerebral infarction 

435 Transient cerebral ischemia 

Includes: 

cerebrovascular insufficiency (acute) with transient focal neurological signs and symptoms 

insufficiency of basilar, carotid, and vertebral arteries 

spasm of cerebral arteries 

436 Acute, but ill-defined, cerebrovascular disease 

Apoplexy, apoplectic: 

NOS 

attack 

cerebral 

seizure 

Cerebral seizure 

437 Other and ill-defined cerebrovascular disease 

438 Late effects of cerebrovascular disease 

Note: This category is to be used to indicate conditions in 430-437 as the cause of late effects. 

The "late effects" include conditions specified as such, or as sequelae, which may occur at any 

time after the onset of the causal condition. 

DISEASES OF ARTERIES, ARTERIOLES, AND CAPILLARIES (440-448) 

440 Atherosclerosis 

Includes: 

arteriolosclerosis 

arteriosclerosis (obliterans) (senile) 

arteriosclerotic vascular disease 

atheroma 

degeneration: 

arterial 

arteriovascular 

vascular 

endarteritis deformans or obliterans 

senile: 

arteritis 

endarteritis 

Excludes: 

atheroembolism (445.01-445.89) 

atherosclerosis of bypass graft of the extremities (440.30-440.32) 
F-9 

440.0 Of aorta 

440.1 Of renal artery 

440.2 Of native arteries of the extremities 

440.3 Of bypass graft of the extremities 

440.8 Of other specified arteries 

440.9 Generalized and unspecified atherosclerosis 

Garshick, 2005:6

 Diseases of the heart (390-398, 402, 404, 410-14, 420-429); Other diseases of 

the circulatory system (401, 403, 405, 415-417, 430--38, 440-459); Diseases of the arteries, 

veins, and pulmonary circulation (415-417,440-459). 

DISEASES OF THE CIRCULATORY SYSTEM (390-459) 

ACUTE RHEUMATIC FEVER (390-392) 

CHRONIC RHEUMATIC HEART DISEASE (393-398) 

402 Hypertensive heart disease 

403 Hypertensive kidney disease 

405 Secondary hypertension 

415 Acute pulmonary heart disease 

416 Chronic pulmonary heart disease 

417 Other diseases of pulmonary circulation 

CEREBROVASCULAR DISEASE (430-438) 

DISEASES OF ARTERIES, ARTERIOLES, AND CAPILLARIES (440-448) 

DISEASES OF VEINS AND LYMPHATICS, AND OTHER DISEASES OF CIRCULATORY 

SYSTEM (451-459) 

Analytical framework for pooled analysis of prevalence of cardiovascular diseases in adults with 

chronic SCI.

Prevalence was calculated as number of CVD events among total number of SCI patients in the 

study, standard error and confidence interval for population prevalence were calculated with 

Wilson estimate as followed:7

SEρ=√ [ρ*(1-ρ)]/[n+4] 

95% level C confidence interval ρ±1.96*SEρ

Where p – prevalence, n- sample size 

Pooled estimate as a weighted average:8

Weights are inverse of variance (standard error): 

∑

∑

=

i

i

i

i i

IV

w

wθ

θ

2 ( )

1

i

i SE

w

θ =
F-10 

Standard error of pooled estimate: 

Heterogeneity (between-study variability) measured by: 

Assumptions for random effects model: true effect sizes qi have a normal distribution with mean 

q and variance t2; t2 is the between-study variance 

Between study variance: 

Where: 

wi are the weights from the fixed effect inverse-variance method 

Q is the heterogeneity test statistic from before (either from inverse-variance method or MantelHaenszel method) 

k is the number of studies, and 

t2 is set to zero if Q<k-1 

Random effect pooled estimate is weighted average: 

Weights used for the pooled estimate are similar to the inverse-variance, but now incorporate a 

component for between-study variation: 

Standard error of pooled estimate 

Heterogeneity between studies was quantified using the I-squared statistic.9

. Statistical 

significance was analyzed at the 95% confidence level. All calculations were conducted using 

STATA software.10

∑ =

i

i

IV

w

SE 1 (θ )

2 ( ) i IV

i

Q = ∑wi θ −θ

∑ ∑

∑

⎟

⎟

⎟

⎠

⎞

⎜

⎜

⎜

⎝

⎛

−

− − =

i

i

i

i

i

i

w

w

w

Q k

2

2 ( 1)

τ

∑

∑

=

i

i

i

i i

DL

w

w

'

' θ

θ

2 2 ( )

1 ' θ + τ =

i

i SE

w

∑ =

i

i

DL

w

SE '

1 (θ )
F-11 

References for Appendix E 

1. National Library of Medicine (U.S.), National 

Center for Biotechnology Information (U.S.), 

National Institutes of Health (U.S.). PubMed 

central: an archive of life science journals. NCBI 

U.S. National Library of Medicine NIH Dept. of 

Health and Human Services [Digital archive 

searchable database]. Available at: 

http://www.pubmedcentral.nih.gov/ 

2. Centers for Disease Control and Prevention 

(U.S.) NCfHSUS. ICD-9-CM, international 

classification of diseases, ninth revision, clinical 

modification. U.S. Dept. of Health and Human 

Services Centers for Disease Control and 

Prevention Health Care Financing Administration. 

3. Groah SL, Weitzenkamp D, Sett P, et al. The 

relationship between neurological level of injury 

and symptomatic cardiovascular disease risk in 

the aging spinal injured. Spinal Cord 2001 Jun; 

39(6):310-7. 

4. McGlinchey-Berroth R, Morrow L, Ahlquist M, et 

al. Late-life spinal cord injury and aging with a 

long term injury: characteristics of two emerging 

populations. J Spinal Cord Med 1995 Jul; 

18(3):183-93. 

5. DeVivo MJ, Black KJ, Stover SL. Causes of 

death during the first 12 years after spinal cord 

injury. Arch Phys Med Rehabil 1993 Mar; 

74(3):248-54. 

6. Garshick E, Kelley A, Cohen SA, et al. A 

prospective assessment of mortality in chronic 

spinal cord injury. Spinal Cord 2005 Jul; 

43(7):408-16. 

7. Moore DS, McCabe GP. Introduction to the 

practice of statistics. 4th ed. New York: W.H. 

Freeman and Co.; 2003. 

8. DerSimonian R, Laird N. Meta-analysis in clinical 

trials. Control Clin Trials 1986 Sep; 7(3):177-88. 

9. Higgins JP, Thompson SG, Deeks JJ, et al. 

Measuring inconsistency in meta-analyses. BMJ 

2003 Sep 6; 327(7414):557-60. 

10. Egger M, Smith GD, Altman DG. Systematic 

Reviews in Health Care. London: NetLibrary, Inc. 

BMJ Books; 2001.