399

Traumatic Brain Injury

Chapter 15

TRAUMATIC BRAIN INJURY

LOUIS M. FRENCH, PsyD*; MARIA MOURATIDIS, PsyD†; BRAD DICIANNO, MD§; and BRADLEY IMPINK, BSE¥

INTRODUCTION

DEFINITION OF TRAUMATIC BRAIN INJURY

BASIC PATHOPHYSIOLOGY OF TRAUMATIC BRAIN INJURY

BLAST EFFECTS

NEUROBEHAVIORAL SEQUELAE OF TRAUMATIC BRAIN INJURY AND POSTCONCUSSIVE DISORDER

TRAUMATIC BRAIN INJURY IN THE AMPUTEE

TREATMENT OF TRAUMATIC BRAIN INJURY 

ACUTE MEDICAL CARE

REHABILITATION

SUMMARY

*

Director, TBI Program, Departments of Orthopaedics and Rehabilitation, Walter Reed Army Medical Center, Military Advanced Training Center, Building 2A, 6900 Georgia Avenue, NW, Washington, DC 20307; Assistant Professor of Neurology, Uniformed Services University of the Health Sciences, 

4301 Jones Bridge Road, Bethesda, Maryland 20814

†

Command Consultant and Subject Matter Expert for Traumatic Brain Injury and Psychological Health, National Naval Medical Center, 8901 Wisconsin 

Avenue, Bethesda, Maryland 20889

§

Assistant Professor, Human Engineering and Research Labs, VA Pittsburgh Healthcare System, 7180 Highland Drive, 151R1-H, Building 4, 2nd Floor 

East, Pittsburgh, Pennsylvania 15206

‡

Predoctoral Fellow, Human Engineering Research Laboratories, VA Pittsburgh Healthcare System, 7180 Highland Drive, 151R1-H, Building 4, 2nd 

Floor East, Pittsburgh, Pennsylvania 15206; formerly, Graduate Student Researcher, Department of Bioengineering, University of Pittsburgh, Pittsburgh, Pennsylvania
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Care of the Combat Amputee

INTRODUCTION

Traumatic brain injury (TBI) is a global public health 

issue that is the leading cause of death and disability 

in young adults in the United States. The Centers for 

Disease Control and Prevention (CDC) estimates that 

1.4 million individuals in the United States sustain TBI 

annually; 50,000 of those injuries are fatal.1 Around 

80,000 to 90,000 individuals per year sustain permanent disability as a result of TBI. The CDC estimates 

the monetary cost of TBI to the public to be almost $50 

billion annually when treatment costs, lost wages, disability, and death are considered.2,3

TBI can significantly impair functioning and may 

negatively impact an individual’s relationships, health, 

and happiness. Military service, even during peacetime, increases the risk of brain injury. In wartime, 

combat operations add to that risk. The incidence of TBI 

in young female service members is similar to that of 

young adult male civilians, the group with the highest 

rate of TBI in the civilian population.4 TBI impacts the 

military as a whole by compromising the health and 

well-being of service members and their families and 

hindering operational readiness.

The survival rate for those injured in Operation 

Iraqi Freedom (OIF) and Operation Enduring Freedom (OEF) is much higher than in past wars. The 

current ratio of wounded to killed in Iraq is over nine 

to one,5 compared to a ratio of fewer than three to one 

in Vietnam and Korea and about two to one in World 

War II.6 This rate of survival is related to numerous 

factors, including advanced in-theater medical care, 

rapid evacuation, and advanced protective equipment. 

Concurrent with these survival rates, the military has 

observed an increased number of those who may have 

experienced TBI. The most common causes of injury in 

OEF and OIF are roadside bombs, improvised explosive devices, and explosively formed projectiles. The 

resultant blast wave from these weapons may cause TBI 

either through the direct blast effect or the secondary or 

tertiary effects (impact of an object against a person or 

a person against an object, respectively). Additionally, 

many service members deployed in support of OIF 

and OEF have been exposed to a multitude of blasts. 

Although a specific injury may be attributed to one 

of these events, the effect on the brain by cumulative 

blast exposures has not yet been clearly elucidated. 

Therefore, it is important that all healthcare providers 

who work with injured military service members be 

aware of the potential for existing TBI. 

TBI is typically identified soon after injury. However, 

delayed recognition, especially when the injury is relatively mild, is not uncommon. These “silent injuries,” 

whether occurring in a military or civilian setting, typically resolve without long-term consequences. Under 

some circumstances though, they have implications for 

functioning and may significantly impact the recovery 

and rehabilitation of other, more visible injuries.

As of March 31, 2008, Defense and Veterans Brain 

Injury Center sites reported 6,602 US service members 

have sustained TBI related to the global war on terror 

since January 1, 2003. The majority of those (1,523) were 

seen at Walter Reed Army Medical Center. Thirty-two 

percent of those arriving via air from Iraq and Afghanistan were diagnosed with TBI, often in association with 

another injury. Of all US service members medically 

evacuated from Iraq or Afghanistan, 25% reportedly 

sustained injuries to the head or neck.7 Additionally, 

military screening of service members returning from 

deployment (not medically evacuated) have determined 10% to 20% sustained a concussion or mild TBI 

(MTBI) at some time during their tour. 8

DEFINITION OF TRAUMATIC BRAIN INJURY

TBI is described as either closed or penetrating injury. 

A penetrating brain injury occurs when a foreign object 

or bone penetrates the dura surrounding the brain. In a 

military setting, this is most commonly a bullet or metal 

fragment, but it can involve bone from the skull or other 

foreign bodies, such as stones. Although the dura is not 

penetrated in a closed TBI, large external forces may 

act on the head, leading to significant brain damage. 

Although there is some variability in the definition of 

TBI, especially with respect to defining milder injuries, 

most accepted definitions (those advanced by the CDC, 

American Congress on Rehabilitation Medicine, American Psychological Association, and the World Health 

Organization) share common elements. The Department 

of Defense’s current definition was drafted in 2007 by a 

consensus panel of experts (Exhibit 15-1, Table 15-1).

BASIC PATHOPHYSIOLOGY OF TRAUMATIC BRAIN INJURY

The severity of closed TBI is typically characterized 

by the duration of loss of consciousness; duration of 

posttraumatic amnesia; and initial, postresuscitation 

Glasgow Coma Scale score. In addition to these criteria, 
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Traumatic Brain Injury Traumatic Brain Injury

neuroimaging results also play a role in injury severity. 

For example, an individual who loses consciousness 

or sustains posttraumatic amnesia consistent with 

MTBI will be classified as having a moderate injury 

if abnormality is evident on brain images because 

those individuals have similar outcomes.9,10 Current 

definitions and designations of TBI only describe the 

severity of the brain injury itself, and do not necesEXHIBIT 15-1

DEPARTMENT OF DEFENSE CONSENSUS ON TRAUMATIC BRAIN INJURY DEFINITION

The Department of Defense Consensus on Traumatic Brain Injury (TBI) defines TBI as a traumatically induced structural injury or physiological disruption of brain function as a result of an external force that is indicated by new onset 

or worsening of at least one of the following clinical signs immediately following the event:

•	 any period of loss of or decreased level of consciousness;

•	 any loss of memory of events immediately before or after the injury;

•	 any alteration in mental state at the time of the injury (eg, confusion, disorientation, slowed thinking);

•	neurological deficits (eg, weakness, balance disturbance, praxis, paresis/plegia, change in vision, other 

sensory alterations, aphasia) that may be transient; or 

•	intracranial abnormalities (eg, contusions, diffuse axonal injury, hemorrhages, aneurysms).

External forces include the following:

•	 an object striking the head; 

•	the head striking an object;

•	the brain undergoing an acceleration or deceleration movement without direct external trauma to the head;

•	 a foreign body penetrating the brain;

•	forces generated from an event such as a blast or explosion; or 

•	 other forces yet to be defined.

Sequelae of TBI may resolve quickly, within minutes to hours after the neurological event, or they may persist. Some 

sequelae of TBI may be permanent. Most signs and symptoms will manifest immediately following the event; however, 

other signs and symptoms may be delayed from days to months (eg, subdural hematoma, seizures, hydrocephalus, and 

spasticity). Signs and symptoms may occur alone or in varying combinations and may result in functional impairment. 

The following signs and symptoms are not better explained by preexisting conditions or other medical, neurological, 

or psychological causes, except in cases of an exacerbation of a preexisting condition:

•	 cognitive (eg, attention, concentration, memory, speed of processing, new learning, planning, reasoning, 

judgment, executive control, self-awareness, language, or abstract thinking);

•	physical (eg, headache, nausea, vomiting, dizziness, blurred vision, sleep disturbance, weakness, paresis/

plegia, sensory loss, spasticity, aphasia, dysphagia, apraxia, balance disorders, coordination disorders, or 

seizure disorders); and

•	 emotional/behavioral (eg, depression, anxiety, agitation, irritability, impulsivity, or aggression).

Cognitive, physical, or emotional/behavioral manifestations that cannot be better explained by another process may 

be casually related to the blast event, even when there is no identifiable evidence of structural brain injury on imaging 

studies or altered brain function immediately following the event. Further study is needed to determine if an episode 

of altered brain function at the time of the trauma is required for a diagnosis of TBI resulting from an explosion or 

blast.

Injury severity is determined at the time of the injury. Although this severity level has some prognostic value, 

it does not necessarily reflect the patient’s ability to function. Serial assessments of the patient’s cognitive, emotional/behavioral, and social functioning are required. The patient is classified as mild, moderate, or severe (see 

Table 15-1).

Data source: US Department of Defense Consensus Traumatic Brain Injury Definition. Developed at: DoD Force Health Protection 

and Readiness TBI Consensus Meeting; 2007.
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Care of the Combat Amputee

Level Structural 

Imaging

Loss of 

Consciousness

Alteration of 

Consciousness

Posttraumatic 

Amnesia

Mild Normal 0–30 min a moment–24 hrs 0–1 day

Moderate Normal or abnormal > 30 min–24 hrs 24 hrs; severity based on other 

criteria

1–7 days

Severe Normal or abnormal > 24 hrs 24 hrs; severity based on other 

criteria

> 7 days

TABLE 15-1

BRAIN INJURY SEVERITY LEVELS

sarily correlate with resultant symptomatic sequelae, 

clinical outcomes, or functionality. There is generally 

a greater chance for persistent problems in those with 

severe injuries, but it is not uncommon for individuals 

diagnosed with severe TBI to have a better functional 

recovery than those diagnosed with MTBI, who may 

have resultant catastrophic changes in personal, social, 

and occupational functioning. Fortunately, such poor 

outcomes are relatively rare and are often mediated 

by a variety of factors.11 Further research is required 

to determine if the typical outcomes seen in a civilian 

population, especially in the case of recovery from 

MTBI, are similar to those seen in the combat-injured 

population. Contextual issues, such as the high rate 

of comorbid medical, physical, or psychological problems, may also significantly impact TBI recovery in this 

patient population.

The two most common injury mechanisms associated with TBI are contact and acceleration/deceleration. A third mechanism, blast, has become the subject 

of increasing debate given the large number of blast 

casualties returning from OEF and OIF. Blast injuries 

may have some different characteristics than those 

resulting from contact or acceleration/deceleration 

injuries. TBI, regardless of its severity, can result in 

damage to the structure and function of the brain. 

Contact injuries can result in focal brain damage, such 

as lacerations, contusions, skull fractures, penetration 

wounds, and intracranial hemorrhage. Acceleration/deceleration injuries can result in diffuse brain 

damage, such as diffuse axonal injury and cerebral 

edema.12–16 Immediately following TBI, cerebral blood 

Data source: US Department of Defense Consensus Traumatic Brain Injury Definition. Developed at: DoD Force Health Protection and 

Readiness TBI Consensus Meeting; 2007.

flow regulation and glucose metabolism are impaired. 

Cerebral blood flow may decrease significantly, and 

cerebral ischemia is common.17–25 Cerebral metabolism 

is often diminished following TBI, which is related to 

mitochondrial dysfunction and reduced production 

of adenosine triphosphate. Reduced cerebral blood 

flow causes an ischemic-like state wherein anaerobic 

glycolysis leads to lactic acid accumulation. Anaerobic 

glycolysis cannot provide sufficient energy for cellular 

function and, because of adenosine triphosphate depletion, the energy-dependent membrane ion pumps 

fail. This results in a secondary pathophysiological 

response, which includes membrane depolarization, 

excessive neurotransmitter release, and ion flux.12,26

The primary excitatory neurotransmitter released is 

glutamate, which over-stimulates ionotropic glutamate 

receptors, resulting in Ca2+, Na+, and K+ fluxes. This 

leads to a catabolic state, increasing the intracellular 

concentrations of toxic products, such as free fatty 

acids and free radicals. Ultimately, the activation of 

various enzymes (proteases, peroxidases, phospholipases, caspases, translocases, and endonucleases) 

leads to membrane degradation, blood–brain barrier 

breakdown, necrosis, and apoptosis. Breakdown of 

the cerebral-vascular barrier results in increased cell 

membrane permeability, ultimately resulting in cerebral edema, which may further exacerbate the ischemic 

state.27,28 This process is more pronounced as the severity of the trauma increases.29

While not considered TBI in itself, secondary brain 

insults, like systemic hypotension and hypoxia, reportedly worsen outcomes in patients with TBI.30

BLAST EFFECTS

In 20th-century military conflicts such as Vietnam, 

the focus of attention in combat-related brain injuries 

has been on the penetrating craniocerebral injury.31

In the current global war on terror, concussive forces 
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Traumatic Brain Injury

and resultant MTBI have proven challenging. A recent 

report states that 88% of injuries seen at an echelon 

II medical unit during OIF were due to explosions.32

This figure is generally consistent with official reports 

on mechanism of injury in US troops in Iraq, in which 

80% of casualties were due to blast.33 Sophisticated 

body armor and protection against penetrating head 

wounds allow US troops to survive explosive attacks 

they would not have survived in previous wars. Because of the frequency of TBI and its impact on service 

members, the military has increased its efforts to screen 

for MTBI.

Levi and colleagues reported on a series of headinjured patients during the 1982–1985 Lebanese war 

and found the majority of TBI reported was penetrating.34,35 One subset (n = 17) of the patients who suffered 

blast injury were identified. Blast was defined as “a) 

primary—due to the air blast, b) secondary—due to the 

impact of blast energized debris (either on the victim 

or vice versa), and c) tertiary—due to the effects of 

fire, gases or collapse of a building.”35(p555) The authors 

commented on the high frequency of pathology identified by computed tomography, including diffuse brain 

injury. They concluded that there was a “unique character of head injuries sustained during explosion.”34

In one study of injuries in the Balkan conflicts, 30% of 

the blast injured had long-term (greater than 1 year) 

symptoms reflecting central nervous system disorders, 

as compared to just 4% of the non-blast–injured patients.36 Building on experience with soldiers, Cernak 

et al conducted animal studies in the laboratory to 

examine blast wave effects on the central nervous system. The studies showed structural, biochemical, and 

cognitive impairments in rat brains after either wholebody or local (chest) overpressure while the head was 

protected. Both groups of animals showed neuronal 

injury in the hippocampus. The whole-body–exposed 

group showed significant decline in performance on a 

previously learned task that persisted at least 5 days. 

In the local (chest overpressure) group, there was also 

a significant drop in performance, but with normalization by 1 day after injury. There was a significant linear 

relationship between blast injury severity and decline 

in task performance in each group.37

Interest in combat-blast–related injury in the central nervous system dates back to at least World War 

I and is again discussed in the scientific literature of 

the World War II era.38,39 The effects of physical and 

psychological injuries on soldiers’ symptom presentation and functioning was often debated. A more modern understanding fully appreciates the relationship 

between cognitive functioning and emotional stress; 

it has been shown that combat exposure puts individuals at higher risk for health-related problems, 

partly because of potential TBI.40

Whether blast-induced brain injury demonstrates 

a different course of illness and recovery than more 

traditional causes of TBI is the subject of ongoing 

investigation, as is whether cognitive and emotional 

profiles affect outcomes. It has been suggested that 

differences may result from the effect of the blast 

wave itself, the added emotional factors associated 

with military service and combat, and the potential 

that blasts may cause greater overall extracranial injury. In a study of victims of terror-related activities, 

Peleg and colleagues showed that gunshot wounds 

and injuries from explosions differ in the body 

regions of injury, distribution of severity, hospital 

length of stay, and length of stay in the intensive 

care unit.41 In the blast victims, it was reported that 

multiple body regions were more often affected. 

The blast victims also had more critical and fatal 

injuries compared to the gunshot victims. Traumatic 

vasospasm has also been reported in a substantial 

number of patients with severe blast neurotrauma 

(80.8%–86.7% of those injured). Additionally, it was 

noted that clinical outcomes were worse for those 

with this condition.6 TBI was noted in 56% of patients 

seen in the Veterans Affairs polytrauma system. 

Those with blast-related TBI demonstrated unique 

patterns of injury. Soft tissue, eye, oral and maxillofacial, otologic, and penetrating brain injuries; 

symptoms of posttraumatic stress disorder (PTSD); 

and auditory impairments were more common in 

blast-injured patients than in those with other warrelated injuries. Despite these differences in injury 

profiles, functional outcome was not predicted by 

the mechanism of the injury.42

NEUROBEHAVIORAL SEQUELAE OF TRAUMATIC BRAIN INJURY AND POSTCONCUSSIVE DISORDER

Neurobehavioral changes are a common consequence of TBI. The characteristics, extent, and duration of these changes are dependent on a multitude 

of factors, including the type and location of injury, 

genetic predisposition, environment, and psychosocial 

support system. Psychosocial functioning has also 

been shown to be affected by TBI. The extent of these 

functional limitations is related to the demographics 

of the population injured, existing comorbid injuries, 

and severity of the head injury itself. As would be expected, more severe head injuries are associated with 

poorer outcomes, including greater reliance on family 

and social subsidy systems, greater unemployment, 

and lower income. The severity of the TBI is also more 

closely related to objective indices of psychosocial 

outcome (eg, employment) than to self-perceived 
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Care of the Combat Amputee

psychosocial limitations.43

Cognitive changes are among the most frequently 

reported difficulties following TBI and can be the most 

debilitating. In at least one study, physical deficits were 

not related to the ability to return to employment, but 

the presence of cognitive, behavioral, and personality 

changes was significantly related to work failure.44 The 

extent of cognitive difficulties is based largely on the 

nature and extent of damage to the brain, especially 

the severity of the diffuse axonal injury suffered.45

Potential cognitive difficulties are wide ranging and 

encompass disruptions in various aspects of attention, learning and memory, language, and executive 

functioning (the ability to plan, organize, and selfmonitor). These key aspects of executive functioning, 

which are necessary for the execution of goal-directed 

activities in daily life, are increasingly disrupted with 

anterior brain lesions because of the anatomic localization of these critical neural substrates in the anterior 

forebrain.46

In general, MTBI is unlikely to cause persistent, significant cognitive difficulties. In a study of MTBI, Belanger and colleagues conducted a metaanalysis of the 

relevant literature based on 39 studies involving 1,463 

cases of MTBI and 1,191 control cases to determine 

the impact of MTBI across nine cognitive domains 

(global cognitive ability, attention, executive functions, fluency, memory acquisition, delayed memory, 

language, visuospatial skill, and motor functions).47

The overall effect of MTBI on neuropsychological 

functioning was moderate, and was found to correlate 

with patient characteristics, time since injury, and the 

cognitive domain affected. Acute (less than 3 months 

after injury) effects of MTBI were greatest for delayed 

memory and fluency. In unselected or prospective 

groups of patients, the overall analysis revealed no 

residual neuropsychological impairment by 3 months 

after injury. In contrast, clinic-based groups of patients 

and those groups including participants in litigation 

were associated with greater cognitive sequelae of 

MTBI. In another study by the same investigators, 

a metaanalysis of sports concussion literature from 

1970 to 2004 found 21 studies meeting inclusion criteria, leading to a total of 790 cases of MTBI and 2,016 

control cases.48 TBI only modestly effected cognitive 

functioning, with delayed memory, memory acquisition, and global cognitive functioning showing the 

greatest effects acutely. No residual effects were found 

from the group tested over 1 week after injury. Iverson 

illustrated that moderate and severe TBI have a significant, negative effect on cognition, but, after the acute 

recovery period, MTBI has essentially no measurable 

effect.29 Larger effects were observed in conditions such 

as depression, bipolar disorder, and attention deficit 

hyperactivity disorder than from MTBI.

A World Health Organization analysis of MTBI outcomes concluded that although acute symptoms are 

common, MTBI symptoms resolve in the vast majority 

of individuals by 3 months after injury, often sooner.11

However, the authors acknowledge that a subset 

of those with MTBI continue to manifest persistent 

symptoms. This has also been clinically observed in 

both military and civilian settings. In a review article 

on outcomes from MTBI, Iverson et al report that postconcussion symptoms are common in healthy subjects, 

including those without history of TBI. These findings 

have important implications for symptom attribution 

and recovery.49 In some cases, without education about 

recovery and expected course of illness, patients who 

have suffered MTBI (ie, concussion) may attribute 

symptoms related to the combat environment or the 

challenges of everyday life to the effects of a remote 

brain injury.

The issues surrounding persistent symptoms after 

MTBI, especially as related to military deployment, has 

led to debate. The first controversy relates to the scope 

of the problem itself. Although it has been reported that 

10% to 20% of those with MTBI will develop chronic 

persistent symptoms, it is likely that this figure is 

closer to 5%.49 An equally controversial topic is the 

theoretical cause of persistent symptoms after MTBI. 

Various authors have attributed MTBI symptoms to 

different causes, some believing they are related to 

the type and location of injury, others purporting a 

multicausal etiology, influenced by premorbid personality characteristics, social-psychological factors, 

and exaggeration of symptom manifestation (either 

conscious or unconscious).

TRAUMATIC BRAIN INJURY IN THE AMPUTEE

For those who have sustained limb amputation as 

a result of combat operations, there is concern about 

other conditions that may be a consequence of combat 

exposure, such as TBI, acute stress, and PTSD. Hoge 

et al surveyed four US combat infantry units either 

before theirdeployment to Iraq or 3 to 4 months after 

theirreturn from combat duty in Iraq or Afghanistan. 

Those who had been deployedto Iraq reported a high 

number of combat experiences, with more than 90% 

reporting being shot at and a high percentage reporting handling dead bodies, knowing someone who

was injured or killed, or killing an enemy combatant.50

Soldiers who servedin Afghanistan reported lower but 

still substantial rates of similar combat experiences. 
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Traumatic Brain Injury

The percentage of individuals whose responses met 

the screening criteria for major depression, PTSD, 

or alcohol misuse was significantly higher among 

soldiers after deployment than before deployment. 

Among service members in OIF, the prevalence of 

PTSD increased with the number of firefights during

deployment, reaching 19.3% for those involved in more 

than five firefights. Additionally within this group, 

it was found that the rates of PTSD were associated 

with having been wounded or injured (odds ratio for

those deployed to Iraq was 3.27; odds ratio for those 

deployed to Afghanistan was 2.49). This latter finding is consistent with Koren’s study of PTSD rates in 

injured Israeli war veterans.51 In that study, findings 

indicated that bodily injury is a risk factor for PTSD, 

with odds of developing PTSD following traumatic 

injury approximately eight times higher than following 

injury-free emotional trauma.

Although myriad factors influence the overall 

functional outcome of a service member with a major 

limb amputation, it is clear that both emotional and 

cognitive factors play a significant role in recovery. The 

presence of disorders such as depression or anxiety 

is associated with greater overall use of healthcare 

resources.52 There is limited literature on the predictive 

value of mental disturbances and cognitive impairments on functional outcome in an amputee population. In general, and representative of the war-injured 

population, younger men have more difficulties 

adjusting to amputations, presumably because of concerns over body image, social stigma, or other related 

factors.53 These concerns may contribute to the high 

rates of self-reported sexual problems in those with 

lower extremity amputations.54

In a study of the physical, mental, and social predictors of functional outcome in geriatric, unilateral lower 

limb amputees, Schoppen et al reported that memory 

ability was the most important of the mental predictors 

for functioning after leg amputation,55 suggesting that 

good memory may be important for relearning daily 

tasks. Depression level 2 weeks after amputation was 

also found to be predictive of outcome at 1 year. In 

another study of geriatric amputees, records of 2,375 

lower extremity amputees treated in Veterans Affairs 

hospitals were examined to determine which patient 

factors may influence the prescription of a prosthesis.56

Those with high cognitive Functional Independence 

Measure (FIM) scores were 1.67 times more likely to 

be prescribed a prosthesis than those in the lowest 

FIM category (the FIM, a widely accepted functional 

measure in the research community, is an 18-item, 

7-level ordinal scale intended to be sensitive to change 

in an individual over the course of a comprehensive 

inpatient medical rehabilitation program). Taylor et 

al investigated the relationship between a variety of 

preoperative clinical characteristics after major lower 

limb amputation and postoperative functional outcome.57 Among other factors, the presence of dementia 

was significantly associated with failure to maintain 

independent living status. Because TBI may disrupt 

cognitive functioning, some aspects of amputee rehabilitation may be complicated, such as learning new 

tasks, remembering appointments, and regaining 

independence.

TREATMENT OF TRAUMATIC BRAIN INJURY

Because the majority of TBI that occurs in the 

civilian and military settings is mild, symptoms can 

generally be expected to improve over time and, in 

most cases, completely resolve.29 MTBI is characterized by immediate physiological changes in the brain, 

but in the first week after injury, the brain undergoes 

a dynamic restorative process. This is often seen in 

athletes, who are typically able to return to preinjury 

functioning (cognitive and self-report) within 2 weeks 

after a concussion. Trauma patients usually take longer 

to return to preinjury functioning because of factors 

such as preexisting psychiatric or substance abuse 

problems, poor general health, concurrent orthopaedic 

injuries, pain, or various psychosocial problems.29 The 

clinical team should communicate the expectation of 

a full recovery with the patient while simultaneously 

assessing the patient’s symptom complex and providing treatment as indicated. The extent of intervention 

or rehabilitation required will be determined by a 

patient’s comorbid injuries rather than the degree of 

brain injury.42

Symptom treatment for MTBI includes four areas 

of focus: pharmacological management, educational 

interventions, rest and return to duty decisions, and 

targeted therapies. Evidence for the efficiency of 

various pharmacologic interventions is prolific.58,59

Pharmacological interventions are often indicated 

for sleep regulation,60 headache,61,62 pain,63 and depression.64 Treating these associated conditions improves quality of life and rehabilitation outcomes. 

Educational and psychological therapies have 

also proven effective in treating MTBI. Mittenberg 

compared two groups of patients with MTBI. Group I 

(n = 29) participated in a cognitive-behavioral model 

of symptom maintenance and treatment, learned 

techniques for reducing symptoms, received printed 

educational manuals, and met with a therapist 

prior to hospital discharge to review the nature and 
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Care of the Combat Amputee

incidence of expected symptoms and instructions 

for gradual resumption of premorbid activities.65

The control group (n = 29) received routine hospital treatment and discharge instructions. After 6 

months, Group I reported significantly shorter average symptom duration (33 compared to 51 days) 

and significantly fewer symptoms at follow-up. 

The conclusion was that brief, early psychological 

interventions are effective in reducing the incidence 

of postconcussive symptoms. Ponsford et al have 

shown similar results.66 Individuals seen 1 week after 

injury and given informational material reported 

fewer symptoms overall and were significantly less 

stressed at 3 months after the injury than a group 

that did not receive the same education. A number of 

educational materials are available from public and 

private sources, including the Defense and Veterans 

Brain Injury Center.67

ACUTE MEDICAL CARE

Emergency preadmission care is aimed at preventing hypoxia and hypotension, which can lead 

to secondary neurological injury.68 When admitting 

a patient for neurosurgical services, care is geared 

toward stabilizing the patient, treating infection, and 

detecting operable lesions that may prevent further 

neurological deterioration. The role of decompressive 

craniectomy remains controversial because it does not 

result in improved outcomes in all cases. Once the patient is stabilized, treatment is focused on creating an 

environment in which the brain has the best chance of 

neural recovery; this involves managing temperature, 

intracranial pressure, and perfusion and oxygenation; 

glycemic control; and early nutrition.68,69 Drug-based 

neuroprotection is one aspect of the acute management 

of TBI. Medications, such as N-methyl-d-aspartate antagonists, are being studied in clinical trials and have 

shown potential long-term benefit.69

The risk of posttraumatic seizures is high in some 

subpopulations, especially those with war injuries.70 Steroid therapy has not been shown to have 

any beneficial effect on seizures.69 It is also clear from 

the literature that long-term use of anticonvulsants, 

such as phenytoin, does not prevent late seizures.69

Managing early seizures with anticonvulsant therapy 

remains controversial. One study showed that lateseizure risk factors include brain contusion with subdural hematoma, skull fracture, loss of consciousness 

or amnesia (lasting > 1 day), and being older than 65 

years.70 However, in another study by four National Institute on Disability and Rehabilitation Research model 

system sites, bilateral parietal contusion, penetration of 

the dura, and multiple intracranial operations resulted 

in the highest risks for late seizures.71

Heterotopic ossification (HO), defined as pathologic 

ectopic bone formation in the soft tissue surrounding 

the joints, often afflicts patients after TBI, and this can 

have a significant impact on the rehabilitation and 

recovery of the amputee. The incidence of HO in TBI 

varies from approximately 10% to 70%, with a clinically 

significant incidence reported in the range of 10% to 

20%.72–75 HO typically causes pain and limits range of 

motion. Larger joints, like the hips, knees, and elbows, 

are most commonly affected. The pathogenesis of HO 

is unknown, but several risk factors have been identified, including prolonged coma after TBI, spasticity, 

immobilization, and increased serum alkaline phosphotase levels. HO is best diagnosed using sonography, three-phase bone scanning, or plain radiography. 

Range-of-motion therapy is often used to prevent 

HO. Although there is little evidence to support this 

theory, some believe active range-of-motion therapy 

may promote HO, therefore passive range-of-motion 

therapy is often recommended. Surgical excision, 

when indicated, is typically delayed until bone fully 

matures (typically 12–18 months). This waiting period 

is thought to reduce the risk of reoccurrence, but recent 

data suggests that early excision may be better and 

that recurrence is unlikely.72 Literature concerning HO 

treatment is generally limited to surgical case studies 

without control groups.

Preventing and treating deep venous thrombosis 

(DVT) in patients with TBI can be complicated by concerns for intracranial bleeding. However, many recent 

studies show that chemical prophylaxis can help prevent DVT in certain populations that are at increased 

risk of bleeding. The importance of screening for 

DVT in these populations by ultrasound, computed 

tomography, and now by D-dimer testing (despite 

its high false-positive rates) remains critical because 

the risks of DVT and subsequent fatal pulmonary 

embolism are high, especially for those with blast 

injuries.76 Although there is no consensus on national 

clinical practice guidelines,77 Walter Reed Army 

Medical Center has developed its own guidelines 

specific to trauma patients.76

Diffuse spasticity is a relatively common complication in individuals with severe TBI. Management 

can often be challenging, but begins with a wellstructured and consistent program of stretching and 

range-of-motion exercises administered by trained 

therapists. Family members can often be taught how 

to help facilitate range-of-motion exercises. Oral 

medications, such as tizanidine78 or baclofen (which 
407

Traumatic Brain Injury

is more effective at managing lower limb tone),79 may 

also be helpful. Unfortunately, oral management 

may be limited by side effects, such as sedation. For 

focal spasticity, interventional injections with botulinum toxin can be efficacious.80 Intrathecal baclofen 

pumps have also proven to be effective in a number 

of trials for more diffuse spasticity and may also be 

useful in managing dysautonomia (the inability to 

regulate the autonomic nervous system).69 Dysuatonomia can manifest with tachycardia, tachypnea, 

fever, or hypertension. This process is less well understood, but a collection of case studies suggests 

that beta blockers, morphine, chlorpromazine, or 

midazolam may be effective treatments. Caution is 

needed any time such sedation medications are used 

in patients with TBI.69

REHABILITATION

When discussing TBI rehabilitation, it is important 

to note that “we have really only recently begun to 

evaluate the efficacy of approaches being used and 

the development of alternatives to optimize functional 

outcomes for TBI.”70 As noted earlier in this chapter, 

given the heterogeneity of the patient population with 

TBI and the complexity of the brain, it is difficult to 

categorize patients with TBI into clear diagnostic 

groups. Moreover, because recovery is dependent 

on a multitude of factors (eg, mechanism, location 

and circumstances surrounding the injury, an individual’s premorbid constitution, environmental and 

psychosocial issues), examining outcomes in this 

patient population is challenging. These challenges 

are compounded when trying to evaluate optimal 

rehabilitation strategies to care for the military service 

member who sustains TBI in association with other 

combat-related injuries.

TBI rehabilitation begins with a careful evaluation 

of an individual’s injuries. This evaluation should 

include a thorough cognitive, neurologic, motor, and 

extremity examination, as well as a full assessment 

of any sensory difficulties in vision, hearing, balance, 

and sense of smell.81,82 It is also important for all rehabilitation disciplines to perform a thorough functional 

assessment of the patient, determining areas of function in hygiene, eating, mobility, dressing, toileting, 

and communication. This thorough, multidisciplinary 

evaluation facilitates the development and implementation of a comprehensive treatment approach. 

Assessment and treatment approaches that focus on 

the entire person, including physical, psychological, 

cognitive, social, occupational, academic, and spiritual 

aspects will have the greatest potential for maximizing 

a patient’s functioning and quality of life. A multidisciplinary treatment team is necessary to treat complex 

patients recovering from polytraumatic injuries, such 

as those returning from OEF and OIF. Rehabilitation 

teams may include:

	 •	 physiatrists,

	 •	 rehabilitation nurses,

	 •	 prosthetists,

	 •	 neuropsychologists,

	 •	 rehabilitation psychologists,

	 •	 clinical psychologists,

	 •	 health psychologists,

	 •	 deployment health psychologists,

	 •	 marriage and family therapists,

	 •	 psychiatrists,

	 •	 neurologists,

	 •	 speech pathologists,

	 •	 occupational therapists,

	 •	 physical therapists,

	 •	 rehabilitation engineers,

	 •	 rehabilitation counselors,

	 •	 vocational rehabilitation therapists,

	 •	 clinical social workers,

	 •	 nurse case managers,

	 •	 substance abuse counselors, and

	 •	 chaplains.

In some cases, this team, combined with a patient’s 

community and case managers, will be needed to provide care across the lifespan of the injured individual. 

In addition to the challenges presented immediately 

after TBI, symptom complexes may change over time. 

Symptoms of depression and reduced motor or cognitive function may result from a variety of life factors, 

such as the development of cardiovascular disease, 

arthritis, and dementia. Therefore it is important to 

provide individuals with TBI life-long coordinated 

health services and access to healthcare to promote 

the highest quality of life.83 This is especially relevant 

for polytrauma patients who have multiple comorbid 

injuries, such as TBI, traumatic amputation, visual 

impairment, and psychological illness.84 Polytrauma 

patients require an integrated treatment approach 

whereby patients receive care for all injuries simultaneously, as opposed to sequentially. 

The role physical therapists play in assessing and 

treating TBI-related deficits is wide-ranging.85 Physical 

therapy has proven effective in treating pain,63 balance 

impairment, and postural instability, which are common symptoms in polytrauma patients with TBI.86

Physical therapy is also helpful in assessing and treat-
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Care of the Combat Amputee

ing motor impairments, especially those associated 

with severe TBI.87 Paresis, ataxia, postural instability, 

tandem gait disturbances, and other motor neuron abnormalities are common and can be addressed through 

physical therapy interventions. 

In addition to helping build independence in activities of daily living, occupational therapy has demonstrated efficacy in improving self-awareness after TBI.88

Its role as part of a long-term strategy in more severe 

TBI patients is also well established.89 Occupational 

therapists are critical to managing upper limb and 

hand spasticity positioning and functioning in those 

with motor deficits. They are also valuable partners 

to vocational rehabilitation experts, performing work 

assessments and helping integrate assistive technology 

to facilitate independence in the workplace.90

Evidence suggests that early rehabilitative interventions after TBI improve outcomes.91,92 Polytrauma patients often have treatment targets in various domains. 

For example, if an injury was severe enough to require 

amputation, other areas of the patient’s health may 

also have been affected. Blast-exposed patients may 

sustain TBI and psychological injuries in addition to 

the blast injury. Considering all of these factors, a patient’s impairments, strengths, and functioning must 

be assessed to enhance the rehabilitation outcome from 

a major limb amputation.

 Because so many patients undergoing rehabilitation 

for amputation suffer from brain injury, it is important 

to explore the particular needs and approaches for 

treating this dual condition. The presence and severity of TBI can have significant implications on the 

rehabilitation process. Patients with TBI may have 

restricted awareness of their injuries or limitations, 

may process information differently, and are likely to 

have difficulty participating in treatment at the same 

pace as amputees without TBI. An undiagnosed TBI 

or a treatment plan that is not modified based on a 

patient’s cognitive impairment is likely to result in 

poor treatment response.

A complete neuropsychological evaluation not only 

reveals if a patient sustained cognitive deficits secondary to blast-related brain injury or other mechanisms, 

but also identifies the patient’s strengths. For the purposes of this discussion, the term “neuropsychological 

evaluation” means the administration, scoring, and 

interpretation of empirically validated and normed 

neuropsychological tests by a neuropsychologist. 

Cognitive and psychological function reciprocate 

and share several mechanisms. Identifying the origin 

of a symptom will inform the treatment approach. For 

example, if a patient has poor motivation, it is important to determine if that symptom is primarily due to 

frontal lobe dysfunction or to depression. In addition, 

MTBI and PTSD share a similar cognitive dysfunction 

profile. Trudeau et al have suggested that blast patients 

may suffer from a complex chronic concussive disorder 

with overlapping cognitive deficits, depression, and 

PTSD. Neuropsychological testing can help tease apart 

these symptoms.93

A comprehensive neuropsychological evaluation 

comprises empirically validated cognitive testing 

and a complete mental health evaluation. Recommended cognitive testing includes a survey of all 

major domains of cognitive functioning (Table 15-2). 

Some caution is warranted when using inventories or 

questionnaires that have been developed for use in a 

civilian TBI population. There may be differences in 

the demographics (eg, education, employment status, 

etc) or the circumstances of the injury (eg, combat 

and related emotional factors) in military patients as 

compared to their civilian counterparts.

The recommended mental health assessment portion of a neuropsychological evaluation includes a 

review of the patient’s personal history, including 

academic, occupational, military, social, family, medical (especially history of prior TBI or concussion), substance use and family substance abuse, mental health, 

deployment, and combat history. Patients with amputations may suffer from a number of mental health 

disorders, not likely limited to PTSD. Among the disorders of concern are depression and possible narcotic 

dependence secondary to overuse of pain medications. 

Clinical interviews focus on how amputees and their 

families are adjusting to daily living, as well as on the 

patient’s strengths and resilience factors. Gathering a 

thorough history and performing a complete mental 

health examination is necessary in order to approximate a patient’s baseline and to appropriately interpret 

results from the neuropsychological evaluation. 

The results of the neuropsychological evaluation 

inform the treatment plan, and there are several ways 

in which the results from a neuropsychological evaluation can be clinically applied. They can be used to 

modify rehabilitation strategies based on a patient’s 

cognitive abilities, or used to directly treat cognitive 

dysfunction and psychological injuries. They can also 

facilitate adjustment to amputation.

In order for many patients to effectively participate 

in the physical aspects of their rehabilitation, their 

cognitive deficits must be recognized and addressed. 

Patients with cognitive deficits often have difficulty 

participating in “treatment as usual.” Many patients 

are considered “treatment failures” when the expected 

treatment outcome is not obtained. However, cognitive deficits often interfere with patients’ abilities to 
409

Traumatic Brain Injury

TABLE 15-2

DOMAINS OF COGNITIVE FUNCTIONING AND REPRESENTATIVE NEUROPSYCHOLOGICAL 

TESTS

Cognitive Function Test

Verbal memory: immediate and delayed California Verbal Learning Test II 

Visual memory: immediate and delayed Rey-Osterrieth Complex Figure, copy and delayed visual 

reproduction subtests from the Wechsler Memory Scale III

Executive functioning Stroop Test, Wisconsin Card Sorting Test, Trail Making Test 

(part B)

Attention Conners’ Continuous Performance Test, Paced Auditory 

Serial Addition Test, digit span subtest from the Wechsler 

Adult Intelligence Scale III

Psychomotor speed Trail Making Test (part A), finger tapping test, grooved 

pegboard test

General intellectual functioning Wechsler Abbreviated Scale of Intelligence

Psychological functioning Clinical interview, collateral interview, Personality Assessment Inventory, Detailed Assessment of Posttraumatic 

Stress

Effort/motivation Test of Memory Malingering, Word Memory Test

understand and follow directions, follow sequences 

or schedules, practice on their own, remember what 

they have learned, manage their behavior, maintain 

sufficient motivation, or work cooperatively with others. Substance abuse, dementia, and stroke literature 

discuss the value of modifying patients’ treatment 

plans in accordance with their cognitive deficits. Several studies address either comprehensive rehabilitation of patients with cognitive deficits or interventions 

for specific cognitive deficits.70 Such approaches also 

show strong support from the brain injury advocacy 

community.94 Treating psychological injuries that occurred with a traumatic event is important for overall 

clinical improvement. Similarly, as a patient begins to 

make gains in physical rehabilitation, improvements 

in mental health symptoms are often observed. 

The experience and management of pain also appears to be related to mental health and, more specifically, to PTSD. Patients with depression experience 

higher subjective pain levels,95 and pain-related variables have been shown to be significant predictors of 

PTSD symptom cluster scores in both male and female 

veterans.96 These findings suggest that managing pain 

for the amputee may improve mental health prognosis. Similarly, treating mental health symptoms may 

improve an amputee’s ability to engage in physical 

rehabilitation because of decreased pain perception. 

Facilitating patient and family adjustment to TBI and 

amputation, the rehabilitation process, and return to 

daily life are integral to patients being able to maintain 

treatment gains, achieve the highest level of independent functioning, and maximize quality of life. 

SUMMARY

In times of peace and during times of active 

military operations, TBI is a significant and important health issue for US military service members. 

Even with the best efforts at prevention, a relatively 

large number of service members can be expected 

to sustain TBI each year. To optimize treatment and 

rehabilitation, the complicated interplay between 

physiologic insult to the brain, the disruption of 

the mind, and the injury to the body must be better 

understood. An assessment and appreciation of how 

these factors act together to ameliorate or hinder an 

individual’s functioning is necessary to maximize 

outcomes and promote recovery across a patient’s 

lifespan.
410

Care of the Combat Amputee

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