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Traumatic Brain Injury in the Military Population

Chapter 15

TRAUMATIC BRAIN INJURY IN THE 

MILITARY POPULATION

LOUIS M. FRENCH, PsyD*; KATHERINE H. TABER, PhD†; KATHY HELMICK, MS, CNRN, CRNP‡; ROBIN 

A. HURLEY, MD§; and DEBORAH L. WARDEN, MD¥

INTRODUCTION

ETIOLOGY AND DIAGNOSIS OF TRAUMATIC BRAIN INJURY

Forces That Cause Traumatic Brain Injury

Vulnerable Areas and Injury Evolution

DETERMINING SEVERITY OF TRAUMATIC BRAIN INJURY

Structural Neuroimaging

Combat-Related Traumatic Brain Injury

COMMON COGNITIVE SEQUELAE

Postconcussive Disorder

The Relationship Between Posttraumatic Stress Disorder and Traumatic Brain 

Injury

In-Theater Management

The Relationship Between Substance Abuse and Traumatic Brain Injury

SYMPTOM TREATMENT 

Educational Interventions

Rest and Return-to-Duty Issues

SUMMARY

*Director, Traumatic Brain Injury Service, Defense and Veterans Brain Injury Center and Department of Orthopaedics and Rehabilitation, Walter Reed 

Army Medical Center, 6900 Georgia Avenue NW, Washington, DC 20307; Department of Neurology, Uniformed Services University of the Health 

Sciences, Bethesda, Maryland 20814

†

Research Health Scientist, Department of Research and Education, WG Hefner Veterans Affairs Medical Center, Mailstation 11M, 1601 Brenner Avenue, 

Salisbury, North Carolina 28144; formerly, Research Fellow, School of Health Information Sciences, University of Texas at Houston 

‡

Senior Executive Director, Traumatic Brain Injury, Defense Center of Excellence for Psychological Health and Traumatic Brain Injury, 1335 East-West 

Highway, 9th Floor, Suite 700, Silver Spring, Maryland 20910; formerly, Deputy Director, Defense and Veterans Brain Injury Center, Walter Reed 

Army Medical Center, Washington, DC 

§

Associate Director, Education, WG Hefner Veterans Affairs Medical Center (Mailcode 11F), 1601 Brenner Avenue, Salisbury, North Carolina 28144; 

formerly, Associate Director, Mental Health, WG Hefner Veterans Affairs Medical Center, Salisbury, North Carolina 

¥

Formerly, National Director, Defense and Veterans Brain Injury Center Headquarters; Departments of Neurology and Psychiatry, Walter Reed Army 

Medical Center, 6900 Georgia Avenue NW, Washington, DC 20307; Departments of Neurology and Psychiatry, Walter Reed Army Medical Center, 

6900 Georgia Avenue NW, Washington, DC 20307-5001
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INTRODUCTION

Traumatic brain injury (TBI) is a very significant 

public health issue and the leading cause of death and 

disability in young people. The Centers for Disease 

Control and Prevention (CDC)1

 estimates that 1.4 

million individuals sustain a TBI in the United States 

annually, with 50,000 deaths. About 80,000 to 90,000 

individuals suffer permanent disability. The monetary 

cost to society is almost $50 billion annually when 

treatment costs, lost wages, disability, and death are 

considered.2,3 Even more significant, at its most severe, 

TBI robs individuals of important aspects of their relationships, well-being, and happiness. 

Service in the military, which includes both rigorous and often dangerous training, and exposure to 

the combat environment, places individuals at greater 

risk than the general population. Surprisingly, young 

adult men (the group with the highest rate of TBI in 

the civilian population), have about the same rate of 

TBI as young women in the military, a figure that underscores the inherent risk in service.4

 However, Ivins 

and colleagues,5 in a recent paper examining trends 

in TBI-related hospitalizations in the active duty US 

Army during the 1990s, reported that the Army’s TBIrelated hospitalization rates decreased for all severity 

levels, both sexes, and all age categories during that 

decade. The paper also indicated that in the first half 

of the 1990s, many of the Army’s adjusted TBI-related 

hospitalization rates, including the overall rate, were 

higher than the rates for US civilians 17 to 49 years of 

age. In the second half of the 1990s, most of the Army’s 

adjusted TBI-related hospitalization rates, including 

the overall rate, were lower than civilian rates, with a 

75% reduction overall. These decreases resulted in a 

relative improvement in the Army’s TBI-related hospitalization rates over civilian rates by the late 1990s. 

This may be related to successful educational efforts 

or other factors.

Somewhat more difficult to quantify is the effect 

of TBI on military readiness. Because some potential 

consequences of TBI include slowed reaction, reduced 

speed of cognitive processing, and mood changes, 

the effects of even transitory symptoms could have 

implications for the deployability or fighting effectiveness of the service member. Additionally, there is 

the risk that the TBI, especially at the milder end of 

the spectrum, will be unrecognized. This chapter will 

describe (a) what TBI is, (b) how severity is determined, 

(c) common consequences of the injury, and (d) some 

treatment strategies. Furthermore, the identification 

and management of TBI in a military operational setting will be discussed. Although the entire spectrum of 

brain injury severity will be discussed, the focus of the 

chapter is on those with mild TBI (mTBI), as that is the 

population that is most likely to come to the attention 

of the military behavioral health provider. Additionally, the overlap of typical postconcussive symptoms 

with symptoms of mood, anxiety, or other disorders 

may make referral to such providers probable when 

an individual with such symptoms of unclear etiology 

is recognized. 

The current conflicts in Iraq (Operation Iraqi Freedom) and Afghanistan (Operation Enduring Freedom) 

are different than past wars in terms of the survival 

rates of those injured. The current wounded-to-killed 

ratio in Iraq is more than 9:1,6

 compared to less than 

3:1 in Vietnam and Korea, and approximately 2:1 in 

World War II.7 This increased survival of wounded 

personnel is related to numerous factors including 

advanced in-theater medical care and superb protective equipment. With these new survival rates come increased numbers of those who may have experienced 

a TBI. Because the most common injury mechanism in 

the current conflict is blast, there are possibilities for 

TBI either through direct blast effect or secondary or 

tertiary blast effects. It is essential for the healthcare 

provider to be aware of the possibility that an injured 

service member may also have sustained a TBI. In 

many cases, this identification is early after the injury. 

There is greater potential, however, for more delayed 

recognition of such an injury, especially if the TBI is at 

the milder end of the severity spectrum. These “silent 

injuries” may have implications for functioning over 

the short or long term, and may affect recovery and 

rehabilitation of other more visible injuries.

ETIOLOGY AND DIAGNOSIS OF TRAUMATIC BRAIN INJURY

TBI is described as either penetrating or closed. A 

penetrating brain injury occurs when a foreign object 

or bone penetrates the dura surrounding the brain. 

(In the military setting, the object is most commonly a 

bullet or fragment.) In a closed TBI, penetration does 

not occur, but forces acting on the head cause damage 

to the brain. Although there is some variability in the 

definition of TBI, especially at the milder end of the 

spectrum, most accepted definitions (CDC,8

 American 

Congress of Rehabilitative Medicine [ACRM],9

 American Psychiatric Association [APA],10 and World Health 

Organization [WHO]11) have common elements. The 

Defense and Veterans Brain Injury Center (DVBIC) 

defines mTBI in a military operational setting as an 
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Traumatic Brain Injury in the Military Population

injury to the brain caused by an external force, with 

either an acceleration or deceleration mechanism 

(or both in some instances), from an event such as a 

blast, fall, direct impact, or motor vehicle accident. 

This trauma causes an alteration in mental status, 

typically resulting in the temporally related onset of 

symptoms such as headache, nausea, vomiting, dizziness or balance problems, fatigue, insomnia or other 

sleep disturbances, drowsiness, sensitivity to light or 

noise, blurred vision, and difficulty remembering or 

concentrating. 

This operational definition of mTBI was established 

in 2006 by a workgroup of experts in the field of military operational medicine and TBI.12 They drew from 

widely accepted definitions, such as those already 

mentioned (CDC, ACRM, APA, and WHO), as well 

as the National Athletic Trainers’ Association position 

statement on management of sport-related concussion,13 and the Prague sports concussion guidelines,14

incorporating common criteria. These established 

definitions endorse biomechanical forces as the cause 

of concussion that results in an alteration of consciousness (AOC), including loss of consciousness (LOC), 

posttraumatic amnesia (PTA) or retrograde amnesia, 

or being dazed or confused at the time of the injury. 

An important aspect of this new operational definition of TBI is that LOC is not a required characteristic 

of concussion. That is, a service member does not 

have to have an LOC to have sustained a concussion 

or mTBI (these terms are used interchangeably). The 

group acknowledged the continued usefulness of these 

parameters and adopted them with a few changes. 

Variations from the established definitions included 

adding common combat-related mechanisms such as 

exposure to blast as a possible mechanism of injury, 

as well as adding a comprehensive list of TBI-related 

symptoms.

The majority of TBI experts in this workgroup 

agreed that symptoms are common following mTBI, 

but the presence of these symptoms is not mandatory 

to establish the diagnosis of mTBI. That is, although 

concussion to the brain may have occurred, it does 

not always result in self-reported symptoms. In some 

circumstances there may be measurable changes in 

functioning or performance, such as increased latency 

of response on measures of reaction time, even in the 

absence of changes noticeable to the injured individual.15 It should be noted that wide consensus among the 

members of the workgroup supported the inclusion of 

an AOC in the definition of mTBI, including reports of 

feeling “dazed and confused” after a traumatic event. 

There are instances, both in the sports literature and 

military arena, of individuals who were involved in 

a traumatic event but did not report any AOC, yet 

these patients subsequently developed symptoms 

consistent with concussion, with onset temporally 

related to the event. Given these cases, a conservative 

approach might be that those individuals involved 

in events with an associated high risk for TBI, who 

report subsequent symptoms, be evaluated further. 

However, without supporting diagnostic evidence, 

these individuals do not meet the criteria for having 

sustained an mTBI. More research is needed to better 

characterize this group.13

Closed-TBI severity is characterized by duration of 

length of LOC and PTA, and initial, postresuscitation 

Glasgow Coma Scale (GCS) score (Table 15-1). Those 

individuals who meet these criteria as having sustained an mTBI, but have positive findings on imaging 

of the brain, are classified as having suffered a TBI of 

moderate severity, as these individuals are known to 

have outcomes similar to those who meet criteria for 

moderate TBI on the basis of length of coma or duration 

of LOC.16,17 It is important to note that these designations describe the severity of the brain injury itself, and 

do not necessarily describe clinical outcomes or functionality in the future. Although there is greater chance 

for persisting problems as injury severity increases, 

many patients at the more severe end of the spectrum 

can have good outcomes, while some patients who 

were initially diagnosed as having a “mild” TBI go on 

TABLE 15-1

TRAUMATIC BRAIN INJURY DESCRIPTION

Severity GCS* LOC PTA

Mild 13–15 < 20 min–1 h < 24 h

Moderate 9–12 1–24 h 24 h– < 7 days

Severe 3–8 > 24 h > 7 days

GCS: Glasgow Coma Scale

LOC: loss of consciousness

PTA: posttraumatic amnesia

*The Glasgow Coma Scale (GCS) is the most commonly used scale to 

determine the severity of a brain injury. It must be noted, however, 

that a GCS score signifies the patient’s “best” response. A patient 

could have a serious deficit that is not indicated by the GCS. Also, the 

score does not indicate the amount of stimulation required to get the 

patient to score at that level. A severe brain-injured patient usually 

has a GCS score of 3–8 and presents with a significant neurological 

deficit. The lowest GCS score is 3 (no neurological functioning). A 

patient with a severe brain injury also will experience loss of consciousness for more than 1 hour. Posttraumatic amnesia (PTA) refers 

to the loss of memory of events immediately following the injury. A 

typical question to ask to assess for PTA is, “What is the first thing 

you remember after your injury?” If the first memory occurred more 

than 24 hours after the injury, then, by definition, the patient has 

suffered a moderate-to-severe traumatic brain injury. 
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to have seemingly catastrophic changes in personal, 

social, and occupational functioning. Persistent postconcussional syndromes are discussed more fully later 

in this chapter.

Forces That Cause Traumatic Brain Injury

Traumatic brain injury may arise from many causes, 

including accidents, assaults, falls, and exposure to 

explosions. The physical forces exerted on the brain 

during most of the events that can cause TBI are 

reasonably well understood (Figure 15-1). The brain 

can be physically displaced within the skull by linear 

forces. It can also be rotated or twisted by angular or 

rotational forces. These forces make the lower-density 

tissues, particularly the outer layer of the brain (the 

cerebral hemispheres), move more quickly than the 

higher-density tissues that make up the core of the 

brain. They can also twist the brain around its central 

axis. Both types of movement result in stretching and 

shearing forces within the brain. Explosion-related 

brain injury is a new area of investigation. Although 

it is not yet proven that the changes in pressure that 

characterize the blast wave directly injure the brain as 

they do other parts of the body (eg, air-filled organs 

such as the lungs, tympanic membrane, and abdominal viscera), preliminary evidence suggests that this 

can occur.18 It is clear that both the blast wave and 

the blast wind propel objects, including people, with 

sufficient power to cause TBI due to both linear and 

angular forces. 

Vulnerable Areas and Injury Evolution 

The most common primary injuries in TBI are traumatic axonal injury (TAI), contusion (bruising), and 

subdural hemorrhage. Movement of the brain within 

the skull can tear the surface veins that bridge from the 

brain to the dural venous sinus, resulting in a traumatic 

subdural hemorrhage (Figure 15-2).19 The most common locations are the frontal and parietal convexities 

on the same side as the injury.20 Subdural hemorrhage 

is crescent shaped on neuroimaging and conforms to 

the cerebral surface.19,20 Its spread is limited by the dural 

reflections, and it rarely crosses the midline. When the 

brain moves within the skull enough to impact bone, 

Figure 15-1. The physical forces exerted on the brain during 

most of the events that can cause traumatic brain injury are 

reasonably well understood. Both linear (green) and rotational (blue) forces can arise. The brain can be physically 

displaced within the skull. It can also be rotated or twisted. 

Rotational forces make the lower-density tissues (eg, cerebral 

cortex) move more quickly than the higher-density tissues 

(eg, subcortical white matter), resulting in stretching and 

shearing forces.

Figure 15-2. Traumatic subdural hemorrhage occurs when the brain moves within the skull enough to tear the vessels that 

bridge from the brain surface to the dural venous sinus (a). The most common locations are the frontal and parietal convexities on the same side as the injury (b).
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Traumatic Brain Injury in the Military Population

it can cause contusion of the brain parenchyma (Figure 

15-3). The most common locations are the superficial 

gray matter of the inferior, lateral, and anterior aspects 

of the frontal and temporal lobes; the occipital poles or 

cerebellum are less often involved.20

The most likely injury to occur in mTBI is TAI, also 

called diffuse axonal injury. Certain areas of the brain 

are particularly vulnerable to TAI (Figure 15-4). One 

is the corticomedullary (gray matter–white matter) 

junction, particularly in the frontal and temporal lobes. 

Areas of very concentrated white matter, such as the 

corpus callosum and internal capsule, are also quite 

vulnerable. Finally, the deep gray matter and upper 

brainstem are also frequent sites of TAI.20 TAI is the 

result of shearing, stretching, or angular forces pulling 

on axons and small vessels.21

The old view of TAI was that these forces produced 

mechanical tearing of axons. Although this can occur, it is now considered to be unusual. The present 

understanding is that TAI is a progressive injury.22,23

Stretching of the axon and its enclosing myelin sheath 

results in increased permeability, allowing an influx 

of calcium. This, in turn, triggers events that loosen 

the normally tight myelin sheath in the vicinity of the 

injury and also cause damage to the axon’s cytoskeleton (a complex network of microtubules and neurofilaments that form the internal supporting structure 

for neurons). 

The integrity of the cytoskeleton is essential for 

many vital functions, including transport of substances from the cell body out to the axon and dendrites 

Figure 15-3. Contusions occur when the brain moves within the skull enough to impact bone, causing bruising. The most 

common locations are the superficial gray matter of the inferior, lateral, and anterior aspects of the frontal and temporal 

lobes, with the occipital poles or cerebellum less often involved.

Figure 15-4. Traumatic axonal injury (TAI) results when 

shearing, stretching, or angular forces pull on axons and 

small vessels. Impaired axonal transport leads to focal 

axonal swelling and (after several hours) may result in 

axonal disconnection. The most common locations are the 

corticomedullary junctions (particularly frontotemporal), 

internal capsule, deep gray matter, upper brainstem, and 

corpus callosum.
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(axoplasmic transport). Breakdown of the cytoskeleton 

disrupts transport of materials within the axon. Material collects proximal to the injury, leading to focal 

axonal swelling. If the swelling continues to progress, 

the axon eventually detaches. The proximal end seals 

and continues to swell, leading to the formation of 

the classic axonal retraction ball. The distal portion 

of the axon undergoes Wallerian degeneration, a process that can take several months in humans.24 (This 

account is based primarily on the study of heavily 

myelinated, large-diameter axons, such as those that 

make up the majority of the corpus callosum and 

internal capsule.) 

Growing evidence suggests that the injury cascade may be quite different in other populations of 

axons (eg, small-diameter, unmyelinated axons) and 

vulnerable areas (eg, injuries close to cell bodies, as 

occurs at the corticomedullary junction and in deep 

gray matter).24 This has important implications both 

for neuropathological identification of TAI and for 

potential therapeutic targets.24 Secondary processes 

can cause further brain injury.24–27 For example, there 

may be a widespread release of glutamate (an excitatory neurotransmitter), with the potential for lethal 

overstimulation of neurons (excitotoxicity). Release of 

blood into brain tissue has toxic effects, including the 

possibility of triggering cerebral vasospasm, which 

increases the risk for ischemia. 

DETERMINING SEVERITY OF TRAUMATIC BRAIN INJURY

Structural Neuroimaging 

TAI is characterized by multiple small injuries, often 

widely dispersed in the brain rather than clustered. As 

a result, its identification on structural neuroimaging 

can be quite challenging. Although magnetic resonance 

imaging (MRI) is more sensitive than computed tomography in detecting this type of brain injury, even 

MRI is often negative.20,22,28–31 Gradient-echo MRI is 

especially useful because it can visualize even very 

small areas of hemorrhage, as often occur in conjunction with axonal injury.32–36 This type of MRI is sensitive to alterations in magnetic susceptibility. Presence 

of blood within tissue creates a local magnetic field 

disturbance, causing a decrease in signal intensity in 

the area containing blood. Areas of TAI not containing 

hemorrhage are better seen on T2*-weighted spin-echo 

MRI, where they will appear bright. Particularly useful is the FLAIR (fluid attenuated inversion recovery) 

sequence, in which the normally high signal intensity 

of cerebrospinal fluid is suppressed, making lesions 

near the ventricles much easier to identify.37 A newer 

method of MRI that shows great promise for improved 

imaging of TAI is diffusion tensor imaging, in which 

the image is made sensitive to the speed and direction 

of water diffusion.38,39 In gray matter and fluid, water 

diffuses at the same speed in all directions (isotropic 

diffusion). In white matter, water diffuses much more 

quickly along the length of axons (fibers, tracts) than 

across them (anisotropic diffusion). Thus, diffusion 

tensor imaging provides a way to examine the structural integrity of the white matter. 

Combat-Related Traumatic Brain Injury

There is increasing evidence that combat-related 

TBIs are a frequent occurrence. Approximately one 

half of combat-related injuries, many a result of explosions, involve the head or neck.40,41 Several studies 

from the DVBIC document the presence of TBI in soldiers returned from Afghanistan or Iraq.42–45 Common 

postconcussive symptoms included headache (47%), 

irritability or aggression (45%), difficulty with memory 

(46%), and difficulty with concentration (41%).43 Studies of active duty soldiers suggest that the majority of 

brain injuries would be classified as mild, as indicated 

by either no or only brief LOC.44,46 In most cases these 

less severe injuries would not have required medical 

evacuation.45

It is well known that mTBI in civilians is underrecognized by both medical personnel and patients, 

resulting in significant underreporting.47,48 A similar 

situation exists in the military in that combat-related 

mTBI may often be unrecognized by both medical 

personnel and service members.44,46,49 DVBIC has recently released a new assessment tool—the Military 

Acute Concussion Evaluation (MACE)—to facilitate 

identification and evaluation of postconcussive symptoms following combat-related brain injuries. The 

literature on concussion strongly supports the need 

to fully evaluate anyone experiencing alteration in 

mental status (eg, dazed, confused, “saw stars,” LOC) 

as a result of exposure to conditions that can injure 

the brain.26 Of particular importance is evaluation of 

memory, as presence of PTA appears to be associated 

with higher rates of cognitive difficulties during the 

first few weeks after injury.49

Postconcussive symptoms may include altered 

consciousness (drowsiness, confusion, lethargy), headache, amnesia, nausea or vomiting, fatigue, irritability, 

restlessness, auditory or vestibular disturbances (balance problems, ringing in the ears, dizziness, hearing 

changes, sensitivity to noise), visual disturbances 

(blurred vision, sensitivity to light, double vision), gait 
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Traumatic Brain Injury in the Military Population

abnormalities, and problems sleeping.50,51 Although 

most patients recover well from mTBI, the rate of recovery is highly variable. During this period of healing 

individuals are likely to perform below their normal 

level on both physical and cognitive tasks. Evidence 

also suggests that the brain is more vulnerable to reinjury during this period. Therefore, in the context of 

active combat, premature return to duty increases risks 

for both the individual and the team.26

Many mild brain injuries will not become evident 

until after the service member returns home. Although 

the majority of people recover well following mTBI, a 

significant minority do not.25 Common problems in the 

chronic phase following TBI include headaches, dizziness, fatigue, sleep disturbances, spasticity, vestibular 

impairments, visual difficulties, personality changes, 

and cognitive or emotional deficits. Some studies 

indicate that as many as one third of these patients 

may have psychiatric symptoms within the first year 

postinjury.52–54

COMMON COGNITIVE SEQUELAE

An examination of cognitive dysfunction following 

TBI must take into account myriad factors, including 

severity and nature of the injury (focal vs diffuse), 

time since injury, motivation of the subject, and other 

injuries. In the case of mTBI, there is agreement that 

there are short-term cognitive consequences of the 

injury, affecting various aspects of attention, speed of 

processing, and other cognitive domains. Even in the 

absence of self-reported cognitive dysfunction or other 

symptoms, decrements in reaction time have been 

reported.14 The longer-term cognitive consequences 

from mTBI are less clear.

Iverson and colleagues55 report data on a group of 

young adult patients seen in the trauma service of a 

Pennsylvania general hospital (1991–1994) with mTBIs 

(based on postinjury GCS scores) who completed neuropsychological testing within the first week postinjury. Those who met severity inclusion criteria and 

were under age 40 accounted for 484 of the 1,695 total 

patients. Most were men, with motor vehicle accidents 

being the most common cause of injury. Most patients 

(82%) had GCS scores of 15, with the remaining ones 

having GCS scores of 14. About 56% had known LOC, 

with about 18% negative, and the rest unclear or unknown. The prevalence of intracranial abnormalities 

on day-of-injury computed tomography was 11.8%. 

The rest of these patients had negative (68.6%) or missing (19.6%) results. The patients were split into two 

groups on the basis of differences on the Galveston 

Orientation and Amnesia Test (GOAT). The groups 

were relatively evenly split by scores above 90 and 

those below (range 0–100). Scores between 90 and 75 

are not low enough to indicate frank PTA, but do suggest some ongoing confusion. All those patients were 

administered a brief (30–45 minutes) but wide-ranging 

neuropsychological test battery. Overall, the results 

suggested that when trauma patients are evaluated 

shortly after an mTBI, the presence of posttraumatic 

confusion is related to worse short-term neuropsychological outcome in that subjects with lower GOAT 

scores had significantly worse scores on measures of 

simple attention, verbal learning, verbal and visual 

memory, and some aspects of executive functioning 

than did subjects in the above-90 range on GOAT. Furthermore, brief traumatic LOC (less than 5 minutes) is 

not related to short-term neuropsychological outcome 

(there were no significant differences in scores based 

solely on whether or not there was brief LOC).

Belanger and colleagues56 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—(1) global cognitive ability, (2) attention, (3) 

executive functions, (4) fluency, (5) memory acquisition, (6) delayed memory, (7) language, (8) visuospatial 

skill, and (9) motor functions. The overall effect of 

mTBI on neuropsychological functioning was moderate (d = .54). However, findings were influenced by 

cognitive domain, time since injury, patient characteristics, and sampling methods. Acute effects (less than 3 

months postinjury) of mTBI were greatest for delayed 

memory and fluency. In unselected or prospective 

samples, the overall analysis revealed no residual neuropsychological impairment by 3 months postinjury. In 

contrast, clinic-based samples and samples including 

participants in litigation were associated with greater 

cognitive sequelae of mTBI.

In another metaanalysis focused on the sports concussion literature, the authors reviewed studies from 

1970 to 2004 from which 21 studies met inclusion criteria, with 790 cases of mTBI and 2,016 control cases.57

The overall effect for size of concussion on cognition 

was 0.49, 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 postinjury.

Postconcussive Disorder

A WHO analysis of outcome in mTBI concludes 

that although acute symptoms are common, the vast 

majority of individuals have good resolution of their 
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Combat and Operational Behavioral Health

mTBI symptoms by 3 months postinjury and many 

quite sooner.58 The authors acknowledge (and this is 

consistent with clinical practice in both military and 

civilian settings) that there are individuals who show 

persistent symptoms. The fourth edition of the Diagnostic and Statistical Manual for Mental Disorders proposed 

diagnostic criteria for a postconcussional disorder in 

its appendix of provisional diagnostic criteria sets.10

Diagnosis of a postconcussional disorder required 

a “significant cerebral concussion” with measured 

cognitive deficit and the presence of at least three of 

eight symptoms—(1) fatigue, (2) sleep disturbance, 

(3) headache, (4) dizziness, (5) irritability, (6) anxiety/

depression, (7) personality change, and (8) apathy—

with onset after injury and persistence past 3 months. 

(See Exhibit 15-1 for full criteria for postconcussional 

disorder.) Criteria have also been included in the International Classification of Diseases, 10th Revision (ICD10).59 These criteria require a history of TBI and the 

presence of three of eight symptoms—(1) headache, (2) 

dizziness, (3) fatigue, (4) irritability, (5) insomnia, (6) 

concentration problems, (7) memory difficulty, and (8) 

reduced tolerance of stress, emotion, or alcohol. 

Boake et al60 compared these two diagnostic sets and 

concluded that there was a large difference between the 

prevalence of postconcussive syndrome using these 

two criteria sets, with the ICD-10 criteria being more 

inclusive. The differences suggest that there could 

be disagreement in diagnosis depending on which 

criteria set is used. Furthermore, they concluded that 

both criteria sets had limited specificity to TBI (if the 

history of TBI itself was removed as a criteria), as 

the other criteria could be met after general trauma, 

whether or not the brain was injured. The authors 

point out that this finding is supportive of previous 

CDC recommendations—namely that postconcussional symptoms in themselves are not sufficient to 

make a diagnosis of mTBI. Iverson and colleagues,61

in a review article on outcome from mTBI, also report 

that postconcussion symptoms are common in healthy 

subjects, those without a history of TBI, and in various 

patient groups.

The existence of a group of patients with persistent 

symptoms has been controversial. The scope of the 

problem itself is difficult to determine (clinical lore has 

set the figure at 10%–20% although it is likely less than 

5% of the total number of individuals who suffer mTBI; 

see Iverson55 for a complete discussion). There is also 

disagreement concerning the cause of these persistent 

symptoms. Various authors have attributed them to different causes, some believing them to reflect the injury 

itself, and others attributing these symptoms to a multicausal etiology, with premorbid personality characteristics, social-psychological factors, and exaggeration 

EXHIBIT 15-1

RESEARCH CRITERIA FOR POSTCONCUSSIONAL DISORDER

A. History of closed head injury:

	 •	 Causing cerebral concussion

	 •	 Symptoms include:

 ° loss of consciousness

 ° posttraumatic amnesia

 ° posttraumatic onset of seizuers (less common)

B. Difficulty (based on cognitive evaluation) in: 

	 •	 attention, such as:

 ° concentration

 ° shifting focus of attention

 ° performing simultaneous cognitive tasks

 or

	 •	 memory, such as:

 ° learning

 ° recalling information

C. Three or more of the following occuring posttrauma (and lasting 3 or more months):

	 •	 easy fatigue

	 •	 disordered sleep

	 •	 headache

	 •	 vertigo/dizziness

	 •	 irritability/aggression on little or no provocation

	 •	 anxiety/depression/affective lability

	 •	 changes in personality

	 •	 apathy/lack of spontaneity

D. “B” and “C” symptoms:

	 •	 have onset following head trauma

 or

	 •	 represent a substantial worsening of preexisting symptoms

E. Disturbance causes significant impairment/significant worsening in:

	 •	 social/occupational functioning (adults)

	 •	 school/academic performance (school-age

children)

F. Symptoms do not meet criteria for/not better accounted for by:

•	 dementia due to head trauma

	 •	 another mental disorder such as:

 ° amnestic disorder due to head trauma

 ° personality change due to head trauma

Adapted with permission from American Psychiatric Association. Diagnostic and Statistical Manual. 4th ed. Washington, DC: 

APA; 2000: 761–762.
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Traumatic Brain Injury in the Military Population

(either conscious or unconscious) playing a role.

The Relationship Between Posttraumatic Stress 

Disorder and Traumatic Brain Injury

Posttraumatic stress disorder (PTSD) can result from 

highly stressful experiences, such as being in combat 

or being injured in combat. Hoge and colleagues62 reported that for all groups surveyed after their deployment, there was a strong relationship between intensity 

of combat experiences (killing the enemy, being shot 

at) and exposure to traumatic combat-related events 

(handling dead bodies, knowing someone who was 

killed), and the prevalence of PTSD. Among service 

members in OIF, the prevalence of PTSD increased 

with the number of firefights during deployment (with 

increases to 19.3% for those involved in more than five 

firefights). The rates of PTSD were significantly associated with having been wounded or injured (odds 

ratio for those deployed to Iraq, 3.27; odds ratio for 

those deployed to Afghanistan, 2.49). This is consistent 

with the findings of Koren et al63 in a small but welldesigned study looking at rates of PTSD in injured 

Israeli war veterans. That study clearly 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. The authors suggest that even this 

rather high figure might be an underestimate of the 

rate because 35% of these injured combat veterans had 

refused to participate in the study. 

Controversy exists, however, regarding the rate 

and risk factors for PTSD following TBI. Bombardier 

and colleagues64 report a cumulative rate of 11.3% in 

a mixed sample of those with TBI ranging from mild 

to severe over a 6-month period. Furthermore, their 

findings were consistent with those of previous studies suggesting that more severe TBI may be protective with regard to the development of PTSD, that is, 

the AOC or LOC associated with TBI may lessen the 

individual’s ability to reexperience the trauma.65 Risk 

factors for developing PTSD following TBI include 

having less education, feeling terrified or helpless, and 

having major depression.64

In-Theater Management

The in-theater management of TBI depends on its 

severity. (There are guidelines recently released on 

the management of more severe combat TBI,66 but 

in-depth discussion of these guidelines is beyond the 

scope of this chapter.) The clinical management of the 

mTBI patient in a military occupational setting was 

addressed in the 2006 DVBIC workgroup. A graphical 

representation of the level-I practice guideline is shown 

in Figure 15-5. This guideline relies on the use of the 

MACE (see Exhibit 15-2 for full instrument), a tool developed by the DVBIC. The MACE has both a history 

and evaluation component. The history component 

can confirm the diagnosis of mTBI after establishing 

that a trauma has occurred and during the course of 

this traumatic event, the service member experienced 

an AOC. An AOC can be defined on a continuum from 

“dazed and confused,” to not remembering the injury, 

to an LOC. The evaluation component, designed to be 

easily used by medics and corpsmen, can be administered within 5 minutes. It utilizes the Standardized 

Assessment of Concussion67 to preliminarily document 

neurocognitive deficits in four cognitive domains: (1) 

orientation, (2) immediate memory, (3) concentration, 

and (4) delayed recall.

The Relationship Between Substance Abuse and 

Traumatic Brain Injury

The relationship between TBI and substance use 

and abuse is an important one that presents a number 

of complexities for understanding their interrelatedness. Intoxication is in itself a risk factor for TBI. That 

is, TBI can result from unintentional alcohol-related 

causes such as motor vehicle accidents or falls while 

intoxicated. More intentional alcohol-related TBI 

can result from other causes such as assault while 

intoxicated (both on the part of the victim and perpetrator), mate-related abuse, and direct self-harm such 

as suicide attempts.1

 Savola, Niemelä, and Hillbom68

investigated the relationship of different patterns 

of alcohol intake to various types of trauma. They 

examined the alcohol consumption in a series of 385 

consecutive trauma admissions. On admission, 51% of 

the patients had alcohol in their blood. Binge drinking was the predominant (78%) drinking pattern of 

alcohol intake, and assaults, falls, and biking accidents 

were the most frequent causes of trauma. Dependent 

alcohol drinking and binge drinking were found to be 

significantly more common among patients with head 

trauma than in those with other types of trauma. The 

relative risk for head injury markedly increased with 

increasing blood alcohol levels. 

A TBI can also exacerbate previous substance 

abuse or lead to behavioral and personality changes 

that could lead to alcohol or drug misuse. Prior history of a substance abuse disorder is a risk factor for 

greater morbidity69 and excessive use following TBI.70

Substance-use disorders following TBI adversely affect 

neuropsychological functioning, subjective well-being, 

employment, and involvement with the criminal justice system.71–74
234

Combat and Operational Behavioral Health

Traumatic Event Occurs: Possible Concussion

(blast exposure, fall, motor vehicle collision, etc)

Assess for loss of consciousness (LOC)/alteration 

of consciousness (AOC): dazed, “bell rung,” “seeing stars,” memory loss, etc

• If positive AOC/LOC after trauma, diagnose con-

 cussion and 

 (1) Administer MACE

 (2) Assess for red flagsa

 and symptomsb

Red flagsa present?

Symptomsb present or MACE < 25?

Perform exertional testing,e

 followed by alternate version of MACE cognitive examination

Refer to level 3

Primary care management

Reevaluate q1 3 days up to 7 days

Symptoms resolved?

Positive symptoms or MACE < 25

Provide education

Return to duty

Continue PCM

Screen for depression & acute stress reaction

Consider combat stress referral

Consider referral 

to level 3

Continue concussion 

& combat stress manage- ment up to 14 days (consider longer if rapidly improving)

a

Red Flags

1. Progressively declining LOC

2. Progressively declining neurological exam

3. Pupillary asymmetry

4. Seizures

5. Repeated vomiting

6. Clinical verified GCS < 15

7. Neurological deficit: motor or sensory

8. LOC greater than 5 minutes

9. Double vision

10. Worsening headache

11. Cannot recognize people or disoriented to place

12. Slurred speech

13. Weakness

bSymptoms

1. Confusion (< 24 h)

2. Unusual behavior

3. Irritability

4. Unsteady on feet

5. Vertigo/dizziness

6. Headache

7. Photophobia

8. Phonophobia

c

Primary Care Management (PCM)

 1. Give educational sheet to all mTBI 

 patients

 2. Reduce environmental stimuli

 3. Ensure adequate rest

 4. Be aggressive in headache manage-

 ment: use acetaminophen q 6 h × 48 h. After 48 h, may use naproxen 

 pm

 5. Avoid tramadol, narcotics

 6. Consider nortriptyline or amiltriptyline, 

 25 mg po q h for persistent head-

 aches (> 7 days); prescribe 10 days 

 maximum

 7. Implement duty restrictions

 8. Send consult to 

 triconsult@us.army.mil for further 

 guidance if needed

 9. Consider for evacuation to higher 

 level care if clinically indicated

10. Document concussion diagnosis in 

 electronic medical recordd

dICD-9 Codes

850.0 Concussion w/o LOC

850.11 Concussion w/ LOC < 30 min

E979.2 Injury from terrorist ex-

 plosion/blast

e

Exertional Testing Protocol

1. Achieve 65%–85% THR 

 (THR = 220 – age), using 

 pushups, step-aerobic 

 treadmill, hand crank

2. Assess for symptoms 

 (headache, vertigo, pho-

 tophobia, balance, dizzi-

 ness, nausea, tinnitus, 

 visual changes, others) or 

 MACE < 25.

†

Return-to-Duty Evaluation

1. Neurocognitive testing if 

 available and expertise for 

 interpretation available

Yes

No

Yes

No

Yes

Yes

No

No

No Neg Pos
235

Traumatic Brain Injury in the Military Population

Figure 15-5 (left page). Initial management of concussion in a deployed seting. Defense and Veterans Brain Injury Center 

decision algorithm for battlefield mild traumatic brain injury at a Level I setting. Definitive assessment and care is given 

by providers to include a more detailed assessment, management recommendations, and consideration for evacuation to a 

higher level of care. 

AOC: alteration of consciousness

GCS: Glascow Coma Scale

HS: at bedtime

ICD-9: International Statistical Classification of Diseases, 

9th edition

LOC: loss of consciousness

MACE: Military Acute Concussion Evaluation

mTBI: mild traumatic brain injury

po: by mouth 

q: every

THR: target heart rate

w/: with

w/o: without

Reproduced from: US Army Institute of Surgical Research. Joint Theater Trauma System Web site. Available at: http://www.

usaisr.amedd.army.mil/cpgs/mTBIDplydSet0811.pdf. Accessed December 15, 2009.

SYMPTOM TREATMENT

Symptom treatment for mTBI can be discussed from 

four areas: (1) pharmacologic management, (2) educational interventions, (3) rest/return-to-duty decisions, 

and (4) targeted therapies. An extensive discussion of 

the pharmacologic interventions in TBI is beyond the 

scope of this chapter. The reader is referred to reviews 

of the evidence for various pharmacologic interventions.45,73–76 In general, however, symptomatic treatment strategies can be the most effective, including 

regulation of sleep through pharmacologic and nonpharmacologic strategies,77 headache management,78

pain management,79 and treatment of depression.80

Treatment of all of these has been associated with 

improved quality of life or outcomes. 

Educational Interventions

Educational and psychological therapies have also 

proven effective in mTBI. Mittenberg et al81 compared 

two mTBI groups: a treatment group (n = 29) and a 

control group (n = 29). The treatment group received a 

printed manual and met with a therapist prior to hospital discharge to review (a) the nature and incidence 

of expected symptoms, (b) the cognitive-behavioral 

model of symptom maintenance and treatment, (c) 

techniques for reducing symptoms, and (d) instructions for gradual resumption of premorbid activities. 

The control group received routine hospital treatment 

and discharge instructions. After 6 months, the treated 

patients reported significantly shorter average symptom duration (33 days vs 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 and colleagues82 have shown similar results 

in a group of individuals with mTBI. Those who were 

seen at 1 week postinjury 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 effective for 

individuals with brain injuries and their families are 

available at a number of sources including the Defense 

and Veterans Brain Injury center Web site (www.dvbic.

org/cms.php?p=Education).

Rest and Return-to-Duty Issues

Other palliative interventions such as bed rest have 

been shown to have some efficacy in treating postconcussive symptoms over the short term (eg, decreased 

dizziness), but have not proven to have long-term 

outcomes better than individuals who did not get 

such rest.83 Return-to-duty issues in the military operational setting are addressed in the algorithm above 

(see Figure 15-5). Most of the decisions are based on 

the resolution of self-reported TBI symptoms as well 

as the integration of clinical data based on testing a 

service member to see if symptoms may return when 

physically stressed. 

SUMMARY

In modern warfare, TBI is a common occurrence that 

has significant implications for the health and welfare 

of the troops, as well as overall fighting effectiveness. 

Early identification of less obvious (usually milder) 

TBI is important, as is a basic understanding of when 

individuals may be treated in situ and ways to maximize recovery. Even in peacetime, there are concerns 

about TBI because it occurs at high rates in the military. 

It is essential, therefore, that healthcare providers and 

the fighting force both have a basic understanding of 

the need for prevention of these injuries, and early 

identification when they do occur.
236

Combat and Operational Behavioral Health

Exhibit 15-2 

military acute concussion evaluation form

 (Exhibit 15-2 continues)
237

Traumatic Brain Injury in the Military Population

Reproduced from: Defense and Veterans Brain Injury Center, Walter Reed Army Medical Center. Military Acute Concussion Evaluaton 

(MACE) form.

Exhibit 15-2 continued
238

Combat and Operational Behavioral Health

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