Traumatic Brain Injury

L I F E L O N G L E A R N I N G I N N E U R O L O G Y®
TRAUMATIC BRAIN INJURY

Volume 16 Number 6 December 2010
Authors
JACK W. TSAO, MD, DPhil, FAAN, Guest Editor

Associate Professor of Neurology and Neuroscience, Uniformed Services University of
the Health Sciences, Bethesda, Maryland; Director, Traumatic Brain Injury Programs,
US Navy Bureau of Medicine and Surgery, Washington, DC
*Dr Tsao has received grants from the US Army Medical Research and Materiel
Command, the Dana Foundation, and the US Navy.
†Dr Tsao has nothing to disclose.
GARY M. ABRAMS, MD, FAAN

Professor of Clinical Neurology, University of California, San Francisco, San Francisco,
California; Rehabilitation Section Chief, San Francisco VA Medical Center,
San Francisco, California
*Dr Abrams has received research support from Innovative Neurotronics for investigation
of a functional electrical stimulation–based orthotic device for gait after stroke.
Dr Abrams has received or plans on receiving personal compensation for serving as
an expert witness and consultant for cases involving the long-term consequences and
rehabilitation issues in brain injury.
†Dr Abrams discusses the unlabeled use of tricyclic antidepressants for sleep. Unlabeled
usage is cited when necessary.
ANTHONY G. ALESSI, MD, MMM, FAAN

Associate Clinical Professor of Neurology, University of Connecticut, Farmington,
Connecticut
*†Dr Alessi has nothing to disclose.
VICTORIA C. ANDERSON-BARNES, BA
Center for Neuroscience and Regenerative Medicine, Uniformed Services University
of the Health Sciences, Bethesda, Maryland
*†Ms Anderson-Barnes has nothing to disclose.
*Relationship Disclosure
†Unlabeled Use of Products/Investigational Use Disclosure
Copyright @ 2010 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
JUSTIN S. CAMPBELL, PhD
Adjunct Assistant Professor, Embry-Riddle Aeronautical University, Andrews Air Force Base,
Maryland; Senior Analyst, Psychological Health Programs, US Navy Bureau of Surgery and
Medicine, Washington DC
*Dr Campbell has received grants from the Office of Naval Research.
†Dr Campbell has nothing to disclose.
KEVIN E. CRUTCHFIELD, MD
Director, Comprehensive Sports Concussion Program, Sinai Hospital, Baltimore, Maryland;
Assistant Professor of Neurology, Military and Emergency Medicine, Uniformed Services
University of the Health Sciences, Bethesda, Maryland
*Dr Crutchfield has received or anticipates receiving personal compensation for acting as
an expert witness in a medical liability case.
†Dr Crutchfield has nothing to disclose.
JAY C. ERICKSON, MD, PhD

Assistant Professor of Neurology, Uniformed Services University of the Health Sciences,
Bethesda, Maryland; Neurology Program Director, Madigan Army Medical Center,
Tacoma, Washington
*Dr Erickson has received an investigator-initiated research grant from Merck & Co., Inc.,
and a traumatic brain injury research program grant from the US Department of Defense.
†Dr Erickson discusses medications and other treatments that are not US Food and
Drug Administration approved for posttraumatic headache.
FREDERICK G. FLYNN, DO, FAAN

Medical Director, Traumatic Brain Injury Program, Chief, Neurobehavior, Madigan Army
Medical Center, Tacoma, Washington; Clinical Professor of Neurology, University of
Washington School of Medicine, Seattle, Washington
*†Dr Flynn has nothing to disclose.
CHRISTOPHER C. GIZA, MD
Associate Professor in Residence, Division of Pediatric Neurology, Department of
Neurosurgery, Brain Injury Research Center UCLA, Los Angeles, California; David Geffen
School of Medicine at University of California, Los Angeles, California; Mattel Children’s
Hospital, University of California, Los Angeles, California
*Dr Giza has received or plans to receive personal compensation for speaking
engagements at academic centers and hospitals and for medicolegal consulting.
Dr Giza is a Thrasher Research Foundation grant recipient.
†Dr Giza discusses the use of advanced neuroimaging and computerized
neuropsychological testing, but does not mention them by brand name.
GRAHAM A. GLASS, MD
Assistant Clinical Professor, University of California, San Francisco, San Francisco,
California; Deputy Director, Parkinson’s Disease Research, Education, and Clinical Care
Center, San Francisco VA Medical Center, San Francisco, California
*Dr Glass has received personal compensation from Schlesinger Associates for blinded
market research and from other entities for reviewing legal medical research for
reviewing legal medical records.
†Dr Glass has nothing to disclose.
JEFFREY S. KUTCHER, MD, MPH

Assistant Professor, Director, Michigan NeuroSport, University of Michigan, Ann Arbor,
Michigan
*†Dr Kutcher has nothing to disclose.
DALILA W. LEWIS, MD
Child/Adolescent Neurology Fellow, National Capital Consortium, Walter Reed Army
Medical Center, Washington DC; Associate Professor of Pediatrics, Uniformed Services
*†Dr Lewis has nothing to disclose.
GEOFFREY S. F. LING, MD, PhD, FAAN

Professor and Interim Chair, Department of Neurology, Uniformed Services University of
the Health Sciences, Bethesda, Maryland
*Dr Ling has received personal compensation for speaking engagements from
Bristol-Myers Squibb and Sanofi-Aventis. Dr Ling holds stock and/or stock options in
Wyeth Pharmaceuticals.
†Dr Ling has nothing to disclose.
SCOTT A. MARSHALL, MD
Major, Medical Corps, US Army; Assistant Professor of Neurology, Uniformed Services
*Dr Marshall has received personal compensation as an expert witness.
†Dr Marshall discusses the unlabeled use of hypertonic saline in the treatment of
traumatic brain injury.
DAVID F. MOORE, MD, PhD
Visiting Professor, Massachusetts Institute of Technology, Boston, Massachusetts
*†Dr Moore has nothing to disclose.
EDWARD T. NEELY, MD
Assistant Professor of Neurology, Uniformed Services University of the Health
Sciences, Bethesda, Maryland; Medical Director, Traumatic Brain Injury Clinic, Walter
Reed Army Medical Center, Washington, DC
*Dr Neely has nothing to disclose.
†Dr Neely discusses medications and other treatments that are not US Food and Drug
Administration approved for posttraumatic headache.
KAREN LYNN PARKO, MD, FAAN

Associate Professor of Clinical Neurology, University of California, San Francisco,
San Francisco, California; Director, Comprehensive Epilepsy Center, San Francisco
VA Medical Center, San Francisco, California; Chair, National VA Epilepsy Centers
of Excellence
*†Dr Parko has nothing to disclose.
RONALD G. RIECHERS II, MD

Medical Director, Polytrauma Team, Cleveland VA Medical Center, Cleveland, Ohio;
Assistant Professor, Department of Neurology, Case Western Reserve University,
Cleveland, Ohio
*Dr Riechers has nothing to disclose.
†Dr Riechers discusses the trial using prazosin for sleep improvement in military
patients with traumatic brain injury but does not give a specific recommendation for
its use.
JAY H. ROSENBERG, MD, FAAN

Neurologist, The Neurology Center of Southern California, Encinitas, California
*Dr Rosenberg has received personal compensation from Biogen Idec; EMD Serono,
Inc.; and Teva Neuroscience as a member of their speakers’ bureau, and from Acorda
Therapeutics and Allergan, Inc., as an advisory board member. Dr Rosenberg has
received or anticipates receiving personal compensation for a professional report for
plaintiff reference and serving as a defendant’s expert witness for a multiple sclerosis
case for a school district.
†Dr Rosenberg has nothing to disclose.
ROBERT L. RUFF, MD, PhD, FAAN
Chief of Neurology, Cleveland VA Medical Center, Cleveland, Ohio; Professor of
Neurology and Neuroscience, Case Western Reserve University, Cleveland, Ohio
*†Dr Ruff has nothing to disclose.
MICHAEL B. RUSSO, MD, FAAN

Medical Director and Chief of Neurology, Pacific Sleep Technologies, Inc., Honolulu,
Hawaii; Adjunct Associate Professor of Neurology, Uniformed Services University of the
Health Sciences, Bethesda, Maryland; Associate Professor of Medicine, John A. Burns
School of Medicine, University of Hawaii, Honolulu, Hawaii
* †Dr Russo has nothing to disclose.
STEPHEN J. SHARP, MD
Assistant Professor, Neurology and Pediatrics, Uniformed Services University of the
Health Sciences, Bethesda, Maryland
*†Dr Sharp has nothing to disclose.
BRETT J. THEELER, MD
AMEDD Student Detachment, 187th Medical Battalion, United States Army Medical
Corps, Fort Sam Houston, Texas
*Dr Theeler has nothing to disclose.
†Dr Theeler discusses medications and other treatments that are not US Food and
Drug Administration approved for posttraumatic headache.
SHARON R. WEEKS, AB
Research Associate, Military Amputee Research Program, Walter Reed Army Medical
Center, Washington, DC
*†Ms Weeks has nothing to disclose.
MULTIPLE-CHOICE QUESTION WRITERS
RONNIE BERGEN, MD
Assistant Professor of Clinical Neurology, University of Arizona College of Medicine,
Tucson, Arizona
*†Dr Bergen has nothing to disclose.
JULIE E. HAMMACK, MD, FAAN

Assistant Professor, Mayo College of Medicine, Rochester, Minnesota
*†Dr Hammack has nothing to disclose.
EDITOR FOUNDING PROGRAM DIRECTOR

Aaron E. Miller, MD, FAAN Theodore L. Munsat, MD
New York, New York
Relationship Disclosure: Dr Miller has received personal EDITORIAL BOARD*
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Company, Ltd.; EMD Serono, Inc.; GlaxoSmithKline; Merck & Cynthia L. Comella, MD, FAAN, Chicago, Illinois
Co., Inc.; Novartis; Ono Pharmaceutical Co, Ltd.; Pfizer Inc;
Sanofi-Aventis; and Teva Neuroscience as a consultant and
Matthew E. Fink, MD, New York, New York
speaker. Dr Miller has received personal compensation from Carlayne E. Jackson, MD, FAAN, San Antonio, Texas
the AAN for serving as the editor of Continuum: Lifelong
Learning in Neurology and from Lippincott Williams &
Steven L. Lewis, MD, FAAN, Chicago, Illinois
Wilkins for serving as an editorial advisory board member for Laszlo Mechtler, MD, Amherst, New York
Real Living with Multiple Sclerosis. Dr Miller has received
research support from Acorda Therapeutics, Inc.; Biogen
Jonathan W. Mink, MD, PhD, FAAN, Rochester,
Idec; Genzyme Corporation; Immune Tolerance Network; New York
Sanofi-Aventis; and Teva Neuroscience.
Jennifer R. Molano, MD, Cincinnati, Ohio
ASSOCIATE EDITOR Joel R. Saper, MD, FAAN, Ann Arbor, Michigan
Steven L. Lewis, MD, FAAN Mark J. Tullman, MD, New York, New York
Chicago, Illinois Charles Zollinger, MD, Canton, Ohio
Relationship Disclosure: Dr Lewis has received personal
compensation in an editorial capacity for Neurology. EDITORIAL STAFF*
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ASSOCIATE EDITOR OF ETHICS
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Baltimore, Maryland Cecelia Adams, Production Editor
Relationship Disclosure: Dr Williams’ life partner holds stock Amanda Doering Tourville, Editorial Administrator
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EDITOR’S PREFACE
Readers can scarcely open In the first article, ‘‘Mild
a newspaper today with- Traumatic Brain Injury Up-
out being confronted date’’, Victoria Anderson-
by the subject of this Barnes and Sharon Weeks
issue of . join Dr Tsao to intro-
Traumatic brain injury— duce the subject, pro-
especially mild traumatic viding appropriate def-
brain injury (mTBI)—is initions, describing the
the subject of article after scope of the problem,
article on the sports pages and addressing patho-
of our daily newspapers physiology and symp-
as athletic authorities de- tomatology. The sub-
bate its consequences and jects of diagnosis and
seek ways to prevent it, The brain is not a management are ex-
especially in such vio- panded in the subse-
lent contact sports as foot-
paired organ. Society quent article by Drs
ball. At the same time, in general but we, Geoffrey Ling, Scott
society grapples with the as neurologists, in Marshall, and David
tragedies of modern war- particular, must Moore. The unique as-
fare and the effects of pects of concussion in
terrorism in which the
help to protect it athletes present a num-
widespread use of impro- better and facilitate ber of challenges, which
vised explosive devices has its recovery when Drs Jeffrey Kutcher,
created a new epidemic injured. Christopher Giza, and 15
of blast-induced head Anthony Alessi address,
injuries. including a discussion of specific pedi-
Neurologists have always been in- atric considerations. Neurologists con-
volved in the care of patients with fronted by questions about return to
head injuries, particularly those that activity, especially athletic competition,
are less severe and require no neuro- will benefit greatly from these authors’
surgical intervention. Today, more than insights.
ever and with the increased public at- Frequently, neurologists will first
tention, we must be up-to-date on this encounter patients with TBI well after
subject. In this issue of , the original injury because of the
Dr Jack Tsao and colleagues will provide occurrence of new or persistent spe-
the latest information on this timely cific neurologic symptoms. The next
topic. few articles in this issue address some
Copyright # 2010, American Academy of Neurology. All rights reserved.
" EDITOR’S PREFACE
of these areas. Drs Jay Erickson, Edward Robert Ruff will inform you about
Neely, and Brett Theeler discuss post- these aspects of management.
traumatic headaches, emphasizing the Decisions about returning to com-
similarities to many headache syn- petitive sports may be difficult, and the
dromes quite familiar to neurologists, neurologist may be confronted by the
but also pointing out areas of difference desires of the athlete or the coach to
and controversy. Memory impairment clear the individual to return. This can
after mTBI is, undoubtedly, a source create ethical dilemmas; Drs Michael
of much concern as it represents one of Russo and Kevin Crutchfield describe
the most debilitating consequences of such a situation in this issue’s Ethical
such events and may be progressive, Perspectives in Neurology section. Head
especially in those with repeated head injuries can be devastating, not only to
injury. Dr Frederick Flynn provides a the victim, but also to the families and
detailed analysis of this issue, examining loved ones. Dr Jay Rosenberg discusses
various aspects of memory disturbance strategies for communicating with these
as well as offering guidance about its concerned parties in the Practice Issues
assessment and management. in Neurology section. As usual, we also
In the next article, Drs Karen Parko, provide a coding table, developed by
Gary Abrams, Justin Campbell, and Drs Laura Powers and Marc Nuwer, to
Graham Glass address three other fre- help in your practice with TBI patients.
quent consequences of TBI: epilepsy, After you have read the articles so
sleep disturbances, and psychiatric man- thoroughly organized and prepared by
ifestations. Although these issues may Guest Editor Tsao and the other con-
occur independently, they often coexist tributors, be sure to challenge yourself
in the head-injured patient. Although with the Patient Management Problem
seizures may be more common among and the Multiple-Choice Questions. The
patients with severe head injury, they former, prepared by Drs Dalila Lewis
certainly develop, at times, in patients and Stephen Sharp, will allow you to
with mTBI. Sleep disturbances are prev- integrate your knowledge of the man-
alent among patients with mTBI, partic- agement of a patient with mTBI. The
ularly soon after the injury. Posttraumatic latter, developed for this issue by Drs
stress disorder is a frequent psychiatric Ronnie Bergen and Julie Hammack, will
comorbidity in patients with TBI. While augment your education while simulta-
this may be more likely to occur in a neously permitting self-assessment of
military setting, it is not confined to this your understanding of this subject.
16 population. Your comfort level in dealing The brain is not a paired organ.
with these common problems will rise Society, in general, but we, as neurol-
after reading this chapter. ogists, in particular, must help to
While most patients with mTBI protect it better and facilitate its
fortunately recover rapidly, healing recovery when injured. Next Sunday,
may be a protracted process. For as you sit, popcorn in hand, watch-
those with a slower recovery, rehabili- ing your favorite National Football
tation is an important aspect of care. League team, I hope you will keep
Some rehabilitation may be rendered in your other hand to
or coordinated by neurologists. Even focus your attention on the important
in those patients with minor head subject of head injury.
injury expected to get better quickly,
education is an important dimension —Aaron E. Miller, MD
of care. Drs Ronald Riechers II and Editor-in-Chief
Continuum Lifelong Learning Neurol 2010;16(6)
MILD TRAUMATIC
BRAIN INJURY UPDATE
Victoria C. Anderson-Barnes, Sharon R. Weeks, Jack W. Tsao
ABSTRACT
Traumatic brain injury (TBI) is a prevalent condition throughout the civilian and military
populations. Although TBI can be classified as mild, moderate, or severe, most TBIs
are considered mild. Understanding the pathophysiologic mechanism(s) of mild TBI
through basic science and clinical cohort studies is an area of active research. While it
is well understood that most people recover from a mild TBI with minimal treatment,
some patients experience long-term consequences that require rehabilitation and
specialized care. Common characteristics of brain injury include loss of conscious-
ness (LOC), posttraumatic amnesia (PTA), and postconcussion syndrome (PCS). The
development of LOC, PTA, and PCS greatly depends on the nature of the injury, and
the degrees to which they develop are not necessarily consistent with symptom
presentation. In recent years, sports concussions have become an area of increased
research and public interest in the civilian population; similarly, blast TBI has gained
attention in the military. Depending on the nature of the injury, different outcomes
may result in the two populations. Consequently, treatments for mild TBI are rather
diverse, and early intervention is the key to maximizing outcomes following a TBI.
These topics and more will be discussed throughout this article.
Continuum Lifelong Learning Neurol 2010;16(6):17–26.
EPIDEMIOLOGY true incidence of mTBI is difficult to

Traumatic brain injury (TBI) is respon- determine because of the number of
sible for over 1.7 million deaths, hospi- individuals with TBI-related symptoms
talizations, and emergency department who never seek medical care.3 In fact,
visits each year.1 Over 80% of patients approximately 16% to 25% of the TBI
are treated and released from the emer- population may not seek medical at- 17
gency department, but approximately tention after sustaining an injury.3 As
52,000 deaths and 275,000 hospitaliza- a result, determining a precise break-
tions result.1 TBI can be characterized down of mild, moderate, and severe
as mild, moderate, or severe, depend- TBIs is challenging, and the published
ing on the injury characteristics. Esti- estimates likely are a low reflection of
mates indicate that approximately 75% the actual incidence of TBI in the United
of the TBIs that occur each year are States.
forms of mild TBI (mTBI), otherwise In the civilian population, the lead-
known as concussion.2 However, the ing causes of TBI include falls (35.2%);
Relationship Disclosure: Ms Anderson-Barnes and Ms Weeks have nothing to disclose. Dr Tsao has received
grants from the US Army Medical Research and Materiel Command, the Dana Foundation, and the US Navy.
Unlabeled Use of Products/Investigational Use Disclosure: Ms Anderson-Barnes, Ms Weeks, and Dr Tsao have
nothing to disclose.
" OVERVIEW
KEY POINTS
motor vehicle and traffic accidents at the time of the accident
A Traumatic brain
(17.3%); getting struck by an object, such (eg, feeling dazed, disoriented,
injury (TBI) is a
prevalent as colliding with a moving or stationary or confused); and
condition object (16.5%); and assaults (10.1%).1 4. focal neurological deficit(s) that
throughout Conversely, blasts from improvised ex- may or may not be transient;
the civilian plosive devices are the leading cause of but where the severity of the injury
and military TBI in the active duty military popula- does not exceed the following:
populations. tion.4 In terms of age, the frequency
Most TBIs are
o loss of consciousness of
distribution of TBI is trimodal: children
classified approximately 30 minutes or less;
aged 0 to 4 years, adolescents aged 15 to
as mild. o after 30 minutes, an initial Glasgow
19 years, and adults aged 65 years and
Coma Scale (GCS) score of 13–15;
A The terms older have the highest rates of injury,
and
concussion and with infant males presenting with the
o posttraumatic amnesia (PTA)
mild TBI are highest rate of TBI overall.1 Unlike mod-
not greater than 24 hours.
synonymous. erate and severe forms of TBI, accurately
Concussion is diagnosing mTBI can be complicated. Alternatively, the AAN operational de-
the preferred Mild TBIs do not always result in obvious finition of concussion is ‘‘. . .a trauma-
medical term as physical impairments, and structural ab- induced alteration in mental status that
it provides an may or may not involve loss of con-
normalities may not be readily visible
individual with
on neuroimaging. This topic will be dis- sciousness.’’6 According to this defini-
an expectation tion, ‘‘Confusion and amnesia are the
of a full and
cussed at length in this issue.
hallmarks of concussion. . .[and] may oc-
complete
cur immediately after the blow to the
recovery. DEFINITION head or several minutes later.’’6
The terms mTBI and concussion are Despite having standardized defini-
oftentimes used interchangeably; yet tions, considerable disagreement exists
several definitions have been proposed as to the proper use of the terms mTBI
for each term. The American Congress and concussion. Some authors have sug-
of Rehabilitation Medicine (ACRM), Cen- gested that including the adjective mild
ters for Disease Control and Preven- gives mTBI an inappropriately benign
tion (CDC), World Health Organization connotation. At the same time, some
(WHO) Collaborating Centre Task Force, believe that using the term mTBI is ap-
and the Defense and Veterans Brain propriate because it provides a frame-
Injury Center (DVBIC) have all proposed work that separates these injuries from
operational definitions of mTBI, and the the TBI diagnosis, which typically con-
18 AAN and Concussion in Sport Group jures up thoughts of more obvious struc-
(CISG) have proposed definitions for con- tural damage to the brain and prolonged
cussion. The ACRM definition of mTBI or permanent neurologic dysfunction. It
is perhaps the most commonly used5: has been suggested that the use of one
A patient with mild traumatic brain term over the other is often a product of
injury is a person who has had a how the clinician wants to project the
traumatically induced physiologi- severity of the injury. For example, if re-
cal disruption of brain function, as assurance is the goal, then the term
manifested by at least one of the concussion is stressed, while the term
following: mTBI is used to underscore the need to
1. any period of loss of consciousness; take the injury seriously.7
2. any loss of memory for events In general, an mTBI or concussion is
immediately before or after the an injury to the brain occurring as the
accident; result of biomechanical forces, generally
3. any alteration in mental state characterized by the rapid onset of a
KEY POINT
constellation of symptoms or cognitive symptoms, such as confusion, amnesia,
impairment.1 and loss of consciousness (LOC), are A Concussion is
primarily a
secondary to the diffuse membrane de-
PATHOPHYSIOLOGY functional
polarization. Following the acute hyper-
injury that
The complete pathophysiologic mech- metabolic phase, there is a much longer occurs as the
anism of concussion continues to be period of decreased metabolism (hypo- result of a
explored and elucidated through basic metabolism), lasting 7 to 10 days and complicated
science investigations, clinical studies of correlated with cognitive deficits, that metabolic
athlete cohorts and the military, and has been described in adult rats.13 cascade.
translational research. These efforts are In humans, this pathophysiologic cas-
building on early animal models that cade has been measured primarily after
have shown an indiscriminate release of severe TBI, demonstrating increased glu-
glutamate and massive depolarization of tamate release, altered cerebral blood
neurons following concussive injury.8,9 flow, and perturbations of glucose me-
In vivo, cerebral microdialysis can detect tabolism similar to that described in the
this significant increase in extracellu- animal models. Growing evidence sug-
lar glutamate as well as an increase in gests that these mechanisms occur after
potassium ion concentrations. Mem- milder human TBI, including a period of
brane ionic pumps then work to restore glucose hypometabolism on PET14 and
homeostasis, using adenosine triphos- reduced NAA/creatine levels on mag-
phatase (ATP) as an energy source and netic resonance spectroscopy.15
greatly increasing cerebral glucose me-
tabolism hyperacutely.10 This increase SYMPTOMATOLOGY
in energy demand results in hypergly- Most people recover from mTBI with
colysis, lactate accumulation, calcium minimal treatment and rest, but it is
sequestration and mitochondrial dys- possible that even mTBI can result in
function, and a decrease in ATP produc- serious long-term effects on an individ-
tion that further exacerbates the ongoing ual’s cognitive, physical, and psychologi-
cellular energy crisis.11 This metabolic cal function.1 An estimated 10% to 15%
cascade is presented in Figure 1-1. Dur- of patients with TBI suffer from long-
ing this hyperacute metabolic phase, term complications and require special-
cerebral blood flow cannot keep up with ized care.16 Diagnostic criteria for TBI
the massive increase in metabolic de- remain an area of active research and
mand, putting neurons at risk of fur- debate. Some common features of brain
ther injury. In experimental TBI models, injury include LOC, posttraumatic am-
this period of metabolic uncoupling and nesia (PTA), and postconcussion syn- 19
hyperglycolysis may last from 30 minutes drome (PCS). LOC is often thought to be
to a few hours, depending on the age a hallmark symptom of TBI and has been
and injury model.10,12 Other markers used as a criterion for TBI severity, but
of metabolic disturbance have been re- recent studies have shown this empha-
ported after repeated experimental mTBI sis may be misplaced, particularly in the
using a weight drop, including reductions case of sports concussions, where not all
in N-acetylaspartate (NAA) and increased athletes lose consciousness.17 Further-
NAA acylase gene expression, that are more, Makdissi reported that recent
maximal when repeated mTBIs are sep- studies have shown that LOC does not
arated by 3 days.13 accurately reflect the severity of TBI, nor
Although no studies have been able does it serve as a good predictor of
to show precisely how these particular recovery duration. PTA, including both
mechanisms result in concussive symp- retrograde amnesia and anterograde
toms, it is likely that many of the initial amnesia, frequently occurs after head
" OVERVIEW
FIGURE 1-1 Neurometabolic cascade following traumatic injury.

K = potassium; ADP = adenosine diphosphate; ATP = adenosine triphosphate; Na-K ATPase = sodium- and
potassium-activated adenosine triphosphatase; Glut = glucose transporter; Mg2+ = magnesium; Ca2+ = calcium;
20 NMDA = N-methyl-D-aspartate; AMPA = -amino-3-hydroxyl-5-methyl-4-isoxazole-propionate.
Reprinted with permission from Giza CC, Hovda DA. The neurometabolic cascade of concussion. J Athl Train 2001;36(3):228–235.
injury; longer periods of PTA tend to Brain injury may also result in enceph-
indicate more severe injury.3 The Inter- alopathy, a disturbance of brain function
national Statistical Classification of indicating damage to the brain’s gray
Diseases, Tenth Revision criteria for PCS matter; focal neurologic signs, indica-
require a ‘‘history of head trauma with tions to a neurologist that specific brain
LOC’’ occurring before the onset of three areas are damaged; seizure; and unequal
or more designated symptom categories or unreactive pupils, which can indicate
(Table 1-1).18 PCS symptoms that do not a dangerous rise in intracranial pressure
resolve within a few weeks to months (which may require surgical interven-
may indicate severe injury. tion to relieve pressure).
KEY POINT
TABLE 1-1 International Statistical Classification of Diseases, Tenth A While loss of

Revision Classification of Postconcussion Syndrome18 consciousness
has been
A. History of head trauma with loss of consciousness precedes symptom onset considered
by maximum of 4 weeks the hallmark
B. Symptoms in three or more of the following symptom categories: symptom of
TBI, it may
Headache, dizziness, malaise, fatigue, noise tolerance not accurately
Irritability, depression, anxiety, emotional lability reflect the
severity of TBI
Subjective concentration, memory, or intellectual difficulties without
and does not
neuropsychological evidence of marked impairment
necessarily
Insomnia serve as a
Reduced alcohol tolerance good predictor
of recovery
Preoccupation with above symptoms and fear of brain damage with duration.
hypochondriacal concern and adoption of sick role
Sports concussions have recently be- preinjury factors, such as employment

come an area of increased research and status and alcohol or illicit drug use, may
public interest. According to statistics play a role in determining the ultimate
on morbidity and mortality kept by the outcome.27 In addition, other social
CDC, emergency departments treat an factors, such as family or social issues
estimated 135,000 sports-related and and legal trouble, may have an influence
recreation-related TBIs among children on outcomes following a TBI. This topic
aged 5 to 18 years each year.19 Athletes will also be explored later in this article.
who have previously had a concussion
are at an increased risk for another con- TYPES OF BRAIN DAMAGE
cussion,20 and children and teenagers After a TBI or concussion, focal and dif-
are more likely to get a concussion and fuse damage may occur. Focal brain
take longer to recover than adults.19 In- injuries occur in a particular area of
terestingly, depression is not uncom- the brain, whereas diffuse injuries occur
mon following brain injury,21–23 and throughout the brain and are not local-
research suggests that athletes who have ized to a specific area. When a moving
sustained repeated concussions are at an object directly strikes the head, causing
increased risk of clinical depression.24 the brain to collide with the skull, a fo- 21
Furthermore, repeated concussion has cal injury has likely occurred. This type
been reported to be associated with an of injury is known as a ‘‘coup’’ injury. A
earlier onset of Alzheimer disease25 and second, directly related injury can result
the development of chronic traumatic when the moving head strikes a sta-
encephalopathy.26 Within the military tionary object28; this is referred to as a
population, blast-related TBI has also ‘‘contrecoup’’ injury. The contrecoup
gained attention. It is estimated that injury occurs opposite the side of the
more than 60% of the combat casualties original impact. Diffuse damage, on the
sustained in the Iraq and Afghanistan other hand, is typically caused by an
conflicts are caused by explosive blasts.4 acceleration/deceleration force being
Brain injuries that result in the civilian applied to the brain, as in the case of
population may not follow the same explosive blast. Diffuse axonal injury,
recovery pattern as injuries sustained in the deforming or stretching of brain
the military population. For example, tissue, is an example. Mild TBI and
" OVERVIEW
KEY POINT
concussion can result from both focal driving, therapeutic recreation, and art
A Treatments for
and diffuse damage. Additional injury to therapy.33 After each care provider team
mTBI and
concussion are the brain can result from the shearing meets with a patient, short-term and
rather diverse, and stretching of the brain tissue caused long-term goals are established, and a
and early by motion of the brain structures rela- treatment plan is put into effect.
intervention is tive to the skull and to each other, as In addition to functional rehabilitation,
the key to well as from a vascular response to the patients with persistent symptoms (eg,
maximizing impact.29 This response can include sub- headaches, chronic pain, and depression)
outcomes dural hematoma, decreased blood flow can benefit from pharmacologic manage-
following a TBI due to increased intracranial pressure, ment, educational interventions, and tar-
or concussion. and brain edema. These insults have geted therapies, as well as rest and timely
been investigated thoroughly in animal return to duty (for the military popu-
models.30 lation) or return to play (for sports-
related injuries).34 Pharmacologic inter-
TREATMENTS ventions have been successfully used
Some of the most common impairments in the treatment of somatic symptoms
after sustaining an mTBI or concussion such as headaches35 and chronic pain,36
include headache, sleep disturbances, cognitive dysfunctions such as memory
and sensitivity to light and noise.31 Silver and attention deficits,37 and emotional/
and colleagues divided the symptoms behavioral symptoms such as depres-
of TBI into three categories: (1) somatic sion.37,38 Providing patients with informa-
consequences, (2) cognitive dysfunction, tional pamphlets highlighting common
and (3) emotion and behavior.32 Somatic symptoms associated with mTBI and ex-
consequences include symptoms such pected course of recovery has also been
as headache and sleep disturbance. Cog- effective in treatment management.34,39
nitive dysfunction is characterized by In addition, targeted therapies, such as
attentional impairment and reduced pro- relaxation training and cognitive behav-
cessing speed, among others; and emo- ioral therapy, have played a role in pro-
tion and behavior symptoms include moting restful sleep40; and cognitive re-
impulsivity, irritability, and depression.32 habilitation has been useful in improving
Depending on the nature of the injury, memory, attention, and executive func-
symptoms present themselves differently tions.37,41 Finally, results from neuro-
in each patient. cognitive assessments (discussed in the
Treatments for mTBI and concus- next section) can be used to help make
sion are rather diverse. To begin with, decisions about return to duty or play by
22 individuals with functional deficits are determining current cognitive status in
in need of rehabilitation. However, the service members or athletes.
goals of rehabilitation, as well as the
type and intensity of rehabilitation ad- NEUROCOGNITIVE TESTING
ministered, vary among patients. Accord- One of the most important components
ing to the Defense and Veterans Brain of evaluating a patient with an mTBI or
Injury Center (DVBIC), early interven- concussion is neurocognitive testing. A
tion is the key to maximizing outcomes careful assessment of the patient’s neu-
following a brain injury.33 Rehabilitation robehavioral problems and neurocogni-
efforts are started immediately after a tive abilities is crucial to understanding
patient is determined to be medically the degree of impairment.42 This can
stable. Rehabilitation involves a variety of be done by either a neurologist with
programs, including occupational ther- experience in behavioral testing and
apy, physical therapy, speech and lan- evaluation in conjunction with, or solely
guage pathology, vestibular therapy, by, a neuropsychologist. Determining
the patient’s history (baseline) is the and specificity of each test.44 Tradition-
first step in the evaluation process. ally, neurocognitive assessments were
However, the patient may not be able in a paper-and-pencil format, but over
to give an accurate representation of his/ the past decade, computerized tests
her history because of memory deficits or have been implemented.45 Computer-
difficulty with time sequencing.42 Conse- ized tests are favored in the sports
quently, the neuropsychologist may need world, as the tests can be quickly ad-
to contact others (eg, family, friends, team- ministered to a number of athletes,
mates, coaches, or prior medical or mili- and multiple forms are available for
tary records) to obtain an accurate history follow-up testing.45
report. During this stage, the neurologist Finally, a physical examination that
and/or neuropsychologist should obtain includes a full neurologic examination
not only information related to the occur- should be conducted. During the neu-
rence and duration of LOC, PTA, alter- rologic examination, the neurologist
ation of mental status, and the presence should focus on primitive reflexes and
or absence of focal neurologic deficits, neurologic ‘‘soft signs.’’43 Standard neu-
but also information on any prior con- roimaging (head CT or MRI) may also
cussions or TBIs, neurologic diseases or prove useful during this phase, although
disorders, psychiatric disorders, substance some issues surround the sensitivity
use, academic history, social and family of these scans. CT scans, for example,
history, and employment history.43 Two are typically performed in the emer-
primary reasons for conducting such a gency department because of their abil-
thorough review of the patient’s history ity to detect hemorrhagic lesions and
are (1) to approximate the patient’s base- other structural injuries.3 Typical imag-
line and (2) to be able to properly assess ing modalities (CT and MRI) have poor
and interpret findings from the neuro- sensitivity, however, when it comes to
cognitive tests.34 When a clear history is detecting abnormalities in mTBI. Issues
not defined, there is a chance that long- surrounding neuroimaging will be dis-
standing deficits may be incorrectly at- cussed in other articles.
tributed to the brain injury.42 For that
reason, baseline data should be obtained CONCLUSION
as soon as possible after the injury. In the forthcoming articles, the patho-
Once the patient’s history has been physiology and symptomatology of mTBI
acquired, the next step is to review the and concussion will be reviewed. Fur-
functional domains that are typically thermore, the progression and mani-
affected by the injury. McAllister42 lists festation of the condition in the civilian 23
these as cognition, personality, mood and military populations will be dis-
regulation, speech/language, mobility, cussed. Finally, mTBI and concussion
and higher-order domains. It is vital that will also be examined with respect to
the test battery is able to assess multiple acute management, sports-related in-
aspects of cognitive function, as neglect- juries, seizures, sleep dysfunction, men-
ing a domain may lead to an inaccurate tal disorders including posttraumatic
conclusion regarding return to duty, stress disorder, cognitive impairment,
for example. A psychometrist may ad- and the use of neurocognitive testing
minister the test battery, but a trained for assessing brain injury status. This
neurologist or neuropsychologist must issue is designed to pro-
interpret the results. Other aspects to vide the reader with a general overview
consider when selecting an appropriate of TBI, focusing on mTBI and concus-
test battery include the length of assess- sion, as well as highlight recent advan-
ments, and the sensitivity, reliability, ces in mTBI/concussion research.
" OVERVIEW
The reader is directed to useful Giza, MD; and Anthony G. Alessi, MD,
references in Appendix A for addi- FAAN, the authors of the sports neurol-
tional details about topics in the rest of ogy article for contributions to the
this issue. In addition to the guidelines pathophysiology section of this article.
cited in Appendix A, the following
websites may be useful: www.dvbic.org DISCLAIMER
(Provider section) and www.cdc.gov/
traumaticbraininjury/index.html. The opinions or assertions contained
herein are the private views of the au-
ACKNOWLEDGMENTS thors and are not to be construed as offi-
cial or as reflecting the views of the De-
The authors would like to thank Jeffrey partment of the Army, the Department of
S. Kutcher, MD, MPH; Christopher C. the Navy, or the Department of Defense.
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Arlington, VA: American Psychiatric Publishing, 2005.
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Service-Members—Veterans/Recovery—Rehabilitation.aspx. Accessed July 12, 2010.
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combat amputee. www.bordeninstitute.army.mil/published_volumes/amputee/
CCAfrontmatter.pdf. 2009. Accessed August 25, 2010.
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42. McAllister TW. Neurobehavioral sequelae of traumatic brain injury: evaluation and
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44. Grindel SH, Lovell MR, Collins MW. The assessment of sport-related concussion: the
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from behavioral to brain imaging measures. J Neurotrauma 2009;26(12):2365–2382.
KEY POINTS
DIAGNOSIS AND A The actual

number of mild
MANAGEMENT OF traumatic brain

injury (mTBI)
TRAUMATIC BRAIN cases is

uncertain as
many patients
INJURY may receive

care by
nonmedical
Geoffrey S. F. Ling, Scott A. Marshall, David F. Moore professionals
or do not
seek medical
ABSTRACT attention at all.
This article will provide an overview of the initial evaluation and management of A The total cost
traumatic brain injury (TBI). In cases of mild injury, conventional imaging in the of TBI is
absence of focal neurologic deficits is generally unrevealing. In the case of moderate estimated to be
or severe TBI, a review of neurocritical care is provided. a staggering
$60 billion
Continuum Lifelong Learning Neurol 2010;16(6):27–40. per year.
INTRODUCTION many as 8 million head injuries occur

Traumatic brain injury (TBI) is unfortu- each year in the United States alone.1–4
nately an all too common disorder. In TBI afflicts patients of all ages and both
the United States, an estimated 1.7 mil- sexes. However, prevalence is greater
lion new TBI cases occur per year. TBI among males, the very young (younger
may result in significant long-term con- than 4 years), adolescents (aged 15 to
sequences, including death and chronic 19 years) and older adults (older than
disability in severe cases. Approximately 65 years). Close to 500,000 of all TBI
1.4 million emergency department visits emergency department visits (or approxi-
per year are for TBI. Of these visits, about mately one-third of the total) are for
275,000 patients are admitted to the hos- children younger than 4 years old, where
pital. In addition, close to 52,000 patients consideration of nonaccidental injury is
with TBI die each year. TBI accounts important.2
for almost one-third of all injury-related The etiology of TBI varies with age. 27
deaths, highlighting the importance of Falls and nonaccidental trauma are more
primary prevention.1,2 frequent in the very young. Sports-
Mild TBI (mTBI) and acute concus- related injuries and motor vehicle acci-
sion account for approximately 75% of all dents are more common among adoles-
TBI cases. However, the actual number cents, while falling is usually the reason
of mTBI cases is uncertain as many pa- for TBI in older adults.5
tients may receive care by nonmedical The total cost of TBI is estimated to
professionals or do not seek medical be a staggering $60 billion per year. Di-
attention at all. Estimates suggest that as rect medical costs for treating a patient
Relationship Disclosure: Dr Ling has received personal compensation for speaking engagements from Bristol-
Myers Squibb and Sanofi-Aventis and holds stock and/or stock options in Wyeth Pharmaceuticals. Dr Marshall
has received personal compensation as an expert witness. Dr Moore has nothing to disclose.
Unlabeled Use of Products/Investigational Use Disclosure: Drs Ling and Moore have nothing to disclose.
Dr Marshall discusses the unlabeled use of hypertonic saline in the treatment of traumatic brain injury.
" DIAGNOSIS AND MANAGEMENT
KEY POINTS
with mTBI can be as high as $85,000 and tuational awareness. mTBI and concus-
A Concussion
for a patient with severe TBI, $3 million. sion are often associated with brief (less
refers to altered
function. mTBI In terms of human and family suffering, than 5 minutes) loss of consciousness
describes a it is incalculable. An estimated 80,000 or situational awareness in which the
pathologic survivors from civilian injury each year person experiences a performance dec-
state of brain are left with residual neurologic deficit rement within the required environ-
after the that results in loss of function. These mental context.11
concussive patients require extended rehabilita- In clinical practice, concussion and
event. tion. Many of these patients are younger mTBI are often used synonymously.
A The AAN than 40 years and are otherwise in good However, they are distinct terms. Con-
concussion physical health and, thus, may live for cussion refers to altered function. mTBI
grades are decades following the injury. Beyond describes a pathologic state of brain
grade 1, the direct medical expense, invisible after the concussive event. Three grades
altered mental costs come into play when a previously of concussion have been identified ac-
status less than productive member of society, usually cording to AAN criteria. The grades are
15 minutes; at an early age, has instead become differentiated by duration of altered
grade 2, dependent.1,6–8 mental status and any of loss of con-
altered mental
Even mTBI or concussion can lead to sciousness. Amnesia, although not part
status more
significant disability. A study of patients of the AAN criteria, is an independent
than 15
who sustained relatively minor injuries diagnostic indicator of TBI severity, with
minutes; and
grade 3, loss of revealed up to 7% to 9% had residual the loss of memory preceding (retro-
consciousness. symptoms 3 months after injury. One- grade) or following (posttraumatic or an-
third of these patients were unable to terograde) injury. A grade 1 concussion is
return to their previous jobs.3,4 defined as having altered mental status
lasting less than 15 minutes without loss of
consciousness. In grade 2, concussion is
SEVERITY OF TRAUMATIC altered mental status lasting more than 15
BRAIN INJURY minutes, again without a loss of conscious-
TBI traditionally has been divided into ness. Grade 3 concussion according to the
three major categories. These are mild, AAN scale is characterized by any loss of
moderate, and severe. The Glasgow consciousness.11
Coma Scale (GCS) score may used to Moderate TBI occurs when a patient
differentiate among the three.9 A trau- sustains a head injury that results in
matic injury to the brain resulting in a a GCS of 9 to 12, and usually is asso-
GCS of 13 to 15 is defined as mild. If the ciated with prolonged loss of con-
28 GCS is 9 to 12, the TBI is defined as sciousness and/or neurologic deficit.12
moderate. If the GCS is 8 or less, the TBI Patients with moderate TBI require ad-
is defined as severe. vanced medical care, including neu-
mTBI is further defined by the Mild rosurgical consultation. Later, as they
Traumatic Brain Injury Section of the recover, they may develop postconcus-
American Congress of Rehabilitation sive syndrome or persistent postconcus-
Medicine (1993)10 as the loss of con- sive symptoms.13
sciousness for less than 30 minutes, loss Severe TBI occurs when the injury
of memory preceding or following in- causes the patient to be obtunded or
jury (amnesia) for less than 24 hours, comatose (ie, the presenting GCS is 8 or
alteration in mental status at time of less). Such injury is typically associated
injury, and/or focal neurologic deficit.10 with significant neurologic injury, often
The level of mTBI severity (as described with structural lesions revealed by neu-
below) is based mainly on the duration roimaging (eg, head CT scan revealing
of altered mental status or altered si- skull fracture, intracranial hemorrhage,
and early diffuse cerebral edema). These injury. The processes that contribute
patients usually require advanced medi- to this ‘‘neuronal suicide’’ include hyp-
cal care even in the prehospital setting. oxia, effects of free radicals, excitatory
After initial resuscitation and stabilization amino acids, certain ions (eg, calcium),
in the field, patients with severe TBI ischemia, and inflammation.16
should be evacuated to the nearest level For practical reasons based on the
1 trauma center with neurosurgical ca- time and effort to develop therapeutics,
pability. Such patients will need airway approaches to TBI have focused on sec-
protection, mechanical ventilation, neu- ondary injury processes. Although sig-
rosurgical evaluation, and intracranial nificant research efforts have been de-
pressure (ICP) monitoring with skilled voted to this issue, current clinical
nursing neurocritical care in a trauma treatment for mTBI is largely confined
unit or neuro-intensive care unit. It is to symptomatic relief, rest, and recu-
expected that recovery will be prolonged peration. For moderate to severe TBI,
and often incomplete, with many pa- focus is on supportive measures with
tients not surviving beyond one year.12–14 particular emphasis on maintaining ce-
rebral perfusion pressure, minimizing
intracranial hypertension, and treating
MECHANISM OF INJURY indirectly cerebral edema. Efforts to de-
Two distinct phases are associated with velop neuroprotective treatments that
TBI. The first phase is the tissue injury are clinically effective in patients are
that is a direct consequence of the pri- ongoing.
mary traumatic event, resulting in stress-
induced strain deformation of the CNS
tissue and skull. The second phase is ETIOLOGIES OF INJURY
multiple related neuropathologic pro- TBI can be caused by a number of dif-
cesses that are responses to the trau- ferent mechanisms that involve varying
matic event. This later secondary phase strain rates of brain deformation, rang-
can last for days to weeks.15 ing from lower strain rates in direct
The primary injury phase occurs al- impact TBI to ballistic-induced head in-
most immediately and is not generally jury to blast-associated neurotrauma at
thought to be amenable to treatment. high strain rates. Injuries can be divided
When sufficiently severe, it can lead to into two main categories—penetrating
death. The damage that occurs from and nonpenetrating (or open head and
this primary phase is often complete by closed head) (Case 2-1). Penetrating or
the time medical care can be instituted. open head TBI is caused by violation of 29
The best approach to mitigating primary the skull. This can result from foreign
injury is prevention with the use of body entry, such as a bullet or knife. It
personal protective equipment, such as can also be caused by direct blunt force,
an appropriately quality-assured helmet such as being struck with an object (eg,
for sports-related concussion. baseball bat), as well as mild to mod-
The secondary injury phase is de- erate explosive blast injuries. TBI as-
layed, which offers an opportunity for sociated with penetration is typically
therapy. This phase begins very quickly moderate to severe (Case 2-2). Non-
after the primary phase and can con- penetrating or closed head injury is most
tinue for an extended period of time. often caused by direct blunt force. Other
Injury usually involves both neurons pathoanatomic features of TBI include
and glia. It is thought that most neu- focal contusions, hypoxic-anoxic injury,
rologic injury occurs after the primary diffuse axonal injury, and diffuse micro-
event and is related to this secondary vascular injury.
Case 2-1
An armed service member in full-body armor and helmet faced incoming firepower that
detonated an ammunition storage area with multiple ensuing explosions. Thinking it was safe,
she stepped out from a bunker but experienced a large blast occurring on the left side at an
approximately 125-m (410-ft) standoff. She reported head and chest pressure, with a sensation of
having her ‘‘bell rung’’ associated with a brief loss of situational awareness. The intensity of
incoming fire and ammunition dump explosions forced her to remain inside the open bunker for
over 2 hours.
Immediately after the large blast, she experienced severe headache, ringing in the left ear,
and aching ribs. Ten hours later, she began vomiting and was medically observed for 2 days
while receiving IV hydration. Symptoms of dizziness, balance difficulties, problems with
thinking, anxiety, insomnia, and nightmares developed and continued prominently for
2 weeks. Medical evacuation to the United States occurred 3 months later, as she
continued to have severe headaches. Neurologic consultation confirmed a normal neurologic
examination. MR imaging showed an area of T2 hypointensity in the left internal auditory
canal consistent with a hematoma and a larger area of hyperintensity of the left cerebellum.
Diffusion tensor imaging tractography demonstrated more robust cerebellar fiber pathways
on the right side than on the left, especially those traveling from right to left. Fluid-attenuated
inversion recovery (FLAIR) imaging was consistent with a subacute vascular event of a
segmental artery.
Comment. This case represents an account of primary blast injury with symptoms
consistent with a concussion (grade 1). The abnormality noted on FLAIR imaging was
consistent with a segmental arterial infarct of the cerebellum possibly due to traumatic
cerebral vasospasm.
Adapted from Warden DL, French LM, Shupenko L, et al. Case report of a soldier with primary blast brain injury. Neuroimage 2009;47(suppl 2):
T152–T153. Copyright # 2009, with permission from Elsevier.
Focal injuries occur at the site of im- rebral arterial territories and the deep
pact, and neurologic deficits are there- penetrating cerebral vessels. It has also
fore referable to the injured areas. The been hypothesized that delayed neu-
orbitofrontal region and anterior tempo- rologic compromise can be attributed
ral lobes are most commonly affected. to delayed ischemia in TBI, particu-
Particular vigilance must be made to larly when traumatic cerebral vasospasm
identify the development of delayed he- occurs.17,18
matomas, which can manifest days after Diffuse axonal injury is a result of
30 injury.16 rapid acceleration and deceleration, as is
Hypoxic and hypoperfusion injuries often experienced in motor vehicle acci-
are well recognized as leading contrib- dents. This leads to shearing of axons in
utors to secondary brain injury. In TBI, the cerebral white matter, which causes
a transient increase occurs in systemic neurologic deficits such as encephalop-
arterial pressure. Apnea and cerebral athy. The consequences of this type of
dysfunction may develop. Depending injury can be delayed for up to 12 hours
on the degree of injury, spontaneous following initial trauma.19
resolution may be delayed. Laceration Diffuse microvascular damage is
of microvasculature will exacerbate this caused by an early loss of cerebral vas-
type of injury. Furthermore, the injured cular autoregulation and a loss of blood-
brain is more susceptible to hypoxic brain barrier integrity. This leads to
ischemia. The most commonly affected endothelial changes, such as the forma-
areas are the hippocampus and vascular tion of intraluminal microvilli. Although
‘‘watershed’’ areas between external ce- the clinical significance of this injury is
KEY POINT
Case 2-2 A Second-impact

A 28-year-old man in combat received a penetrating bullet wound to syndrome
the left occiput with lodging of the bullet in the corpus callosum. He arrived is another
3 days later at a tertiary medical center intubated and having been put potentially
into pentobarbital coma. In addition, he had received a left-sided serious
hemicraniectomy. Over the course of the next week, he had diffuse cerebral complication
edema extending past the craniotomy margins that resolved. He received of mTBI.
medical treatment in the intensive care unit and after 1 month was
transferred to a regular hospital bed with a hemianopsia and a
right-sided hemiplegia. After rehabilitation, he was discharged home with
persistent upper quadrantanopsia and mild right lower limb weakness.
He later returned to the hospital to have a replacement skull plate inserted.
Comment. This case illustrates the changing prognosis for severe brain
injury. It is likely that the hemicraniectomy, which allowed brain swelling, may
have avoided further neuronal injury and an evolving herniation syndrome.
This case also illustrates persistent neuroplasticity occurring during the
rehabilitation period, even in an older-age individual.
uncertain, it may play a role in cerebral consequence of this re-injury.22 Iden-

edema associated with TBI.20 tified in boxers, dementia pugilistica, a
Explosive blast TBI results when physi- form of CTE, is arguably the first clearly
cal forces from detonation of explo- described syndrome in which permanent
sive devices couples to neuronal tissue. neurocognitive deficits develop as a result
Which of the many physical forces is of repeated head blows.23 An increasing
important is not known, but likely can- concern is that other professional ath-
didates include blast overpressure and letes who are at risk for repeated con-
underpressure; and acoustic, electro- cussions are also at risk for CTE. A recent
magnetic, and thermal energy; with toxic case series of autopsies of former pro-
agents such as chemical products of fessional athletes (two boxers and one
detonation perhaps also involved. Fol- American football player) demonstrates
lowing these insults, brain cells can that significant structural brain damage
undergo both apoptotic and necrotic can occur in these high-risk patients.22
changes, with subacute to chronic neu- Second-impact syndrome (SIS) is
rodegeneration also potentially occur- another potentially serious complica-
ring. Brain vascular endothelial structures tion of mTBI.24 A disorder that seems 31
may also be injured, leading to vasospasm to affect children more than adults, SIS
and pseudoaneurysm formation.18 When occurs as a consequence of sustain-
vascular injury is mild, the primary neu- ing another TBI before fully recovering
rologic deficits are cognitive and neuro- from the initial one. Tragically, patients
behavioral. As vascular injury severity with SIS develop rapid cerebral edema,
increases, the neurologic state worsens leading to severe neurologic deficits,
from focal neurologic deficits to coma.21 including coma and death. The fatality
rate of this fortunately rare disorder is
REPEATED INJURY very high, approaching 50%.
There is a growing appreciation that The mechanism underlying SIS de-
repeated re-injury, even years later, may velopment is uncertain. A leading hy-
lead to a worse neurologic outcome. pothesis is that cerebral autoregulation
The syndrome of chronic traumatic en- is impaired. Subsequent injury initi-
cephalopathy (CTE) is thought to be a ates the secondary injury cascade, often
KEY POINTS
exacerbating the presumed underlying thology. The presence of intracranial
A Most patients
inflammatory condition, thus allowing blood, intracranial air, skull fracture, or
with mTBI
recover from cerebral edema to develop, which in parenchymal contusion on routine CT
this disorder turn leads to intracranial hypertension. or MRI suggests a more severe traumatic
with full The existence of this disorder has not brain injury. Patients with such findings
resolution of been fully accepted as limited cases of will need neurosurgical evaluation.
symptoms. SIS have been reported. Given its po- The indication for neuroimaging is a
tential for high morbidity and mortality, presenting history of trauma and signs
A In mTBI, the most
common head
however, patients are usually counseled and symptoms concerning for struc-
CT or MRI not to return to prior high-risk activities tural lesions, such as focal neurologic
finding is a until a period of convalescence has signs and prolonged depressed levels
normal image. passed. of consciousness. These patients are at
highest risk following concussion and
POSTCONCUSSIVE SYNDROME should have neuroimaging (ie, AAN
mTBI can lead to headache, confusion, grade 2 or 3 concussion). Moderate-
amnesia, difficulty concentrating, mood risk patients are those who have had a
alteration, sleep disturbance, and anxi- recent history of brief altered mental
ety.25 Typically, these symptoms re- status only, eg, an AAN grade 1 con-
solve within a few hours or days. cussion. Patients at minimal risk are
Often, a patient with mTBI may not asymptomatic, experience only head-
recognize it as such. The first indication ache or scalp laceration, and thus do not
of injury may be the manifestation of meet criteria for having sustained a con-
postconcussive symptoms. These are cussion. This last group should not have
typically headaches, vertigo, short-term neuroimaging for mTBI.27,28
memory loss, or difficulty concentrating In mTBI, the most common head
or with multitasking.26 As these symp- CT or MRI finding is a normal image.29
toms can be subtle, a detailed mental Patients with mTBI typically do not
status evaluation is necessary. An im- require hospital admission and can be
portant part of this evaluation should followed as outpatients. It is generally
be objective neuropsychological testing, recommended, however, that a friend or
even though initially it may only consist family member monitor them in the
of limited bedside testing. Efforts are acute period (12 to 24 hours after injury)
underway to develop neuropsychologi- for any signs of deterioration.30,31
cal tests that can be automated on a
laptop computer or are more easily
32 interpretable to allow use by less-trained TREATMENT
providers. Recognition that an mTBI has occurred
Fortunately, most patients with mTBI is important. This can be difficult as the
recover from this disorder with full re- history may be unclear in a patient who
solution of symptoms. Some patients, presents with a normal general neuro-
however, have persistent symptoms that logic examination. If mTBI is suspected,
can last 6 months or more. When symp- a detailed mental status examination
toms persist greater than a few days, that includes frontal lobe tasks should
postconcussive syndrome should be be conducted. A useful aid is the De-
considered. TBI of any severity can lead fense and Veterans Brain Injury Center’s
to postconcussive syndrome. military acute concussion evaluation
(MACE),32 a paper-based, rapid bedside
NEUROIMAGING neuropsychological tool modeled after
The decision to obtain neuroimaging is the Standard Assessment of Concussion
based on the risk for intracranial pa- used by the National Football League.
KEY POINT
Other tools, such as computer-based than 90% and systolic blood pressure
A Hypoxia and
reaction time testing and ocular motor greater than 90 mm Hg.34,35
hypotension
testing, are becoming available. The most important treatment for should be
TBI treatment has greatly improved mTBI or acute concussion is the pre- avoided by
over the past 15 years, largely because of vention of further injury. Removal from maintaining
the widespread use of evidence-based play or work followed by adequate rest oxygen
guidelines for clinical management. and recuperation is the mainstay of saturation
In 1995, The Brain Trauma Founda- therapy.11 greater than
tion published the first edition of the Symptomatic treatment is indicated 90% and
‘‘Guidelines for Management of Severe to help ameliorate the condition. The systolic blood
Traumatic Brain Injury.’’ Since then, Veterans Administration and Depart- pressure
greater than
two updated editions have been rement of Defense have issued clinical
90 mm Hg.
leased, with the most recent in 2007.33 practice guidelines for concussion/
The guidelines were developed jointly mTBI.36 These are evidence-based phar-
by the American Association of Neuro- macologic and nonpharmacologic strat-
logical Surgeons and the Congress of egies designed to be symptom targeted.
Neurological Surgeons. Other guide- For example, it is recommended that
lines have also been released so as to headaches be treated with nonsteroi-
optimize prehospital care and neuro- dal anti-inflammatory agents as well as
surgical intervention. They are the ‘‘Pre- physical therapy, relaxation, and sleep.
hospital Guidelines for Management of Cognitive disorders can be treated with
Severe Traumatic Brain Injury,’’ the selective serotonin reuptake inhibitors
‘‘Guidelines for the Field Management as well as reassurance, sleep, and physi-
of Combat-Related Head Trauma,’’ and cal activity. In general, this condition
the ‘‘Surgical Management of Traumatic will last just a few weeks but, in some
Brain Injury.’’34–36 cases, can persist up to 1 year or
Treatment begins at the site of injury. more.37
Anyone suspected of sustaining a TBI, Moderate and severe TBI are serious
no matter how minor, should be im- conditions that require immediate and
mediately removed from further play or advanced medical care. Initially, attention
work. For mild injury, if the individual must be made to ensure airway patency,
has had no mental status changes and is control of bleeding, and adequate circu-
neurologically normal, he or she may lation, the ABCs. Such patients require
return to previous activity. If any confu- hospital admission, typically to a neuro-
sion is noted, the injured person should critical care unit. Early neuroimaging is
be evaluated by a trained provider. If important as these patients often require 33
any loss of consciousness is present, the neurosurgical intervention.
person should be evaluated by an ex- Clinically deteriorating patients and
perienced medical provider, ideally in a those with GCS scores of 8 or less
hospital emergency department. If the should be intubated as they are unable
TBI is severe, it is a medical emergency to adequately protect their airway. They
requiring rapid evacuation to a level 1 should also be placed in a rigid neck
trauma center with neurosurgical capa- collar with the head elevated 308. The
bility. While in the field and during neck collar performs two important
transport, it is important to remember functions: (1) to protect the cervical
the ABCs, ie, airway protection, mainte- spine so that appropriate neuroimaging
nance of ventilation, bleeding control, can be conducted to ensure there is no
and circulation maintenance. Hypoxia spine injury; and (2) to keep the head
and hypotension should be avoided by midline to avoid compromising venous
maintaining oxygen saturation greater drainage.33
KEY POINT
If any evidence of brain herniation, fast and lasts a few hours but
A Cerebral
such as asymmetric pupils, is present, then rapidly loses efficacy because of
perfusion
pressure should mannitol should be given intravenously local metabolic compensation within
be maintained at a dose of 0.5 g/kg to 1.0 g/kg. There- the CSF and brain tissue. When em-
between after, lower intermittent boluses can ployed, efforts should be made to wean
50 mm Hg and be used with IV doses of 25 g to 50 g the patient from this type of therapy
70 mm Hg, administered every 4 to 6 hours until as soon as other interventions become
with a target of serum osmolality exceeds 315 mOsm/L. effective.33
60 mm Hg. The decision to use induced hypother- If these efforts are unable to control
mia is difficult as it is not yet standard the ICP, other options are to induce
care for TBI. Preclinical studies are barbiturate coma or undertake neuro-
promising, but no compelling human surgical decompression or hemicraniec-
clinical evidence of efficacy has yet been tomy. If barbiturate coma is to be used,
shown.37–40 pentobarbital can be administered at a
An ICP monitor is needed for a TBI loading dose of 5 mg/kg IV followed by
patient with a GCS score of 8 or less. an infusion of 1 mg/kg/h to 3 mg/kg/h.
The external ventricular drainage device The goal is to induce a burst-suppression
or intraventricular catheter has two ben- pattern on EEG, obligating use of con-
efits. The first is that among all ICP tinuous EEG monitoring. Barbiturates
monitors, it provides the most reliable are myocardial depressants and, thus,
data. The second and equally important aggressive cardiovascular management
benefit is that it is also a treatment op- will probably be necessary to maintain
tion as it allows CSF drainage so that ICP systemic blood pressure. Unresponsive
and abnormal intracranial compliance ICP after induction of barbiturate coma is
can be controlled according to Monro- an ominous sign, and neurosurgical con-
Kellie doctrine. This essentially states sideration should be made regarding
that the intracranial volume is a constant frontal or temporal lobe decompression
and that contributing volumes of CSF, and/or hemicraniectomy.33
intracranial blood volume, and brain As ICP issues are being addressed,
parenchyma together with any space- attention must be paid to the cerebral
occupying lesion remain constant. Ther- perfusion pressure (CPP). ICP and CPP
apeutic measures to alter ICP and move are related by
down the intracranial compliance curve
are to reduce the intracranial blood vol- CPP ¼ MAPICP ðequation 1Þ
ume, alter production/drainage of CSF,
34 and use osmotherapy to reduce the CNS in which MAP is the mean arterial
tissue volume. Other options for moni- pressure. The goal is to maintain the
toring ICP, such as subdural bolt and CPP between 50 mm Hg and 70 mm Hg,
fiber optic epidural catheter, are less in- with a target of 60 mm Hg.33,41
vasive but less reliable.33 Addressing CPP begins with placing
ICP should be 20 mm Hg or less. If an arterial line and providing isotonic
ICP remains elevated after the above fluid resuscitation to euvolemia. Ade-
measures, induced hyperventilation quate hydration must be maintained. In
may be tried. Respiratory rate should order to increase the osmolar gradient
be increased to decrease arterial PCO2 to between the systemic vasculature and
34 mm HG to 36 mm Hg. Often the the brain, hyperosmolar IV solutions
respiratory rate to achieve this is about should be used. Normal saline is most
16 breaths per minute. It must be uncommonly used and is hyperosmolar
derstood that this is only a temporizing relative to blood. Another option is hy-
therapy. The clinical response is very pertonic saline.33
Hypertonic saline is a useful adjunc- patient who may be experiencing hem-
tive therapy in managing cerebral edema orrhagic shock.42–44
and intracranial hypertension.42 It can If meeting CPP goals continues to be
be administered either as a 2% or 3% difficult with IV fluids alone, vasoactive
continuous IV infusion. The rate of in- pharmacologic agents, such as phenyl-
fusion is determined to be what is nec- ephrine and norepinephrine, may be
essary to maintain euvolemia. Conceptu- required. Dopamine is less often used
ally, hypertonic saline creates an osmotic as it has the potential to further elevate
gradient, which favors reduction of in- ICP. Invasive hemodynamic monitoring
tracerebral water. This will reduce brain with a central venous catheter or pul-
volume and thus ICP. When 2% or higher monary artery/Swan-Ganz catheter may
saline solutions are used, a mixture of be needed.33
50% sodium chloride and 50% sodium Hypoxia, seizures, and fever need to
acetate is helpful. This helps minimize be avoided. Maintaining PO2 at approxi-
hyperchloremia. Infusions are admin- mately 80 mm Hg to 100 mm Hg is
istered until a serum sodium goal is sufficient. No benefit to higher levels of
met, typically 150 mEq/L to 155 mEq/L oxygen has been documented, but a
or higher as needed. These serum so- potential for toxicity exists. Studies have
dium levels will result in serum osmolal- shown that phenytoin will reduce early
ity of approximately 310 mOsm/kg to posttraumatic seizures, ie, those that
320 mOsm/kg. Once ICP is controlled, occur during the first 7 days after TBI.45
hypertonic saline can be switched to However, further phenytoin treatment
normal saline. When the time is appro- does not appear to reduce the rate of
priate to discontinue the infusion, it developing late posttraumatic seizures,
can be stopped abruptly. Serum sodium ie, seizures that develop beyond 7 days
will normalize over the next 24 to from injury. Thus, phenytoin should be
48 hours. Potential untoward effects administered only for the first 7 days
of hypertonic saline use are thrombo- after injury and then stopped. Only if the
phlebitis, seizures, and central pontine patient should have a seizure thereafter
myelinolysis. By administering the solu- should antiepileptic medications be re-
tion through a central venous line, started. Valproate was also shown to be
thrombophlebitis can be avoided. Sei- effective in reducing early posttraumatic
zure risk is highest with serum sodium seizures, but it, too, did not reduce
levels above 160 mEq/L to 165 mEq/L. late posttraumatic seizure rate. Unfor-
Central pontine myelinolysis is gener- tunately, valproate was also associated
ally not an issue as the rise and fall of with a higher mortality rate. Thus, phe- 35
serum sodium associated with hyper- nytoin is the preferred agent.46
tonic saline infusion and discontinua- Fever increases cerebral metabolic
tion is less than 1 mEq/L/h unless a loop rate and therefore should be minimized.
diuretic is given simultaneously. Although TBI alone can induce a fever,
Another option in the case of acute this should be a diagnosis of exclusion.
herniation syndromes is very high hy- Febrile patients should be appropriately
perosmotic saline (23%) given as a slow worked up for an underlying infection
IV administration of 30 cc to 60 cc (total to include blood count, chest x-ray,
dose). The onset of effect is rapid, often urinalysis, and cultures of blood and
within minutes, and the ICP lowering urine. At the same time, the fever needs
effect can last several hours. One major to be reduced. This can be achieved
benefit of this approach is that intravas- with acetaminophen and cooling blan-
cular volume is not compromised. This kets. If a patient develops severe shiver-
is especially helpful for the polytrauma ing, one should consider administering
KEY POINT
meperidine and/or inducing pharmaco- families must be educated about the
A The AAN’s
logic paralysis, eg, with vecuronium. If need to allow for an adequate period of
guidelines for
concussion using paralysis, sedation is mandatory. recuperation. Potentially the encounter
management Other important clinical issues are with health care providers is an oppor-
include nutrition, stress ulcer prophylaxis, and tunity to facilitate greater awareness of
recommended deep vein thrombosis prevention with primary prevention of TBI in the pa-
periods of sequential compression devices and tient and family members. Typically this
recovery and anticoagulation using low-molecular- entails the effective use of some task-
are a practical weight heparin or low-dose unfraction- specific personal protective equipment,
clinical guide. ated heparin, with or without mechanical such as a helmet.
compression devices such as graduated The AAN’s guidelines for concussion
compression stockings and sequential management include recommended pe-
compression devices.33,47 If intracerebral riods of recovery and are a practical
blood is present, it is recommended that clinical guide.25 Other guidelines that
only sequential compression devices be can also be used are the Cantu Grading
used until the risk of further bleeding system, the Colorado Medical Society
decreases, at which time anticoagula- Guidelines, and the Zurich Consensus
tion may be started.33,47 To ensure ade- Guidelines, which have been developed
quate nutrition, a nasogastric or orogas- for sports-related TBI but are widely
tric tube should be placed. Since most applied and meaningful for the manage-
patients with TBI have some cerebral ment of both civilian and military pa-
edema, hypo-osmotic feeds should not tients with head injury.48–54
be used to minimize free water, which
could worsen cerebral edema. Again, the
injured brain is hypermetabolic so pa- CONCLUSION
tients with TBI typically require 140% of TBI is not a new disorder. It has existed
their basal metabolic caloric needs.33 as long as man has existed. However,
While in the acute period, all patients recent insights are improving the un-
with TBI should be examined neurologi- derstanding of the pathophysiology of
cally on a regular basis—at least every this condition as well as directing new
hour for the first 24 hours, which is a efforts to improve diagnosis and treat-
hyperacute period, and then less often ment. Although a specific brain rescue
as clinically indicated. For patients with drug remains elusive, evidenced-based
intracranial lesions, continuous ICP and clinical practice guidelines for treatment
CPP measurements should be made. and return to play/work/duty provide a
36 In general, the period of time after injury rational approach to managing these pa-
during which cerebral edema is greatest tients and improving outcome.
is from 48 to 96 hours. Thereafter, edema
should begin to resolve, and the patient
should improve clinically. DISCLAIMER
The opinions expressed herein belong
RETURN TO PLAY OR WORK solely to the authors. They are not, nor
The decision to return to play or work is should they be interpreted as, represen-
difficult as many patients do not recog- tative of or endorsed by the Uniformed
nize the need for convalescence, espe- Services University of the Health Sci-
cially in the case of mTBI. This lack of ences, the Defense Advanced Research
insight may be attributed to the rela- Projects Agency, the Defense and Vet-
tively mild symptoms experienced by erans Brain Injury Center, the United
the patient or be a direct result of the States Army, or the Department of
brain injury itself. Patients and their Defense.
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40
KEY POINT
SPORTS CONCUSSION A Between 1.6

and 3.8 million
Jeffrey S. Kutcher, Christopher C. Giza, Anthony G. Alessi sporting
concussions
occur each year
in the United
ABSTRACT States.
Concussion is an injury to the brain occurring as the result of biomechanical forces,
generally characterized by the rapid onset of a constellation of symptoms or cognitive
impairment, which is typically self-limited and resolves spontaneously. Concussion as
the result of playing sports is particularly common, estimated to occur up to 3.8 million
times each year in the United States. Although most concussions can be considered
benign, the symptoms are often severe enough to interfere with daily function.
A small percentage of concussions can be more serious, resulting in a prolonged
symptom course, significant morbidity, or even death. The management of concussion
in the athlete presents a unique set of challenges for the clinician, requiring not
only a detailed neurologic history and examination, but also careful consideration
of an athlete’s risk of further injury and possible long-term sequelae.
INTRODUCTION frequent media reports as well as be-

Because of the violent nature of many ginning governmental attempts to regu-
popular sports, concussion has long late certain aspects of sports concussion
been considered to be ‘‘part of the management have resulted in an in-
game.’’ Even in many of the so-called creasing public awareness of the pos-
noncontact sports, such as soccer, sible serious manifestations of concus-
baseball, and field hockey, the veloc- sion. Table 3-1 presents the states that
ities of the athletes and the presence have enacted or proposed legislation
of multiple ballistic objects or fixed specific to sports concussion within the
impediments make concussion a com- past 2 years. An increasing interest from
mon injury on the playing field. The the scientific community can be demon-
Centers for Disease Control and Pre- strated as well by performing a PubMed
vention estimate that between 1.6 and search that crosses the terms sports
and concussion. The results of this
41
3.8 million sporting concussions occur
each year in the United States alone.1 search, stratified by decade, are shown
In the high school population, con- in Figure 3-1. The heightened aware-
cussion is estimated to account for al- ness in public, government, and scien-
most 9% of all athletic injuries.2 tific sectors highlights the need for neu-
Despite their long-standing high prev- rologists to increase their involvement
alence, sports concussions have only in sports concussion clinical care, edu-
recently garnered significant public at- cation, and research. At the same, the
tention. Over the past few months, both need to include sports-specific issues
Relationship Disclosure: Drs Kutcher and Alessi have nothing to disclose. Dr Giza has received or plans to
receive personal compensation for speaking engagements at academic centers and hospitals and for
medicolegal consulting. Dr Giza is a recipient of the Thrasher Research Foundation grant.
Unlabeled Use of Products/Investigational Use Disclosure: Drs Kutcher and Alessi have nothing to disclose.
Dr Giza discusses the use of advanced neuroimaging and computerized neuropsychological testing but does
not mention them by proprietary name.
" SPORTS CONCUSSION
KEY POINT
classified into three ‘‘grades’’ based on
A Loss of TABLE 3-1 States or Other
Jurisdictions the duration of symptoms and the
consciousness
may be a With Sports Concussion– presence of LOC.3 This document also
manifestation Specific Legislation made recommendations regarding the
of concussion Enacted or in Process management of concussed athletes by
but is not suggesting return-to-play timing based
required for " Legislation Passed on this grading system. Clinical prac-
diagnosis. Maine tice has shown, however, that predict-
Oregon
ing the course of any one concussion
based on its initial presentation is ex-
Texas tremely difficult.6–8 More recent con-
Washington sensus efforts have concluded that little
" Legislation Pending clinical value can be ascribed to classi-
fying concussion in the acute setting.9
California
Current clinical trends favor treating
New Mexico each concussion individually, further
" Legislation Introduced highlighting the value of a clinician’s
experience in managing sports concus-
Connecticut
sion over the availability of a written
Florida management protocol. Understanding
Howard County, Maryland this, the AAN has formed a multidisci-
plinary panel that is currently working
Massachusetts
to produce a new evidence-based
Missouri guideline on sports concussion.
New Hampshire
DEFINING CONCUSSION
North Carolina
Concussion is a biomechanically in-
Oklahoma duced brain injury resulting in neuro-
Pennsylvania logic dysfunction.3 It is most commonly
Rhode Island characterized by the rapid onset of a
constellation of symptoms or cognitive
Suffolk County, New York
impairment that is self-limited and re-
Virginia solves spontaneously.
LOC may be a manifestation of con-
cussion but is not required for diagnosis.
42 Concussions have been defined as in-
in traditional neurologic training is juries that do not produce an abnormality
brought to the fore. on standard structural neuroimaging.9
With that in mind, it should be noted
TRENDS that a concussion can also be present in
In order to improve sports concussion the setting of other, more structural in-
management and outcomes, several juries such as fracture or hemorrhage.
attempts have been made to establish
a clinically relevant classification sys- CONCUSSION IN THE ATHLETE
tem for concussion.3–5 For several reasons, the neurologist
Early efforts focused on classifying needs to be aware that providing con-
the injury based on the presence or cussion care for athletes presents a
absence of a loss of consciousness unique set of challenges. In contrast to
(LOC). In 1997, the AAN published the concussions seen in the general popu-
recommendation that concussions be lation, the insulting force is not always
FIGURE 3-1 Number of publications returned for the
PubMed search crossing the terms sports and
concussion, by decade.
obvious. In contact sports, such as foot- illustrates this point. When a football
ball, ice hockey, or wrestling, the athlete player reports a headache after a full-
may experience dozens of impacts dur- contact practice, for example, it may
ing the course of a game or practice. be the result of a concussion, an exer-
There may not always be one obvious tional migraine headache, or the effect
extraordinary hit, but several routine of an ill-fitting helmet. In the general
hits, and it may be difficult at times to population, the impacts are unintended
clearly diagnose a concussion. Case 3-1 and, therefore, much more obvious, such
Case 3-1
A 21-year-old college football player sustained a blow to the left side of
the neck and body during a game. He developed paresthesias in the
left arm and leg with no objective deficits on examination. The symptoms
resolved completely over several hours. Imaging studies of the neck were
normal. The following week, he suffered a head injury on the opening
kickoff. He then reported a severe headache, left lower extremity
paresthesias, and visual changes. Paresthesias and visual symptoms
43
resolved in 3 hours, but the headache persisted for 2 days. Neurologic
examination, MRI of the brain, and CT angiogram of the head and neck
were normal.
Comment. Further investigation reveals a previous event in high school
during which the athlete lost part of his visual field followed by a
severe throbbing headache. A family history of migraine headache is
also confirmed. With these additional pieces of history, it becomes
more likely that the traumatic events described triggered a migraine
headache. Not all reports of headache in the setting of contact sports
are the direct result of concussion. Migraine headache presents with
many of the typical symptoms of concussion, putting emphasis on the
importance of careful neurologic history. Previous headache and family
history can help establish the diagnosis, but the most telling aspect may be
the pattern of the symptom timing that emerges after multiple events.
" SPORTS CONCUSSION
KEY POINTS
as a motor vehicle accident or a slip Clinical Presentation
A Concussion
and fall. In the acute setting, the signs and
symptoms and
deficits are Another difference is the presence of symptoms of concussion typically begin
often more third-party influences or the motivation immediately or within a few minutes
notable when of a patient to be less than forthright of the impact in question. They may be
the patient is about the history. In cases of concus- maximal at onset or worsen over the
trying to sion in the general population, one can minutes to hours following the injury.
perform at a expect, for the most part, that patients In some cases, symptom onset may be
high level, are providing an accurate history to the delayed completely for up to several
either physically best of their ability, or if they are not, hours, especially when the athlete has
or cognitively. they are much more likely to be exag- continued with physical exertion after
A The return-to- gerating rather than minimizing their the impact or if a second impact oc-
play decision symptoms. Conversely, athletes are more curs.10 Because of the possibility of a
presents a likely to possess the unique motivation delay in symptom onset or symptom
unique array of to hide or minimize their symptoms in worsening, it is extremely difficult to
challenges that order to return to participation sooner. clearly define a minimum duration of
may be foreign This same motivation often exists in the symptoms required to make a diagnosis
to the patient’s family, coach, and teammates, of concussion. As noted earlier, LOC
neurologist.
making the history extremely difficult is not a requirement for diagnosis. The
A The signs and to ascertain. common acute signs of concussion
symptoms of Neurologists should also be aware include headache, disorientation, con-
concussion that many athletes are looking to return fusion, amnesia, dizziness, and incoor-
typically begin to a level of physical activity and per- dination. A more complete list of the
immediately or formance that would be considered ex- acute signs and symptoms is presented
within a few in Table 3-2. Continued symptoms are
traordinary in the general population.
minutes of likely caused by the neuronal metabolic
Concussion symptoms and deficits are
the impact in
often more notable when the patient is mismatch described in the article ‘‘Mild
question.
trying to perform at a high level, either Traumatic Brain Injury Update.’’ This
They may be
maximal at physically or cognitively. Exertion in relationship may explain why contin-
onset or either realm may also be a risk factor ued participation and physical exertion
worsen over for symptom exacerbation and a pro- are sometimes felt to result in a delayed
minutes to longed injury course. presentation of symptoms or symptom
hours. Perhaps the most important differ- worsening. It is widely held that in up to
ence, however, lies in the nature of the 90% of concussions, signs and symp-
return-to-play decision. In the general toms are short-lived, resolving com-
44 patient population, it is typically the pletely between 7 and 10 days.8
case that the insulting biomechanical
force is the result of an accident that Acute Assessment and
would not be expected to recur in a Management
short period of time. In sports, and in When a concussion is suspected, the
contact sports particularly, the risk of first consideration should always be for
recurrence is significantly higher. The the athlete’s safety. A careful assessment
clinician must become familiar with the of airway, breathing, and circulation
nature of the patient’s chosen sport (ABCs) and the possibility of cervical
and the possible implications of a re- spine injury should be closely followed
current concussion, such as a wors- by estimating the need for emergency
ening symptom complex, prolonged medical services. It is essential that ath-
symptom course, postconcussion syn- letes who are suspected to have had
drome, or even the possibility of a dev- a concussion be removed from the con-
astating, life-threatening injury. test or practice until a certified health
KEY POINT
mechanism of injury as well as the
TABLE 3-2 Common Signs A Any athlete with
and Symptoms presenting signs and symptoms. The
a suspected
of Concussion athlete should not be left alone for concussion
the subsequent 3 to 4 hours in case of should be
" Signs clinical worsening. A significant change removed from
Amnesia prior to or after
in mental status, especially level of con- the contest or
injury sciousness, within this time frame may practice until
be an indication of a developing intra- evaluated by a
Behavior or personality certified
change
cranial hematoma. In these cases, emer-
gent evaluation with CT is required, medical
Confabulation along with the appropriate neurosurgi- caregiver.
Delayed verbal and motor cal consultation.
responses The hallmark of concussion diagnosis
Disequilibrium lies in a thorough history and physical
examination. The history should in-
Disorientation
clude a detailed account of the injury,
Emotional lability the symptom and deficit course, and
Loss of consciousness the athlete’s physical and cognitive
Slurred/incoherent speech
exertion levels between impact and pre-
sentation. The physical examination is
Vacant stare critical, with many of the findings in
" Symptoms concussion being subtle and dynamic.
Blurry vision/double vision The mental status portion of the physi-
cal examination is particularly impor-
Confusion
tant, with deficits in attention span and
Dizziness memory being most pertinent. Distur-
Excessive drowsiness, sleep bances in mood and affect are also
difficulty common. These potentially subtle men-
Feeling hazy, foggy, or
tal status examination findings speak to
groggy the value of the clinician having at least
some preinjury knowledge of the con-
Headache
cussed individual. A team physician, for
Inability to focus, concentrate this reason, is in a unique position to
Nausea and/or vomiting manage the concussed athlete. More
objective physical findings may also in-
Not feeling right
clude incoordination, nystagmus, or 45
Photophobia/phonophobia even subtle weakness demonstrated by
a pronator drift. It can be very difficult to
attribute such findings to a concussion
alone, versus a more malignant injury,
care professional or physician knowl- such as an intracranial hematoma. The
edgeable in concussion evaluates them. timing of these findings in relation to the
If a concussion is diagnosed, the most injury and how the findings themselves
prudent management is to remove the may be changing over time are both
athlete from participation for the re- extremely important concepts to keep
mainder of that day, with further eval- in mind. Any worsening of the clinical
uation to be performed on subsequent presentation should be considered care-
days prior to making a return-to-play fully and in the first few hours following
decision. At the time of the injury, it is the impact should be considered an
important to document the time and emergency until proven otherwise.
" SPORTS CONCUSSION
In the acute setting, or even on the liberally, and avoid any exacerbating
sidelines, several assessment tools can activities, which may include television,
be used to help document the clinical video games, computer use, or texting.
presentation or, in some cases, aid in the
diagnosis. The most recently published Return-to-Play Decisions
tool, the Sport Concussion Assessment As previously noted, it is important for
Tool 2 (SCAT-2), is a product of the the neurologist to understand the com-
consensus statement from the 3rd In- plex nature of the return-to-play deci-
ternational Conference on Concussion sion. The clinician is essentially deciding
in Sport held in Zurich, Switzerland, in that it is reasonable for the patient to
the fall of 2008.9 The SCAT-2 includes resume the same high concussion risk
aspects that track concussion symp- activity that caused the injury in the first
toms, cognitive performance, and bal- place. This ‘‘return-to-risk’’ decision is
ance. Several other assessment tools complicated by several factors, includ-
exist, with none having clear superiority ing the athlete’s desire to compete and,
or a data-driven evaluation that provides therefore, misrepresent symptoms. Ad-
a quantitative estimation of its clinical ditionally, one needs to consider the in-
value.11 Whatever assessment tool is creased risk of worsening or additional
used, it is more valuable to have a injury if the athlete returns too quickly.
preinjury baseline score for the athlete One study showed that collegiate foot-
for reasons of comparison. These tools ball players who had suffered one con-
should be used with care, noting that cussion were 3.4 times more likely than
environmental factors can act as sig- uninjured teammates to sustain a sub-
nificant distractions and affect perfor- sequent concussion during the same
mance. It is also important that no one season.10 This same study showed that
tool be used in isolation, but rather prolonged symptom recovery may be
as part of a comprehensive concussion associated with a history of prior con-
management program, which is discussion, although eventual full recovery
cussed in greater detail later in this to baseline is expected.
article. The underlying management princi-
Once a concussion is diagnosed, at- ple is not to allow a concussed athlete to
tention should turn to symptom man- return to participation until it is reason-
agement. It is typically obvious to the ably certain that the physiologic effects
clinician that environmental variables, of the concussion have abated. This
such as bright lights, loud noises, and process is anchored by a rigorous, artful,
46 movement, are all exacerbating factors. and, if necessary, serial history to elu-
In this way, the typical concussed pa- cidate the athlete’s symptom burden.
tient is very similar to a person suf- Perhaps no area of concussion manage-
fering from migraine headache. The ment is better suited to the particular
concussed patient should be instructed skill set of the neurologist.
to avoid physical and cognitive exertion If the athlete is felt to be symptom
as much as possible. Acetaminophen free without the use of medications, and
can be used immediately following the the physical examination is completely
injury for headache control. A few hours normal, the neurologist should inquire
after the injury, when the possibility as to the presence of any preinjury
of an undiagnosed intracranial hemor- objective data that may have been col-
rhage has been minimized, the use of lected as part of a comprehensive con-
anti-inflammatory medications is rea- cussion management program. Athletic
sonable. The patient should be in- programs at all levels are increasingly
structed to maintain oral intake, sleep utilizing differing modalities, including
computerized neurocognitive testing, simple cardiovascular challenge, such
scored balance systems, and reaction as 30 minutes on a stationary bike. The
time mechanisms, in order to better es- level of exertion should be enough to
timate an athlete’s neurologic baseline induce an obvious increase in meta-
preconcussion. These tests are then bolic demand. If the concussive symp-
repeated, typically after the patient is toms recur, the trial should be stopped
symptom free, for comparison. The use and the athlete should not attempt
of these objective tests is covered in another trial until the next day, assum-
greater detail later in this article. ing that he or she is symptom free
If an athlete’s performance on ob- again at rest. If that challenge is toler-
jective testing is similar to that seen in ated, the athlete can proceed to increas-
the preinjury setting and the athlete ing levels of exertion as presented in
is completely symptom free and has a Table 3-3.
normal neurologic examination, the When considering the current in-
moratorium on physical activity can be jury alone, the return-to-play decision
lifted. Physical activity should be rein- requires close and careful monitoring
troduced, however, in a very careful of signs and symptoms as the athlete
and graded manner. The purpose of this progresses along this paradigm of
approach is to increase the demand on graduated exertion, but a clear path
the brain in a stepwise fashion, giving to participation exists. When the injury
the clinician the opportunity to deter- is placed in the larger context of the
mine whether the concussion’s physio- athlete’s overall sports and concussion
logic mechanism is still present, without experience, as well as the complete
exposing the brain to unnecessary risk. medical history, additional factors may
This process typically begins with a still complicate the decision.
TABLE 3-3 Graduated Return-to-Play Protocol
Rehabilitation Functional Exercise at Each Objective of

Stage Stage of Rehabilitation Each Stage
(1) No activity Complete physical and Recovery

cognitive rest
(2) Light aerobic exercise Walking, swimming, Increase heart rate
47
stationary bike
(3) Sport-specific exercise Running drills in soccer, Add movement
skating drills in hockey, etc
(4) Noncontact drills More complex training Coordination and
drills, may start cognitive load
resistance training
(5) Full-contact practice With medical clearance, Restore confidence
participate in normal and assess functional
training activities skills by coaching staff
(6) Return to play Normal game play
Adapted with permission from McCrory P, Meeuwisse W, Johnston K, et al. Consensus statement on Concussion in
Sport 3rd International Conference on Concussion in Sport held in Zurich, November 2008. Clin J Sport Med
2009;19(3):185–200.
" SPORTS CONCUSSION
The most common complicating factor sider adding further diagnostic evalua-
is the presence of previous concussive tion with a formal neuropsychological
injuries. No accepted absolute number of evaluation, and possibly consider spe-
concussions that any one individual must cialized neuroimaging, such as diffusion-
experience before retiring from sports can tensor imaging (DTI). At some point,
be set. Each concussion is unique, and the symptom burden may be signifi-
therefore each concussion history should cant enough to recommend that the
be carefully fleshed out and judged on its athlete retire from sports, thus hoping to
own. For each previous concussion, the avoid the next concussion and minimize
clinician should attempt to ascertain the the potential for chronic sequelae.
details of the injury, including the mech- Other cases can be complicated by
anism, degree of force, and symptom additional intracranial pathology. Intra-
duration. It is also very important to un- cranial hemorrhage and skull fracture as
derstand any subtle changes in cognition the result of head injury add a layer of
or personality that may be occurring over complexity to the decision-making pro-
time. It is extremely difficult to appreciate cess. Given the tremendous variability
these types of changes during the typical in the size and possible locations of
clinic visit; thus the clinician should be sure these structural lesions, no single well-
to ask about academic or job performance established guideline to follow exists.
and the presence of social difficulties. Each case should be considered indi-
In some cases, it is clear that with vidually. The governing principle is to
each subsequent concussion, the ath- best estimate the increased risk that any
lete is experiencing a greater symptom additional variable adds. Case 3-3 dis-
burden for a longer period of time. A cusses how the presence of a previous
typical example is presented in Case 3-2. head injury resulting in a small hemor-
In these situations, it is important to rhage might affect the return-to-play
approach the return-to-play decision decision. If a hemorrhage is discovered
more conservatively, perhaps elongate as part of the evaluation of a mild trau-
the period of time that the athlete matic brain injury (mTBI), it is worth in-
spends at each exertional level of the vestigating the possible presence of a
graded exercise paradigm, strongly con- structural lesion, such as an arteriovenous
48 Case 3-2
A 23-year-old hockey player presented after his fourth career concussion. Each of the first three
concussions was related to hockey, included symptoms that resolved after 7 to 14 days, and did
not involve LOC. The fourth and most recent event resulted in chronic and persistent dizziness,
headache, and insomnia. Neurologic examination and imaging studies of the brain remained
normal. Symptoms gradually resolved, and neuropsychometric scores returned to baseline over a
period of 6 months. The patient never resumed his hockey career.
Comment. This case emphasizes one of the possible effects of multiple concussions, the prolonged
symptom course. In these cases, it is essential to understand any additional factors that may be adding to
the symptom burden. It is certainly possible that preexisting pathologies, including mood and sleep
disorders, might also be at play. Alternatively, these ongoing problems may be the direct result of the
injury itself. In either case, each symptom should be addressed and treated individually while alternative
explanations are sought. Sleep difficulties, including insomnia and excessive fatigue, are especially
common in individuals with a history of concussion. Adequate amounts of sleep are a crucial element to
concussion recovery. Insomnia must be addressed as part of the treatment plan and may require
medications, such as tricyclic antidepressants, which can address both the headache and sleep issues.
Case 3-3
A 15-year-old boy suffered a head injury as the result of a motorcycle accident, causing a small
bleed in the left caudate head that is noted with CT. Headache and ataxia persisted for 2 weeks.
Two years later, he suffered a concussion during a basketball game. Symptoms included
anterograde amnesia lasting seconds, ataxia lasting minutes, and a headache that persisted for 2
weeks. Neuroimaging was negative, and he was able to resume running and lifting weights
without symptoms. Should this athlete return to contact sports and, if so, when?
Comment. The question of when it is safe for an athlete to return to contact sports after
neurologic injury is always a challenge. No specific formula has been determined, and many
variables must be considered. In this case, it is worth noting that the second head injury
produced a relatively typical concussion with normal neuroimaging. Given the remote history of
the small caudate bleed, one can assume that this patient does have some increased risk from
subsequent injury. However, considering that this bleed may not have been unexpected given the
circumstances (motorcycle accident), no preexisting underlying structural abnormality is
present, and the second injury did not cause hemorrhage, the actual increased risk of
complicating a subsequent concussion with repeat hemorrhage is likely quite low. It is also
important to note the lack of a skull fracture in the initial injury, which would have
added another layer of increased, although difficult to quantify, risk.
Some consideration should also be given to the fact that this patient has had two concussions.
Given the appropriate time to heal and a careful return to exertion with a graded paradigm,
however, this patient may not have any long-term sequelae or suffer from a more complicated
course if he were to sustain a third concussion. Estimating this risk is extremely difficult, and
particular attention should be paid to family history variables, such as intracerebral hemorrhage,
frequent concussions, and dementia. Close attention should also be paid to the patient’s baseline
cognition and personality. Future return-to-play or retirement decisions could be aided by the
presence of objective baseline data, which should only be obtained once the patient is
asymptomatic from the current injury.
malformation, that may have been the DTI, fMRI, MR spectroscopy (MRS),
origin of the hemorrhage. and PET.
Each of these modalities has poten-
NEUROIMAGING tial advantages and disadvantages for
mTBIs that result in concussion typi- use in concussion. Both MRS and PET
cally do not cause abnormalities on provide images that demonstrate func-
traditional neuroimaging studies—CT tional cerebral metabolism and could 49
and standard MRI. While some struc- potentially be used to delineate the
tural injury may occur in the setting of physiologic changes seen in concus-
concussion, it is beyond the sensitivity sion, while fMRI provides real-time
of these modalities.12 As such, most con- feedback on cerebral metabolism dur-
cussions do not lead to neuroimaging ing specific cognitive or motor tasks.
studies. Given that concussion manage- DTI provides a modality for measuring
ment is still based primarily on clinical white matter integrity and connectiv-
measures, such as symptom checklists, ity. Each of these technologies requires
physical examination, and computerized relatively long collection times, and
neurocognitive testing, tremendous inter- other than PET, they all require post-
est exists in investigating more advanced imaging data processing. PET involves
neuroimaging techniques that may bet- the injection of a radioisotope and the
ter quantify the functional disturbances need for not only a PET scanner but also
of the concussed brain. These include a cyclotron to produce radioisotopes.12
" SPORTS CONCUSSION
While none of these modalities has a demiologic phenomenon driven by the

widespread clinical role in the current low prevalence of a particular genetic
management of sports concussion, con- trait, such as a mutation in a calcium
tinued investigation into their sensitivity channel gene, and the age structure
and specificity for concussion, their of the athletic population. Given that,
ability to estimate injury severity, and as of this writing, fewer than 30 cases
their role in documenting long-term of suspected SIS or malignant cerebral
sequelae are important aspects of im- edema have been described, it may
proving sports concussion care. not be surprising that all of the cases
have been described in the age group
SECOND-IMPACT SYNDROME that has the highest head trauma
Second-impact syndrome (SIS) is a rare exposure risk.
form of re-injury that occurs prior to the
complete resolution of a previous con-
cussion.13 SIS diagnoses have been CHRONIC CUMULATIVE EFFECTS
described in a series of case reports in- It is widely accepted that the symptom-
volving a second, sometimes minor, atic effects of up to 90% of concussions
head trauma that leads to a devastating are short-lived, lasting only 7 to 10 days.9
injury or death. In such cases, diffuse This viewpoint puts sports concussion
cerebrovascular dysregulation is thought in the light of being a transient phe-
to lead to massive cerebral edema and nomenon with little or no long-lasting
subsequent herniation. Some disagree- effects. There is increasing concern,
ment exists, however, about the preva- however, that this may not be the case.
lence of this diagnosis and the accuracy On the extreme side of the sports con-
of the proposed mechanism. Cases of cussion spectrum, professional boxers
delayed-onset diffuse cerebral edema are well known to have a risk of de-
following relatively minor head traumas, veloping permanent alterations in brain
without a previously documented injury, function.18 A growing body of literature
have also been described.14,15 An attempt is now raising concern, however, that
to investigate the similarities among 17 cumulative effects may also be occurring
of the published case reports of sug- in athletes who sustain more ‘‘routine’’
gested SIS found that none fulfilled all injuries as a function of playing a contact
four diagnostic criteria that were pro- sport such as football or ice hockey.19,20
posed by the author and only five could Possible long-term effects include chronic
be classified as ‘‘probable’’ SIS.16 It is motor and neuropsychological deficits.21,22
50 certainly possible that all of these cases, Recently, de Beaumont and colleagues
regardless of their terminology, have a found that former ice hockey and football
common pathophysiology. Recently, a players who had a remote history of con-
mutation in the CACNA1A calcium chan- cussion, up to 30 years prior to testing,
nel subunit gene that is associated with showed cognitive and motor deficits when
familial hemiplegic migraine was linked compared to those without a concussion
to cases of fatal malignant brain edema.17 history.22 Conversely, a separate study found
Interestingly, almost all of the sus- no such association in college athletes.23
pected cases of SIS have occurred in A separate concern is the possibility
athletes younger than age 20, with most that repetitive concussion may be a risk
being 18 years old or younger. This may factor for, or lead directly to, a dementing
implicate an, as yet undefined, unique illness. Termed chronic traumatic brain
quality of the still-developing brain that injury, dementia pugilistica, or chronic
significantly determines the risk of these traumatic encephalopathy (CTE), this re-
types of injuries. It may also be an epi- lationship has been classically described
in retired boxers.24,25 More recent work mind. As much as possible, the base-
has shed light on the possibility that a line and postinjury testing environments
similar relationship may be seen in re- should be free of distraction and similar
tired football players. Guskiewicz and to each other. Finally, any additional physi-
colleagues described retired profes- ologic variables, such as sleep depriva-
sional football players with a history of tion, medication use, or illness, should
three or more concussions who were be noted. Whatever modality is used,
5 times more likely to have mild cog- the clinician should make an informed
nitive impairment.26 Speaking more di- judgment as to the value of the data that
rectly to possible tau-related dementing are being presented.
pathology, McKee and colleagues re- As difficult as this process may be,
viewed the autopsy findings of three especially for a large team or athletic
professional athletes as well as the pub- program, the data can be invaluable when
lished reports of 48 cases of suspected making return-to-play decisions. We sug-
CTE and concluded that CTE is a ‘‘neu- gest that the sports medicine staff respon-
ropathologically distinct. . .tauopathy with sible for performing these tests become
a clear environmental etiology.’’27 very familiar with the particular nuances of
their chosen modality, program, or pro-
tocol. Sports concussion care providers
BASELINE TESTING should become familiar with the nature
The management of sports concussions of the data that are being collected, how
remains highly dependent on clinical they are interpreted, and how they may
information and is particularly depen- be affected by the influences mentioned
dent on subjective symptom reporting. above. Several options are available for
Any objective data that can be used to measuring cognitive performance, both
help diagnose concussion and, more computerized and more traditional man-
importantly, manage it appropriately, ual tests. We do not emphasize the validity
can be very helpful. Objectively measur- of one over the other or recommend one
ing brain function can be an extremely particular program. Rather, we urge their
difficult task, given the wide range of careful and prudent use.
what one would consider to be normal
functional output. Consequently, a large
portion of concussion management is PEDIATRIC CONSIDERATIONS
not about detecting a truly abnormal Recognizing that children and adoles-
finding but being able to quantify the cents are not just little adults, recent
change that is seen in the concussed consensus guidelines have indicated a 51
athlete’s functional abilities. need for pediatric-specific modifications
Baseline data typically come from to adult concussion management plans.9
three domains: cognitive, balance, and Although no evidence-based pediatric
motor reaction time. Although poten- guidelines are yet available, an increasing
tially useful, baseline data can be difficult number of studies indicate that age ef-
to obtain and use correctly. The first fects are relevant in determining the ap-
significant hurdle is in obtaining baseline propriate postconcussion management
data that are a true reflection of the plan. Field and colleagues compared
athlete’s ability. Several factors, including symptom checklists and neuropsycho-
motivation, environmental conditions, logical testing between concussed high
and poor effort can produce abnormally school and collegiate athletes and found
low baseline scores in any domain. Prac- those in high school demonstrated im-
tice effects and expected test-retest dif- pairments of learning and memory up
ferences are other variables to keep in to 7 days postinjury, while collegiate
" SPORTS CONCUSSION
athletes recovered to control levels by genesis of cognitive deficits after con-

postinjury day 3.28 Prolonged (6-day to 7- cussive brain injury. Not all experimen-
day) neurocognitive recovery in high tal data point to worse pathophysiology
school athletes after concussion has been in the young brain, however. Recovery
reported in at least two other studies, from delayed cerebral glucose hypome-
suggesting that return-to-play guide- tabolism appears to occur more rapidly
lines may need to be more conservative in immature rats than in adults.37
in younger concussed athletes.29,30
Furthermore, in the Field and col- CONCLUSION
leagues study, neurocognitive impair- Concussion is perhaps the single most
ments in the concussed high school common form of acquired brain injury,
athletes were still demonstrable at time and the role for neurologists in the proper
points at which their clinical symptom assessment and management of this
checklists had returned to baseline lev- entity is likely to grow. In distinction to
els.28 In a related finding, high school prior perceptions of concussions as
athletes with rapid resolution of postcon- benign events, and a mentality, particu-
cussive symptoms (less than 15 minutes) larly in sports, to ‘‘tough it out,’’ more
were reported to develop measurable recent evidence suggests that even mTBI
cognitive impairment and worsening of can induce a neurometabolic cascade of
symptoms several days after these seem- dysfunction that may predispose the
ingly mild concussions.31 These data imply brain to ongoing impairment and poten-
that measurable deficits in learning and tial for recurrent or cumulative damage.
memory may occur in younger athletes in Proper management of sports concus-
the absence of significant symptomatology sions depends on identification of rele-
or in a delayed fashion after an apparent vant signs and symptoms, removal of the
rapid resolution of acute symptoms. athlete from potential repeat injury, and
The underlying reasons for these serial assessment of neurologic function.
developmental distinctions are not en- In general, individuals with uncompli-
tirely clear. Age-dependent differences cated concussions are able to recover
seen clinically may result from physio- fully. However, even after the patient
logic vulnerabilities, genetic predispo- becomes asymptomatic, a prudent ap-
sition, parental perceptions,32 or even proach is to recommend a graded return
differences in neuropsychological test to activity, particularly when contact sports
sensitivity due to rapidly changing de- are involved. Increasing evidence demon-
velopmental baselines.33 strates that recurrent concussive (or per-
52 Using animal models, data following haps even subconcussive) injuries may
experimental concussive TBI in the im- lead to chronic neurocognitive impairment
mature brain have shown impairment of or even early onset of dementia, factors
neuroplasticity and delayed development that should be considered when evaluating
of cognitive deficits.34 Other animal data and informing the multiply concussed
indicate that unmyelinated fibers may athlete of the risk of returning to play.
be more vulnerable to biomechanical Finally, increasing animal and human data
forces.35 Myelination, particularly in the suggest that the developing brain’s reac-
frontal lobes, is incomplete in humans tion to concussive injury is distinct from
until the early adult years, and clinical the mature brain, and that age-specific
studies of white matter integrity using clinical guidelines for concussion manage-
DTI have shown abnormalities after ment be developed, with perhaps a more
mTBI in adolescents.36 These data sup- conservative approach to assessment
port a role for axonal dysfunction in the and recovery.
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19. Collins MW, Grindel SH, Lovell MR, et al. Relationship between concussion and
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23. Bruce JM, Echemendia RJ. History of multiple self-reported concussions is not
associated with reduced cognitive abilities. Neurosurgery 2009;64(1):100–106.
24. Martland H. Punch drunk. JAMA 1928;91(15):1103–1107.
25. Critchley M. Medical aspects of boxing, particularly from a neurological standpoint.

Br Med J 1957;1(5015):357–362.
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30. McClincy MP, Lovell MR, Pardini J, et al. Recovery from sports concussion in high
school and collegiate athletes. Brain Inj 2006;20(1):33–39.
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35. Reeves TM, Phillips LL, Povlishock JT. Myelinated and unmyelinated axons of the
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36. Wozniak JR, Krach L, Ward E, et al. Neurocognitive and neuroimaging correlates of
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KEY POINT
POSTTRAUMATIC A No defining
clinical features
HEADACHE of posttraumatic
headaches
(PTHAs), other
Jay C. Erickson, Edward T. Neely, Brett J. Theeler than onset
after trauma,
distinctly
ABSTRACT separate them
from other
Headache is a common symptom after traumatic head injury and is a frequent feature headache
of the postconcussive syndrome. A variety of headache subtypes can be precipitated disorders.
by head trauma, although posttraumatic headaches most often resemble migraine
or tension-type headache. A lack of clinical trials limits evidence-based treatment
recommendations for both acute and chronic posttraumatic headaches. However,
numerous pharmacologic and nonpharmacologic interventions can be used to suc-
cessfully manage posttraumatic headaches. This article reviews the classification,
epidemiology, prognosis, and pathophysiology of headaches after head trauma and
provides a practical clinical approach for evaluating and treating patients with post-
traumatic headaches.
INTRODUCTION headaches are not caused by an identi-

Headache is the most common symptom fiable underlying illness, injury, or expo-
following concussion or mild traumatic sure. In contrast, secondary headaches
brain injury (TBI). This condition fre- are attributable to a specific inciting event,
quently develops as part of the acute post- exposure, or condition, such as traumatic,
traumatic syndrome and may continue infectious, neoplastic, inflammatory, sys-
to occur for months or years after the temic, or toxic processes. The most com-
injury. Posttraumatic headaches (PTHAs) mon primary headache disorders are
contribute to disability, lost productivity, tension-type headache and migraine
health care costs, and decreased quality headache. PTHAs are classified as sec-
of life among patients with TBI. Under- ondary headaches because they are
standing proper headache diagnosis caused by head, face, or neck trauma
and management are therefore essen- and are among the most common types 55
tial skills for clinicians who care for pa- of secondary headache disorders.
tients with TBI. This article highlights No defining clinical features of
the classification, epidemiology, clini- PTHAs, other than onset after trauma,
cal features, evaluation, and diagnosis of distinctly separate them from other
PTHAs and provides a framework for headache disorders.2,3 According to the
formulating an effective treatment plan. International Classification of Headache
Disorders, 2nd edition (ICHD-2), head-
CLASSIFICATION aches attributed to head or neck trauma
Headache disorders are classified as include seven different secondary head-
either primary or secondary.1 Primary ache syndromes: (1) acute PTHA, (2)
Relationship Disclosure: Dr Erickson has received an investigator-initiated research grant from Merck & Co., Inc.,
and a Traumatic Brain Injury Research Program grant from the US Department of Defense. Drs Neely and Theeler
have nothing to disclose.
Unlabeled Use of Products/Investigational Use Disclosure: The authors discuss medications and other treatments
that are not US Food and Drug Administration approved for posttraumatic headache.
" POSTTRAUMATIC HEADACHE
KEY POINTS
chronic PTHA, (3) acute headache at- either a migraine or as both a migraine
A Acute PTHAs
tributed to whiplash injury, (4) chronic and a PTHA per the clinician’s judg-
begin within 7
days of head headache attributed to whiplash injury, ment.1 Marked worsening of the primary
trauma and (5) headache attributed to traumatic headache disorder in close temporal
may continue intracranial hematoma, (6) postcraniot- relation to trauma or development of
for up to 3 omy headache, and (7) headache attrib- different headache features after trauma,
months after uted to other head or neck trauma.1 including ineffectiveness of medications
the injury. Head trauma, especially in the acute to that had previously been effective, are
PTHAs that subacute period, may result in head- some factors that support adding a di-
persist beyond aches associated with a variety of struc- agnosis of PTHA in patients with preex-
3 months after tural lesions that may have serious isting primary headache disorders.
the inciting sequelae. Most patients with PTHAs at-
head trauma EPIDEMIOLOGY
tributable to mild head trauma, how-
are classified as
chronic.
ever, have no identifiable structural lesion. Every year in the United States, an es-
The criteria for classifying acute and timated 1.8 million individuals develop
A The prognosis of chronic PTHAs are summarized in acute PTHA and 400,000 individuals de-
acute PTHA is Table 4-1.1 By definition, PTHAs must velop chronic PTHA.5 The incidence of
generally begin within 7 days after head trauma or acute headache following mild traumatic
favorable, and after regaining consciousness. New head injury ranges from 31% to 96%.5–9
most patients
headaches that develop beyond 7 days Headaches occur after moderate to se-
can expect to
after the injury are not classified as vere traumatic head injury in 4.3% to
experience
headache
PTHAs. Acute PTHAs begin within 7 37.0% of patients.10–13 The prognosis of
remission days of head trauma and may continue acute PTHA is generally favorable, and
within 6 months. for up to 3 months after the injury. most patients can expect to experience
PTHAs that persist beyond 3 months headache remission within 6 months
after the inciting head trauma are clas- (Case 4-1). PTHAs persist in 32% to 78%
sified as chronic. PTHAs are further clas- at 2 to 3 months after trauma, 8% to 35%
sified according to the severity of head at 1 year, and 20% at 3 to 4 years.5–9,14
trauma (Case 4-1). The criteria for The prevalence of PTHAs plateaus at
acute and chronic headache attributed about 6 months, after which time most
to whiplash injury are similar but imply a patients who are still experiencing
traumatic mechanism with acceleration- PTHAs will probably continue to do so
deceleration of the neck associated with for many more months.14 The incidence
neck pain at the time of injury. of acute PTHAs in children is similar to
The current classification criteria for that seen in adult populations.15 How-
56 PTHAs do not include the characteristics ever, chronic PTHAs develop less often
or accompanying features of the pain or in children, occurring in only 7% of cases
the specific cause of injury (eg, blunt in one study.16
impact, explosive blast). Moreover, the A review of 1670 patients from 12
time criteria are somewhat arbitrary and studies revealed that chronic headaches
not based on pathophysiologic mecha- occur in 58% of patients with TBI of
nisms.4 The different causes of head any severity.17 This analysis did not dis-
trauma, the variability of PTHA pheno- tinguish between primary headaches,
types, and an incomplete understand- PTHAs, or other types of secondary
ing of the pathophysiology of PTHA headaches. Although it is evident that
pose challenges to any classification chronic headaches are the most com-
system. mon category of pain disorders after TBI,
When a preexisting headache disor- it is important to recognize that not all
der, such as migraine, is made worse headaches in patients with TBI are
by head trauma, it can be classified as attributable to trauma or classifiable as
TABLE 4-1 Criteria for Classifying Acute and Chronic
Posttraumatic Headaches1
5.1.1 Acute posttraumatic headache attributed to moderate or severe head injury

A. Headache, no typical characteristics known, fulfilling criteria C and D
B. Head trauma with at least one of the following:
(1) Loss of consciousness for > 30 minutes
(2) Glasgow Coma Scale < 13
(3) Posttraumatic amnesia for > 48 hours
(4) Imaging demonstration of a traumatic brain lesion
C. Headache develops within 7 days after head trauma or after
regaining consciousness
D. One of the following:
(1) Headache resolves within 3 months after head trauma
(2) Headache persists but 3 months have not yet passed since
head trauma
5.1.2 Acute posttraumatic headache attributed to mild head injury
B. Head trauma with all of the following:
(1) Either no loss of consciousness, or loss of consciousness
< 30 minutes
(2) Glasgow Coma Scale 13
(3) Symptoms and/or signs diagnostic of concussion
C. Headache develops within 7 days after head trauma
D. One of the following:
(1) Headache resolves within 3 months after head trauma
(2) Headache persists but 3 months have not yet passed since
head trauma
5.2.1 Chronic posttraumatic headache attributed to moderate or severe
head injury 57
B. Head trauma with at least one of the following:
(1) Loss of consciousness for > 30 minutes
(2) Glasgow Coma Scale < 13
(3) Posttraumatic amnesia for > 48 hours
(4) Imaging demonstration of a traumatic brain lesion
C. Headache develops within 7 days after head trauma or after
regaining consciousness
D. Headache persists for > 3 months after head trauma
continued on next page
KEY POINTS
A It is important to TABLE 4-1 Continued
recognize that
not all
5.2.2 Chronic posttraumatic headache attributed to mild head injury
headaches in
patients with A. Headache, no typical characteristics known, fulfilling criteria C and D
TBI are
B. Head trauma with all of the following:
attributable to
trauma or (1) Either no loss of consciousness, or loss of consciousness < 30 minutes
classifiable as (2) Glasgow Coma Scale 13
PTHAs.
(3) Symptoms and/or signs diagnostic of concussion
A Headaches tend
C. Headache develops within 7 days after head trauma
to occur more
frequently and D. Headache persists for > 3 months after head trauma
are more likely Reprinted from Headache Classification Subcommittee of the International Headache Society. The international
to persist after classification of headache disorders: 2nd edition. Cephalalgia 2004;24(suppl 1):8–160. Copyright # 2004, with
permission from SAGE.
mild head injury
compared to
moderate or
severe head PTHAs. Patients with TBI can have to 23.4% in patients with severe TBI
injury.
primary headache disorders such as mi- (GCS less than or equal to 8, coma du-
graine, which affects 12% of the general ration 3 to 14 days) in this study.12 The
population, or secondary headaches that presence of an abnormal CT scan of the
are not directly related to head trauma brain or a prolonged period of amnesia,
such as medication-overuse headache both features of a more severe head
(MOH). injury, are associated with fewer re-
The epidemiology of headache after ported headaches.10 Other symptoms
whiplash injury is less well defined. One of the posttraumatic syndrome may also
percent to 6% of individuals may have occur more often after a concussion or
chronic whiplash symptoms.7,18 Head- mild head injury.22
aches occur immediately after whiplash Significant disparity exists in the
injury in 49% to 82% of patients.19,20 prevalence of PTHA in different coun-
Headaches persist 1 year or longer after tries. In Lithuania, for example, only 4%
whiplash injury in 8% to 82% of patients of individuals reported posttraumatic
in different study populations.7,21 Ac- headaches that continued for more
cording to the current classification than 1 month after a concussion.23
58 system, headaches that develop beyond The lower prevalence of PTHA in certain
7 days after whiplash injury are not clas- countries may be explained by different
sified as a PTHA. cultural and social expectations of post-
An inverse relationship exists between traumatic symptoms as well as lower
the severity of head injury and incidence rates of litigation.7 The role of litigation
of PTHA. Headaches tend to occur more in the persistence of PTHA continues to
frequently and are more likely to per- be a matter of considerable debate. The
sist after mild head injury compared to preponderance of evidence, however,
moderate or severe head injury.7,10,11 Of does not support resolution of head-
377 patients with severe head trauma, ache coincident with resolution of liti-
only 4% to 23% had headaches 1 year gation or compensation claims.24
later.12 Further, the rate of headache af- Military troops are at risk for PTHA
ter very severe TBI (Glasgow Coma Scale resulting from head or neck trauma
[GCS] less than or equal to 8, coma du- sustained during combat operations.25
ration 15 to 60 days) was 4.3% compared Of United States Army soldiers returning
Case 4-1
A 30-year-old man was thrown from a motorcycle at approximately 40 mph. He was wearing a
helmet. He lost consciousness for 30 minutes with a period of confusion and amnesia lasting for
1 week. The patient was emergently evaluated and found to have a small subarachnoid
hemorrhage over the right parietal convexity on head CT. The patient developed severe headache
as well as concentration difficulties and disequilibrium beginning immediately after the injury.
Neurologic examination revealed difficulty with short-term memory and concentration as well as
some behavioral disinhibition. The patient had severe vertigo resulting in gait disequilibrium.
MRI of the brain performed 5 days after the injury revealed three punctate, right posterior
juxtacortical and subcortical areas of blooming signal on gradient-echo sequence
(Figure 4-1 A and B) consistent with microhemorrhages and an area of increased T2 signal in the
splenium of the corpus callosum (Figure 4-1D) consistent with axonal injury. The patient reported
severe and constant headache immediately upon regaining consciousness. Headaches were
holocephalic,
throbbing, and
associated with
photophobia,
phonophobia,
and nausea.
Rest, ibuprofen
800 mg every
8 hours, and
acetaminophen
500 mg every
6 hours were
administered
on a scheduled
basis for the
first week and
then used
as needed.
The initial
continuous
headache
evolved into
a daily,
intermittent
headache after 59
approximately
2 weeks. Over
the next
4 weeks the
headaches
decreased in
frequency and
severity. The
patient’s vertigo, Gradient-echo MRI images (A and B) showing punctate areas of bloom artifact
FIGURE 4-1 in the juxtacortical and subcortical regions in the right cerebral hemisphere
disequilibrium, (black arrows). Fluid-attenuated inversion recovery (FLAIR) image (C ) showing
memory, hyperintense signal in the sulci over the right parietal convexity (white arrow) consistent with
cognitive, and subarachnoid hemorrhage. FLAIR image showing area of hyperintensity in the splenium of the
corpus callosum (D, white arrow).
behavioral
continued on page 60
Continued from page 59

symptoms also gradually resolved over this period. Six weeks after the injury he
reported no headaches. He completed a course of neurorehabilitation and
returned to his demanding professional career after 2 months.
Comment. The ICHD-2 classifies PTHA as acute if lasting less than 3
months and as chronic if lasting longer than 3 months.1 These headaches
are further classified based on the severity of head trauma.1 Using this
classification system, this patient had acute PTHA attributable to moderate
to severe head trauma. Despite the presence of a moderate head injury,
the headaches were adequately controlled with a combination of
nonsteroidal anti-inflammatory drug (NSAID) and acetaminophen, and
completely resolved within 6 weeks. This case illustrates the favorable
prognosis of acute PTHAs, which often resolve within 3 months after
injury. This case also demonstrates the paradox of headaches resolving
after a moderate to severe head injury accompanied by abnormal brain
imaging, whereas patients with a mild injury and normal neuroimaging
may have headaches that persist well beyond the acute period.
from Iraq or Afghanistan, 10% to 25% pain stimuli of the head. The trigeminal
have sustained a concussion.26,27 In a nerve contains nociceptive afferents
study of 978 returning US soldiers who from the anterior scalp, anterior cranium,
had a concussion in Iraq or Afghanistan, face, mouth, teeth, temporomandibu-
the prevalence of any type of headache lar joints, sinuses, cranial blood ves-
was 98% and the prevalence of PTHA sels, and meninges. Injury to any of
was 37%.28 these structures can cause head pain.
A number of risk factors for devel- The greater and lesser occipital nerves,
oping chronic PTHA have been iden- which arise from the C2 and C3 cervical
tified. These include female sex, lower spinal roots, convey nociceptive stim-
educational level, low socioeconomic uli from the posterior head and scalp.
status, prior history of headaches, mild Painful stimuli from structures of the
severity of head trauma, short dura- cervical spine are conveyed largely by
tion of posttraumatic amnesia, and the cervical nerve roots.
medication overuse.6,8,9,11,29 Although The central processes of trigeminal
60 a causal relationship has not been pain neurons and cervical pain neurons
proven, psychiatric symptoms, such as converge within the CNS in the upper
depression, anxiety, anger, and per- cervical spinal cord. The convergence of
sonality change, are increased in these two anatomic pain pathways is
patients with PTHA and may contrib- known as the trigeminocervical com-
ute to the development of chronic plex.35 Some second-order neurons in
PTHA and increased headache-related this region receive inputs from both
disability.30–34 cervical and trigeminal pain afferents.
Thus, peripheral activation of one pain
system (trigeminal or cervical) can pro-
PATHOPHYSIOLOGY duce central activation of the other sys-
The major neuroanatomic pathways tem. The trigeminocervical complex
involved in head pain are shown in helps explain why injury of neck struc-
Figure 4-2. The trigeminal nerve is the tures can cause head pain. It also helps
major peripheral nerve for transmitting explain why activation of the trigeminal
KEY POINTS
pain pathway can produce pain in the significant role in the genesis of PTHA.
A Headaches
posterior head and neck. Theoretically, damage to central antino-
following mild
Headaches following mild head injury ciceptive systems or activation of central head injury are
are rarely associated with an identifiable pronociceptive systems could contribute rarely
underlying structural injury. A number to posttraumatic head pain, although associated with
of neuronal biochemical and cellular this has not been definitively established. an identifiable
changes induced by head trauma have The multiple mechanisms of head underlying
been identified and may contribute pain described above are not exclusive structural
to the development of PTHAs in the of one another. An individual patient injury.
absence of identifiable structural in- may have multiple mechanisms acting in A The current
jury.5–7,36 Changes include widespread concert. Identifying all potential sources criteria for
neuronal depolarization, indiscriminant of head pain in each patient is important PTHA require
release of glutamate and other neuro- for developing a successful therapeutic onset of
transmitters, altered glucose and energy plan. headache
utilization, and decreased magnesium within 7 days of
levels among other changes.6,36,37 These CLINICAL FEATURES head or neck
events may create conditions that are PTHAs are highly heterogeneous, and trauma, but do
not require the
ripe for the generation of head pain and many different headache types have been
presence of any
recurrent headaches, although the pre- reported after head trauma.41 PTHAs do
particular
cise mechanisms are uncertain. not possess any unique clinical symptoms
headache
PTHAs, especially those possessing that clearly distinguish them from non- characteristics.
migraine features, may share the same traumatic headache disorders, other than
pathophysiology as migraines, includ- having onset in close relation to head,
ing activation of the trigeminovascular face, or neck trauma. The current criteria
system, release of neuropeptides from for PTHA require onset of headache
trigeminal nerve terminals, changes in within 7 days of head or neck trauma,
cerebral vasoreactivity, central sensitiza- but do not require the presence of any
tion, altered cerebral neurotransmitter sig- particular headache characteristics.1
naling, and cortical hyperexcitability.36,38
Trauma has been implicated as a trig-
ger for migraine in previously asymp-
tomatic individuals.39 Patients with post-
traumatic migraines may have a latent
genetic predisposition to migraine that
clinically manifests after concussion or
mild head trauma. 61
Irritation, activation, or compres-
sion of the occipital nerve(s), trigem-
inal nerve(s), or their branches are
other potential sources of persistent or
recurrent head pain after trauma. This
can result in neuralgic pain in the
distribution of the involved nerve. Trau-
matic injury to muscular, skeletal, and
ligamentous structures of the cervical
spine can cause pain to be referred to the
head.40
It is uncertain whether injury to cen- Major neuroanatomic pathways conveying
tral neural pathways involved in pain FIGURE 4-2
pain from the head and neck.
transmission or pain modulation plays a
KEY POINT
In civilian populations, approxi- Approximately 33% of PTHAs resem-
A PTHAs most
mately 72% of headaches attributed to ble tension-type headaches with a wide
commonly
resemble head trauma are bilateral in location.41 range from 6% to 85% reported in dif-
tension-type In one study, a frontal location was seen ferent studies.13 Tension-type headache
headache or in 50%, followed by holocephalic (18%), is typically bilateral and of mild or
migraine hemicranial (13%), and bitemporal moderate severity. The pain quality is
headache. (10%).41 Over 80% of PTHAs in civilian pressing or tightening in nature and not
populations are nonthrobbing.13,41 The aggravated by routine physical activity.
pain may be described as either dull Tension-type headache may be accom-
or sharp in 43% and 35% of patients, panied by either light or sound sensi-
respectively.13 Seventy-one percent of tivity, but not nausea.1
PTHAs are aggravated by physical activity Approximately 28% to 60% of PTHAs
or exertion, and over 60% are mild to resemble migraine.28,41 Migraine head-
moderate in severity.41 Sensitivity to light aches are the most common form of
and sound occurs in 35% and 29% of PTHA after military-related mild head
patients, respectively.41 Nausea occurs trauma.28 Migraine characteristics in-
in 16% to 31%, while vomiting occurs in clude head pain that is moderate or
12% to 14% of patients with PTHAs.9,41 severe, unilateral or asymmetric, throb-
Headaches after whiplash injury are bing or pulsatile in quality, aggravated
located in the occipital region in 46% of by or cause avoidance of routine physi-
patients. Generalized head pain or non- cal activity, and accompanied by either
occipital locations occur in 54% of nausea and vomiting or both light and
cases.42 One study found that head pain sound sensitivity.1 The headache attacks
associated with whiplash injury was last several hours to several days without
rarely severe.20 Other features that may treatment. Aura, a transient focal neuro-
be seen in postwhiplash headaches in- logic symptom that is most often visual
clude aggravation of symptoms by exer- in nature and precedes or accompanies
tion or activity, photosensitivity, and the headache, occurs in a minority of
phonosensitivity.41 patients with migraine and is not re-
Headaches developing after head quired for a headache to be considered a
trauma often possess the same character- migraine. The term posttraumatic mi-
istics as primary headache disorders.2,3,41 graine is sometimes used to describe
Between 70% and 96% of headaches PTHAs that would otherwise meet di-
attributed to head trauma would other- agnostic criteria for migraine, although it
wise meet ICHD-2 criteria for a primary is not listed as a diagnosis in the ICHD-2.
62 headache disorder at some time follow- Posttraumatic migraines may not be dis-
ing head injury.2,9,41 PTHAs most com- tinguishable from idiopathic migraine by
monly resemble tension-type headache clinical features or by responsiveness to
or migraine headache.2,3 This is clini- treatment.39
cally relevant because treatment is based Rarely, head trauma can precipitate
on the type of headache that the PTHA the development of trigeminal auto-
most resembles. Thus, it is useful for nomic cephalalgias.42 Trigeminal auto-
clinicians to classify PTHAs according to nomic cephalalgias manifest as unilateral
well-recognized headache types or syn- headache accompanied by prominent
dromes. As noted above, the major sub- autonomic manifestations, such as con-
groups of headaches after trauma include junctival injection, lacrimation, ptosis,
tension-type headache, migraine, cranial miosis, eyelid edema, rhinorrhea, or
neuralgias, cervicogenic headaches, and facial sweating abnormalities.1 Specific
MOH. Each of these is briefly described subtypes of trigeminal autonomic cephal-
in the following paragraphs. algias (TACs) include cluster headache,
KEY POINTS
paroxysmal hemicrania, hemicrania con- tributor to chronic headaches following
A Occipital
tinua, and short-lasting, unilateral, neural- head trauma. Of patients with PTHAs,
neuralgia is
giform headache attacks with conjunctival 19% to 42% develop this secondary probably the
injection and tearing (SUNCT). headache disorder.2,3 MOH develops in most common
Cranial neuralgias can result from susceptible patients when frequent use neuralgiform
head trauma.5,6,42 Occipital neuralgia is of acute analgesic medication is contin- disorder
probably the most common neuralgi- ued over a prolonged period of time. following head
form disorder following head or neck MOH is most common in patients with or neck injury
injury and typically presents with persis- migraine but may also occur in the set- and typically
tent, moderate, side-locked unilateral ting of tension-type headache or cluster presents with
head pain with episodes of brief, severe, headache. Analgesic overuse is defined persistent,
moderate,
lancinating pain radiating from the oc- as use of acute analgesics 15 or more
side-locked
cipital area to the side of the head. days per month for more than 3
unilateral head
Trigeminal neuralgia and neuralgias in- months.1 MOH is typically bilateral, mild pain with
volving the terminal branches of the to moderate, and nonthrobbing. It oc- episodes of
trigeminal nerve, such as supraorbital curs at least 15 days per month and often brief, severe,
neuralgia and infraorbital neuralgia, occurs daily. The headache usually be- lancinating pain
can also occur after head trauma. Com- gins a number of hours after consuming radiating from
pression, stretching, or other forms of the offending analgesic. The patient be- the occipital
injury to these peripheral nerves, their comes trapped in a cycle of escalating area to the side
branches, or their central connections headaches and increasing medication of the head.
can cause pain in the distribution of use. The diagnosis is confirmed when A Analgesic
the affected nerve. The pain is typically headaches improve after cessation of the overuse is
stabbing, jabbing, or lancinating. Se- overused analgesic. Typically the head- defined as use
vere brief paroxysms of pain that are aches worsen for 2 weeks after analgesic of acute
superimposed on persistent, less severe cessation and then gradually improve analgesics 15 or
pain in the distribution of the nerve over the next 4 to 6 weeks. Opioids, more days per
may occur. Usually tenderness over the combination medications, and triptans month for more
than 3 months.
nerve is present, and sensory impair- have significant potential to cause MOH,
ment in the distribution of the nerve whereas NSAIDS are less likely and di-
may occur. hydroergotamine and antiemetics are
Cervicogenic headaches occur when unlikely to induce MOH.43
pain is generated or referred from a
source in the cervical spine, such as DIFFERENTIAL DIAGNOSIS
cervical discs, facet joints, or myofascial Most patients with PTHAs after concus-
structures.40 Patients with this category sion or mild head trauma do not have an 63
of headaches typically have persis- underlying, life-threatening condition.
tent or intermittent neck discomfort However, the clinician must ask the
as part of their presentation. Neck or question, ‘‘Are the headaches a harbin-
occipital tenderness with or without ger of a serious underlying disorder that
trigger points may be present. Head- would significantly alter prognosis or
aches may be precipitated by certain require specific treatment?’’ Table 4-2
neck movements or positions. Cervico- lists specific causes of headaches after
genic headache is often located in the head trauma. It is beyond the scope of
occipital area or posterior head region this article to describe each of these
but may also affect anterior head re- disorders in detail. Clinicians who eval-
gions. The head pain can be unilateral uate patients after head trauma should
or bilateral. be familiar with the key features of these
MOH, previously called analgesic re- disorders in order to avoid delays in
bound headache, is an important con- diagnosis.
KEY POINT
A number of red flags should alert the
A Red flags that
clinician to the possibility of a potentially TABLE 4-2 Continued
should alert the
serious medical condition as an under-
clinician to the
possibility of a lying cause of a headache. Red flags " Other Causes
potentially Medication-overuse
serious medical Causes of Headache (rebound) headache
TABLE 4-2
condition as an After Trauma Medication side effect
underlying
cause of a " Dangerous Causes of Headache Sinus injury
headache Temporomandibular joint
Cerebral vein or sinus
include altered thrombosis (TMJ) disorders
mental status,
Subdural or epidural hematoma Postcraniotomy headache
focal neurologic
symptoms or Intracerebral hemorrhage Ocular pain (various causes)
deficits, Chemical meningitis
Subarachnoid hemorrhage
progressively
worsening Low or high intracranial Headache due to a
headache pattern, pressure nontraumatic cause
intractable Hydrocephalus Headache due to a psychiatric
headache, new condition
onset of Carotid or vertebral artery
dissection Somatization
headache after
50 years of age, Carotid-cavernous fistula Malingering
and headaches
Cerebral aneurysm
induced by
position or Skull fracture
include altered mental status, focal neu-
Valsalva Cervical vertebra fracture rologic symptoms or deficits, prog-
maneuver.
Cervical disc protrusion ressively worsening headache pattern,
intractable headache, new onset of head-
" Primary Headache Disorders
ache after 50 years of age, and headaches
Migraine induced by position or Valsalva maneu-
Tension-type headache ver.44 Headaches with atypical features
Cluster headache
failing to conform to common headache
phenotypes, fever or other constitution-
Other al symptoms, and persistent rhinorrhea
" Neuralgiform Headaches (suspect CSF leak) are other signs of a
64 potentially serious underlying abnormal-
Occipital neuralgia
ity. Unfortunately, headaches fully re-
Supraorbital or infraorbital
sembling primary headaches can occur
neuralgia
in patients with serious underlying medi-
Trigeminal neuralgia cal conditions.
Scalp laceration–associated
neuralgia
CLINICAL EVALUATION
" Cervicogenic Headaches
The major goals of the clinical evalua-
Cervical disc protrusion
tion are to exclude serious underlying
Cervical ligament strain medical etiologies, establish an accurate
Cervical myofascial pain headache diagnosis, determine the im-
pact of the headaches on the individ-
C2-C3 facet joint dysfunction
ual, and identify important comorbid
conditions that may be perpetuating
KEY POINTS
or exacerbating the headaches. This ence of MOH. Common pitfalls in
A An individual
information is essential to formulating headache treatment include prescribing
patient may
an effective therapeutic plan. nonoptimal doses, failing to treat with have more than
prophylactic agents for a sufficient pe- one type of
History riod of time, and continuing to prescribe headache, so it
The history obtained from the patient is medications causing MOH. is important to
the most important part of the clinical Standardized instruments can aid in obtain a detailed
evaluation. A detailed description of the the evaluation of patients with PTHAs. description of
headache should be obtained, including Visual or verbal analog pain scales are each headache
onset, location, quality, frequency, se- useful for grading pain severity and type.
verity, duration, associated symptoms, tracking changes in pain over time. A Common pitfalls
triggers, functional impact, and changes Studies have demonstrated the benefit in headache
in pattern over time. of using a headache disability instru- treatment
The specific characteristics of PTHAs ment to more effectively guide patient include
can be used to classify them into cate- care.45,46 The Headache Impact Test prescribing
gories that have treatment implications. (HIT-6) and the Migraine Disability nonoptimal
Assessment Scale (MIDAS) are two doses, failing to
It is useful to categorize PTHAs into
treat with
those resembling migraine, tension-type widely used disability scales, although
prophylactic
headache, cervicogenic headache, neu- neither one has been specifically vali-
agents for a
ralgiform headache, or MOH. An indi- dated in patients with PTHA.47,48 A head- sufficient
vidual patient may have more than one ache log or headache calendar can also period of time,
type of headache, so it is important to be helpful. and continuing
obtain a detailed description of each to prescribe
headache type. It also important to ask Physical Examination medications
about headaches that existed prior to Patients with headaches should un- causing
the traumatic injury and whether there dergo a careful neurologic examina- medication-
has been a marked change in the pattern tion, including vital signs and evalua- overuse
of preexisting headaches. tion of mental status, cranial nerves, headache.
Patients should be asked about the motor function, sensation, coordina-
occurrence of focal neurologic symp- tion, gait, and reflexes. It is important
toms, either during or between head- to examine the optic discs for papil-
ache attacks, as well as other red flags ledema, the pupils for anisocoria, the
(see previous section). Posttraumatic eyelids for ptosis, and the eyes for
migraines may be accompanied by an chemosis, proptosis, or orbital edema.
aura, which typically manifests as tran- Most patients with headaches in the
sient visual disturbance. Other focal neu- subacute phase after concussion or mild 65
rologic symptoms in patients with a head injury will have a normal neuro-
history of head trauma should not be logic examination. Careful palpation
attributed to a migraine aura without first for cranial, occipital, or cervical trigger
excluding other causes. points also should be performed.
The clinician must ascertain all cur-
rent and previously attempted headache Imaging
therapies to include both medications All patients with moderate or severe
and nonpharmacologic treatments. The traumatic brain injury and many pa-
dose, effectiveness, tolerability, side ef- tients with mild head trauma should
fects, and duration of each therapy have a head CT during the acute eval-
should be determined. This information uation.49–51 When patients are sub-
is essential for determining whether a sequently evaluated for persistent or
specific therapy has received an ade- recurrent headaches during the sub-
quate trial and for identifying the pres- acute phase, perhaps weeks or even
KEY POINTS
months following head trauma, the exclude infectious or inflammatory eti-
A Specific signs
clinician must consider whether ad- ologies of headache in selected cases.
that suggest
the need for ditional (or initial) neuroimaging is
needed. Head CT or MRI has been Comorbidities
neuroimaging
in patients with recommended in patients whose head- Patients with PTHA often have concurrent
nonacute aches worsen or persist longer than medical and psychological conditions that
headache one week after concussion.51 Specific can perpetuate or exacerbate headaches.
include signs that suggest the need for neu- Common comorbidities include sleep
abnormal roimaging in patients with nonacute disorders, psychosocial stressors, post-
neurologic headache include abnormal neuro- traumatic stress disorder (PTSD), de-
examination logic examination findings, progres- pression, anxiety, alcohol or drug abuse,
findings, sively worsening headache pattern, and concurrent physical injuries (eg, explo-
progressively
headaches induced by position or Val- sive blast injuries may be accompanied
worsening
headache
salva manuever.44 Headaches that fail by amputation, eye injury, hearing loss,
pattern, and to respond to an appropriate trial of or polytrauma), or sequelae of a pre-
headaches therapy or possess atypical features not vious head injury.23,52 Cognitive im-
induced by conforming to common headache phe- pairment, primarily involving executive
position or notypes are additional indications for dysfunction as well as attentional defi-
Valsalva imaging. cits, memory impairment, and increased
maneuver. Brain MRI is more sensitive than CT impulsivity, is another feature often seen
A It is critical to and is the imaging study of choice in in patients with chronic PTHA.31,34,53
identify and the subacute setting. MR or CT angio- The prevalence of psychiatric comor-
treat gram should be used in patients in bidities differs according to injury sever-
comorbidities whom arterial dissection, aneurysm, ity, duration from injury, and diagnostic
to most vasospasm, or carotid-cavernous fistula criteria. Major depression in TBI has
optimally affect are considerations. MR or CT venogram been reported in a wide range of 10% to
PTHA as well as should be performed in patients with 77%.54 In an analysis of 10 studies,
the overall possible cerebral vein thrombosis, a con- the prevalence of major depression after
well-being of
dition that can be triggered by trauma TBI was 44%.55 The incidence of PTSD
the patient.
and has variable manifestations, includ- appears to be inversely related to the
ing headache. Cervical spine MRI may be severity of the injury. In one study, the
used in patients with suspected cervico- incidence of PTSD was 27% among pa-
genic headaches to assess for structural tients who had less than 1 hour of loss
abnormalities, such as herniated discs of consciousness compared to only 3%
or cervical nerve root impingement. among those who were unconscious for
66 more than 12 hours.56 This relationship
is not universally accepted, however.
Other Diagnostic Tests It is critical to identify and treat co-
Lumbar puncture is not necessary in morbidities to most optimally affect
most cases of PTHA. However, mea- PTHA as well as the overall well-being
suring the opening pressure is an im- of the patient. Standardized instruments
portant diagnostic tool for excluding can aid in detecting and monitoring
low or high CSF pressure in selected comorbid conditions (Table 4-3). Treat-
cases. Patients with low CSF pressure ment of conditions other than headache
headaches caused by a dural tear, which is discussed in other articles in this is-
can be caused by mild trauma, have sue. Comorbid conditions may limit
positional head pain that is triggered headache treatment options or provide
by moving to an upright posture and therapeutic opportunities. The clinician
relieved by lying back to a supine po- should strive to avoid headache treat-
sition. CSF analysis may also be used to ments that may exacerbate comorbid
KEY POINT
TABLE 4-3 Screening of Important Comorbid Conditions in A Nonsteroidal

Patients With Posttraumatic Headache anti-inflammatory
drugs (NSAIDs)
Comorbidity Assessment Tools/Referrals are a good first
choice for most
Sleep impairment Pittsburgh Sleep Quality Index types of PTHA.
Epworth Sleepiness Scale

Polysomnography
Cognitive impairment Automated Neurocognitive Assessment Metrics
Neuropsychologic evaluation
Depression Patient Health Questionnaire-9
Beck Depression Inventory
Psychologic/psychiatric evaluation
Various postconcussive symptoms Neurobehavioral Symptom Inventory
Posttraumatic stress disorder (PSTD) PTSD checklist
Primary care PTSD screen
Psychologic/psychiatric evaluation
Drug/alcohol dependence Cut down, annoyance, guilt, eye-opener (CAGE)
questionnaire and modified CAGE questions
conditions and select headache treat- ache frequency, reduce disability, and
ments that simultaneously benefit one or prevent chronicity. As discussed in the
more comorbid conditions. following sections and outlined in
Figure 4-3, a wide variety of pharma-
TREATMENT cologic and nonpharmacologic therapies
The treatment of PTHAs can be both can be used to optimize the outcome
challenging and rewarding. To date, no of PTHAs.
randomized, controlled clinical trials
evaluating the efficacy of any therapies Headache Abortive
for PTHAs have been done. No treat- Medications
ments have been developed specifically Abortive headache treatments provide 67
for PTHA, nor are any US Food and Drug acute relief of individual attacks of head-
Administration (FDA)-approved medica- ache. The goal is to achieve complete
tions with this indication available. Treat- relief or nearly complete relief of head
ment of PTHA is therefore based on pain as rapidly as possible so the patient
treatments for phenomenologically sim- can resume normal activities. A practical
ilar headaches (eg, PTHAs with migraine goal is to achieve headache relief within
features are treated like migraine). Clas- 2 hours of onset.
sification of the headache type, along NSAIDs are a good first choice for most
with careful identification of each source types of PTHA. NSAIDs are effective for
of head pain, is thus an important step in migraine, tension-type headache, and
developing an individualized treatment cervicogenic headache.44,57–59 The spe-
plan. cific NSAID agent is not especially impor-
The major goals of treatment are to tant, although naproxen and ibuprofen
abort headache attacks, decrease head- are the most widely used. Naproxen, as a
KEY POINT
long-acting agent, may be especially fa- tients with migraine. Patients who have
A The triptan class
vorable. Ketorolac injection may be help- rapid-onset headaches or who develop
of medications
should be tried ful for patients who cannot take or do not severe nausea or vomiting early in the
in patients with respond to oral medications. headache attack may benefit from a nasal
migraine-type The triptan class of medications or subcutaneous route of administra-
PTHAs that fail should be tried in patients with mi- tion. Triptan medications have an excel-
to respond graine-type PTHAs that fail to respond lent safety record, although they should
adequately to adequately to NSAIDs (Case 4-2). Trip- be used with caution in patients with
NSAIDs. tans are serotonin-receptor agonists that vascular risk factors and should be
are selectively effective for migraine pain avoided in patients with uncontrolled
and are FDA approved for the treatment hypertension because of their vaso-
of acute migraine. Uncontrolled studies constrictive properties. Patients who ex-
suggest that these agents are effective perience nausea or vomiting during
for aborting attacks of PTHA.41 Oral acute migraine attacks should be pre-
triptan agents are effective for most pa- scribed an antiemetic agent, such as
68
FIGURE 4-3 Posttraumatic headache treatment algorithm.

NSAID = nonsteroidal anti-inflammatory drug; bid = twice a day; tid = three times a day; HA = headache;
HS = at bedtime.
Case 4-2
A 33-year-old man presented to the emergency department 24 hours after
sustaining blunt head trauma from falling on the sidewalk. He was not
certain whether he lost consciousness but remembered falling and then
recalled finding himself on the ground some seconds to minutes later. The
patient reported headache, nausea, photophobia, imbalance, drowsiness,
and difficulty concentrating. On physical examination, the patient had a
large ecchymosis on the right forehead and a normal neurologic
examination. CT of the head was normal. The patient was treated in
the emergency department with IV ketorolac 60 mg and promethazine
25 mg, resulting in a decrease in headache severity and nausea. He was
discharged from the emergency department with instructions to use
ibuprofen 800 mg every 8 hours as needed for pain. The patient was
referred to neurology 1 week later because of persistent, nearly
continuous, severe, daily headaches only partially relieved by ibuprofen.
He still reported mild imbalance, drowsiness, and difficulty concentrating,
although these symptoms were gradually improving. His headaches
were holocephalic, throbbing, and associated with nausea and light
sensitivity. Neurologic examination was still normal. Sumatriptan 100 mg
orally once daily for 5 days was initiated. The headaches immediately
improved and fully resolved after 5 days of therapy.
Comment. This case demonstrates a fairly typical case of acute PTHA
after mild head trauma. A dearth of evidence is available to guide the
management of PTHAs in the acute and early subacute settings. After
ruling out an intracranial hemorrhage and skull fracture with a head CT,
conservative management with rest, NSAIDs, and antiemetics, as was done
in this case, is a common approach. When frequent headaches persist in
the subacute period and significantly interfere with the patient’s function
despite these measures, the most effective management strategy has
not been rigorously established. We recommend initiating headache
therapy according to the specific headache phenotype (Figure 4-3). In this
case, the patient’s headaches closely resembled migraine, so he was
treated with a triptan medication with satisfactory results. Although not
necessary in this case, initiation of headache prophylactic medication can
be considered as early as 2 weeks after injury if headaches are occurring
multiple days per week and are not adequately relieved by abortive
therapies. Aggressive early treatment of PTHA may reduce the risk of
developing a chronic, refractory headache syndrome.
69
metoclopramide, prochlorperazine, or aminophen/aspirin/caffeine (Excedrin).

promethazine.44,57 Triptan agents may These agents contain multiple active
be given in combination with an NSAID drugs and may be helpful for patients
for increased effectiveness. with infrequent attacks of mild-moderate
A variety of combination analgesic migraine headache. The efficacy of any
products are marketed for acute treat- of these agents for PTHA has not been
ment of headaches. Such products in- studied. These agents have a significant
clude butalbital/acetaminophen/caffeine risk for overuse and dependence.44 Pa-
(Fioricet), butalbital/aspirin/caffeine tients using these medications must,
(Fiorinal),acetaminophen/isometheptene/ therefore, be educated about their
dichloralphenazone (Midrin), and acet- potentially addictive properties and the
KEY POINTS
risk of developing MOH. These prod- daily headache complicated by medica-
A Opioid
ucts are not first-line treatments for tion overuse.62
medications are
generally not PTHAs and should not be used in pa-
highly effective tients who have two or more head-
aches per week. Headache Prevention
for most
headache types Opioid medications are generally not Medications
and should not highly effective for most headache types Patients who experience frequent head-
be used as and should not be used as first-line aches may benefit from daily use of
first-line headache headache abortive agents.44,57 How- headache prophylactic medication. Be-
abortive agents. ever, opioids may be used as infrequent cause many patients with PTHAs expe-
A Treatment of rescue therapy for severe, intractable rience spontaneous resolution in the
medication- headache attacks not responding to first month or two after injury, most
overuse multiple first-line abortive agents. IV or practitioners do not initiate prophylac-
headache requires oral corticosteroids (eg, prednisone 60 tic therapy in the acute or early sub-
cessation of the mg daily for 5 days), IV valproate, or IV acute stage. It remains to be determined
causative magnesium are options to consider in- whether initiation of headache prophy-
analgesic agent. stead of opioids for treating intractable lactic therapy in the first few days
A Patients who migraine headache. or weeks after injury mitigates acute
experience two Treatment of MOH requires cessa- PTHAs or decreases the likelihood of
or more tion of the causative analgesic agent.60 developing chronic PTHAs. At this time,
moderate-severe Sudden cessation of the offending agent insufficient evidence is available to
headache can usually be accomplished, although guide the decision as to when after the
attacks per
large amounts of butalbital-containing injury headache prophylaxis should be
week or 3 or
products (Fioricet or Fiorinal) should started. However, many practitioners
more days of
impaired be tapered gradually to prevent drug- would agree that patients who continue
activities per withdrawal seizures. Likewise, large doses to experience frequent headache more
month over a of opioids may need to be tapered down than 2 months after the injury are ap-
period of or monitored to prevent severe with- propriate candidates for prophylactic
several months drawal symptoms. Cessation of anal- therapy. In the setting of multiple co-
despite use of gesic medication inevitably results in morbidities and stressors, such as those
abortive worsening daily headaches for about occurring in a military combat environ-
medications are 2 weeks followed by a gradual improvement, one of the authors (ETN) rec-
good candidates ment back to an episodic headache ommends initiation of prophylaxis as
for headache
pattern within 6 weeks. Patients must early as the second week postinjury
prophylactic
understand that withdrawal headaches if headaches are occurring more than
70 medication.
are expected for at least 2 weeks and twice weekly.
must be fully committed to the treat- In general, patients who experience
ment plan. A short course of prednisone two or more moderate-severe headache
may be used to minimize withdrawal attacks per week or 3 or more days of
headaches.61 A long-acting triptan or impaired activities per month over a pe-
NSAID combined with an antiemetic riod of several months despite use of
agent may be used sparingly for severe abortive medications are good candidates
exacerbations.60 Sleep-inducing medi- for headache prophylactic medication. A
cation and adequate hydration may be practical treatment goal of prophylactic
helpful during the withdrawal period. medication is a 50% or greater reduction
Multidisciplinary inpatient treatment with in headache attack frequency. Prophylac-
IV dihydroergotamine, drug withdrawal, tic medications require a minimum of
cognitive-behavioral therapy, anesthesio- 4 weeks to take effect. Treatment should
logic interventions, and other treatments begin at a low dose to minimize side ef-
may be needed for refractory chronic fects and be gradually increased over
KEY POINTS
weeks or even months until the fre- Tricyclic antidepressants, such as
amitriptyline or nortriptyline, are ap-
A Amitriptyline,
quency of headaches decreases, side ef-
propranolol,
fects develop, or the highest target dose propriate first-line agents for prophy-
topiramate,
is reached. Patience on the part of both laxis of PTHAs resembling tension-type and valproate
the patient and provider is critical. Switch- headaches (Figure 4-3).59 Other pro- have strong
ing prophylactic agents prematurely, with- phylactic agents that may be helpful for evidence of
out first titrating up the dose or treating tension-type headache are tizanidine, efficacy as
for a minimum of 6 weeks, should be mirtazapine, and topiramate. prophylaxis for
avoided. PTHAs with neuralgiform pain, such migraines and
No randomized controlled trials of as occipital neuralgia or trigeminal neu- are first-line
prophylactic medications for PTHAs ralgia, may benefit from an anticonvul- options for
sant (Figure 4-3). Carbamazepine is the prevention of
have been done. Prophylactic agents ef-
posttraumatic
fective for primary headache disorders most established agent for trigeminal
migraine
are typically used to treat patients with neuralgia but has not been studied for
headaches.
PTHAs. Selection of a specific prophylac- occipital neuralgia. Gabapentin is often
tic agent for PTHA is based primarily on selected for treating occipital neuralgia A Tricyclic
when nerve blocks are declined or in- antidepressants,
the type of headache (Figure 4-3). Un-
effective. Lamotrigine is another option such as
controlled studies provide some evi-
amitriptyline or
dence supporting the effectiveness of for neuralgiform headache, being well
nortriptyline, are
amitriptyline, propranolol, and valproate tolerated with minimal adverse cognitive
appropriate
for prophylaxis of chronic PTHAs.41,63–65 side effects, but the dose must be slowly first-line agents
Amitriptyline, propranolol, topiramate, titrated up to minimize the risk of a se- for prophylaxis
and valproate have strong evidence of rious mucocutaneous reaction. of PTHAs
efficacy as prophylaxis for migraines resembling
and are first-line options for prevention Nonpharmacologic Therapies tension-type
of posttraumatic migraine headaches A variety of nonpharmacologic inter- headaches.
(Figure 4-3).44,57 Other medications that ventions may be helpful in treating A A variety of
can be useful for migraine prevention PTHAs. Such treatments include behav- nonpharmacologic
include nortriptyline, gabapentin, calcium ioral therapies, physical modalities, and interventions
channel blockers, pregabalin, and quetia- injection procedures. No randomized may be helpful
pine.44,57,66,67 Selection of a migraine controlled trials have evaluated the ef- in treating
prophylactic agent is influenced by the fectiveness of any of these approaches PTHAs. Such
patient’s comorbid conditions. Amitripty- for PTHAs, but evidence supports their treatments
line and quetiapine are options in the include
use in other headache disorders. Most
behavioral
setting of comorbid insomnia. Proprano- nonpharmacologic techniques have mini-
lol or another beta-blocker is a good mal to no adverse effects, making them
therapies, 71
physical
choice for patients with comorbid hyper- very suitable options in patients with po- modalities, and
tension or tremor. Topiramate is optimal tential cognitive impairment and other injection
for patients with comorbid obesity or comorbidities, and may be used as an procedures.
epilepsy. Valproate is particularly appro- adjunct to pharmacologic treatments.
priate in the setting of comorbid bipo- All patients with PTHAs should re-
lar disorder or epilepsy. Gabapentin or ceive education about their diagnosis
pregabalin are good options when the and treatment plan. Patients with acute
patient has comorbid fibromyalgia, myo- PTHAs should be reassured that their
fascial pain, or neuropathic pain disor- headaches are likely to improve over
der (such as stump pain following limb time. Patients with chronic PTHAs
amputation). Occasionally, combination should be informed that numerous
therapy with multiple prophylactic med- therapies that may alleviate headaches
ications is needed to achieve satisfactory are available, but multiple trials may be
control of headaches (Case 4-3). needed to optimize treatment. Patients
Case 4-3
A 35-year-old male army officer hit his helmeted head on the roof of a
military vehicle after it was struck by an explosive device in Iraq. He did not
lose consciousness but was dazed for several minutes and had brief
posttraumatic amnesia. He subsequently had daily left retro-orbital, dull,
constant pain, 1-2/10 at baseline with exacerbation to 8/10 occurring 3 to
5 times per week, worsening with movement, associated with
photosensitivity, phonosensitivity, nausea, and blurred vision. He was
treated in Iraq with isometheptene plus dichloralphenazone plus
acetaminophen (Midrin) and ibuprofen, but these were not helpful. The
patient completed his tour in Iraq despite continued symptoms and was
referred to neurology postdeployment. He had a history of multiple blast
exposures within 100 m (328 ft), multiple prior concussions from intramural
football and a parachute injury, and chronic neck and low back pain.
He also reported poor balance, poor concentration, forgetfulness,
difficulty making decisions, slowed thinking, anxiety, depressed mood,
difficulty falling or staying asleep, repeated disturbing memories,
nightmares, and angry outbursts. Physical examination revealed
tenderness on palpation of the cervical paraspinal muscles from C4 to C6
and mild decreased range of motion in all directions. MRI of the brain
with and without contrast was normal. C-spine MRI revealed mild
uncovertebral joint degenerative changes and mild neuroforaminal
narrowing bilaterally at several levels without root impingement from
C2-3 to C6-7. Neuropsychological testing revealed moderate to severe
impairments in delayed verbal and nonverbal memory. The patient was
treated with zolmitriptan 5 mg for acute headache attacks, prednisone
60 mg daily for 10 days, and nortriptyline 10 mg at bedtime with an
increase to 25 mg after 1 week. He was also referred to physical therapy for
neck and back pain and to the behavioral health service for treatment
of PTSD. The headaches temporarily resolved while he was on prednisone
but became daily again after the prednisone was stopped. Gabapentin
300 mg daily was then added and gradually titrated up to 1200 mg in
divided doses. He was also given botulinum toxin type A injections to the
bilateral frontalis and corrugators, bilateral temporalis, bilateral splenius
capitis, midcervical paraspinal, and bilateral lumbar paraspinal muscles.
Two months later, he reported having had only two headaches in the
previous month, which were effectively relieved by zolmitriptan, as well as
72 decreased cervical and lumbar pain.
Comment. This case illustrates a number of points: (1) headache onset
following multiple bouts of mild head injury; (2) persistence of chronic
headaches despite mild severity of head injury; (3) presence of PTSD,
insomnia, and neck and back pain, which likely exacerbated the headache
syndrome and contributed to the patient’s impairment; (4) normal brain
imaging despite multiple physical, cognitive, and psychological symptoms;
and (5) in the chronic stage, headache management that required
several modalities to achieve an effective response.
should be given clear instructions about participation of the patient will improve
the goals and proper uses of any pre- compliance.
scribed medications. Establishing realis- Lifestyle modification is a simple, yet
tic expectations and enlisting the active often overlooked, technique. Patients
KEY POINT
should be encouraged to establish efficacy of these treatments for PTHA has
A Occipital nerve
healthy meal, sleep, and exercise pat- not been rigorously studied. Nonethe-
blocks,
terns. Patients may identify specific less, these approaches are well suited for performed by
triggers for their headaches that can be patients with myofascial pain and muscle injecting local
avoided. Caffeine overuse, smoking, and tenderness as prominent features.40,58,72 anesthetic with
alcohol use can contribute to head- Botulinum toxin injections are also ap- or without
aches. A headache log may help identify propriate for PTHAs resembling chronic steroid, can be
potential triggers in some cases. migraine and occipital neuralgia.73–76 helpful for a
Uncontrolled studies of cognitive- Headaches secondary to C2-C3 facet variety of
behavioral therapy, relaxation therapy, joint dysfunction can be treated with headaches,
and biofeedback have shown favorable facet joint blocks or cervical medial most notably
occipital
results in PTHA.68,69 These techniques branch blocks.40,58
neuralgia.
seem to be especially helpful for patients Occipital neurolysis, occipital nerve
with PTHAs who have significant muscle decompression surgery, and implanta-
tightness, anxiety, or insomnia. The ef- tion of occipital nerve stimulators are
ficacy of these treatment modalities for potentially useful treatments for re-
migraine headache is well established.44 fractory headaches but are not widely
Physical modalities such as physical used. Studies are needed to validate
therapy, osteopathic manipulation ther- the usefulness of these more invasive
apy, acupuncture, and massage have techniques before they can be recom-
not been fully evaluated for PTHA. mended for PTHA.
These techniques are useful as adjuncts
to medical therapy, particularly in pa- SUMMARY
tients with suspected cervical sources of PTHA is a heterogeneous syndrome that
pain (Case 4-3). Physical therapy is an can be both challenging and rewarding
important initial step in treating post- to treat. A comprehensive diagnostic
traumatic cervicogenic headache. and therapeutic approach is needed to
establish an individualized treatment
Injections and Procedures plan that addresses all of the potential
Occipital nerve blocks, performed by underlying causes of head pain as well as
injecting local anesthetic with or without comorbid conditions that can perpe-
steroid, can be helpful for a variety of tuate the headache syndrome. PTHAs
headaches, most notably occipital neu- often resemble primary headache dis-
ralgia.70 One case series showed an 80% orders and are treated in a similar
response rate of PTHA following occipital manner. Classifying the phenotype of
nerve blockade.71 Occipital nerve blocks PTHA helps guide treatment. A combi- 73
can also alleviate cervicogenic headache nation of pharmacologic and nonphar-
and migraine.70 Other useful injection macologic interventions as well as a
techniques include botulinum toxin in- multidisciplinary approach may be nec-
jections and trigger point injections of essary to remedy the headache and pre-
craniocervical muscles (Case 4-3). The vent chronicity.
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78
KEY POINT
MEMORY IMPAIRMENT A Of the somatic,

cognitive, and
AFTER MILD TRAUMATIC neuropsychiatric

symptoms
BRAIN INJURY experienced

after a mild
traumatic brain
Frederick G. Flynn injury (mTBI), a
problem with
memory is one
of the most
ABSTRACT common
Concerns of memory impairment are common after mild traumatic brain injury (mTBI). concerns.
Acute effects after mTBI may include posttraumatic amnesia, which may last up to
24 hours. In the postacute phase, memory concerns are usually linked with increased
distractibility; impaired attention, working memory, retrieval; and executive dys-
function. These acute and postacute impairments have distinct neuroanatomic and
pathophysiologic correlates. Cognitive assessment should be undertaken during the
acute phase after an mTBI using a standardized tool that can be administered quickly
and is sensitive to cognitive impairment. Early validation of the patient’s symptoms and
concerns (especially the expectation of recovery), coupled with educational and emo-
tional support after the mTBI, remains the core approach to treatment. The effects of
comorbidities, recurrent mTBIs, and blast exposures in military personnel on protracted
symptoms and long-term cognitive deficits will be discussed.
INTRODUCTION symptoms commonly attributed to mTBI

Approximately 75% of all civilian trau- with those of comorbidities such as de-
matic brain injuries (TBIs) are mild by pression and posttraumatic stress disor-
definition.1 The estimate for military der (PTSD).4
populations is slightly higher.1 Estimates Of the somatic, cognitive, and neuro-
of 11% to 23% of deployed service mem- psychiatric symptoms experienced after
bers screen positive for a history of mTBI an mTBI, a problem with memory is one
(the term mild TBI is used interchange- of the most common concerns of pa- 79
ably with the term concussion).2,3 These tients.5 Acute, subacute, and chronic
figures may be spurious as most screen- memory problems after an mTBI have
ing tools are based on self-report, usually been reported.
completed months after the event oc- In the acute phase after an mTBI, the
curred, rather than on clinician-confirmed patient may experience posttraumatic
examination. Thus, the actual incidence of amnesia (PTA), whether or not a loss of
mTBI and prevalence of mTBI-associated consciousness (LOC) has occurred as a
persistent symptoms is unknown. Com- result of the concussion. The patient’s
pounding this uncertainty are the limita- inability to learn new information dur-
tions of specific diagnostic tools, the lack ing this period (which can last from
of biological markers, and the overlap of minutes up to 24 hours postinjury) may
Relationship Disclosure: Dr Flynn has nothing to disclose.

Unlabeled Use of Products/Investigational Use Disclosure: Dr Flynn has nothing to disclose.
" MEMORY IMPAIRMENT
be falsely interpreted later as LOC be- symptoms usually occurs within the
cause the patient is unable to remem- first 3 months following the injury.7,8
ber that period of time.1 The PTA period Of patients with mTBI, 10% to 15%
is defined as the length of time from may continue to manifest persistence
the injury until continuous memory of symptoms that may result in func-
resumes.6 Retrograde and anterograde tional impairment and limitations in
PTA may diminish over time with events daily life activities.9 A recent review,
closest to the time of trauma being most however, suggests that in sports-related
resistant to recall (Case 5-1).1 concussion, persistent symptoms be-
In 85% to 90% of civilian patients yond 1 month exist in fewer than 3% of
with mTBI, recovery with resolution of affected athletes.10 Among patients with
Case 5-1
A 21-year-old soldier was riding in a military vehicle when a roadside bomb exploded
approximately 40 m (131 ft) in front of him. He was wearing a Kevlar helmet at the time.
The concussive blast hurled him out of the vehicle, where he was witnessed to strike his head
on a large rock. A medic rendered aid and found the soldier to be unresponsive. He remained
this way for approximately 12 minutes before gradually regaining consciousness. He was confused
and not able to answer questions concerning where he was or what had happened to him.
The last thing he remembered was eating breakfast at his Forward Operating Base, which
occurred 45 minutes prior to the explosion. The medic administered the Military Acute Concussion
Evaluation (MACE). The soldier could repeat only three digits forward and on immediate recall
was able to repeat 0/5 words on the first trial, 1/5 on the second trial, and 2/5 on the
third trial. After a few minutes of distraction by having the patient perform tests of balance and
coordination, he was asked to recall the list of words. He could not recall any of the words,
and cueing failed to help. The MACE score was 11/30 (normal is greater than 25/30). He was sent
to the base medical facility, where he was placed under observation. For the next 6 hours he
continued to ask the same questions repeatedly. He reported being dizzy and having a ‘‘bad’’
headache but had no focal neurologic deficits on examination. A noncontrast CT scan was normal.
About 12 hours after the explosion the medics observed that the patient was starting to recall
some events that transpired during the previous half hour. The following day the patient was
administered the MACE with a different word list than the first. This time his immediate
recall trials were 1/5, 2/5, and 4/5. Five-minute delayed free recall was 0/5, but he was able to
identify 4/5 words with cueing. The MACE score improved to 15/30. Over the next 2 weeks his
symptoms improved and he was able to gradually return to duty. He continued to demonstrate
80 improvement in his memory with the MACE score improving to 27/30. He began to recall riding
in the vehicle shortly before the explosion. However, he never regained any memory of the
events that occurred at the time of the explosion or during the first 6 hours after the blast.
Comment. The presence of LOC less than 30 minutes, PTA less than 24 hours, and no focal
neurologic findings categorize this patient’s injury as an mTBI. This patient had PTA. The initial
retrograde component was for a period of 45 minutes prior to the explosion. The anterograde
component lasted between 6 and 12 hours initially, but even after recovery the patient had no
memory recall of a 6-hour period after the explosion. After the patient could once again acquire
new information in long-term memory, he continued to have some problem with retrieval
after a delayed recall. The fact that he improved significantly with cueing suggests that the process of
consolidation and storage of information was once again functioning. Persistent problems with
memory retrieval with improvement with cueing are not uncommon during the postacute period
after an mTBI. Even after the patient becomes asymptomatic, return to work should take place
gradually, as increased cognitive challenges during this time require significantly more effort and
may unmask deficits from which the patient had previously recovered.
KEY POINTS
persistent symptoms, chronic memory In addressing the sequelae of mTBI,
A Although the
concerns are very common. one must exercise caution because of
term memory
Although a ‘‘memory problem’’ may the potential misattribution of persistent problem may
be a common concern among patients symptoms to an mTBI that occurred be a common
with postconcussive symptoms, the prob- months or years ago.2,4,16 Many comor- concern among
lem may actually involve impaired atten- bidities, such as PTSD, depression, anxi- patients with
tion and concentration, forgetfulness, ety, physical pain, sleep disturbance, postconcussive
distractibility, slowness of mental pro- alcohol and substance abuse, and family- symptoms, the
cessing and reaction time, impaired related and job-related stressors, may problem may
mental flexibility, working and prospec- produce or exacerbate similar physical, actually involve
tive memory, and memory retrieval.11 cognitive, and neurobehavioral symp- impaired
Patients may also have difficulty with attention and
toms that are commonly seen after mTBI
concentration,
executive functions, including strategic (Figure 5-1) (Case 5-2).4
forgetfulness,
planning, the poor use of semantic orga- Memory concerns are common among distractibility,
nization on memory tests, and, conse- patients with one or more of the above slowness of
quently, impaired free recall.12 Unlike comorbid conditions, even when no mental
the consolidation and storage deficits of substantiated history of mTBI is pres- processing
PTA, which are thought to be mediated ent.2,17 It has also been suggested that and reaction
by the medial temporal-hippocampal in a blast-related LOC or dazed and con- time, impaired
system,13 the memory retrieval prob- fused state, the etiology may be misat- mental
lems common in patients with persis- tributed to an mTBI when the actual flexibility,
tent symptoms after an mTBI involve cause of the symptoms may be an acute working and
impairment of function in frontal net- stress response with autonomic features prospective
memory,
works.14 This is felt in part to be caused due to the life-threatening nature of the
and memory
by dysfunction of the prefrontal cortex’s event.17
retrieval.
role in the activation and maintenance In many cases it is not a question of
of working memory (Case 5-1).15 ‘‘either/or’’ (mTBI versus psychological A Many
comorbidities,
such as
posttraumatic
stress disorder
(PTSD),
depression,
anxiety, physical
pain, sleep
disturbance,
alcohol and
81
substance
abuse, and
family-related
and job-related
stressors, may
produce or
exacerbate
similar physical,
cognitive, and
neurobehavioral
symptoms that
FIGURE 5-1 Conditions that may affect recovery of posttraumatic memory concerns are commonly
or impairments. seen after mTBI.
TBI = traumatic brain injury; mTBI = mild traumatic brain injury.
" MEMORY IMPAIRMENT
Case 5-2
A 36-year-old male soldier, with a history of previous concussion during high school, sustained an
mTBI from an improvised explosive device (IED) blast while in Afghanistan. He was knocked
unconscious for 10 minutes and had a 12-hour period of PTA. The MACE score was 11/30 with
inability to recite more than three digits forward. Immediate recall trials were 0/5, 1/5, and 3/5
words. Delayed recall was 0/5 with no improvement on cueing. Within 2 weeks his MACE score
improved to 23/30. He continued to have headaches, insomnia, problems with concentration,
and forgetfulness. He had trouble multitasking and remembering appointments. Cognitive
assessment 1 month after the injury demonstrated difficulties with working memory, especially
in the visuospatial domain; delayed free recall, which improved significantly with cueing; and
some difficulty with executive functions. Effective treatment of the headaches helped to improve
sleep. The use of mnemonics and notebooks, removing distracters, and working on one task
at a time helped the patient to improve day-to-day functions.
One month prior to returning to the United States (and the most current evaluation), the
patient experienced another IED blast. He was dazed and confused but without LOC. The
patient witnessed the death of fellow soldiers, including his best friend. On initial assessment in
the United States he complained of headaches, dizziness, irritability, and problems thinking.
Cognitive testing demonstrated two digits forward with immediate recall testing of 0/5, 0/5,
and 1/5 words. Delayed free recall was 0/5, giving a total MACE score of 7/30. He correctly
identified the first three words with cues but then said, ‘‘My memory is shot.’’ Over the ensuing
months his symptoms worsened. He also developed nightmares, flashbacks, increased startle,
hypervigilance, heart palpitations, impulsive anger, and social withdrawal. During repeat
cognitive testing he demonstrated little effort and frequently stated, ‘‘I can’t concentrate.’’ Digit
span was only two forward. Immediate memory recall was 0/5 on all three trials. Delayed free
recall was 0/5 with no improvement on category cueing. When given multiple choices, his
response was delayed, but he correctly identified all five words on recognition. Total cognitive
score was 6/30.
Comment. This patient has a history of multiple concussions. The first concussion occurred in
high school with an unknown period of LOC or PTA. The second event, an IED blast, involved
the LOC and PTA within the limits that defined it as an mTBI. Deficits of attention, working
memory and recall, and executive function persisted long after the PTA had resolved. A problem
with memory retrieval, with improvement on cueing, is typical of the pattern seen during the
recovery period after an mTBI. Headaches and sleep disturbance often exacerbate problems
with attention and memory retrieval. Effective treatment of these problems will usually have
a positive effect on cognition. The patient also used practical compensatory techniques to assist
him in day-to-day functions. The history of a previous mTBI, the duration of the LOC and PTA,
headaches, and insomnia may all have contributed to protracted recovery.
82 It is uncertain whether the most recent IED caused an mTBI. Being dazed and confused
may have been consistent with an mTBI, but it may also have been caused by an acute stress
reaction because of the intense fear and the emotional impact of witnessing fellow soldiers
killed. Physical and cognitive concerns are common after an mTBI but are not specific to mTBI.
The same symptoms may be seen with psychological stress. The worsening of his symptoms
over the subsequent month is not consistent with the usual recovery pattern from an mTBI.
It is consistent with the development of PTSD, which he clearly manifested. His lack of motivation
and effort on cognitive testing was felt to be predominantly related to depression. The
absence of delayed free recall and no improvement with cueing are not compatible with
his obvious day-to-day learning. The patient was treated through a multispecialty interdisciplinary
team focusing on mental health care for depression and PTSD as well as symptomatic treatment
of headaches and sleep disturbances. The patient should continue to be followed and
reassessed in the future as the history of multiple concussions poses a higher risk for future
TBI and for dementia. The comorbidities of mTBI and PTSD are also a higher risk for long-term
disability.
KEY POINTS
factors) but rather the neurobiologi- a greater challenge than forward digit
A mTBI may
cal consequences of the coexistence of span. The prefrontal cortex appears to
impair cognitive
both conditions.18 It has been proposed be vital to normal working memory, as resources
that mTBI may result in dysfunction to damage to this area in humans often involved in
prefrontal cortical regions that serve results in impairment of this function.22 creating
to regulate the response to acute and Long-term memory is the ability to adaptive
chronic psychological stress.18,19 Mild learn new information and be able to strategies to
TBI may also impair cognitive resources recall the information after a delay of deal with
involved in creating adaptive strategies minutes to hours. Patients with amnesia psychological
to deal with psychological stress20 and lose long-term memory. The memory stress This may
thus predispose to a greater incidence loss may be transient (eg, transient global predispose
of PTSD.19 Some of these same pre- to a greater
amnesia or a posttraumatic anterograde
incidence
frontal cortical networks involved in amnesia) or permanent (eg, damage to
of PTSD.
working memory, memory retrieval, both medial temporal lobes). Long-term
and cognitive processing are commonly memory may be tested in the clinical A The prefrontal
affected after mTBI as well.14 setting with recall of a word list after cortex appears
An overview of the functional neu- a short delay of a few minutes during to be vital to
normal working
roanatomy and pharmacology of ex- which the patient is distracted with an-
memory, as
plicit memory, the clinical correlation other task. The amnestic patient will fail
damage to this
with memory problems of patients with to recall the list and show very little, if area in humans
mTBI, and the assessment and man- any, improvement with cueing. often results in
agement strategies for coping with, and Long-term memory can be divided impairment of
rehabilitation of, cognitive problems as- into two major categories: (1) explicit or this function.
sociated with mTBI will be presented. declarative and (2) implicit or nondeclar-
Clinical case histories with emphasis on ative. Explicit memory is conscious learn-
A Long-term
memory can be
the challenges posed by combat-related ing, whereas implicit learning does not divided into
mTBI and persistent cognitive concerns require conscious awareness. Implicit two major
will be included. memory can be subdivided into priming; categories:
procedural skills; associative learning, explicit or
OVERVIEW OF FUNCTIONAL including classic and operant condition- declarative and
NEUROANATOMY OF MEMORY ing; and nonassociative learning, includ- implicit or
The most accepted terms for categoriz- ing habituation and sensitization. Explicit nondeclarative.
ing memory include short-term, long- memory may be further divided into Explicit memory
term, and remote.14 Short-term memory episodic and semantic memory.23 Epi- is conscious
represents the ability to hold informa- sodic memory represents the personal learning,
tion in mind temporarily, usually for a events in one’s life (eg, what one had for whereas 83
implicit learning
period of just seconds unless repeatedly breakfast or what one did at work the
does not
rehearsed. Short-term memory involves day before). Semantic memory rep- require
working memory, defined as the ability resents learned facts and principles conscious
to maintain short-term storage of infor- about the world and the universe (eg, awareness.
mation that is inaccessible in the envi- the earth rotates around the sun; George
ronment and the processes that keep Washington was the first US president).
the information active for later use.21 Just as new learning occurs in our per-
The classic example is the ability to re- sonal lives on a daily basis (episodic),
tain a telephone number in mind long new learning about the world also occurs
enough to find a writing instrument and on a daily basis (semantic) (Table 5-1).
put the number on paper. In mental Explicit and implicit memory func-
status assessment, the digit span test is tions do not always occur in isolation.
an example of a short-term and working For example, a boy, while riding his
memory test, with reverse presenting bike, encounters a barking dog that
" MEMORY IMPAIRMENT
KEY POINTS
including the striatum, amygdala, cere-
A Explicit memory TABLE 5-1 Two Forms of
Long-Term bellum, brainstem, and spinal reflex
processing
consists of Memory pathways.
four different Explicit memory processing consists
elements: " Explicit (Declarative) of four different elements: encoding,
encoding, Events: episodic
consolidation, storage, and retrieval. En-
consolidation, coding occurs when new information
storage, and Facts: semantic is attended to and processed when
retrieval. " Implicit (Nondeclarative) first encountered. In order to be re-
A Retrieval is Priming membered later, information must be
dependent on strongly encoded. This usually involves
Procedural (skills and habits)
prefrontal increased attention to the material and
cortical Associative learning: classic associating it with knowledge already
function, as it and operant conditioning known. Motivation may also increase
involves an Nonassociative learning: encoding. Consolidation is the process
active effort habituation and sensitization by which newly encoded or stored in-
and strategy formation is altered in order to make
and is critically labile memory more stable for long-
dependent on
term storage. This process involves
short-term
begins to chase him. A year ago the boy long-term potentiation and the expres-
workingmemory.
had been bitten by a dog. While the sion of genes and protein synthesis
sight and sound of the attacking dog is within neurons, which leads to struc-
consciously being laid down in long- tural changes resulting in memory sta-
term memory (episodic memory), his bilization. Storage is the mechanism by
racing heart and cold sweat (conditional which memory is retained over long
fear and emotional memory), as well as periods of time in distributed cortical
the reflex response of accelerating the sites. The storage process has a vast ca-
pedals and maneuvering the bike at pacity unlike short-term working mem-
high speed (procedural memory), oc- ory, which is very limited.14
cur automatically. The emotional va- Retrieval, the process that permits
lence of the event serves to strengthen the recall and use of stored informa-
the encoding and storage of the explicit tion, involves bringing together differ-
memory. When the event is consciously ent kinds of information that are stored
recalled at a later time, the emotional in separate cortical network sites. Be-
effect (fear) and the autonomic effects cause this is a constructive process, it is
84 (racing heart, cold sweat) may be re- subject to distortion. Retrieval is most
experienced along with the explicit effective when it occurs in the same
memory. The amygdala and its limbic, context in which the information was
neocortical, hypothalamic, and brain- originally acquired and in the presence
stem connections play a central role in of the same cues that may have been
the emotional component of memory available during the learning process.13
and the strength by which episodic in- Retrieval is dependent on prefrontal
formation is encoded, consolidated, cortical function as it involves an ac-
and stored.24 tive effort and strategy and is criti-
The anatomy of implicit memory will cally dependent on short-term working
not be discussed in detail here, but it memory.14
should be noted that other than prim- The processing of new information
ing, which is felt to be a neocortical is first and foremost dependent on in-
process, the elements of implicit learn- tact attention. Inattention or impaired
ing take place in subcortical regions, attention will interfere with the ability
to acquire new information in long- filtering of other sensory input. This fil-
term memory. Information from the tering appears to be a dynamic function
external world arrives in the brain of the reticular nucleus of the thalamus
through the five senses. Although any with continuous feedback from the pre-
new learning can take place through the frontal and specific sensory association
senses of smell, taste, and somatosen- cortices to raise or lower the gain or
sory input, the most prevalent learning change sensory modality preference
takes place through visual and auditory (Figure 5-2).25 Specific sensory mo-
input. Language plays a critical role in dality input is processed in respective
the learning process. Any lesion of the unimodal association cortices (eg, visual
brain that affects language will impair at processing in the occipital-temporal cor-
least some form of language-dependent tex). Information from polymodal sen-
learning (eg, a patient with a Wernicke sory input (eg, auditory and visual) is
aphasia will have impairment in audi- processed in the heteromodal associa-
tory learning). tion areas of the temporal, parietal, and
Modality-specific information enters prefrontal cortices.25 Processed informa-
the brain through the respective sen- tion then passes to the parahippocampal
sory pathways. With the exception of gyrus, as well as the perirhinal and en-
olfaction, all sensory pathways synapse torhinal cortex of the medial temporal
in their respective thalamic nuclei prior lobe. From the entorhinal cortex projec-
to projecting to their respective primary tions to the hippocampus arrive via the
sensory cortices. Selective attention to a perforant pathway. Sequential process-
specific sensory modality requires some ing at the cellular level in the dentate
85
FIGURE 5-2 Explicit long-term memory pathways—primary and selective attention.

LG = lateral geniculate nucleus; MG = medial geniculate nucleus; VP = ventral posterior nucleus;
nuc = nucleus.
" MEMORY IMPAIRMENT
KEY POINT
gyrus projects axons of granule cells via the fornix gives off an anterior projec-
A The hippocampal
the mossy fiber pathway of the hippo- tion to the septal region and the basal
network is felt
to be important campus to CA3. CA3 subsequently proj- forebrain (Figure 5-3). This region pro-
in encoding ects pyramidal cell fibers via the Schaefer vides rich cholinergic input from the
new facts and collateral pathway through CA2 to CA1, medial septal nucleus to the hippo-
experiences which in turn projects to the subiculum campus. The substantia innominata of
and in before exiting back to the entorhinal the basal forebrain also projects cho-
consolidation cortex.13 Excitatory projections from linergic neurons to widespread areas of
of new CA1 also enter the columns and body the neocortex, amygdala, and paralimbic
information of the fornix and project to the mamillary regions.25 The hippocampus receives
over time and bodies and, from there, to the anterior predominantly excitatory input from
the distribution thalamic and intralaminar nuclei. Pro- the entorhinal cortex and subiculum
of the memory
jections from the thalamus go to the with glutaminergic, cholinergic, dopami-
representations
throughout
cingulate cortex, pass through the retro- nergic, noradrenergic, and serotonergic
cortical regions splenial area to the parahippocampal inputs. The prominent efferent neuro-
for long-term gyrus, the entorhinal cortex, and even- transmitter of the hippocampus is gluta-
storage. tually back to the hippocampus. Prior to mate, providing excitatory transmission
projecting fibers to the mamillary bodies, via the fornix.14 These hippocampal
86
FIGURE 5-3 Explicit long-term memory and emotional valence pathways.
KEY POINTS
efferents also project back to unimodal are stored in neural networks of the re-
A When damage
and heteromodal association cortices spective sensory association neocortex.
to the association
(Figures 5-2 and 5-3). This circuit serves Episodic knowledge, on the other areas of the
to provide dynamic unimodal and inte- hand, is stored long term in association prefrontal
grated sensory input to the prefrontal areas of the prefrontal cortex. This re- cortex occurs,
cortex for higher processing and recip- gion works in harmony with other areas the person
rocally modulates sensory information of the neocortex to recall the when and may develop
originating in unimodal and heteromo- where an event took place. When dam- a ‘‘source
dal cortical regions. -Aminobutyric acid age to this region of the prefrontal cor- amnesia,’’ which
(GABA) inhibitory input to the hippo- tex occurs, the person may develop a involves the loss
campus is predominantly provided by ‘‘source amnesia.’’ A source amnesia in- of memory for
when and
the contralateral hippocampus.14 volves the loss of memory for when and
where an event
The hippocampal network is felt to where an event occurred, despite retain-
occurred, despite
be important in encoding new facts and ing information of the event itself. For retaining
experiences but also in consolidation example, one may remember the details information of
of new information over time and the of a movie but forget when they saw it, the event itself.
distribution of the memory representa- whether it was in a theater or on DVD,
tions throughout cortical regions for and even whether they were with some- A Explicit memory
long-term storage.26 one at the time. that has
been stored
Another important memory circuit is Remote memory is actually a form of
long-term may
the amygdala–dorsomedial thalamus– long-term memory, but that in which
be subject to
prefrontal cortex–amygdala loop (Figure 5-3). information was learned, consolidated, modification
This circuit most likely participates in and stored in the past. This includes upon recall. In
prefrontal network functions contribut- autobiographic, episodic, and semantic many cases
ing to memory. These may include inte- memories learned and stored months this is due to
grating emotional importance of the and years ago. It is extremely rare to newly acquired
explicit memory, sustained attention, have a deficit of remote memory after an information
retrieval, temporal and spatial organiza- mTBI. When individuals who sustained about the
tion of memory, judgment of one’s own an mTBI claim to have lost memory of recalled event.
knowledge of his or her memory ability their past life and even self-identity, an A For the few
(metamemory), the ability to recall de- underlying psychogenic basis for their patients with
tails of a future event (prospective mem- concerns should be considered. mTBI who have
ory), and the ability to apply strategies Explicit memory that has been stored persistent
to improve learning.14 The prefrontal long term may be subject to modification memory
cortex also has reciprocal connections upon recall. In many cases this is due to problems,
with unimodal and heteromodal asso- newly acquired information about the some evidence 87
ciation cortices (Figures 5-2 and 5-3). recalled event. For example, one’s recall indicates reduced
Semantic knowledge is stored in a of a particular scene or line from a fa- cognitive
information-
distributed fashion throughout the neo- vorite movie may be discovered upon
processing
cortex. Pieces of associative information viewing the film again to be slightly dif-
efficiency,
reside in different neocortical regions ferent from how it was originally re- impaired vigilance,
but upon recall are integrated in the membered. Changes to the memory prolonged
heteromodal cortex to form a complete store, based on the new information ac- reaction time,
memory. For example, when asked to quired, may later be recalled in its newly and deficits
recall a fire truck, descriptors that may modified form. The hippocampus is also in sustained
come to mind include the size, shape, responsible for accessing these new and focused
color, type of vehicle, function, sound of memories for future modulation and attention months
the siren, and all associated equipment consolidation.27 Patients with amnesia after injury.
(eg, helmet, boots, hose, and even a who have lost their ability to learn new
dalmatian). All of the individual features information may still be able to recall
" MEMORY IMPAIRMENT
KEY POINTS
remote memories. However, new infor- function of storage processing, a more
A Patients who
mation used to modify a remote memory passive function commonly seen with
sustain an mTBI
and recover to cannot be learned. In the patient with temporal and diencephalic lesions.33
apparent normal amnesia, therefore, the remote memory The memory problems and execu-
function remain will repeatedly be recalled in its original tive dysfunction experienced by pa-
susceptible stored form despite exposure to new tients with mTBI after resolution of PTA
to the information, which would result in mo- are linked to increased sensitivity to
reemergence dulation and reconsolidation in a person interference, difficulty organizing mate-
of cognitive with intact long-term memory. rial to be learned, and difficulty with
impairment The memory problems experienced generating an effective search mecha-
during periods by patients with mTBI can be better nism for locating material stored in
of physical or
understood through familiarity with memory. This results in poor perfor-
psychological
the functional anatomy and categories mance because of the inability to focus
stress. This
suggests that
of memory processing. attention and control interference, which
even when affects both registration and retrieval of
normal function information.33 These patients, just as
EXECUTIVE DYSFUNCTION IN those with amnesia, have difficulty with
ostensibly
returns, cerebral MEMORY PROCESSING immediate memory and delayed free re-
recovery may mTBI generally does not lead to per- call on a word list, but patients with mTBI
not be sistent significant compromise in mem- will significantly improve on recognition
complete. ory function.28 For the few patients whereas the amnestic patients will not
A The memory with mTBI who have persistent memory improve. Patients with mTBI are also
problems and problems, however, some evidence in- less likely to use semantic clustering as a
executive dicates reduced cognitive information- strategic technique in order to enhance
dysfunction processing efficiency,29 impaired vigi- memory recall.33 For example, if patients
experienced by lance, prolonged reaction time,30 and with mTBI are presented a list of 12
patients with deficits in sustained and focused atten- words randomly listed, but including
mTBI are linked tion months after injury.31 In addition, three semantic categories of four words
to increased patients whose cognitive test scores nor- each (eg, four musical instruments, four
sensitivity to malize may still not have full neurophys- fuels, and four food products), they are
interference,
iologic recovery.1 Evidence also suggests far less likely than healthy controls to use
difficulty
that patients who sustain an mTBI and a strategy of word grouping by category
organizing
material to be
recover to apparent normal function re- (semantic clustering).33 Patients with
learned, and main susceptible to the reemergence of mTBI also tend to have more intrusions
cognitive impairment during periods of and a higher incidence of false-positives
88 difficulty with
generating an physical or psychological stress.32 This on recognition when a distracter list is
effective search suggests that even when normal func- presented after the target list of words.33
mechanism for tion ostensibly returns, cerebral recovery This appears to have ‘‘real-life’’ applicabil-
locating material may not be complete.1 ity in that a common concern associated
stored in The subtlety of past mTBI residual with mTBI patients is easy distractibility
memory. cognitive deficits may lead to the inac- and forgetfulness, which are often im-
curate conclusion that patients have proved with reminders.
returned to a normal baseline when in In addition to problems with mem-
fact they continue to demonstrate im- ory recall, retrieval, and sustained atten-
pairments with appropriate executive tion, patients with mTBI and executive
function challenges. After an mTBI, a memory dysfunction manifest deficits
higher incidence of executive dysfunc- of working memory, recall of temporal
tion of memory including defective re- order, prospective memory, source mem-
trieval, a function that requires strategy ory, and metamemory,33 as well as deficits
and effort, exists, in contrast to a dys- in the application of strategies to improve
KEY POINTS
learning and memory.14 It is common for memory trace. This rehearsed material
A Patients with the
patients with a history of an mTBI to is actively held in phonologic short-term
inability to
present with a concern of ‘‘my memory is storage. The visuospatial sketch pad focus attention
shot.’’ Yet during the history intake they (visual domain) retains small amounts and control
may be able to discuss in great detail the of visuospatial information in working interference,
events that have taken place from the memory. The visuospatial loop is fur- just as those
time of the injury up to the present time, ther divided into visual object and with amnesia,
clearly demonstrating their ability to learn spatial components.36 For example, if have difficulty
new information. However, the patient’s one were to enter the room of a house with immediate
significant other or friend may reveal that for the first time and then suddenly memory and
if the patient is asked to perform a task move to another room, the ability to delayed free
recall on a
and then is interrupted before the task is recall after a short delay that a black
word list, but
executed, the patient may completely recliner chair (visual object compo-
the patients
forget to do the task, unless once again nent) was located in the far left corner with mTBI will
reminded (difficulty with working mem- of the room (spatial component) would significantly
ory). It may also be revealed by another represent the visuospatial sketch pad’s improve on
that the events recalled during the history role in working memory. The interac- recognition
intake did occur, but not necessarily in tion with the articulatory loop (eg, re- whereas the
the temporal order presented by the hearsal of the words black recliner patients with
patient or in the location ascribed to the chair and far left corner) may serve to amnesia will
event (source memory deficit). Another strengthen the memory trace but is not not improve.
common concern of the patient with an necessary for visual object and spatial A In addition to
mTBI is forgetting to keep an appoint- recall. Patients given a test of simple problems with
ment or an engagement (prospective visual reaction time while being pre- memory recall,
memory deficit). A prospective memory sented with a dual task of digit span retrieval, and
contains two components, retrospective demonstrate a decrement in reaction sustained
and prospective.34 Retrospective memory time compared to healthy controls.37 attention,
is the ability to remember what action This kind of test stresses the central patients with
needs to be taken in the future and when executive system, thereby adversely af- mTBI and
it needs to be taken (eg, meet the boss fecting the allocation of attentional re- executive memory
dysfunction
for lunch on Thursday). The prospective sources as well as planning, analysis of
manifest deficits
component is remembering to actually optional responses, and selection of
of working
perform the action when the appropriate cognitive strategies.36 This scenario also memory, recall
event and time occurs (eg, going to lunch has real-life applicability as patients with of temporal
with the boss when Thursday arrives). mTBI often demonstrate difficulty with
A functional working memory model sustained attention, distractibility, and
order, prospective
memory, source
89
has been proposed that includes a multitasking. memory, and
central executive system with connec- As previously mentioned, executive metamemory,
tions to subsidiary storage mechanisms function is often used synonymously as well as deficits
known as the articulatory loop and the with frontal lobe function but is ac- in the application
visuospatial sketch pad systems.35 The tually dependent on neural networks of strategies to
central executive system is believed to that connect frontal areas with specific improve learning
and memory.
coordinate and schedule mental opera- subcortical and diffuse cortical regions,
tions, including the allocation of atten- including unimodal and heteromodal
tional resources as well as the planning association cortex; medial temporal and
and selection of cognitive strategies.36 cingulate cortex; amygdala; and other
The articulatory loop (verbal domain) is limbic, thalamic, striatal, and brainstem
believed to recycle or rehearse verbal regions (Figure 5-3). The prefrontal
material, such as a word list or digits, cortex serves as the central executive
automatically in order to enhance the of these networks, processing and
" MEMORY IMPAIRMENT
KEY POINTS
analyzing selectively attended-to sen- ferred to as being fluid, while those that
A A functional
sory information in the context of pre- require retrieval of overlearned infor-
working memory
model has been viously stored applicable knowledge, mation are referred to as being crystal-
proposed that from which goal-directed strategies are lized.39 Fluid processes appear to have a
includes a central constructed, planned, and executed higher association with visual memory
executive system, through a motor response. compared to verbal memory.40 Busch
with connections This whole process may be influ- and colleagues posited that patients
to subsidiary enced by the emotional significance for with executive dysfunction would per-
storage the individual. For example, the license form more poorly on tests of visual
mechanisms plate number of the vehicle driven by an memory functions.40 In patients with
known as the individual who just robbed you may be mild executive dysfunction who were
articulatory
held in working memory (with stronger tested 1 year after injury, deficits in vi-
loop, and the
efficiency) until it can be written down, sual memory performance remained,
visuospatial
sketch pad
compared to a list of words you are whereas verbal memory function had
systems. asked to remember in a doctor’s office. returned to a normal range. The more
The neural circuitry of working mem- crystallized function of verbal memory
A The prefrontal ory appears to have somatotopic func- normalized, while the more fluid func-
cortex serves as tional components as well. Verbal working tion of visuospatial memory remained
the central
memory has greater left hemisphere defective.40 This suggests that the vi-
executive
participation, but recruitment of homolo- suospatial sketch pad is more strongly
system,
processing
gous contralateral regions may occur with linked to the central executive than
sensory increasing task demand.38 Verbal working is the verbal articulatory/phonologic
information memory involves a storage component in loop.39 Therefore, episodic visual mem-
from which the posterior parietal area, a rehearsal ory tasks place greater demands on
goal-directed component in frontal speech area (inferior cognitive processing, planning, organi-
strategies are frontal gyrus and supplemental motor zation, and overall executive function-
constructed, area), and an execution component in ing than do verbal memory tasks.40 This
planned, and the prefrontal cortex.36 finding has clinical applicability for many
executed. This Visuospatial working memory involves patients who continue to have memory
whole process greater right rather than left hemisphere problems months to years after an mTBI.
may be
involvement but, like verbal working Many of the short mental status exami-
influenced by
memory, recruits from the opposite he- nations used in outpatient settings by
the emotional
significance for
misphere when increased task demand primary care providers and neurolo-
the individual. occurs.38 Bilateral parietal and cingulate gists test exclusively for verbal memory
cortex provide the substrate for content- through word lists. Rarely are visuospa-
90 specific attention to task, and the tial working memory tests administered
prefrontal cortex serves to store and ma- by primary providers months to years
nipulate information. A hierarchy of pre- after an mTBI. Subtle persistent deficits
frontal function is composed of the in visuospatial executive function there-
ventral lateral area, which serves to store fore may be missed because the sensitive
and maintain information online, and the tools used to detect these deficits are not
dorsal lateral prefrontal cortex (DLPFC), utilized. Formal testing of visuospatial
which monitors and manipulates the working memory and executive function
allocation of resources.36 Spatial working under the supervision of a skilled neu-
memory storage of information also oc- ropsychologist may be required to de-
curs in more dorsal lateral regions of the tect these deficits.
prefrontal cortex, while object recall in- Other common problems noted in
formation occurs more ventrally.36 patients after an mTBI include slowness
Cognitive processes that require of mental processing, delayed reaction
novel problem solving have been re- or response time, difficulties switching
KEY POINTS
or completing tasks, multitasking, and acute assessment tool, the Military Acute
A Cognitive
temporal monitoring of both past and Concussion Evaluation (MACE). The
processes that
future events.1,11,41 All of these prob- MACE includes the Standardized Assess- require novel
lems affect the mediation of goal- ment of Concussion test in addition to problem solving
directed behavior and subsequently historical information of the event, in- have been
the ability to function normally in real- cluding whether an LOC or any PTA referred to as
life, day-to-day experiences.15 Patients occurred and the duration of each, and being fluid,
with mTBI may also manifest deficits of the performance of a general neurologic while those that
metamemory, demonstrating poor judg- screening examination.43 Based on the require retrieval
ment of what they think they know and acute assessment of the military service of overlearned
how well they think they know it.41 member in a combat theater who sus- information
The concerns of many patients with tains an mTBI, the Defense and Veterans are referred
to as being
a history of mTBI who continue to Brain Injury Center (DVBIC) developed
crystallized. The
manifest persistent cognitive symptoms a detailed algorithm of ongoing assess- fluid processes
have been attributed to psychological ment, care, and return-to-duty clinical appear to
factors.2,32 Psychological factors such practice recommendations, which can have a higher
as depression and chronic stress can- be found at www.dvbic.org. Other fre- association with
not be ignored, as they do represent com- quently used acute brief assessment visual memory
mon comorbidities associated with mTBI. tools for concussion include the Repeat- compared to
However, sensitive neuropsychological able Battery for the Assessment of Neu- verbal memory.
testing and modern functional neuro- ropsychological Status (RBANS) and the A Episodic visual
imaging are shedding new light on the memory tasks
presence of neural network dysfunction place greater
that may persist for months to years in TABLE 5-2 Tools for
demands on
Assessment of
patients after an mTBI who on general Concussion cognitive
mental status testing have ostensibly processing,
returned to a ‘‘normal’’ baseline. planning,
" Automated
Neuropsychological organization,
COGNITIVE ASSESSMENT Assessment Metrics (ANAM) and overall
OF MEMORY executive
" CNS Vital Signs VS7 functioning
A number of measures have been de-
veloped to assess cognitive function in " Cognistat than do verbal
memory tasks.
both the acute and postacute-chronic " HeadMinder Cognitive
This finding
stages after an mTBI (Table 5-2). Many Stability Index (CSI)
has clinical
of the acute assessment tools were " Immediate Post-Concussion
initially developed for the sideline eval- Assessment and Cognitive
applicability for
many patients
91
uation of athletes after a witnessed Testing (ImPACT) who continue to
concussion. One such instrument, the " MicroCog have memory
Standardized Assessment of Concussion, problems
" Military Acute Concussion
was developed to acutely assess con- months to years
Evaluation (MACE)
cussed athletes who experienced no after an mTBI.
" Repeatable Battery for
LOC.42 This tool is a 30-point assessment the Assessment of
of orientation, immediate memory recall Neuropsychological
(three trials of five words), concentration Status (RBANS)
(digits in reverse and months in reverse), " Sports Concussion
and delayed free recall. A series of Assessment Tool (SCAT)
exertional physical maneuvers are con-
" Standardized Assessment
ducted between the immediate and of Concussion (SAC)
delayed recall component of the evalu-
ation.42 The military developed its own
" MEMORY IMPAIRMENT
KEY POINTS
Immediate Post-Concussion Assessment chological Assessment Metrics (ANAM),
A It is rare that tests
and Cognitive Testing (ImPACT).44 An- a computerized assessment tool that
of visuospatial
working other standardized tool, recently modi- takes approximately 20 minutes to com-
memory are fied at the 2008 Third International plete. Using the ANAM, the military is
administered Conference on Concussion in Sports, is in the process of acquiring baseline neu-
by primary the Sports Concussion Assessment Tool rocognitive data on all service members
providers (www.sportsconcussion.co.za). prior to deployment. Consequently a
months to Unlike a concussion witnessed by personal baseline comparison will be
years after an others in an athletic contest, a combat- available for any service member who
mTBI. Subtle related mTBI, such as that caused by might sustain a TBI and be tested while
persistent an IED explosion, is often unwitnessed in the acute postconcussive state during
deficits in
and compounded by serious bodily in- the period of recovery and remotely af-
visuospatial
jury, immediate fear of death or serious ter the event.
executive
function
injury, acute stress reaction, and wit- A number of issues may cloud the
therefore may nessing the death or maiming of fellow accuracy of the baseline cognitive per-
be missed service members or innocent victims formance. A few examples include pre-
because the (Case 5-2). All of these events may ex- deployment anxiety, sleep deprivation,
sensitive tools acerbate the cognitive, physical, and neu- fatigue, pain, medication, alcohol or
used to detect ropsychiatric sequelae of an mTBI.18,45 drug use, psychological problems, fam-
these deficits Because detailed screening for a his- ily and psychosocial stressors, effort of
are not utilized. tory of mTBI (often by questionnaire performance, and inattention for any
A Patients with
and self-report) occurs after deployment number of reasons (Figure 5-1).
mTBI may also (sometimes months after the event), Postdeployment cognitive assess-
manifest there is concern of misattribution of the ment may identify deficits and serve in
deficits of service member’s current symptoms to part as a basis for treatment strategies;
metamemory, the remote mTBI, if an mTBI did in- however, the presence of deficits does
demonstrating deed occur. Belanger and colleagues not confirm that an mTBI did occur.
poor judgment and Hoge and colleagues have sug- Even when the history strongly suggests
of what they gested that even the initial event (eg, that an mTBI did occur, the presence
think they exposure to an IED explosion) that re- of deficits does not confirm that the
know and how sulted in an LOC or being dazed or con- patients’ symptoms or cognitive testing
well they think
fused may be the result of an acute stress results can be attributed to the mTBI.
they know it.
reaction with autonomic changes rather In like manner, the absence of self-
A The concerns of than an mTBI.17,46 reporting does not necessarily mean
many patients In the process of developing clinical that an mTBI did not occur. It is widely
92 with a history practice guidelines and recommendations accepted that many of the same so-
of mTBI who for the acute management of mTBI in matic, cognitive, and neuropsychiatric
continue to military operational settings, the DVBIC symptoms that may be present after an
manifest
working group addressed neurocognitive mTBI also occur in patients with medi-
persistent
assessment.44 The working group be- cal or psychiatric problems who have
cognitive
symptoms have
lieved that a good assessment tool should never had a TBI.46 Furthermore, even
been attributed test attention/concentration, memory, pro- in patients who have had a history of
to psychological cessing speed, reaction time, and execu- mTBI, the results of cognitive testing
factors. tive function. may be predominantly due to medical
DVBIC members presented a number or psychological factors, or to these in-
of factors related to applicability, utility, tegrated comorbidities with mTBI.
and practicality of neurocognitive assess- In postdeployment screening and
ment in an operational environment. assessment, the importance of a face-
These are detailed in their report.44 The to-face interview cannot be overempha-
military chose the Automated Neuropsy- sized. It has been shown that patients
with mTBI tend to significantly endorse Resnick49 identified three categories
more symptoms and the severity of of malingering. (1) Pure malingering in-
symptoms when completing a ques- volves feigning illness when none exists.
tionnaire than they actively endorse (2) Partial malingering is characterized
during a face-to-face interview.47 by either the exaggeration of symptoms
If it is determined that formal neuro- or the allegation that symptoms result-
psychological testing be performed, the ing from an injury still persist when in
testing should be conducted by a skilled truth they have resolved. (3) False im-
neuropsychologist. In addition to the putation occurs when symptoms that
selection of the battery to be used and actually exist are consciously falsely as-
its interpretation, the neuropsycholo- cribed to the injury when a patient
gist should conduct a face-to-face inter-
view and observation of the patient in
order to help determine validity of per- TABLE 5-3 Neuropsychological Tests Commonly
formance, including effort and whether Used to Assess Patients With
any responses are exaggerations.11 It is Persistent Cognitive Concerns After
Mild Traumatic Brain Injury
also up to the neuropsychologist to de-
termine whether the results across test
" Neuropsychological Tests
batteries make neurologic sense based
on what is known about normal brain Brief Visuospatial Memory Test-Revised (BVMT-R)
function. It is important to note that California Verbal Learning Test-Second Edition
‘‘abnormalities’’ on neuropsychological (CVLT-II)
testing do not necessarily mean that the Category Test
patient has acquired brain dysfunction.
Continuous Performance Test (CPT)
Intraindividual variability and low scores
are occasionally seen in healthy adults.48 Controlled Oral Word Association Test (COWAT)
Table 5-3 includes a partial list of neu- Digit span
ropsychological tests that are commonly
Digit Symbol-Coding (from Wechsler Adult
used in the evaluation of mTBI. Intelligence Scale-III)
Table 5-4 lists cognitive effort tests
Hopkins Verbal Learning Test-Revised (HVLT-R)
commonly associated with detection of
malingering.28 Performance on forced- Paced Auditory Serial Addition Test (PASAT)
choice measures of cognitive function Rey-Osterreith Complex Figure (ROCF)
is typically at a below-chance level in
Stroop Color and Word Test
malingerers. Caution is advised to not
use performance on effort tests alone Symbol Digit Modalities Test (SDMT) 93
in making a diagnosis of malingering. Trail Making Tests A and B
Some patients with medical, neuro-
Wechsler Memory Scale-III Logical Memory I and II
logic, and psychiatric illness may be
depressed, apathetic, lethargic, or ex- Wisconsin Card Sorting Test (WCST)
hausted and exert very little effort on " Personality Inventories
these tests. Determining level of ef- Minnesota Multiphasic Personality Inventory,
fort is important in establishing the Second Edition (MMPI-2)
validity of performance on other neuro-
Personality Assessment Inventory (PAI)
psychological assessment measures. Mis-
attribution of low raw scores to cognitive " Self-Report Measures
impairment due to mTBI may lead to Neuropsychological Impairment Scale (NIS)
misdiagnosis, inappropriate treatment,
Neuropsychological Symptom Inventory (NSI)
perpetuation of illness behavior, and
compensation where none is warranted.
" MEMORY IMPAIRMENT
KEY POINT
knows they are due to another cause. A history of a single mTBI is usually
A Sensitive
not associated with long-term persistent
For example, concerns of difficulty
neuropsychological
concentrating may be consciously and neuropsychological deficits.7 However,
testing and
modern volitionally ascribed to an mTBI that even when standard neuropsychological
functional occurred many months previously, testing of patients with mTBI is within
neuroimaging when the symptom actually arose after normal limits, specialized tests of at-
are shedding the onset of a recent significant psycho- tention, working memory, and reaction
new light on the logical stressor.28 Testing for and deter- time may reveal subtle deficits.11 In ad-
presence of mination of malingering by a skilled dition, it has been demonstrated that
neural network clinician is important in establishing an when a group of patients were informed
dysfunction that accurate diagnosis, avoiding inappro- that they were undergoing neuropsy-
may persist for priate or unnecessary evaluation and chological testing because of their his-
months to tory of mTBI, they performed more
treatment and secondary gain rewards,
years in patients
maintaining the morale of the group to poorly as a group than another group
after an mTBI,
and in whom, on which the patient belongs (eg, the of patients who had a history of mTBI
general mental military), and avoiding the long-term but were not told that the testing was
status testing, economic burden to society for future linked with their previous mTBI.51 There-
have ostensibly medical and disability costs (Case 5-3). fore, even the ‘‘diagnostic threat’’ of
returned to a Tools for use in cognitive screening association can negatively impact per-
normal baseline. and assessment of mTBI continue to formance on neuropsychological tests.51
evolve. Recently a Concussion Symp- In certain circumstances, especially
tom Inventory was developed to mon- after multiple concussions, persistent
itor progress in recovery for sports- neuropsychological deficits may be
related concussions.50 Since screening manifested. This topic will be dis-
questionnaires may sometimes lead to cussed further in ‘‘Management and
misattribution of common symptoms Outcomes.’’
to a previous possible mTBI, and the
absence of reported history or symp- NEUROIMAGING AND
toms may lead to overlooking a pa- COGNITIVE CORRELATION
tient who actually had a prior mTBI, Most patients who have sustained a
it is important to seek objective diag- single mTBI have had normal conven-
nostic biomarkers for mTBI not only tional brain imaging with either CT or
for accurate diagnosis but also for MRI.52 MRI is more sensitive than CT in
prognosis. patients with mTBI, but over two-thirds
of symptomatic patients who undergo
94 routine MRI show no signs of struc-
tural abnormality. T2-weighted fluid-
TABLE 5-4 Effort Tests Commonly Associated
With the Detection of Malingering attenuated inversion recovery (FLAIR)
and gradient-recalled echo (GRE) MRI
" Test of Memory Malingering (TOMM) sequences have been shown to be more
sensitive to traumatic lesions and hem-
" Victoria Symptom Validity Test (VSVT)
orrhages than routine MRI. Diffusion-
" Medical Symptom Validity Test (MSVT) weighted imaging (DWI) on MRI has
" Green’s Word Memory Test been even more sensitive than T2/FLAIR
and GRE in demonstrating injuries
" Effort index—Repeatable Battery for the
Assessment of Neuropsychological Status (RBANS) caused by shearing.53
TheVeteransAdministration/Department
" Forced choice on California Verbal Learning
of Defense (VA/DoD) Clinical Practice
Test—Second Edition (CVLT-II)
Guideline for Management of Concussion/
mTBI states that CT is still the imaging
Case 5-3
A 32-year-old male soldier was medically evacuated from Iraq to the United States because of
subjective symptoms of PTSD. While on the psychiatry service he was observed to have no problem
sleeping, no hypervigilance or startle, and showed no social withdrawal. He reported poor
memory but was able to present a detailed history of events while he was deployed. He claimed
that he had over 24 concussions, half of which were associated with LOC for over 20 minutes
each. He said he had been exposed to 15 IED blasts, estimating his proximity within .9 m
to 1.5 m (3 ft to 5 ft) of the explosions. He sought no medical attention after any of these
events, nor was there any objective documentation by a medic or physician of these self-reported
injuries.
On questionnaires, the patient had the highest score possible for headaches, neck and back
pain, and general fatigue. He stated that he could barely function. General physical and
neurologic examination was normal. He was oriented to only 3/5 parameters. His word list
immediate recall was 0/5 on all three trials. Delayed free recall was 0/5, with no improvement on
cueing and multiple choice. He became very angry when the provider suggested that he might
not be exerting good effort. He was a very muscular individual who was witnessed by other
soldiers to frequent the gym’s weight room when not at the hospital for evaluations.
On a subsequent visit the patient underwent neuropsychological assessment. He was able to
discuss in detail the events in his life that occurred between appointments. He stated that his
memory had become so bad that he could no longer remember his brothers’ and sisters’ names
or where he grew up. He said that he had to relearn how to tie shoelaces. His overall performance
on the Neuropsychological Assessment Battery (NAB) was in the second percentile. On the two
trials of the Test of Memory Malingering he scored 25/50 and 27/50 (cutoff score is 45/50).
The expressed intent of the patient was to receive a medical board from the military for
which he felt entitled to 100% disability. This desired plan would release him from active duty
and provide both a medical retirement income and full benefits, including medical, for life for
him and his family.
Comment. Many inconsistencies appear in this patient’s reported history. His repeated poor
performances on tests of memory and effort are incongruent with his ability to function on a
day-to-day basis and his detailed recall of personal events between appointments. His claim to fail
to remember family names (remote memory) or how to tie shoes (procedural memory) is not
usually associated with the attention and retrieval deficits seen with mTBIs or PTSD. His lack
of recall improvement with cues and multiple choice is the pattern seen in a confusional
state or amnesia. Clinically he manifested neither condition. None of these findings makes
neurologic sense.
His reported history of the IED explosions and concussions raises the question of complete
fabrication or at least embellishment. The patient stated that he was within 1.5 m (5 ft) of the 95
explosions, which apparently caused concussions, but no other bodily injury. This proximity to a
blast is lethal in almost 100% of cases. The fact that the patient never sought medical care after
these apparent blasts provides no objective basis for even a single TBI having been documented.
Despite the extreme scores on the intake questionnaires, the patient was able to continue to
function in daily life and was frequently seen working out in the gym without any apparent
difficulty. The anger with which he responded to the examiner who questioned his effort is
typical of the behavior seen when patients who are intentionally feigning feel that they are being
‘‘discovered.’’ The less-than-chance performance on the Test of Memory Malingering strongly
suggests a conscious and intentional effort to deceive. Although the patient reported most
symptoms associated with PTSD, there was little objective evidence of the condition under
observation.
The patient’s history and performance on cognitive measures, associated with the intended
secondary gain of receiving a medical retirement and disability, as well as full benefits for life, was
felt to constitute malingering. He received a less than honorable discharge from the service
without disability or benefits.
" MEMORY IMPAIRMENT
KEY POINTS
study of choice during the acute phase tion, attention, and memory among
A A combat-related
to rule out potentially life-threatening injured patients compared to healthy
mTBI is often
compounded intracranial pathology when certain red controls.58 This further suggests that
by serious bodily flag symptoms are present. These may executive dysfunction in mTBI may also
injury, immediate include progressively declining level of arise from injury to subcortical neural
fear of death or consciousness and/or neurologic exam- networks that interact with prefrontal
serious injury, ination abnormalities, pupillary asymme- regions rather than requiring discrete
acute stress, and try, seizures, repeated vomiting, double lesions in prefrontal cortex to explain
witnessing the vision, progressively worsening head- clinical executive dysfunction.
death of others. ache, failure to recognize familiar people Functional imaging studies, such as
All of these events or places, increasing confusion and fMRI, PET, and SPECT are being uti-
may exacerbate
irritability, slurred speech, unsteadiness lized more frequently to detect changes,
the cognitive,
and weakness, and/or numbness in the both acutely and chronically, after mTBI.
physical, and
neuropsychiatric
arms or legs.54 The guideline further SPECT has been shown to be more sen-
sequelae of states that neuroimaging is not recom- sitive to detecting abnormalities after
an mTBI. mended for patients who sustained an mTBI than CT scans.59 When performed
mTBI/concussion and are beyond the 72 within the first few weeks after an mTBI,
A Even when the hours postinjury phase if red flags are not SPECT reveals hypoperfusion, usually in
history strongly present or the condition is not deterio- frontal and temporal regions, in over
suggests that an
rating.54,55 One may also access these 60% of patients who had a normal CT.60
mTBI did occur,
guidelines at www. pdhealth.mil/TBI.asp. However, few SPECT studies to date
the presence of
deficits does not
A growing body of literature dis- have investigated neuropsychological
confirm that the cusses newer structural and functional correlation with metabolic function,
patients’ symptoms imaging techniques used to study acute findings in asymptomatic patients who
or cognitive and chronic effects of mTBI. A number had an mTBI, and long-term outcomes
testing results of these studies have revealed both after an mTBI.60
can be attributed acute and chronic structural and func- Functional MRI and PET studies look-
to the mTBI. tional changes after mTBI not seen ing at changes in brain activation or
A Many of the
on routine neuroimaging. A number of metabolism with cognitive challenges
same somatic, newer imaging techniques are being have produced interesting results. Some
cognitive, and used to investigate TBI. The reader is of these results provide new insights
neuropsychiatric referred to current detailed reviews of into different changes that occur in
symptoms that the topic.52,56 the brain in patients with mTBI com-
may be present Some of these new neuroimaging pared to healthy controls, even when
after an mTBI techniques are used primarily as in- cognitive task performance between
96 also occur in vestigational tools for their correlation the groups is often no different. One
patients with with acute and chronic neurocogni- such study demonstrated that among
medical or tive symptoms and deficits. Diffusion- patients with mTBI at 1 month post-
psychiatric
tensor imaging fractional anisotropy, injury, an increase occurred in activa-
problems who
which is a measure of white matter tion in predominantly right parietal and
have never
had a TBI.
integrity, has been used for correlation DLPFC when a progressive-load work-
with cognitive performance, especially ing memory task was administered.
in attention, working memory, and re- Healthy controls demonstrated bipa-
action time in both healthy controls rietal and bifrontal activation to low-
and patients with mTBI.57 A recent load working memory tasks, but the
study demonstrated that fractional an- activation did not significantly increase
isotropy changes seen in projection on higher-load tasks. Cognitive perfor-
fibers from ventral and anterior ven- mance on the tasks was not significantly
tral thalamus to the frontal cortex ac- different between the groups.61 In a
counted for variance in executive func- subsequent study, the patients with
KEY POINTS
mTBI demonstrated disproportionately McAllister and colleagues62 have stated
A Patients with
increased activation compared to con- that injury-related changes in the ability
mTBI tend to
trols when the task load went from low to activate or modulate working mem- significantly
to moderate, but when the load in- ory processing resources may underlie endorse more
creased to high, the cortical activation the persistent memory concerns that symptoms and
changed very little from the moderate- many patients with mTBI manifest. This the severity of
load activation. Once again, task perfor- is consistent with the real-life experi- symptoms on a
mance did not differ significantly be- ences of many patients who struggle questionnaire
tween groups.62 with cognitive challenges, despite ob- than they
In a study that included patients with jective normal mental status testing. actively endorse
mTBI up to 14 months after their injury, Correlation of functional imaging with during a
patients were found to have decreased face-to-face
consistent use of selected cognitive
interview.
activation in the frontal cortex and evaluation tools during acute and
increased activation in temporal and chronic postconcussive phases is essen- A Abnormalities on
parietal areas relative to healthy con- tial in future investigations and may neuropsychological
trols, despite similar performance be- assist in better understanding the differ- testing do not
tween both groups on working memory ences in the brain, if any, between those necessarily mean
tasks.63 The same group of investigators individuals who have resolution of their that the patient
studied a group of patients with mTBI has acquired
symptoms and those whose symptoms
brain dysfunction.
who had persistent postconcussive symp- persist.
Intraindividual
toms 1 to 9 months after injury. They New imaging studies require norms
variability and
were restudied 9 to 23 months after the with which to compare selected study low scores are
first study. An initial decreased activa- groups with a history of mTBI. In addi- occasionally seen
tion of DLPFC occurred during a work- tion many patients with mTBI, especially in healthy adults.
ing memory task in the mTBI group. combat related, have comorbidities. The
Upon reassessment, those patients comorbid variables will need to be con-
A Caution is advised
to not use
whose clinical symptoms had resolved trolled as many of these conditions, such performance on
demonstrated an increase in left DLPFC as depression and PTSD, may also cause effort tests
activation compared to those with per- cognitive problems, including reports of alone in making
sistent symptoms.64 memory impairment. a diagnosis of
Another study in concussed athletes malingering.
that was performed a week after injury MANAGEMENT AND OUTCOMES Some patients
demonstrated a correlation between the Most patients who have sustained a with medical,
degree of activation and length of time to single mTBI gradually recover within the neurologic, and
return to play. The longer the increased first 2 weeks after injury with no last- psychiatric
activation on working memory tasks per- ing clinical sequelae.7,66 Management of illness may be 97
depressed,
sisted, the longer the time of recovery.65 these patients should focus on promot-
apathetic,
New structural and functional imaging recovery and avoiding harm. Early
lethargic, or
ing techniques such as diffusion-tensor supportive validation and educational exhausted and
imaging, fMRI, and PET have increased intervention, including the expectation exert very little
sensitivity to changes in the brain after of recovery, are effective in helping in- effort on
mTBI. Some of these functional changes dividuals improve and also avoid the these tests.
may only be appreciated after a cogni- long-term consequences of postconcus-
tive challenge. Performance on cogni- sion syndrome.67
tive testing may return to normal; yet The AAN created guidelines for as-
the effort required to achieve normal sessment, care, and return to play for
cognitive performance may be much athletes who sustained a concussion in
greater in a person who previously sus- sports contests. The VA/DoD also de-
tained an mTBI than in a healthy control veloped an evidence-based clinical prac-
person who has never had a TBI.59 tice guideline for the management of
" MEMORY IMPAIRMENT
KEY POINTS
concussion/mTBI. The reader is re- risk to the service member and to
A A history of a
ferred to this document for details on others if the soldier remained armed
single mTBI is
usually not management and outcome of all symp- and returned to a combat environment
associated with toms associated with mTBI (www. prior to full recovery. Rest, symptomatic
long-term pdhealth.mil/TBI.asp). treatment of somatic concerns, gradual
persistent The specific recommendations in increase in physical activity, and gradual
neuropsychological these guidelines regarding cognitive return to duty are important steps in
deficits. However, symptoms include the early education recovery. When the patient is asymp-
even when of the patient about the nature of the tomatic, a test of exertional activity is
standard cognitive symptoms; consideration of administered to see whether the patient
neuropsychological the effects that common noncognitive remains asymptomatic or once again be-
testing of patients
symptoms, such as pain and sleep de- comes symptomatic, which may include
with mTBI is
privation, may have on exacerbating the the reemergence of cognitive problems.
within normal
limits, specialized
cognitive symptoms; and how to convey If they remain asymptomatic then they
tests of attention, to the patient the expectation of recov- can be returned to their unit with a
working memory, ery. This has a strength of recommen- gradual transition to full-duty activities.
and reaction dation (SR) of A (Box 5-1). The VA/DoD If they once again become symptom-
time may reveal Work Group also recommends a cogni- atic, then they should be given an ex-
subtle deficits. tive evaluation through a structured tended period of rest or transferred to a
A Performance on
interview, although the SR is only rated higher-level medical facility for further
cognitive testing a category C. Comprehensive neuropsy- evaluation.54
may return to chological testing is not recommended Pharmacologic and nonpharmacologic
normal, yet the during the first 30 days after injury (SR management options for cognitive prob-
effort required equals D). In the case that a preinjury lems after mTBI have been established
to achieve neurocognitive baseline has been estab- by the VA/DoD Guidelines Work Group.
normal cognitive lished, then a postinjury comparison At the present time55 medication for cog-
performance may be completed by a neuropsychol- nitive symptoms after mTBI is not re-
may be much ogist but should be determined using commended. This is consistent with the
greater in a reliable tools, and test-retest stability civilian literature in which little evidence
person who
should be ensured (SR equals B).55 In a has been found for effective drug inter-
previously
combat theater it is particularly impor- ventions for patients with an mTBI.68
sustained an
mTBI than in a
tant to assess the service member who A number of recent comprehensive
normal control has sustained an acute mTBI as soon as reviews of neuropharmacologic interven-
person who has possible. The acute cognitive symptoms tions after TBI have been published.69,70
never had a TBI. experienced could create a substantial Most of the studies reviewed involved
98
Box 5-1
Strength of Evidence-Based Recommendations, Veterans
Administration/Department of Defense Clinical Practice
Guidelines: Management of Concussion/Mild Traumatic
Brain Injury
A = Strongly recommended
B = Recommended
C = No recommendation either for or against
D = Not recommended as routine intervention
I = Insufficient evidence to make a recommendation
www.healthquality.va.gov/Rehabilitation_of_concussion_mTBI.asp
KEY POINTS
patients with moderate-severe TBI, but Associated somatic symptoms such
as headache, systemic pain, and sleep
A Injury-related
a few studies included patients of
changes in
mixed severities. A general summary of disturbance, as well as behavioral symp- the ability to
the reviews suggests that methylpheni- toms such as depression or anxiety, may activate or
date may help ameliorate problems be treated with medication if necessary. modulate
with attention and improve processing A provider should exercise good judg- working
speed, concentration, and vigilance. No ment in risk-benefit analysis as a num- memory
clear conclusions can be made about ber of the medications used to treat processing
any specific agent in the treatment of these associated symptoms may ad- resources may
memory or other cognitive problems, versely affect attention, memory, and underlie the
including executive dysfunction. Some executive function. Because the somatic persistent
and behavioral concerns may also ad- memory
preliminary studies using cholinester-
concerns that
ase inhibitors in memory showed prom- versely affect cognitive function, the
many patients
ise; however, further investigations are effective treatment of these symp-
with mTBI
necessary.69 toms may result in improved cognition. manifest. This is
A possible explanation as to why re- Guidelines should serve as a ‘‘guide,’’ consistent with
sults have produced little support for and treatment decisions are still the role the real-life
any specific medication includes the of the provider using best judgment experiences of
fact that multiple neurotransmitters are based on individual patient risk-benefit many patients
involved in attention, encoding, consoli- analysis. who struggle
dation, and storage of explicit memory The only other treatment options for with cognitive
as well as working and prospective mem- cognitive symptoms recommended by challenges,
ory. Norepinephrine, acetylcholine, do- the DVBIC and the VA/DoD guidelines despite objective
during acute postconcussive period normal mental
pamine, serotonin, GABA, and a number
status testing.
of neuromodulators participate in the are to normalize sleep and nutrition,
integrated process of attention, explicit control pain, and encourage graded A Most patients who
memory, working memory, and execu- regularly scheduled aerobic exercise. have sustained
tive function.14 In the future, optimal Follow-up for all patients should occur a single mTBI
pharmacologic success in improving within the first 4 to 6 weeks or sooner gradually recover
within the first
cognitive functions may require combi- to assess progress. A list of practical
2 weeks after
nations of medications that target a num- recommendations for improving mem-
injury with no
ber of neurotransmitters. Some clinical ory can be found in Table 5-5.
lasting clinical
researchers have suggested that response The long-term sequelae after an mTBI sequelae.
to medication may be dose or individual due to a blast in a combat situation
dependent. An example of this is when continue to be under investigation. The A Early supportive
healthy young adults were administered pathophysiology of injury resulting from validation and 99
educational
a baseline working memory task and a blast may differ froman isolated impact
intervention,
then given a dose of bromocriptine fol- or acceleration-deceleration injury. Re- including the
lowed by another working memory task; covery may be impacted by the nature of expectation of
those who had a lower baseline working the injury as well as comorbidities, such recovery, are
memory performance improved on the as an acute stress reaction, anxiety, de- effective in
bromocriptine and those with the higher pression, or the development of PTSD. helping
baseline performance actually worsened The risk of developing PTSD increases individuals
their performance.14 This study result after mTBI, and an mTBI in a patient with improve and
suggests that an optimal level of dopa- PTSD will result in greater disability.71 also avoid the
mine may be necessary in order to maxi- The VA/DoD guidelines also provide long-term
mize working memory performance.14 for assessment of the small percentage consequences of
postconcussion
Doses above or below the optimal level of patients with persistent symptoms.
syndrome.
will produce a decrement in working Within this group of patients cogni-
memory performance. tive symptoms are common. Symptoms
" MEMORY IMPAIRMENT
KEY POINTS
Recommendations by the VA/DoD
A In a combat TABLE 5-5 Ways to Improve
Memory After Guidelines Work Group for patients
theater it is
particularly Mild Traumatic Brain Injury with persistent postconcussive symp-
important to toms include consideration of other
assess the service " Use checklists behavioral health issues, such as stress
member who " Prioritize
and mood disorders; substance abuse;
has sustained an psychosocial and family support sta-
acute mTBI as " Keep a cheat sheet of tus; potential danger to self and others;
soon as possible. important information
with you
premorbid mental health issues; sys-
The acute temic problems such as pain and sleep
cognitive " Get 7 to 8 hours of sleep deprivation; job-related issues, includ-
symptoms " Avoid alcohol, tobacco, ing unemployment; financial and legal
experienced excessive caffeine, and issues; and secondary gain. A suggested
could create a energy drinks
substantial risk to
series of interview questions regarding
the service " Use a pill organizer to each of these factors can be found in
organize your medicines Table C-1 of the guidelines summary
member and to
others if the " Stay physically active (www.pdhealth.mil/TBI.asp).
soldier remained Because of the frequency of co-
" Maintain a healthy diet
armed and morbidities in patients with persistent
returned to a " Avoid further brain injury symptoms, emphasis has shifted from
combat " Focus on one thing at trying to establish attribution of the
environment a time symptoms to focusing on a holistic ap-
prior to full proach to treating the patient’s symp-
recovery.
" Get a routine
toms through a multispecialty interdis-
" Keep mentally active
A Medication for ciplinary team.4,45,71,72
cognitive " Decrease your stress level Management of persistent cognitive
symptoms after " Write it down symptoms may include referral for neu-
mTBI is not ropsychological assessment. This may
Adapted from the Defense and Veterans Brain
recommended. Injury Center. Concussion/mild traumatic brain help to distinguish individual patient
A A provider injury rehabilitation: 10 ways to improve your
memory. www.dvbic.org/images/pdfs/Clinical-
characteristics and performance profile,
should exercise Tools/10_Ways_to_Improve_Your_Memory.aspx. which may help to direct appropriate
good judgment Updated May 4, 2009. Accessed October 19, 2010. treatment options (SR equals B). The
in risk-benefit VA/DoD Guidelines Work Group also
analysis as a suggests that testing should be con-
number of the ducted with reliable and standardized
100 medications tools by trained evaluators under con-
used to treat
may include concerns with memory, trolled conditions and findings should
associated
concentration, and functional limita- be interpreted by trained clinicians. The
symptoms may
adversely affect
tions in their daily lives. As stated above, SR for this suggestion is category C.
attention, caution should be taken not to imme- Deficits on neuropsychological test-
memory, and diately assume that persistent symp- ing should not be automatically as-
executive toms are the direct effect of the mTBI. sumed to be the direct result of an
function. In a review of a large brigade of soldiers, mTBI. Neuropsychological compromise
5% of whom had a suspected history in sustained attention, verbal learning,
of an mTBI with LOC and persistent and visuospatial memory has been dem-
symptoms (including cognitive con- onstrated in deployed service members
cerns), the only symptom found to be compared to nondeployed service mem-
associated with the mTBI, after adjust- bers, even after accounting for head
ment for PTSD and depression, was injury, depression, and stress. Deploy-
headache.2 ment to a combat zone alone, even if no
KEY POINTS
history of TBI was present, was enough mental visual image of a person sitting
A After an mTBI
to account for compromise in cognitive on a motorcycle, holding a football with
due to a blast
function compared to nondeployed ser- a pumpkin on the back of the bike, while in a combat
vice members. Of interest is that the sitting in front of a building with a large situation,
deployed service members had better red cross and a public mailbox in front recovery may
simple reaction times compared to the of the hospital. That image, as bizarre be impacted by
nondeployed service members.73 as it may seem, will assist the individual the nature of
Patients with memory, attention, and/or in recalling the five words. Some draw- the injury
executive function problems who did not backs to this technique include: (1) as well as
respond to initial treatment (previously Patients with significant right medial comorbidities,
mentioned in the acute postconcussive temporal lobe lesions may be incapable such as an acute
recommendations) may be referred to stress reaction,
of generating such visual images. (2) Pa-
anxiety,
therapists with expertise in TBI cognitive tients with mTBI who have the capacity
depression,
rehabilitation. These may include neuro- to utilize this technique may not take or the
psychologists, psychologists, speech path- advantage of it because it requires spon- development of
ologists, and occupational therapists. The taneous generation of an intent and PTSD. The risk of
VA/DaD SR for these treatment strategies strategy to do so, which may be prob- developing
is category C. lematic for some patients because they PTSD increases
Assistive technology for cognition often have some degree of executive after mTBI, and
tools may serve to assist or compensate dysfunction.41 an mTBI in a
for impairment in memory, attention, For real-life tasks, the most practical patient with
and executive function. These devices way of remembering a list is to write the PTSD will result
are also categorized as memory aids or items down on a piece of paper or in a in greater
disability.
cognitive prostheses. The purpose of notebook. For example, taking a written
these tools is to help the individual to list of grocery items to the store is more A Caution should
execute real-life daily tasks by providing practical than rehearsing them mentally be taken to not
cues and limiting demands on impaired by trying to apply visual imagery strat- immediately
cognitive function. egies. Memory prostheses include such assume that
Devinsky and D’Esposito14 catego- items as notebooks, diaries, alarms, per- persistent
rize cognitive remediation therapy into sonal digital assistants, name tags, and symptoms are
three types: (1) memory retraining, (2) posted signs in one’s environment, such the direct effect
compensatory strategies, and (3) tap- as a daily to-do list. Education of sig- of the mTBI.
ping residual memory abilities. Mem- nificant others and family members A Because of the
ory retraining techniques center around to encourage the patient to utilize these frequency of
repetitive practice of memorization; strategies is also very important to comorbidities in
however, this strategy is rarely appli- achieving the benefits of these aids. patients with 101
cable to real-life situations, and it ap- Memory manuals that lay out a daily plan persistent
pears that damaged memory processes of activities should include the possible symptoms,
show little recovery through repetition emphasis has
challenges that may be encountered
shifted from
training.14 throughout the day as well as written
trying to establish
Compensatory strategies are similar plans to deal with them. Support groups
attribution of
to those recommended in the VA/DoD that focus on post-mTBI memory con- the symptoms to
guidelines. These include memory aids/ cerns may also be helpful. These groups focusing on a
prostheses and mnemonics. One strat- are made up of patients experiencing holistic approach
egy for facilitating memory recall is to similar problems, and each member may to treating
link visual imagery with verbal memory play a role in the encouragement and the patient’s
demands. For example, if one is asked support of others. This added socializa- symptoms through
to recall the words motorcycle, hospi- tion may also help patients to develop a multispecialty
tal, pumpkin, football, and mailbox, better strategies for other somatic and interdisciplinary
the individual may develop a surreal psychological comorbidities.14 team.
" MEMORY IMPAIRMENT
KEY POINTS
Tapping residual memory abilities with head injury is a carrier of the APOE
A Deployment to
is primarily directed at patients with 4 allele.76
a combat zone
alone, even if no severe episodic memory impairment, A current avenue of investigative
history of TBI usually after damage to the bilateral interest is the study of long-term se-
is present, is medial-temporal diencephalic circuit. It quelae after cumulative concussions.
enough to involves the use of implicit memory cues Guskiewicz and colleagues75 studied
account for as a method of learning new informa- retired professional football players and
compromise in tion. It has little utility as a strategy for found a significant correlation between
cognitive the common cognitive problems associ- recurrent concussions, self-reported
function ated with mTBI.14 memory symptoms, and clinically diag-
compared to Chen15 recommends an approach to nosed mild cognitive impairment. Players
nondeployed rehabilitation by focusing on training with three or more concussions had a
service
related to executive function. He sug- fivefold prevalence of mild cognitive im-
members.
gests that these training tasks should pairment and a threefold prevalence of
A One strategy for include (1) challenging patients to en- reported significant memory concerns,
facilitating gage top-down modulatory processes compared with players who had no
memory recall mediated by the prefrontal cortex; (2) previous concussion. An earlier onset
is linking visual
developing a goal-based approach; (3) occurred in the players who developed
imagery with
enhancing the transfer and generaliza- AD, compared to age-matched males in
verbal memory
demands.
tion of training effect to new and real- the general population.75
world contexts; and (4) progressively Chronic traumatic encephalopathy,
A Memory and adaptively challenging patients. One which is clinically manifested by memory
prostheses include way to practice executive function re- disturbance, behavioral and personality
such items as
habilitation is through meta-cognitive changes (often with antisocial character-
notebooks,
strategy instruction (MSI),74 which teaches istics), parkinsonism, and speech and
diaries, alarms,
personal digital
patients to plan and manage goals gait abnormalities, is a subject of interest.
assistants, name by breaking down complex tasks into Most patients who have had postmor-
tags, and posted steps. This includes the identification tem evaluation have been boxers and
signs in one’s of a goal and the prediction of their professional football players who had
environment, performance in advance of the activity, sustained repeated concussions during
such as a daily assessing possible solutions based on gen- their careers. Examination of their brains
to-do list. eral predictions, self-monitoring of their demonstrated the presence of a tauop-
A Professional performance during an activity, and or- athy with cerebral atrophy, especially in
football players chestrating a change in behavior if the the medial temporal lobe, as well as the
goal has not been met.15 thalamus, mammillary bodies, and brain-
102 with three or
more concussions Long-term risks after a single mTBI stem, with a prevalence of ventricular
had a fivefold are presently uncertain. Some investi- dilatation and fenestrated cavum septum
prevalence of gators contend that TBI is a potential pellucidum. Amyloid- plaque deposi-
mild cognitive risk factor for the early expression or tion occurred in less than 50% of the
impairment occurrence of neurodegenerative disor- patients but was cytochemically iden-
and a threefold ders such as Alzheimer (AD) or Parkin- tical to those plaques found in AD.78
prevalence of
son disease.75,76 The risk of AD after a No long-term outcome studies have yet
reported
history of head injury doubles in those been done on military personnel who
significant
memory concerns,
who had LOC compared to those who have experienced cumulative concus-
compared with did not. However, those who had no sions due to blast exposure. This is
players who LOC with the head injury still have a clearly a topic for investigation with
had no previous higher risk for developing AD com- long-term follow-up warranted.
concussion. pared to those who have never had a Overall, the key points of outcomes
head injury.77 It appears that the risk of after an mTBI include: (1) symptoms
AD may be even higher if the patient resolve in gradual fashion over days to
KEY POINTS
weeks in most patients; (2) cognitive caused by dysfunction in prefrontal cor-
A In uncomplicated
impairments are usually evident dur- tical networks, which include connec-
mTBI (no imaging
ing the acute phase even when no tions with limbic, subcortical, and other abnormality or
LOC or amnesia has occurred; (3) in heteromodal association cortices. It is cumulative TBIs),
most cases, cognitive impairments re- common to see associated problems persistent
solve over days to weeks with no with planning, organizing, and strategic symptoms and/or
residual objective neuropsychological goal-directed behaviors in patients with poor functional
deficits by 3 months postinjury; (4) these memory concerns. outcomes are
brief unconsciousness or amnesia dur- In assessment of memory, delayed usually linked
ing the acute phase is not predictive free recall is impaired in both patients to noninjury-
of recovery or outcome; (5) most pa- with amnesia and patients with exe- associated
psychological,
tients have a favorable functional re- cutive system–associated memory im-
medical, social,
covery, resuming normal social and pairment. Both groups of patients
and personal
occupational activities within days to manifest retrieval difficulty, but pa- situational factors,
weeks; and (6) in uncomplicated mTBI tients with amnesia fail to improve with despite frequent
(no imaging abnormality or cumulative cues or recognition, whereas the pa- symptom
TBIs), persistent symptoms and/or poor tients with executive system-associated misattribution
functional outcomes are usually linked memory impairment do improve with to the original
to noninjury-associated psychological, cues and recognition. The latter is most mTBI by patients,
medical, social, and personal situational commonly encountered in patients with families, and
factors, despite frequent symptom misat- mTBI who have memory concerns that providers.
tribution to the original mTBI by patients, persist beyond the acute phase. Some A The long-term
families, and providers.59 patients who have ostensibly returned outcome of
It appears that the long-term outcome to normal objective cognitive function patients who
of patients who have had multiple con- after an mTBI may experience a decline have had multiple
cussions may be characterized by per- in performance in the face of a novel concussions
manent cognitive compromise.59 The cognitive challenge or stressor. Modern may result in
long-term effect on cognition of patients functional neuroimaging suggests that permanent
who have sustained mTBI due to blast this may be caused by increased activa- cognitive
and the role that comorbidities, such as tion of neural circuits to achieve the compromise.
PTSD, play in persistent cognitive impair- same cognitive response as a healthy A During the first
ments remain under investigation. control would achieve with less activa- few weeks to
tion. Real-life applicability suggests that a months of
greater cognitive effort is involved in recovery,
SUMMARY achieving goals when the patient with a memory
Memory problems are common after an history of mTBI faces day-to-day chal- problems are 103
common but
mTBI. In the acute phase this may in- lenges. The effort exerted in this pro-
usually affect
clude a period of anterograde and re- cess may account for some of the sustained
trograde PTA, affecting medial temporal- ‘‘mental fatigue’’ often expressed by pa- attention,
hippocampal-diencephalic pathways and tients weeks or months after an mTBI. working
transiently interfering with the ability Patients with ‘‘normal’’ neuropsychologi- memory, speed
to learn new information. In the post- cal performance on routine cognitive of processing,
acute phase and during the first few testing may nevertheless demonstrate and memory
weeks to months of recovery, memory impairments on tests that examine spe- retrieval, rather
problems are common but usually affect cific subtle aspects of complex atten- than the
sustained attention, working memory, tion and working memory.11 Visuospatial consolidation
speed of processing, and memory re- working memory tests may continue and storage
deficits seen in
trieval, rather than the consolidation to demonstrate impairments even after
amnesia.
and storage deficits seen in amnesia. verbal memory tests have returned to
These memory symptoms are felt to be normal.
" MEMORY IMPAIRMENT
KEY POINTS
No recommended medication is The long-term effects of mTBI af-
A It is common to
available for the treatment of mTBI- ter blast exposure may have a differ-
see associated
associated cognitive impairment. Cogni- ent outcome than those of an impact/
problems with
planning, tive remediation methods in use include acceleration-deceleration injury. The
organizing, and memory prostheses for adapting to, prevalence of associated acute and
strategic goal- and coping with, day-to-day challenges. chronic stress in military personnel who
directed Overall, the most effective treatment have sustained a blast-induced mTBI
behaviors in after an mTBI includes validation, educa- may also compound neurobiological
mTBI patients tional support, and conveying prohealth impairment and result in a protracted
with memory expectations of recovery over time. course of recovery even when an op-
concerns. Outcome after a single mTBI is over- timal multispecialty and interdisciplin-
A Patients with whelmingly positive in that functional ary approach to care is instituted.
amnesia fail to recovery and return to normal routine Complexities of the neurobiology of
improve with life usually occurs within weeks. The few memory processing, new tools for mem-
cues or patients who manifest persistent cogni- ory assessment and brain imaging, new
recognition, tive symptoms months to years after a treatment approaches, the influence of
whereas patients single mTBI usually have other psycho- comorbidities on cognitive change after
with executive logical, medical, and/or psychosocial an mTBI, and prevention of injury all
system–associated problems underlying their symptoms. warrant continued investigation.
memory
The long-term effects of cumulative
impairment
mTBIs may result in persistent cognitive
improvewithcues DISCLAIMER
and recognition.
impairment with underlying neuropa-
The latter is thologic changes. Cumulative mTBIs The views expressed in this article are
most commonly and concussions may also increase the those of the author and do not reflect
encountered in risk of the development of neurode- the official policy or position of the
patients with generative disease and neuropsychiatric United States Army, Department of De-
mTBI. comorbidities. fense, or the United States government.
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109
KEY POINT
A Posttraumatic
epilepsy (PTE) is
EPILEPSY, SLEEP
a disorder
characterized DISTURBANCES,
by recurrent
unprovoked
seizures
AND PSYCHIATRIC
occurring later
than a week CONSEQUENCES
following a
traumatic brain Karen Lynn Parko, Gary M. Abrams, Justin S. Campbell, Graham A. Glass
injury.
ABSTRACT
Neurologic impairment after TBI causes serious morbidity for patients and their
families. Prior articles have discussed headache and memory impairment. In this article,
epilepsy, sleep disturbances, and psychiatric consequences will be covered. People
who have suffered traumatic brain injury are at risk for any of these disturbances, and
each person will have a constellation of neurologic symptoms spanning the spectrum
from no difficulty in any area to symptoms in each of these areas.
EPILEPSY IN MILD TRAUMATIC terized by recurrent unprovoked sei-

BRAIN INJURY zures occurring later than 1 week fol-
Seizures and epilepsy are frequent con- lowing a TBI.
sequences of traumatic brain injury (TBI). The public health impact and added
Seizures may occur following TBI and disability of seizures and epilepsy on peo-
they generally are classified as: ple with TBI is significant and marked
by decreased function and a shorter life
o immediate if they occur within the
expectancy. The occurrence of seizures af-
first 24 hours
ter TBI has been shown to worsen func-
o early if they occur between
tional outcome significantly.2 In addition,
24 hours and 7 days, and
veterans with TBI who develop epilepsy
110 o late if they occur after 7 days1
have been shown to have a decrease in life
Early and immediate seizures are con- expectancy when compared to veterans
sidered provoked events secondary to with TBI who do not develop epilepsy.3
the acute physiologic effects of trauma
and thus are not considered epilepsy.
Late seizures that recur are considered Epidemiology
diagnostic of epilepsy. Thus, posttrau- The incidence of PTE varies among
matic epilepsy (PTE) is a disorder charac- studies with reports ranging from 4%
Relationship Disclosure: Dr Parko has nothing to disclose. Dr Abrams has received research support from
Innovative Neurotronics for investigation of a functional electrical stimulation–based orthotic device for gait
after stroke and has received or plans to receive personal compensation as an expert witness and consultant
for cases involving long-term consequences and rehabilitation issues in brain injury. Dr Campbell has received
grants from the Office of Naval Research. Dr Glass has received personal compensation from Schlesinger
Associates for blinded market research and from other entities for reviewing legal medical records.
Unlabeled Use of Products/Investigational Use Disclosure: Drs Parko, Campbell, and Glass have nothing to
disclose Dr Abrams discusses the unlabeled use of tricyclic antidepressants for sleep. Unlabeled usage is cited
when necessary.
KEY POINTS
to 53%.1 The studies vary in several shearing of axons and selective damage
A The relative risk
factors, including population-based ver- to vulnerable brain regions, such as the
for developing
sus admissions to hospitals, time period hippocampus. The clinical, neurophysi- PTE with mild
after injury, age range, the severity ologic, imaging, and neuropathologic TBI is 1.5,
of injury, and the definitions of TBI. features of TBI induced by these mech- moderate TBI
The varying lengths of follow-up of the anisms differ from penetrating brain 4.0, and severe
studies also make comparisons difficult. injury. The incidence of epilepsy with TBI 29.0.
The effects of demographic and psy- blast and closed head injury is unknown
A The incidence
chosocial factors have not been fully and still being researched. of PTE in
explored in relation to the risk for PTE.4 The consequences of TBI form a combat-related
Genetic predisposition for develop- heterogeneous disorder. The patient’s TBI following
ment of epilepsy after an injury is under clinical state (eg, presence and length craniocerebral
research; and endophenotypes (inter- of alteration/loss of consciousness, the missile wounds
nal phenotypes that are intermediate Glasgow Coma Scale score, posttraumatic is 50%.
between epilepsy and the presumptive amnesia, neurologic deficits) at the time
genetic or environmental contribution) of the brain injury determines the se-
A The critical
determinant
of PTE may eventually allow for better verity rating of the TBI. Different types of the
risk stratification. In the general popu- of injuries may have different distribu- development
lation, the relative risk for developing tions of damage and the mechanisms of PTE is the
PTE with mild TBI (mTBI) is 1.5, mod- may be different. The injuries caused can severity of the
erate TBI 4.0, and severe TBI 29.0.5 be primary (those that result as a direct head injury.
Military epidemiology. Substantial consequence of the mechanical force
differences in incidence exist when of the trauma) or secondary (those that
comparing head injuries that occur in result from nonmechanically induced
civilian populations with those sustained secondary complications). Other rele-
during military trauma. In 11 studies of vant clinical factors in epilepsy affecting
armed conflicts during the 20th century, mTBI, such as response to seizure medi-
the development of epilepsy by 10 years cation and surgical outcomes, may also
or more after a craniocerebral missile be present. In a retrospective study
wound shows a consistent pattern. The done at a military hospital, patients with
incidence of PTE in combat-related TBI confirmed medically refractory epilepsy
following craniocerebral missile wounds (epilepsy that is not controlled with medi-
is 50%.6 Within the military setting the cation) from temporal lobe origin had
higher rates of PTE after TBI are at- a higher incidence of prior mTBI.8
tributed to a higher proportion of inju-
ries that involve dural penetration and Risk Factors 111
widespread brain damage. Blast injury Although several independent risk fac-
has been called the signature injury of tors have been established for the de-
the US operations in Iraqi and Afghani- velopment of PTE after TBI, the critical
stan. Blast injury often does not involve determinant of the development of PTE
penetrating injury. The prevalence of is the severity of the head injury. The
mTBI in blast-exposed veterans is very occurrence of early posttraumatic sei-
large, however, and the relationship to zures, age older than 65 years, brain con-
future development of epilepsy is esti- tusion, and intracerebral hematoma are
mated to be significant. Of the 169,738 also independent risk factors (Table 6-1).9
American service men and women who
experienced any severity of TBI between Occurrence of Posttraumatic
2000 and 2009, 77% (129,893) experi- Epilepsy
enced mTBI.7 Closed head injury often In people who have suffered TBI, it is
produces diffuse concussive injury with unclear how long the risk for development
" EPILEPSY, SLEEP, PSYCHIATRIC CONSEQUENCES
KEY POINTS
fered TBI, the potential risk of PTE
A The risk of
seizures is TABLE 6-1 Independent Risk should place seizure high in the differ-
Factors for ential diagnosis. Often patients do not
highest in the Developing Posttraumatic
first year after Epilepsy
relate a trauma occurring many years
trauma and prior with new symptoms, and thus the
decreases " Age older than 65 occurrence and severity of TBI—at the
progressively time of the injury—should be sought in
thereafter. " Brain contusion
the medical history.
" Intracerebral hematoma Adjunct clinical testing may not be
A EEG has not been (especially subdural
shown to be
helpful as demonstrated by Case 6-1.
hematoma)
helpful in Routine outpatient interictal EEG can
predicting the " Occurrence of early be normal, and EEG has not been
(within first week of shown to be helpful in predicting the
development of
traumatic brain injury)
epilepsy after development of epilepsy after TBI.12
posttraumatic seizures
TBI. Brain imaging can disclose evidence
" Severity of injury of a prior insult but can also be normal.
In the Vietnam Head Injury cohort,
brain volume loss 15 years after the
trauma was quantified by CT and the
of PTE persists. Both experimental ani- correlation with occurrence of PTE was
mal models and human observations highly significant, but the location of the
have revealed that there is a latent period lesions appear to be more important
following the brain injury during which than size in determining posttraumatic
no acute seizures occur. The length of seizures.13 At the time of TBI, the need
the latent period is unknown. In most for brain imaging is based on clinical
cases of PTE, the risk of seizures is presentation. In a study done in India
highest in the first year after trauma and that looked at head CT imaging on all
decreases progressively thereafter. Up to patients, regardless of clinical presen-
86% of people with a first posttraumatic tation, in a prospective consecutive un-
seizure will have a second within the selected cohort of mTBI (defined as
following 2 years.10 In a population- Glasgow Coma Scale score of 13 to 15),
based study in a state with a fairly homog- 38% had an abnormal CT (any acute
enous population and a high median injury to the brain and cranium).14 Per-
family income, examining the occurrence haps in the future, imaging may help
of PTE in 2758 patients with mTBI to predict which patients with mTBI
112 showed that the standardized incidence may have more likelihood of developing
ratio was 1.5 with an increased risk during epilepsy, but currently there is usually
the first 5 years following the injury, af- no indication to image most patients
ter which it returned to that of the gen- with mTBI at the time of TBI.
eral, noninjured population. In moderate
TBI, the standardized incidence ratio was Seizure and Epilepsy
2.9, and this elevated risk persisted for 10 Prophylaxis After Traumatic
years. Among the patients with severe TBI Brain Injury
the standardized incidence ratio was 17.0 In mTBI, antiepileptic drugs (AEDs)
and the risk of seizures remain increased should not be administered unless the
for 20 years after the injury.11 person develops PTE. In severe TBI,
phenytoin prophylaxis protects against
Evaluation early (7 days) posttraumatic seizures.15
In the neurologic evaluation of a parox- No evidence suggests that any of the
ysmal event in persons who have suf- AEDs when administered after any
KEY POINT
Case 6-1 A The lack of

A 27-year-old unbelted male driver of a sport utility vehicle veered off evidence for
of the road while he was briefly changing a music CD. A quick attempt prophylactic
to correct the car’s direction resulted in a rollover of the car in which he efficacy of
was not ejected but was thrown into the rear of the car. Help arrived antiepileptic
within 10 minutes. He was alert but confused about what had occurred drugs (AEDs)
and self-reported awakening in the back seat of the car. He was after 7 days
placed in cervical spine stabilization and transported to a local emergency precludes
department, where he was found to have a fracture of his humerus. long-term use
Over the following days he noted severe headache, neck pain, and of AEDs in
musculoskeletal soreness and stiffness, which he treated with nonsteroidal patients with
anti-inflammatory medication and massage. He felt fully recovered from TBI to
the accident after his arm fracture healed within 6 weeks. Two months prevent late
after the accident he reported an unwitnessed episode of ‘‘spacing out’’ posttraumatic
described only as an awareness that time had passed. He denied seizures or PTE.
incontinence or injury. He was evaluated by his primary physician, and
an EEG was obtained and was normal. Three months later he reported
a similar incident. At this time, he underwent MRI imaging of his brain,
which was normal. He was sent for neurologic evaluation. The examination
findings were normal, and the EEG and MRI were reviewed and
confirmed normal. An AED was empirically started, and during the
next month while on a low-dose of the AED, he had a witnessed
generalized tonic-clonic seizure. After titration of the AED he did not
have another seizure.
Comment. This young man suffered an accidental mTBI without any
immediate neurologic consequences. His first seizure was 2 months after
the injury, and his diagnosis of epilepsy was established at 8 months
after injury. The clinical description of the seizure is likely consistent
with a focal seizure with impairment of consciousness (previously called
complex partial seizures). The witnessed generalized tonic-clonic seizure
likely represented a focal seizure that secondarily generalized. Fortunately,
his seizures were controlled with AEDs, and if they remain controlled,
he will be eligible for a trial of tapering off medication 2 years after his last
seizure. It is not unusual that his neurologic examination, routine EEG,
and MRI are normal. It is also not unusual that focal seizures/epilepsy
are not recognized or diagnosed. Not all focal seizures will become
secondarily generalized, which makes them easier to recognize as seizures.
Thus a high suspicion for the etiology of paroxysmal events representing
113
seizures should be maintained when evaluating patients with a history
of TBI.
severity of TBI have any antiepilepto- have been tested. The lack of evidence
genic or disease-modifying effects on for prophylactic efficacy of AEDs after
the development of PTE in humans. 7 days precludes long-term use of
Five drugs (phenytoin, phenobarbital, AEDs in patients with TBI to prevent
carbamazepine, valproate, and magne- late posttraumatic seizures or PTE.
sium) have been tested for antiepilep-
togenic effect and have not shown Treatment
evidence that they prevent or even Treatment of PTE is the same as for
suppress epileptic seizures after TBI.16 treatment of epilepsy in general. Be-
None of the AEDs approved after 1980 cause the seizures often accompany
KEY POINTS
brain injury and are secondary to or Natural History of
A It is critical to
symptomatic of the injury, however, Posttraumatic Epilepsy
choose and use
the best AED they may require lifetime medication Continued use of an AED in a patient
for each usage. It is critical to choose and use should be evaluated by the clinical
individual the suitable AED for each individual course of that individual patient. PTE
patient with patient with attention to other comor- patients with completely controlled
attention to bid diseases. Often patients with PTE epilepsy (no seizures of any type for
other comorbid suffer from coexistent cognitive diffi- a minimum of 2 years) are eligible for
diseases. culty, making AEDs with the least cog- taper or trial off of AEDs. Published
A Published nitive impairment some of the best remission rates of PTE range from 25%
remission rates choices. Surgical therapy may be an op- to 40%.1 It is unclear whether a rela-
of PTE range tion. Patients who are not controlled on tionship exists between the latency to
from 25% AED medication should be referred to a first seizure and PTE duration or per-
to 40%. comprehensive epilepsy center for an sistence. People with PTE who have
evaluation for possible surgical thera- frequent seizures (more than 10) in
pies, including resective cerebral sur- the first year following TBI often con-
gery of an identified seizure focus or tinue to have frequent seizures and
vagal nerve stimulation, which is an elec- have a two-thirds smaller chance of PTE
trical therapy delivered by direct stimu- remission in 15 years than those who
lation of the peripheral vagus nerve. Two have less than three seizures in the first
new surgical therapies for epilepsy are year.16
likely to be approved for epilepsy treat- To better understand the develop-
ment in the near future: deep brain stim- ment and clinical course of PTE, infor-
ulation and responsive neurostimula- mation must be exchanged between
tion (RNS). Deep brain stimulation for the trauma and epilepsy fields. A list of
epilepsy utilizes stimulation of the useful websites for providers and pa-
anterior nucleus of the thalamus. RNS tients with epilepsy is shown in Box-1.
continuously monitors and records
electrocorticography from depth or MILD TRAUMATIC BRAIN INJURY
subdural strip electrodes; when elec- AND SLEEP
trical seizure discharges are detected, Sleep disorders are common after acute
the RNS system delivers electrical stim- TBI of all severities. Castriotta and col-
ulation to suppress ictal discharges leagues,17 using a battery of sleep physi-
before a seizure occurs. It is hoped that ologic studies, found objective changes
114 those patients who are medically refrac- in sleep behavior in nearly half of all
tory but not resective surgery candidates patients recruited from acute TBI reha-
may benefit from these new therapeutic bilitation services. No consistent pattern
approaches. of sleep behavior is associated with TBI
Box-1
o www.aesnet.org: American Epilepsy Society; resource for providers on
practice standards as well as patient support
o www.epilepsy.va.gov: Veterans Affairs National Epilepsy Centers of
Excellence; referral resource for veterans with posttraumatic epilepsy.
o www.epilepsy.com: Patient information
o www.epilepsyfoundation.org: Patient and provider information
KEY POINTS
severity, however. Sleep disorders are crease insomnia symptoms. These co-
A Sleep disorders
also common in chronic TBI. Excessive morbidities include a high prevalence of
are common
daytime sleepiness is the most common depression,24 pain,25 and anxiety.26 Con- after traumatic
presenting symptom, and the spectrum versely, fatigue, mood disturbance, and brain injuries of
of sleep abnormalities seen in TBI is worsening of cognitive deficits may be a all severities
similar to that of the general popula- consequence of insomnia; thus recogni- and are a
tion (Table 6-2).18 Despite methodo- tion of a sleep disturbance may be critical potential
logic problems associated with studies for improving functional performance in source of
of sleep and TBI, at 3 months or longer a variety of domains. Polysomnographic cognitive
after a TBI poor sleepers appear to have measurements suggest that individuals dysfunction.
reduced ability to maintain sustained at- with chronic TBI tend to overstate their Excessive
tention.19 Thus, the recognition of sleep daytime
sleep disturbance. In fact, insomnia is
somnolence is
disturbances in chronic TBI is an impor- not easily characterized by any current
the most
tant issue because of the potential ad- physiologic measurements for sleep. In- common
verse influence of poor sleep on many somnia is a common concern after mTBI, symptom.
daily activities. but the direct relationship of insomnia
In both prospective and retrospective to mTBI is unclear and in most cases A Insomnia is
studies of mTBIs, insomnia was reported has a multifactorial etiology.27 the most
by up to 60% of respondents to ques- An area of public interest and clini- commonly
reported sleep
tionnaires.20–22 According to the Inter- cal controversy is the relationship be-
disorder after
national Classification of Sleep Disor- tween mTBI and posttraumatic stress
mild TBI, but
ders, insomnia is defined as a subjective disorder (PTSD) in military veterans of the incidence
complaint of difficulty initiating or main- the Iraq and Afghanistan conflicts (see of insomnia
taining sleep, waking up too early, or below). The co-occurrence of mTBI directly
having nonrestorative sleep despite ad- and PTSD is common, and insomnia is attributable to
equate opportunity for sleep.23 Al- frequently observed in Vietnam War vet- brain injury
though mTBI may affect brain mecha- erans with PTSD.28 Polysomnographic may be
nisms directly involved with initiating studies of PTSD demonstrate sleep ab- overestimated.
and sustaining sleep, it is also commonly normalities that seem to be directly In many cases,
associated with stressors that could in- attributable to PTSD, despite the many insomnia is
potential comorbid confounders seen caused by
comorbid
Sleep Disturbances with this condition. The abnormalities
TABLE 6-2 conditions
Associated With include reduced stage 1 and slow-wave
such as pain,
Traumatic Brain sleep and greater REM density.29 How- anxiety, and
Injury ever, the substantial overlap in the clini-
cal symptoms of postconcussive syn-
depression. 115
" Behaviorally induced drome and PTSD makes it difficult to
insufficiency sleep
attribute insomnia to a single disorder,
syndrome
given current limitations in diagnostic
" Excessive daytime sleepiness methods.
" Fatigue The prospective study of a group of
" Insomnia
patients with TBIs of all severities by
Baumann and colleagues30 supports the
" Narcolepsy observation that insomnia may be over-
" Obstructive sleep apnea estimated. The most common sleep dis-
" Periodic limb movements orders documented in this study were
of sleep excessive daytime sleepiness/fatigue and
posttraumatic hypersomnia. Short mean
" Posttraumatic hypersomnia
sleep latencies documented by multi-
ple sleep latency testing were more
frequent in patients with TBI and cor- have played an important role in the
related with the subjective concerns of favorable outcomes seen in their pa-
sleepiness. No association was found tients and were probably important in
between excessive daytime sleepiness/ explaining the discrepancy from prev-
fatigue and depression. While the previous studies. Perhaps the most signifi-
alence of subjective excessive daytime cant finding was the reduced vitality
sleepiness in patients with TBI (38%, after TBI as recorded on the 36-item
N = 68) was similar to that seen in gen- short form health survey (SF-36) mea-
eral populations,31 patients with TBI suring quality of life.30 This finding of
were relatively younger (mean age of 39 reduced vitality was consistent with the
versus 57). Nevertheless, given the fre- observation of Emanuelson and col-
quency of sleep disturbances in the leagues,34 who studied a Scandinavian
general population, the diagnosis of ex- population with mTBI.
cessive daytime sleeping or posttrau- Not all insomnia in TBI is caused by
matic hypersomnia should be made either a primary or secondary sleep dis-
with consideration of pretrauma sleep turbance. When sleep does not occur at
and fatigue status, when available.32 In the desired time, individuals may also
this group of 96 patients (mTBI was report insomnia. Ayalon and colleagues
present in 26), only 5% reported insom- described circadian rhythm disorders in
nia at 6 months postinjury. Other iden- patients with TBI who reported insom-
tified sleep disorders included obstructive nia.35 Circadian rhythm disorders arise
sleep apnea, periodic limb movements when the sleep-wake rhythm does not
of sleep, behaviorally induced insuffi- match an individual’s environmental
ciency sleep syndrome, narcolepsy, and and social schedule.23 Similar to primary
depression. insomnia, circadian rhythm disorders may
Acute TBI was associated with reduced be associated with cognitive-behavioral
levels of CSF hypocretin-1. This may be disturbances. In 42 patients with mTBI
due to direct damage to hypothalamic reporting insomnia, 36% were found
neurons or transient disruption of hy- to have a circadian rhythm disorder,
pothalamic function. In most patients 6 either delayed sleep phase syndrome or
months post-TBI, CSF hypocretin-1 levels irregular sleep-wake pattern. These di-
were normal but were lower in those agnoses emerged from examination of
individuals with excessive daytime sleep- sleep-wake patterns and recording of
iness. Lower hypocretin levels were also melatonin and temperature rhythms.
associated with worse functional out- Recognition of these disorders is im-
116 comes. It is therefore unlikely that ab- portant, since treatment of circadian
normalities in hypocretin levels would rhythm disorders focuses on the use of
explain daytime sleepiness in mTBI. Al- melatonin or light therapy for synchro-
though secondary narcolepsy has been nization of the sleep-wake cycle with the
rarely reported in association with dam- environmental dark-light cycle, rather
age to the posterior hypothalamus and than the use of sedative-hypnotics or
low CSF hypocretin levels after severe other agents, which is prevalent in the
TBI may lead to daytime sleepiness,33 treatment of insomnia.
well-documented cases of the full nar- The optimal treatment of sleep dis-
colepsy syndrome associated with mild orders associated with TBI is uncertain.
or severe TBI are lacking. The only sleep Castriotta and colleagues studied a group
disorder that correlated with TBI sever- of patients with TBI (N = 57) who were
ity was posttraumatic hypersomnia. The more than 3 months after acute injury.36
investigators hypothesized that the low Only five subjects in this group had
incidence of pain and depression may mTBI. Individuals with circadian rhythm
KEY POINT
sleep disorder were excluded from the and should be useful in mTBI. It may be
A No specific
study, as were subjects who were using particularly beneficial for insomnia that
pharmacologic
sedating medications. In addition to accompanies common comorbidities of recommendations
detailed sleep evaluations, all subjects mTBI, such as pain and depression. Ad- have been
underwent neuropsychological testing. ditional studies are needed, however.40 established
Of the total subjects, 35 had no sleep Unfortunately, the availability of resources for treatment
disorder; 22 had a sleep disorder; 13 for cognitive-behavioral therapy is limit- of sleep
had obstructive sleep apnea; 3 had nar- ed; therefore, pharmacologic treatments disturbances
colepsy without cataplexy; 2 had post- are the mainstay of treatment. Hypnotics related to
traumatic hypersomnia; and 4 had pe- that are commonly prescribed include mild TBI.
riodic limb movements of sleep. None benzodiazepines (eg, temazepam and Cognitive-
behavioral
of these individuals had an mTBI. In TBI triazolam) and nonbenzodiazepines (eg,
therapy may
patients with identified sleep disorders zolpidem and zaleplon). Zolpidem, for
be the most
who were successfully treated, no im- example, has a short duration of action effective
provement occurred in excessive day- and may be most useful for sleep-onset treatment,
time sleepiness in most (20 of 22), and insomnia, while longer-acting agents may especially when
no significant changes occurred in mood, be more effective for sleep maintenance. pain and/or
quality of life, or cognitive performance. Melatonin is available for use in circadian depression
In a study examining the use of modafinil rhythm disorders. Non–US Food and Drug is present.
for excessive daytime sleepiness in TBI Administration–approved treatments in-
with sufficient severity to require inpa- clude antidepressants (eg, tricyclic anti-
tient rehabilitation, a trend toward im- depressants) that can improve sleep in-
provement in fatigue, but an increase sufficiency but have not been studied
in insomnia, was found.37 In each of for long-term use and are generally not
these studies, a variety of methodologic recommended for short-term use.38 In
problems limited the interpretation of mTBI, a theoretical consideration is that
the results, but treatment of sleep dis- agents such as benzodiazepines or anti-
orders after TBI of any severity may not cholinergic-like drugs may interfere with
satisfactorily resolve symptoms, and no brain neuroplasticity. The complexity of
treatment strategy with proven efficacy managing sleep disturbance after mTBI
is available. is well-illustrated by Case 6-2.
No specific pharmacologic recom-
mendations have been established for MILD TRAUMATIC BRAIN
treatment of sleep disturbances associ- INJURY AND PSYCHIATRIC
ated with mTBI. Treatment options par- COMORBIDITIES
allel those for insomnia and other sleep Psychiatric disorders can either result 117
disturbances in individuals without TBI. from or be associated with TBI (Table 6-3).
For the most common disorders, both The most commonly associated classes
nonpharmacologic and pharmacologic of psychiatric disorders associated with
options are available.38 Nonpharma- TBI are mood and anxiety disorders,
cologic approaches are the best initial with mania and alcohol-related disor-
approach and might include sleep re- ders receiving somewhat less attention.41
striction, sleep hygiene education, or Prominent mood disorders are major
relaxation training. The goals of sleep depressive disorder (MDD) and bipolar
management should be to establish a disorder. Notable anxiety disorders in-
regular, unbroken, nighttime sleep pat- clude posttraumatic stress disorder and
tern and to improve perceptions of the obsessive-compulsive disorder. Although
quality of sleep.39 Cognitive-behavioral the 2005 National Comorbidity Survey
therapy has demonstrated efficacy in Replication (NCS-R) indicates the 12-
treating chronic insomnia of any cause month prevalence of anxiety disorders
Case 6-2
A 27-year-old man presented to the clinic with reports of difficulty falling and staying asleep
through the night since discharge from military service. He indicated that it could take him over
an hour to fall asleep most nights of the week; he would typically sleep for a few hours and then
wake up intermittently throughout the night. He indicated that he probably spent over 2 to 3
hours of his time in bed each night staring at the ceiling. He reported that he had been a good
sleeper prior to sustaining an mTBI after exposure to an improvised explosive device (IED). He
reported that following the blast he had difficulty with staying alert during the day and suffered
from poor concentration and frequent headaches. Within a few weeks the headaches remitted,
but he began to have difficulties with sleep initiation and maintenance that persisted since
his return from Iraq. He reported that despite feeling a lack of energy and having difficulty
concentrating during the day, he still could not sleep at night. Over the past 26 months following
the TBI, his primary care doctor had prescribed trazodone, zolpidem, and temazepam. These had
helped him fall asleep faster, but he continued to wake up multiple times in the night
and remain awake for extended periods of time. Further, these medicines became less effective
after a couple of weeks. He also tried over-the-counter sleep agents, including acetaminophen
plus diphenhydramine HCl (Tylenol PM) and diphenhydramine (Benadryl) without improvement
in sleep quality. He reported significant frustration with his inability to sleep and described a
sense of dread about going to bed every night, as he knew that he would not be able to fall
asleep. Although he knew that he should not, he would end up napping for roughly 45 minutes
each afternoon and felt a little bit better after doing so. He denied drinking caffeine during
the daytime, did not drink alcohol, did not exercise in the evening, and slept in a quiet dark room
without distractions. Further, he reported no abnormal sensations in his legs, had a normal body
mass index, and did not snore according to his bed partner. Other than TBI, his medical history
was significant for anxiety and depression, for which he took citalopram 30 mg per day with
reported modest improvement. On physical examination, the patient was found to have normal
general and basic neurologic examinations.
After discussing the potential therapeutic interventions for the treatment of chronic insomnia
in the setting of TBI, the patient was offered 8 weekly sessions of cognitive-behavioral therapy.
The sessions included a review of a sleep diary, reduction of sleep preoccupation, ‘‘cognitive
restructuring’’ to correct negative sleep thoughts; stimulus control therapy to lessen arousal at
bedtime, limiting wake time spent in bed; sleep restriction therapy; and fatigue management.
After 3 months, the patient reported that on many days he fell asleep in less than 30 minutes and
that although on some days he awoke earlier than he wanted to, he still got at least 6 hours of
good sleep on most nights. Follow-up at 6 months indicated a sustained benefit although still
‘‘not as good as before the injury.’’
Comment. This case highlights the fact that insomnia is a very common post-TBI concern and
118 typically is a chronic struggle for patients. Although very little data regarding the treatment
of insomnia in this patient population are available, the use of cognitive-behavioral therapy
has been shown in small series to be at least as effective, if not more so, than pharmacologic
intervention. Although no long-term studies confirm continued efficacy, studies in other forms
of insomnia would suggest that cognitive-behavioral therapy has a more long-lasting effect than
does pharmacotherapy. An additional point is that insomnia should be treated independently
and in conjunction with therapy for depression and anxiety in these patients. Independent
treatment of the sleep disorder may result in improved management of depression or anxiety.
(18.1%) is more common in the US Depression

general population compared to mood According to the NCS-R, the estimated
disorders (9.5%), it is MDD that has lifetime prevalence of major depression
garnered the most attention with rein the US general population is 16.2%
spect to comorbidity with TBI.42 and 6.6% for 12-month prevalence.43
of MDD.48 Controlling for age and edu-
TABLE 6-3 Psychiatric
Disorders cation, the TBI-injured group lifetime
Associated With TBI prevalence rate was 18.5% compared to
13.4% of those in the non-TBI-injured
" Alcohol-Related Disorders cohort. In another study, an anonymous
" Anxiety Disorders
mental health survey was administered
to a cohort of soldiers 3 to 4 months
Obsessive-compulsive disorder after their return from a tour of duty in
Posttraumatic stress disorder Iraq.49 The percentage of the Iraq sam-
" Mania ple screening at risk for MDD was 22.9%
of the 124 soldiers who reported head
" Mood Disorders
injury with loss of consciousness and
Bipolar disorder 8.4% of 260 soldiers who reported head
Major depressive disorder injury with altered mental status. By
contrast, in the group of soldiers from
this cohort reporting no head injury, the
incidence of soldiers screening at risk
Accumulating evidence in both civilian for MDD was only 3.3%. In sum, re-
and military populations indicates that ported estimates of the prevalence of
persons exposed to mild, moderate, or depression in persons impacted by
severe TBI have a higher 12-month TBI indicate that the risk for develop-
prevalence of depression than the gene- ing depression is more than double
ral population. Starting with the civilian that found in the general population.
population, Jorge and colleagues44 fol- Further, the limited evidence disag-
lowed 91 patients with closed head gregating mild from moderate and
injury (44.3% had mTBI) at 3, 6, and 12 severe TBI is mixed, with one civilian
months. Major depression was ob- study supporting a higher prevalence
served in 33% of patients within 1 year of MDD in patients with mTBI47 and
of presenting with TBI as opposed to another study using a military sample
just 7.4% of a control sample. Another that suggested a higher prevalence of
study that followed a civilian cohort of MDD in cases of more aggravated TBI
559 patients with TBI (no distinction in (loss of consciousness as opposed to
severity) up to 1 year45 found that 53.1% altered mental status).49
of the sample was coded as having MDD Why is depression more likely in pa-
based on a structured interview utilizing tients with TBI? For several years, the
the Patient Health Questionnaire 9-item catecholamine theory of depression sug- 119
depression scale.46 Lastly, Fann and col- gested that a deficiency in norepineph-
leagues47 observed a higher 12-month rine was the primary causal factor in the
prevalence of affective disorder (the development of depression.50 More re-
International Classification of Dis- cently, a deficiency in another mono-
eases code analogous to major depres- amine, serotonin, has received a great
sion) in patients with mTBI (11.3%), deal of attention.50,51 Despite evidence
compared to either patients with mod- that monoanimine deficiency is insuffi-
erate to severe TBI (12.0%) and con- cient to cause depression, documented
trol patients without TBI (5.5%). cases of depression without monoani-
Similar findings have been noted in mine deficiency have prevented a con-
military samples. For instance, World War sensus from declaring that monoamine
II era veterans with TBI (n = 520) and deficiency is also a necessary condition for
without (n = 1198) were interviewed in depression.50,51 Thus, an increasing em-
1997 to evaluate the lifetime prevalence phasis has been placed on the complex
KEY POINT
interaction between biological risk factors aggression and mood irritability/variability,
A Depression is the
(such as serotonin deficiency), stressful which may also be linked to focal brain
most common
co-occurring life events, and individual differences in trauma, complicate the effort to research
psychiatric personality and associated coping mech- whether the symptoms are psychiatric or
condition anisms. Given the emergent appreciation traumatic in origin.
associated of life history as a potential causal agent
with TBI. for the onset of depression, the events Suicide
that incur TBI and the consequences that TBI has been linked to an increased risk
follow are reasonable risk factors for of suicide. Teasdale and Engberg,56 study-
depression (Case 6-3). Taylor and Jung52 ing a Danish cohort of 145,440 persons,
posit one such pathway in which patients reported suicide mortality ratios of 3.0,
with TBI become more at risk for mood 2.7, and 4.1 that indicate increased risk for
disorders caused by the psychological dis- persons coded as having TBI associated
tress experienced in the wake of major with concussion (n = 126,114), brain lesions
complications in daily living wrought by (11,766); and skull fractures (n = 7560),
acquiredneurologicdysfunction.LeDoux51 respectively. Simpson and Tate57 noted
and Duman53 provide further detail to a that post-TBI emotional distress and
model of stress-induced brain dysfunc- substance misuse made individuals 21
tion associated with adrenal steroids times more likely to attempt suicide
and neurotrophic factors that may lead after the TBI injury. In the same study,
to atrophy in regions of the hippocam- self-poisoning was identified as the most
pus responsible for supporting neuro- employed method of self-harm, being
genesis. One possible explanation is employed in 65% of suicide attempts
that additional damage to neural struc- observed in that study, a finding the au-
tures and/or circuits caused by stress thors attributed to the pervasive use of
could likely interact with and exacerbate medications by patients with TBI.
trauma-induced brain dysfunction. In an
attempt to specify specific brain struc- Posttraumatic Stress Disorder
tures most at risk for shared TBI and Turning to anxiety disorders, PTSD is
depression, one research group54 posits often discussed in association with TBI, in
that TBI affecting complex neural cir- part because of the necessity of trauma
cuits, including the prefrontal cortex, in developing either TBI or PTSD. One
amygdala, hippocampus, basal ganglia, major point of contention in the pub-
and thalamus, is more likely to lead to lished literature has been the debate
symptoms of depression. The amygdala, about whether a person with a loss of
120 hippocampus, and prefrontal cortex are consciousness for the traumatic event can
particularly sensitive and vulnerable to indeed form the traumatic memories
prolonged stress exposure.51 once thought to be the sole culprit be-
hind PTSD.54 However, this debate has
Mania diminished in the face of accumulating
Relative to depression, other mood dis- evidence documenting the presence of
orders have received much less attention PTSD following a TBI incident. For in-
as potential sequelae of TBI.55 One re- stance, a PTSD prevalence rate of 27.1%
view put the comorbidity of TBI with was observed in a sample of 96 patients
bipolar disorder to be between 1.6% and with severe TBI who had no firm recall of
1.7%,55 and yet another review cites evi- events during and up to 1 month after
dence of a comorbidity rate with mania their traumatic event.58 Turnbull and
that ranges from 4.2% to 9.0% within 1 colleagues59 reported a 27% incidence
year of the TBI occurrence.54 The nature of PTSD at 6 months following undiffer-
of manic symptoms such as increased entiated TBI; while Gil and colleagues60
Case 6-3
A 42-year-old man was referred to a neuropsychiatry unit for evaluation and treatment of
behavior problems that began after initial treatment and rehabilitation for a severe TBI at
another hospital. The TBI was induced by a fall from a 12.2-m (40-ft)-high ladder and a fracture of the
right orbital wall. The only known procedure to have been performed was the surgical repair of an
orbital fracture. The length of posttraumatic amnesia and Glasgow Come Scale score were unknown.
Following discharge from hospitalization for the initial injury, the patient exhibited socially
inappropriate behavior (eg, arguing with other male coworkers, inappropriate touching and
groping of female coworkers), which ultimately led to a 3-month incarceration, separation from
his wife, and the alienation of family members. Additional presenting behaviors included
frequent outbursts of anger and aggressive behavior.
The patient’s family indicated that he unsuccessfully tried risperidone (1 mg at bedtime)
divalproex sodium (750 mg 2 times a day), quetiapine (dose unknown), and methylphenidate
(dose unknown). The most recent referral came after a gradual increase in disinhibited and
physically aggressive behavior. His primary concern was intermittingly reoccurring episodes
(2 to 3 weeks) of depression, including passive suicidal thoughts. He also noted short, transient
experiences of sadness that would last a few hours after a stressful episode. Prior to the severe
TBI, he had experienced one other episode of mTBI with no complications, and otherwise had no
prior history of the deviant behaviors that he had begun to manifest after the TBI.
Abnormalities revealed during the mental status examination were incongruent mood and
affect, an endorsement of transient passive death wishes, and a limited insight into emotional
difficulties. Neuropsychological assessment revealed frontal-subcortical system dysfunction as
indicated by poor performance on a wide range of tasks evaluating executive function.
Comment. The patient was a middle-aged man with a complicated case that started with two
experiences of TBI (mild and severe), which in turn led to behavior problems. The consequences of
the latter were social isolation and dysfunction, which contributed further to his mood problems.
The treatment course was to apply therapies to address the varied perspectives in which the
case could be conceptualized. Acute inpatient treatment was utilized to engage in behavior
medication of inappropriate behavior, including a tapering of his previous pharmacologic
regimen and replacement with 150 PO mg/d of sertraline for treatment of MDD and amantadine
(gradually increased to 100 mg/d) to address executive function deficits associated with frontal
lobe dysfunction. The inpatient treatment was followed by outpatient treatment that continued
the pharmacotherapy. Moreover, a variety of ongoing therapeutic groups were prescribed,
starting with weekly individual cognitive-behavior therapy, two daily group therapies that
targeted specific social deficiencies (eg, sexual behaviors group), and family therapy every
3 months. Although the patient was not cured, he has, in fact, made significant progress.
Although the treatment model described by Rao and colleagues appeared well conceived and 121
executed, there is little consensus in the literature to guide clinicians who find themselves in a
similar position. For instance, the review by Schwarzbold and colleagues54 noted that little
evidenced-based data are available to guide the treatment of co-occurring TBI and psychiatric
disorders. What data exist consist primarily of case reports, such as that by Rao and colleagues.32
The same review also noted that pharmacologic interventions remain similar to those of the
primary psychiatric disorder, but extreme caution must be taken to avoid side effects and
unwanted drug interactions when the patient has a co-occurring TBI and psychiatric condition.
The same appears to hold with respect to psychotherapy as well. For instance, cognitive-
behavioral therapy utilized for PTSD in isolation is also undertaken for individuals who experience
TBI and PTSD. A commonly occurring therapy for individuals with co-occurring psychiatric
conditions and TBI is family and systems therapy, as the effects of TBI, especially severe TBI, may
impose additional strains on patients’ families.
Case 6-3 is the author’s (JC) review of the case report by Rao V, Handel S, Vaishnavi S, et al.
Psychiatric sequelae of traumatic brain injury: a case report. Am J Psychiatry 2007;164(5):728–735.
KEY POINT
noted a 14% incidence of PTSD at 6 ral lobe lesion, increased lesion volume,
A Posttraumatic
months post-mTBI. Comparatively, the and recall of the injury.41
stress disorder
is the second NCS-R42 reported that the general US
population 12-month prevalence of Obsessive-Compulsive Disorder
most common
co-occurring PTSD was 3.5%, suggesting that patients A second anxiety disorder that has re-
psychiatric who experience a TBI, especially when ceived limited attention as a possible
condition the TBI event causes intense fear, hor- sequel to TBI is obsessive-compulsive dis-
associated with ror, and a concern for one’s physical order (OCD). Behaviors associated with
TBI and can safety, do indeed have an elevated risk OCD, such as perseveration, repetition,
occur even in for the development of PTSD. One such and compulsion, may also stem directly
cases where situation likely to induce both TBI and from TBI damage to structures involved in
individuals lose
fear is exposure to the detonation of memory (eg, the hippocampus) or exec-
consciousness
IEDs seen in wars or other conflicts. The utive control (eg, the prefrontal cortex).61
or have
amnesia for the
prevalence of IEDs and the increased A review of the literature identified two
trauma-inducing survivability of US service-members have studies examining this issue that place the
event. combined to make PTSD and TBI the prevalence of co-occurring TBI and OCD
signature wounds of the US wars in Iraq between 1.6% and 15%.54 As a point of
and Afghanistan. To evaluate the psychi- reference, the NCS-R 1-year prevalence
atric consequences of TBI in service of OCD is 1%. The literature in this area,
members serving in these conflicts, Hoge however, is too limited to reach any
and colleagues49 surveyed 2525 Army in- conclusions regarding changes in risk
fantry soldiers between 3 and 4 months for OCD associated with TBI.
following return from deployment to
Iraq. Although the prevalence of PTSD Psychosis
in service members deployed to combat Aside from mood and anxiety disorders,
zones is higher than that in the general psychosis associated with TBI has also
civilian population as indicated by the received somewhat limited investiga-
9.1% prevalence rate in soldiers who tion. The review by Schwarzbold and
reported no injuries (the general popu- colleagues54 noted prevalence rates for
lation prevalence of PTSD was 3.5% in psychosis in TBI patients ranging from
the NCS-R), the study by Hoge and col- 0.1% to 9.8%. In another review,62 the
leagues showed that the prevalence of rates of diagnosis for psychosis or schizo-
PTSD in combat-deployed soldiers in- phrenia like psychosis ranged from 3%
creases dramatically with the severity of to 26%. It is important to note that
symptoms associated with head trauma, the Diagnostic and Statistical Manual
122 such as altered mental status (27.3% of Mental Disorders, Fourth Edition,
PTSD prevalence) and most especially Text Revision (DSM-IV-TR)63 provides a
loss of consciousness (43.9% PTSD prev- means for clinicians to attribute delirium
alence). The evidence clearly establishes specifically to physical illness, such as
the possibility of developing PTSD fol- TBI, thereby adding further complexity
lowing TBI, with TBI exposure in combat to the study of co-occurring psychosis
veterans of the recent wars in Iraq and and TBI since psychotic symptoms in
Afghanistan perhaps being the most at risk the acute TBI phase may, in some in-
for both maladies. Other risk factors cited stances, be more appropriately labeled
in a review conducted by the American delirium.54
Neuropsychiatric Association Committee
on Research were a loss of consciousness Personality Changes
associated with the TBI incident, use of As with psychosis, personality changes
avoidance coping, female sex, early post- associated with TBI may be directly
injury depression and anxiety, left tempo- attributed to the physiologic brain insult
KEY POINT
according to the DSM-IV-TR,63 thereby tion likely to co-occur with TBI, and
A No consensus
complicating efforts to determine whether the various prevalence rates reported
exists regarding
behaviors typically associated with per- throughout the literature seem to the impact
sonality disorders are more appropri- support depression as the most likely varying
ately labeled a personality change caused psychiatric condition to co-occur with severities of TBI
by TBI. The Schwarzbold and colleagues54 TBI. Some evidence suggests that mTBI might have
review cites prevalence rates of apathy is more likely to result in depression with respect to
(34.5%) after severe TBI, affective lability than moderate or severe TBI, but the developing
(5.0% to 32.7%) after undifferentiated quantity and quality of this evidence are co-occurring
TBI, and aggression (16.4% to 33.7%) not mature enough to reach any strong psychiatric
after undifferentiated TBI. Clearly, the im- conclusions at present. Based on the conditions.
portant executive functions carried out prevalence rates reviewed above, PTSD
by the frontal lobes make damage to this emerged as the second most likely psy-
area of the brain a prime candidate as chiatric condition to co-occur with TBI.
the causal agent behind sudden per- Similarly, persons suffering mild TBI
sonality change. Two additional studies may also be at elevated risk for PTSD
in military populations64,65 indicate in- compared to individuals who exper-
creased aggressive behaviors in person- ience moderate or severe TBI, especially
nel who experienced TBI, making spe- when the latter forms lead to loss of
cial note of the increased risk for verbal consciousness. Although less prevalent,
confrontations in this population, a find- some very limited evidence exists link-
ing that again highlights frontal lobe ing TBI to an elevated risk for mania/
dysfunction (Case 6-3). bipolar disorder and OCD. The rela-
tionship between TBI and personality
Alcohol-Related Disorders changes, especially increased aggres-
Alcohol-related disorders have been sion, and psychotic behavior remain
found to have a high co-occurrence with methodologically challenging to study.
TBI, with pre-TBI prevalence rates rang- The challenge arises from the various
ing from 34.9% to 51.0% in retrospective options for diagnosing commonly oc-
studies using samples undifferentiated curring symptoms; some may directly
with respect to severity of TBI.54 In attribute symptoms to TBI, while others
contrast, a second review noted that might attribute the behaviors to stable
alcohol use tends to decrease in the first dispositional diagnoses of personality
year following a TBI.55 Yet another study disorders. It is clear that the study of
points out that heavy ingestion of al- co-occurring TBI and psychiatric con-
cohol reduces the recovery of neuro- ditions suffers from a lack of criterion- 123
logic function after a TBI.66 Thus, while standard measures that can be employed
alcohol abuse clearly seems to predis- to standardize the definitions used
pose individuals to engage in behaviors to evaluate the prevalence of disor-
that increase their risk for TBI, no clear ders, along with an overreliance on
consensus exists regarding the causal self-report surveys and archival data-
mechanisms and course of alcohol abuse sets. With such methodologic disunity,
that begin post-TBI exposure. one would expect that great advances
lie in wait for a time when more rigor-
Summary ous prospective studies will illuminate
Major depression has received the the psychiatric comorbidity associated
most attention as a psychiatric condi- with TBI.
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REHABILITATION IN THE
PATIENT WITH MILD
TRAUMATIC BRAIN
INJURY
Ronald G. Riechers II, Robert L. Ruff
ABSTRACT
Traumatic brain injury (TBI) has garnered increased public attention in the past
several years because of high-profile athletes with possible long-term effects of their
injuries as well as large numbers of returning combat veterans injured by blast
explosions. Most of these injuries are mild in nature and require no specific surgical
treatment but may benefit from brief rehabilitation interventions. To appropriately
rehabilitate patients with mild traumatic brain injury (mTBI), one must fully un-
derstand its clinical course and the factors that accelerate or delay recovery.
Education is the centerpiece of mTBI treatment and should be included in the
rehabilitation plan. When devising the rehabilitation plan, the neurologist should
take into account the goals of the patient and establish a reasonable time frame
for treatment paralleling the expected recovery course. Cognitive and vestibular
functions are commonly affected after mTBI and are particularly responsive to re-
habilitation interventions. Vocational rehabilitation and community reentry plan-
ning are aspects of the global rehabilitation plan that should not be neglected.
Combat-injured veterans with mTBI present unique challenges to the rehabilitation
team, and assessment of these patients often needs to include assessment of
psychological function.
INTRODUCTION severe, and penetrating TBI is viewed

128 Traumatic brain injury (TBI) has gar- to be a disease treated by the neuro-
nered increasing attention in the public surgeon because the attendant issues
consciousness in recent years in part of elevated intracranial pressure, hem-
because of the impact of explosive orrhage, and skull defects require sur-
blasts on our combat soldiers and vet- gical management. Chronically, these
erans and the high-profile cases of patients frequently transition from sur-
former professional athletes with his- gical services to rehabilitation services,
tory of concussions and abnormalities often under the auspices of a physiat-
on autopsy.1–3 The role of the neurol- rist for their longer-term rehabilitation.
ogist in the treatment of TBI is difficult Because of the often benign natural
to define at times. Acutely, moderate, history of mild TBI (mTBI), the patients
Relationship Disclosure: Drs Riechers and Ruff have nothing to disclose.

Unlabeled Use of Products/Investigational Use Disclosure: Dr Riechers discusses the trial using prazosin for sleep
improvement in military patients with traumatic brain injury but does not give a specific recommendation for its
use. Dr Ruff has nothing to disclose.
KEY POINTS
may never be seen by neurologists with
TABLE 7-1 Postconcussive A Rehabilitation for
only those patients with postconcus- Symptoms traumatic brain
sion syndrome or persisting headaches injury (TBI),
receiving neurologic care. Thus, the view " Physical much like
of rehabilitation for TBI from a neurol- rehabilitation
Dizziness
ogist’s perspective may be skewed by for stroke, is
experience. Fatigue focused on the
Rehabilitation for TBI, much like re- Headache deficits found.
habilitation for stroke, is focused on In TBI, cognitive
Imbalance/incoordination deficits are
the deficits found. These deficits are
predicated on lesion location and se- Insomnia common and
need to be
verity. In TBI, however, the diffuse Light/noise sensitivity
addressed.
axonal injury component increases the " Emotional
possibility of cognitive deficits based on
the damage to white matter structures Anxiety A TBI rehabilitation
requires a team
critical for the network connectivity Depression
of providers
underpinning cognition. Also, regional Emotional lability and therapists
vulnerabilities of the frontal and tem- from multiple
Irritability
poral lobes to contusion injuries con- disciplines and
tribute to the common occurrence of " Cognitive medical
cognitive dysfunction in TBI. As the se- Inattentiveness specialties. The
verity of TBI increases, there is greater rehabilitation of
Memory impairment
occurrence of motor and sensory def- patients with
icits requiring more intensive therapies Organizational difficulties mild TBI (mTBI)
in increasingly acute treatment loca- is often
Slowed information
tions. The focus of this review will be processing impacted by
common
on the rehabilitation of the patient with
postconcussive
mTBI or concussion, as these patients
symptoms,
may be seen by neurologists early in the including pain
course of recovery. outcome. A recent large systematic re- and sleep
Rehabilitation, perhaps more so than view evaluated the prevalence of pain disorders.
any other medical specialty, is centered after TBI.4 Pain, including headache,
on the team concept of care delivery. was prevalent in 57.8% of patients and
TBI rehabilitation is no different. The had a greater association with mTBI as
rehabilitation team can include physi- opposed to moderate or severe TBI.
cal, occupational, and speech therapists; The prevalence of chronic pain of any 129
neuropsychologists; behavioral health type was 51.5% and 43.1% in civilian and
or rehabilitation psychologists; neurolo- military populations respectively, with a
gists; physiatrists; and vocational reha- pattern similar to headaches where pain
bilitation providers, among others. The prevalence was higher among those
role of each discipline in the care of with mTBI. Sleep disorders after mTBI
the patient with mTBI depends on the occur with widely varying frequency
individual’s constellation of clinical symp- (36% to 70%) with much of this var-
toms or deficits (Table 7-1). The re- iability depending on the population
habilitation of patients with mTBI is studied.5 The sleep disorders following
often impacted by common postconcus- mTBI include both ends of the spec-
sive symptoms, including pain and sleep trum, hypersomnia or insomnia. Later
disorders. These symptoms impact the sections of this review will discuss the
individual’s engagement in treatment impact of insomnia, pain, and mental
and subsequently the ultimate functional health diagnoses on the recovery from
" REHABILITATION
KEY POINT
and rehabilitation of mTBI in the special
A Patients with TABLE 7-2 Conclusions of
population of returning veterans. Un- the World Health
mTBI tend to
recover within fortunately, little data on the premorbid Organization
days to weeks prevalence of psychiatric illness among Collaborating Centre Task
after injury; veterans with mTBI are available. Force on Mild Traumatic
Brain Injury
however, a
small
percentage of PROGNOSIS " Common Symptoms After
Mild Traumatic Brain Injury
patients with As discussed in an earlier article, mTBI Include
mTBI will have is a disease predominantly character-
a more Blurred vision
ized by transient disruption of neuro-
prolonged Dizziness
nal function involving an imbalance
course of
between energy expenditure and nu- Headache
postconcussive
symptoms.
trient utilization and supply.6 Given the
Memory impairments
transient nature of the neuronal dys-
function, treatment and recovery are Sleep problems
focused primarily on rest and avoid- Other cognitive concerns
ance of exacerbating factors (recurrent
" Symptoms Are Transitory,
trauma, metabolic disturbances) while Resolving Within Days to
intrinsic tissue recovery is occurring. Weeks in Most Patients
Each individual is affected differently by
" Prognosis Is Generally Good
this transient neuronal dysfunction, and With No Residual Cognitive
the duration of the neurologic signs and or Physical Deficits in Most
symptoms varies significantly. Recovery Patients
after mTBI is an area of some consensus Data from Caroll LJ, Cassidy JD, Peloso PM, et al.
and some controversy. Most clinicians Prognosis for mild traumatic brain injury: results
of the WHO Collaborating Centre Task Force on
will agree with the assertion that pa- Mild Traumatic Brain Injury. J Rehabil Med 2004;
tients with mTBI tend to recover within 43(suppl):84–105.
days to weeks after injury and that a
small percentage of patients with mTBI
will have a more prolonged course of mTBI had generally returned to baseline
postconcussive symptoms. The mecha- cognitive functioning. In those patients
nism of these symptoms and their label with persisting symptoms outside the
are the source of some disagreement typical time frame of expected recovery
within the TBI community. In terms of from mTBI, additional factors frequently
130 recovery from mTBI, the World Health influenced the recovery course. These
Organization (WHO) Collaborating Cen- factors can be as disparate as secondary
tre Task Force on Mild Traumatic Brain gain from ongoing legal issues or occult
Injury’s review of the literature on prog- CNS damage, such as contusion or dif-
nosis of mTBI was published in 2004.7 fuse axonal injury not discovered during
The task force’s conclusions are listed the initial workup. Also, psychiatric diag-
in Table 7-2. As demonstrated with the noses, such as depression or posttrau-
symptomatic recovery of patients with matic stress disorder (PTSD), can in-
mTBI, objective evidence of neuropsy- fluence the course of recovery. The role
chological impairments similarly resolves of the treating neurologist is to seek to
with time. Belanger and colleagues8 re- identify and appropriately treat the con-
viewed the mTBI literature and demon- dition impacting the recovery curve. An
strated that the window for recovery of exhaustive further discussion of the post-
objective neuropsychological deficits was concussion syndrome and recovery after
3 months; ie, by 3 months, patients with mTBI is beyond the scope of this article,
KEY POINT
but we refer the reader to the reviews by of treatment. Case 7-1 illustrates recov-
A mTBI
McCrea and colleagues9 and McCallister ery from mTBI. rehabilitation
and Arciniegas,5 among others. The interventions
understanding of the basic tenets of EDUCATION AS THE FOCUS should focus on
recovery after mTBI is, however, impor- OF TREATMENT functional
tant to take into account when deter- A fundamental role of the treating phy- improvements,
mining the treatment plan for patients. sician is to educate patients on the ex- be paired with
Determining who is referred for rehabil- pected course of recovery as well as the clear goals and
itation after mTBI requires the ‘‘art of time limits, and
normal symptoms that they will expe-
medicine’’ skills of the neurologist. One reinforce the
rience throughout the course of injury.
natural history
must find a balance between the extreme Most patients with mTBI will be initially of mTBI
of denying rehabilitation interventions seen by providers other than neurolo- throughout the
because the disease ‘‘will get better with gists, and these early evaluations are course of
time’’ with the opposite extreme of ex- often focused on ruling out potentially treatment.
cessive referrals for rehabilitative inter- life-threatening conditions and treating
ventions that may misinterpret normal non-neurologic injuries. Thus, delivery
symptoms in the course of mTBI as of education about the expected course
pathologic. Perhaps a mechanism to fos- of recovery may be limited to a patient
ter a balance between these extremes is education handout or be nonexistent.
to offer interventions to improve func- Additionally, patients with mTBI may
tion paired with clear goals and time still be disoriented, confused, or in frank
limits as well as reinforcing the natural posttraumatic amnesia, rendering any
history of mTBI throughout the course educational intervention less effective.
Case 7-1
A 33-year-old man who had sustained mTBI with one episode of loss of
consciousness (LOC) resulting from a fall at work was seen 4 weeks after his
initial emergency department visit. For the first 2 weeks after the accident
he suffered from tension-type headaches that were initially daily and
then diminished in frequency and severity. For the first 2 days after the TBI
he felt fatigued, slept more than 10 hours a day, and was nauseated. Over
time the symptoms diminished in severity. At the time of his neurologic
evaluation 4 weeks after his TBI, he was having about one tension-type
headache per week at an intensity of 5/10. He was sleeping about 9 hours
per night, which is 1 to 2 hours more than his usual sleeping pattern. He
131
still felt fatigued and could not work a full day because of fatigue and
difficulty maintaining concentration. He had impaired olfaction when
tested 4 weeks after the TBI and no other abnormalities on neurologic
examination. He scored 26/30 on the Montreal Cognitive Assessment
(MoCA) test, with points lost for attention and delayed recall. He was
treated initially with a nonsteroidal anti-inflammatory drug for his
headache and given counseling, which consisted of educating the patient
on the usual course of recovery from mTBI. Two months later, his
headaches and fatigue had resolved. He was able to work a full day and
felt that he was back to his baseline state. His olfaction was normal when
tested 6 months after the TBI.
Comment. This case illustrates recovery from mTBI in a civilian setting.
It is important to provide support and provide guidance to the patient. This
patient also illustrated transient posttraumatic hypersomnia.
" REHABILITATION
KEY POINTS
Because of the importance of this edu- TBI were randomized to an educational
A Educational
cation for the treatment of mTBI, it may intervention (in person, telephonic, or
interventions
for mTBI should need to be delivered subsequently in the written) versus standard clinical care. The
validate the neurologic evaluation or even repeated mTBI population receiving this interven-
current during the initial visit. When delivered, tion scored lower on standard measures
symptomatology the approach should be to validate the of postconcussive symptoms than those
while encouraging current symptomatology while encour- receiving no intervention. These studies
the course of aging the course of recovery and the were limited by attrition of participants.
recovery and the importance of realistic functional goals. Despite the minor limitations, the inter-
importance of This education is often best delivered vention is one involving no harm to the
realistic functional with other significant individuals who are patient or provider other than time and
goals.
part of the patient’s life so they too are serves to reinforce the expected natural
A Two neurologic able to set appropriate expectations. history of mTBI. Many resources, from
sequelae of Several large studies of treatment of pocket cards and emergency department
mTBI for which mTBI have evaluated the effectiveness discharge sheets to full workbooks, exist
rehabilitation of an educational intervention on re- for the education of patients following
interventions covery.9 In fact, the WHO Collaborating mTBI. Table 7-3 provides some written
can provide Centre Task Force on Mild Traumatic references as well as some Internet
benefit include Brain Injury reported that educational websites to offer patients.
vestibular and
intervention was the only intervention
cognitive
for mTBI with clear evidentiary sup- NEUROLOGIC DEFICIT-SPECIFIC
dysfunction.
port.10 Ponsford and colleagues11 com- REHABILITATION
pleted a trial to evaluate the benefit of a A patient presenting to a neurologist
specific written educational module on after mTBI injury may experience a
the recovery after mTBI. They random- myriad of symptoms, some of which
ized 202 patients to an intervention or may be appropriate for rehabilitative
nonintervention group where the inter- interventions while others may be best
vention consisted of symptom, psycho- addressed by pharmacologic interven-
logical, and cognitive assessments, as tions. Two neurologic sequelae of
well as provision of a written informa- mTBI for which rehabilitation inter-
tion booklet on the typical symptoms, ventions can provide benefit include
coping strategies, and expected course vestibular and cognitive dysfunction.
of recovery following mTBI. This inter- The initiation of rehabilitation gen-
vention took place within 7 days of in- erally occurs when a deficit has func-
jury. The nonintervention group was
132 simply seen in the emergency depart-
tional impairment with the goal of re-
storing function via recovery of the
ment by acute care providers. Both deficit or adaptation. Similar principles
groups were subsequently followed are applied to both cognitive and ves-
up at 3 months postinjury and under- tibular rehabilitation.
went symptom, psychological, and cog-
nitive assessments. On follow-up, the
patients who received educational inter- Vestibular
vention via an information booklet re- Vestibulocerebellar concerns after mTBI
ported lower symptom levels, statistically include dizziness, frank vertigo, and gait
significant for sleep disturbance and an- instability or incoordination. The inci-
xiety, and scored lower on indices of dence of these symptoms depends on
psychological distress in the domains of how long after injury patients are asked
paranoia and hostility. This work affirmed about them. Dizziness may be reported
the prior study by Wade and colleagues12 by as many as 80% of patients within the
in which patients with all severity levels of first few days following mTBI, whereas
KEY POINT
tibulocerebellar deficits can only begin
TABLE 7-3 Selected A Rehabilitation
Educational after appropriate identification of the site
of the
Resources for of dysfunction. The site of dysfunction vestibulocerebellar
Patients With Mild Traumatic will determine the specific techniques deficits can
Brain Injury employed for the rehabilitation. The re- begin only after
habilitation assessment and treatment appropriate
" Written Resources team for these deficits includes physical identification of
Mason DJ. The mild therapists and audiologists most fre- the site of
traumatic brain injury quently. Assessment of vestibular and ce- dysfunction
workbook: your program rebellar function after mTBI begins with a using bedside
for regaining cognitive examination and
good bedside examination, looking for
function and overcoming occasionally
emotional pain. Oakland, evidence of nystagmus, saccadic/pursuit
advanced
CA: New Harbinger abnormalities, body position shifts evi-
techniques.
Publications, 2004. denced by past pointing or rotation on
Understanding brain injury: the Fukuda stepping test, appendicular
a guide for the family. ataxia via finger-to-nose testing and rapid
Rochester, MN: Mayo Press, alternating movements, and gait func-
1999, 2000. Available at tion. If historical features support the
library.ncrtm.org/pdf/ possibility of benign paroxysmal posi-
321.026.pdf.
tional vertigo (BPPV), performance of the
" Internet Sites Dix-Hallpike maneuver is critical. Addi-
Brain Injury Association of tional tools that can be employed in the
America. www.biausa.org. clinic setting include the Dizziness Hand-
Defense and Veterans Brain icap Inventory (a self-report tool) and
Injury Center. www.dvbic.org. Dynamic Visual Acuity testing (an objec-
tive examination measure). In fact, work
BrainLine.org.
www.brainline.org. by Basford and colleagues14 as well as
Traumatic brain injury: the
journey home. www. Causes of
traumaticbraininjuryatoz.org.
TABLE 7-4
Dizziness After
Mild Traumatic
Brain Injury
chronic dizziness and incoordination " Central

affect up to 30% of patients with post-
concussive symptoms.13,14 The proposed
Brainstem/cerebellar lesion 133
mechanisms of vestibulocerebellar dys- Migrainous vertigo
function after mTBI can be central (ax- Sensory integration/
onal disruption of cerebellar circuits) or vestibular processing deficit
peripheral (otolith or canal dysfunction). " Peripheral
Table 7-4 lists potential causes of dizzi-
Benign paroxysmal positional
ness after mTBI. Vestibulocerebellar dys- vertigo
function can negatively impact physical
performance of activities of daily living Labyrinthine concussion
reliant on higher balance function, such Otolith dysfunction
as bathing or dressing, driving or other Perilymphatic fistula
activities where shifting vision occurs
Posttraumatic endolymphatic
during bodily movement, and when
hydrops
pronounced vertigo can trigger or worsen
headaches. Rehabilitation of the ves-
" REHABILITATION
Gottshall and colleagues15 demonstrated in patients suffering blast injury, vestib-

statistically significant differences in the ular-evoked myogenic potentials may
Dizziness Handicap Inventory between also be tested. When gait instability or
patients with mTBI and healthy controls. balance concerns are significant, the ad-
In addition, the work of Gottshall and dition of posturography provides insight
colleagues15 demonstrated that both the into the integration of sensory, visual,
Dizziness Handicap Inventory and Dy- motor, and vestibular systems. Posturog-
namic Visual Acuity test could be used raphy also will help to identify which
as outcome measures for patients with area(s) may be contributing at the most
mTBI. This work also reinforced the gen- significant levels and demonstrate pat-
eral prognosis of mTBI as positive, dem- terns that are suggestive of an aphysio-
onstrating a significant improvement in logic cause of the gait instability. For a
both measures 4 weeks after injury. more detailed discussion of the specific
When vestibular symptoms are pres- tests, we refer the reader to the article by
ent and functionally limiting and physical Shepherd.16 Obviously, when approach-
examination signs are absent, more ing a patient with dizziness, the specific
detailed examination using formal ves- dysfunction can be varied and historical
tibular laboratory testing is indicated. data can help to hone the approach to
Video or electronystagmography will specific laboratory testing. Scherer and
provide insight into semicircular canal Schubert17 provide a potential frame-
function as well as central oculomotor work for approaching this testing, which
control pathways. Adding rotary chair is summarized in Table 7-5.
testing may further help define the lat- After identification of the specific def-
eralization and severity of deficits of icits, the therapy plan can be tailored to
peripheral function. To assess the oto- focus on the patient’s needs. Typically
lith organs, an area of increasing interest this therapy is delivered by physical
TABLE 7-5 Tests for Evaluation of Specific Vestibular Concerns

After Mild Traumatic Brain Injury
Symptom Vestibular Laboratory Testing
Motion sensitivity Motion sensitivity quotient

Posturography
134 Oscillopsia Computerized dynamic visual acuity
Vertigo Video/electronystagmography with calorics
Rotary chair testing
Positional testing (Dix-Hallpike)
Spatial disorientation Video/electronystagmography
Rotary chair testing
Posturography
Gait/postural instability Posturography
Data from Scherer MR, Schubert MC. Traumatic brain injury and vestibular pathology as a comorbidity after blast
explosure. Phys Ther 2009;89(9):980–992.
Data from Shepherd NT. Use of laboratory testing in the management of the patient with dizziness and balance
disorder. Continuum Lifelong Learning Neurol 2006;12(4):33–45.
KEY POINT
therapists and includes development of (executive functions).18 Individuals closest
A Rehabilitation of
a home exercise plan that the patient to the patient may validate these symp-
the mTBI
practices. Vestibular rehabilitation is di- toms and endorse changes in the patient’s patient with
rected at the capacity for adaptation and level of anger and irritability. In general, dizziness
habituation within the vestibular system the recovery of these deficits following should focus on
as well as the ability to correct conditions mTBI occurs within the first weeks to the domains of
such as BPPV via canalith repositioning months, and recovery often occurs with- motion
techniques. In patients with BPPV, canal- out specific intervention. When this dys- sensitivity,
ith repositioning maneuvers can be function is persistent or causes significant gaze, and
performed directly by the treating neu- functional alteration, however, rehabili- postural
rologist; however in refractory cases, the tation interventions to promote recovery stability.
incorporation of vestibular rehabilitation may be warranted. These techniques
may be beneficial. When approaching should clearly be defined by the domain
the mTBI patient with dizziness, the and level of impairment detected via val-
rehabilitation should focus on three idated testing methods. Additionally, any
domains: gaze instability, motion sen- technique employed should be paired
sitivity, and postural instability. Specific with appropriate educational intervention
exercises to be employed to address to reinforce the expected recovery pattern
each of these domains are detailed in of mTBI. While cognitive rehabilitation is
Table 7-6. Outcome data are somewhat not indicated for all patients with mTBI,
limited in the TBI population, but recent the patient with mTBI fits several ideal
work in patients with blast-associated patient characteristics for cognitive
mTBI has shown improvement in object rehabilitation. Cognitive rehabilitation
measures, including dynamic visual acu- seems to be most effective in patients
ity and dynamic gait index, following with mild to moderate deficits who are
vestibular rehabilitation.17 functional and motivated to partici-
pate.18,19 The delivery of cognitive re-
habilitation should be individualized
Cognitive and designed using knowledge of pa-
Self-reported cognitive symptoms fol- tient strengths and weakness. Also, the
lowing mTBI include impairments of focus should be on functional gains via
sustained and selective attention, short- use of compensatory strategies, adapta-
term memory, and organizational skills tion, and previously learned skills.18,19
TABLE 7-6 Exercises for Vestibular Deficits After Mild Traumatic Brain Injury 135
Domain Exercise Mechanism Notes
Gaze instability Adaptation exercises Vestibuloocular reflex Best with unilateral vestibular
gain facilitation dysfunction
Substitution exercises Improvement of May be used in patients with
compensatory saccades bilateral vestibular dysfunction
Motion sensitivity Habituation exercises Central reorganization, Not to be used with bilateral
decreased sensory mismatch vestibular dysfunction
Postural Static and dynamic Vestibular adaptation of Can be employed in unilateral or
instability gait and posture vestibulo-spinal responses bilateral dysfunction
Data from Scherer MR, Schubert MC. Traumatic brain injury and vestibular pathology as a comorbidity after blast exposure. Phys Ther 2009;89(9):980–992.
" REHABILITATION
KEY POINTS
Cognitive rehabilitation interventions their intervention population, patients
A Cognitive
are typically managed by speech therapists, received cognitive-behavioral therapy
rehabilitation
tools that can
occupational therapists, or neuropsy- as well as cognitive remediation target-
be used in chologists. The treatment can be face- ing attention and memory. At the com-
patients with to-face pencil-and-paper methods or pletion of 11 weeks of the study, the
mTBI include through use of computer or virtual re- intervention group not only demon-
attention ality technology. However, technology strated an improvement in symptom
process alone should not supplant the role of the reporting, anxiety, and depression, but
training, treating clinician.20 The following are also demonstrated improvements in
memory specific cognitive rehabilitation tools that measures of auditory attention. Adding
notebook, and have been used in patients with mTBI: to the significance of their findings is
metacognitive attention process training to address the fact that a significant percentage of
strategy.
attentional deficits, memory notebook patients involved in litigation in the
A Veterans with as a compensatory tool for memory im- treatment group still demonstrated im-
mTBI have pairments, and metacognitive strategy provement. Secondary gain issues have
prolonged instruction to address executive dysfunc- long been viewed as perpetuating fac-
postconcussive tion.19,20 Many of these tools go hand tors in postconcussive symptom per-
symptoms, in hand with assistive technologies, such sistence. Cognitive rehabilitation is a
including as personal digital assistants (PDAs) or treatment that should be used in mTBI,
headache,
smartphones. In fact, the Department of albeit in a selective fashion and with an
impaired
Veterans Affairs/Department of Defense emphasis on functional recovery and
attention, poor
temper control,
TBI treatment guideline specifically ref- the use of compensatory strategies.
and impaired erences the importance of assistive
technology in the symptomatic mTBI IMPACT OF SLEEP, PAIN,
sleep.
population.19 The use of PDAs has been AND POSTTRAUMATIC
beneficial in our mTBI population, im- STRESS DISORDER
proving appointment compliance as well Veterans with mTBI have prolonged
as improving sense of organization and postconcussive symptoms, including
self-efficacy. At times, cognitive reha- headache, impaired attention, poor tem-
bilitation efforts will also be directed per control, and impaired sleep.22,23 Vet-
at social pragmatics. These deficits are erans with mTBI caused by exposures to
more typically seen in the moderate to explosions in combat may have been
severe TBI population with frontal lobe more likely to have persisting postcon-
injuries. cussive symptoms compared to people
Cognitive rehabilitation has been who sustained TBI in civilian life for
136 studied in a controlled fashion in many several reasons. Soldiers with mTBI can
different diseases, including focal le- be returned quickly to combat stress,
sions such as stroke, as well as more which will preclude a rest period that
diffuse injuries such as those seen in might aid in neuronal recovery from
TBI or anoxic brain injuries. It is gen- mTBI. Headache, a common component
erally viewed as a validated treatment of postconcussive symptoms, differs be-
modality, and we refer the reader to the tween civilian and combat mTBI. Head-
works of Cicerone and colleagues for aches caused by combat mTBI often
a more comprehensive discussion of have features of migraine.23,24 In con-
the evidence behind its use in these trast, headaches caused by noncombat
diseases.19 Tiersky and colleagues21 re- mTBI are usually tension type. Headache
cently published a small, randomized, usually resolves within 6 months for ci-
single-blind trial of cognitive rehabili- vilians with mTBI,25 whereas headaches
tation specifically for mTBI. Their study associated with combat mTBI often per-
revealed some interesting findings. In sist for years.23
KEY POINT
A prominent difference between com- to an incidence of PTSD up to 19%
bat and civilian mTBI is the context in
A The context
among veterans with severe TBI. A study
of veterans’
which the injury occurred. Combat mTBI of active duty military personnel noted injuries as well
occurs in stressful situations that are that a history of mTBI increased the as the higher
likely to induce PTSD.26–28 The likeli- likelihood of a diagnosis of PTSD by potential for
hood of an individual developing PTSD more than fourfold.27 A study of veterans multiple injuries
is influenced by many factors, including treated in a Department of Veterans impacts the
the character of the traumatic exposure Affairs Polytrauma Center found a high development of
and the individual’s psychological resil- coexistence of PTSD in veterans with his- posttraumatic
iency and educational history.29 Case 7-2 tories of mTBI.22 Among veterans who stress disorder
illustrates how PTSD can complicate re- did not have head trauma, the frequency (PTSD) and
covery from mTBI. The frequencies of of PTSD was 3%; in contrast 73% of vet- increases the
PTSD among veterans and military per- chances for
erans with mTBI had PTSD. Depression
prolonged
sonnel vary among studies. The Depart- and anxiety are also frequently associated postconcussive
ment of Veterans Affairs published a with mild TBI acquired in combat. Ex- symptoms.
summary of information related to TBI tensive overlap occurs between the
and PTSD.30 In that report up to 89% of symptoms that are usually attributed to
veterans with mTBI had PTSD compared a prolonged postconcussive state and
Case 7-2
A 42-year-old US Army reservist who had been deployed 2 times to Iraq
sustained four episodes of LOC, the last being 2 years earlier. He reported
experiencing daily tension-type headaches and one migraine headache
each week. He had PTSD with interrupted sleep caused by nightmares,
excessive daytime sleepiness, impaired concentration, impaired recall,
short temper, and difficulty relating to his wife. She did not understand
why he was acting differently, in spite of no visible injuries. His recollection
of his last episode of head trauma with LOC illustrated the combat
conditions that led to the development of PTSD. He said, ‘‘I was the gunner
on a Humvee. A suicide bomber was coming at us. In the back seat were
a terrified woman and her daughter. I had to take out the car driver, but
the car still hit our vehicle. The blast knocked me out for several minutes.
Our driver was killed. The woman and her daughter were killed. I see
that girl when I look at my daughter.’’ On neurologic examination he had
impaired olfaction. He scored 25/30 on the MoCA test, with points lost
for visuospatial/executive function, attention, and delayed recall. He was
137
resistant to taking medications that might alter his cognitive function. The
initial intervention involved initiating family counseling so that his wife
understood how his TBI and PTSD changed his behavior. He and his wife
received counseling on sleep hygiene. A slowly increasing dose of prazosin
was started at 1 mg at bedtime and increased weekly to 7 mg at bedtime.
After 9 weeks of treatment, his nightmares abated, his sleep improved,
and he no longer had excessive daytime sleepiness. His migraine headaches
resolved, and his tension-type headaches became less intense and were
occurring only once a week. Six months later, he and his wife felt that his
mood was much improved and his headaches occurred only monthly. His
MoCA score improved to 30.
Comment. This case illustrates that mild combat TBI is often associated
with PTSD. The symptoms associated with the mild TBI and PTSD overlap,
and both conditions need to be addressed.
" REHABILITATION
FIGURE 7-1 Overlap of symptoms and distinct features of

traumatic brain injury and posttraumatic
stress disorder.
PSTD = posttraumatic stress disorder; TBI = traumatic brain injury.
those attributed to PTSD (Figure 7-1). that intrusive remembrances (eg, flash-
Case 7-3 demonstrates the overlap of backs, vivid nightmares) are thought to
symptoms associated with mTBI and be unique to PTSD, and persisting neu-
PTSD. This case also illustrates that rologic deficits and headaches, particu-
PTSD can develop following noncombat larly with a migraine component, are
trauma. Distinguishing differences are usually attributed to TBI.24,28
Case 7-3
A 23-year-old woman who had sustained mTBI with one episode of LOC
during an assault was seen 10 weeks later because of persisting
tension-type headaches and difficulty concentrating at work. The
headaches occurred 6 times a month, lasted 2 to 4 hours, and had an
intensity of 4/10. She had difficulty sleeping with recurrent nightmares and
recurrent intrusive recollections of her assault. She had excessive daytime
sleepiness along with impaired concentration and recall.
138 She had no abnormalities on neurologic examination, but she did meet
Diagnostic and Statistical Manual of Mental Disorders (Fourth Edition)
criteria for a persisting stress reaction presumably related to her assault.
She scored 28/30 on the MoCA test, with points lost for attention and
delayed recall. She was treated initially with psychological counseling
related to her assault. In addition she received sleep hygiene counseling,
and a slowly increasing dose of prazosin was started at 1 mg at bedtime
and increased weekly to 7 mg at bedtime. After 9 weeks of treatment, her
nightmares abated, her sleep improved, she no longer had excessive
daytime sleepiness, and she no longer had intrusive recollections of her
assault. Her tension-type headaches resolved without analgesic
medication. Her MoCA score improved to 30.
Comment. This case illustrates that the recovery from mTBI in a civilian
setting can be complicated by a persisting stress reaction. Resolution of
symptoms requires treating the stress reaction.
KEY POINTS
Veterans with combat mTBI have vilian life for returning Operation Iraqi
often sustained multiple episodes of
A The challenges
Freedom/Operation Enduring Freedom
of social
mTBI.23 Even a single episode of mTBI (OIF/OEF)veterans who sustained mTBI reintegration
can produce brain injury that can be was 82% compared to 19% for veterans following
seen on neuroimaging.31,32 Perhaps the who did not have TBI or PTSD (unpub- combat TBI
brain is able to repair or compensate lished data). The challenges of social may heighten
for the damage produced by isolated reintegration may heighten sleep diffi- sleep difficulties
episodes of mTBI, but the brain may culties and worsen psychological health. and worsen
have reduced ability to accommo- An intriguing question is why com- psychological
date repeated injuries.33,34 Animal stud- bat mTBI increases the likelihood of health.
ies suggest that repeated episodes of developing PTSD.27,28 Perhaps, the loci A The areas of the
head trauma will increase the likeli- of injury in mTBI result in alteration of brain with
hood of persisting cerebral injury.35 brain function that predisposes to the altered function
Combat veterans of conflicts in Iraq emergence of PTSD. The areas of the identified by
and Afghanistan often suffered mTBI brain with altered function identified functional
resulting from exposure to an explo- by functional imaging in PTSD, includ- imaging in
sion. Combat mTBI was thus associated ing inferior frontal lobes and ante- PTSD, including
with two almost simultaneous traumatic rior temporal lobes,32,37,38 are included inferior frontal
events. Veterans with combat mTBI within the areas that are damaged in lobes and
were often close enough to the blast mTBI.31,32,39,40 Veterans with moderate anterior
temporal lobes,
to experience the explosive overpres- to severe TBI appear to be at lower risk
are also areas
sure wave. In addition, veterans often for having PTSD compared to veterans
that can be
sustained explosion-associated concus- with mild TBI.41 The reason for the in- damaged in
sion when thrown by the blast-wind, creased risk of developing PTSD for mTBI.
impacted by shrapnel, or involved in a mild compared with moderate or severe
motor vehicle accident associated with TBI is not known. One possibility is that
the explosion.26 Even though they all with moderate or severe TBI the in-
reported wearing combat helmets, dividual may have little or no residual
these helmets were designed to protect memory of the traumatic events associ-
against projectile injury, not mTBI.26 ated with the head trauma or of events
Another factor that may have com- that preceded the trauma.
promised recovery from mTBI among The extensive overlap of combat
the veterans who were returning from mTBI with psychological comorbidities
combat was adapting to civilian life. has suggested to some that persisting
Reintegration into society is challeng- deficits in veterans with mTBI are solely
ing for combat veterans with histories due to psychiatric conditions such as 139
of mTBI to severe TBI.36 For veterans PTSD.27 An argument made in defense of
with mTBI, readjusting to civilian life this position is that combat mTBI should
presents challenges because behavior behave the same as civilian TBI. Given
patterns useful in a combat setting are that the manifestations of mTBI or con-
often not appropriate for civilian life. cussion occurring in a civilian setting
The families of veterans with mTBI and usually resolves within 6 months,25,42–44
PTSD, but no other physical injuries, pseudologic could be used to argue that
found it difficult to understand why the any residual issues that exist in veterans
veterans were having problems resum- with mTBI must be due to something
ing their predeployment lives.36 The other than the TBI. As stated earlier,
veterans looked the same but did not differences in the circumstances asso-
act the same. Family discord, including ciated with TBI may alter the outcomes
divorce, was common. The divorce rate associated with mTBI. An alternative
in Ohio during the first 2 years of ci- view is that PTSD is tightly entwined
" REHABILITATION
KEY POINT
with combat mTBI; therefore, one needs heighten the perceived pain severity.57
A PTSD, sleep
to consider how to treat both conditions Sleep deprivation can trigger migraine
deprivation,
and chronic simultaneously. and other headaches and increase a
pain are all One way that mTBI and PTSD may person’s perceived pain intensity.53,54,58
factors that be maliciously entwined is that PTSD We previously noted that veterans with
significantly can compromise sleep, and impaired mTBI who had impaired sleep reported
impact the sleep will worsen and likely prolong more severe pain.23
recovery curve postconcussive manifestations. Moder- We examined the impact of improv-
in patients with ate and severe TBI are associated with ing sleep in a group of OIF/OEF veterans
combat-related several types of sleep impairment, such with mTBI who had persistent head-
mTBI. as obstructive sleep apnea, hypersom- aches associated with PTSD.59 The treat-
nia, narcolepsy, and periodic limb ment intervention consisted of providing
movements in sleep.45 However, mTBI sleep hygiene education to regulate and
by itself is unlikely to produce a per- improve sleep onset and prazosin to
sisting sleep impairment.45 Nightmares block nightmares. Sleep hygiene coun-
due to PTSD will disrupt sleep, and anx- seling is a standard educational inter-
iety about having nightmares will in- vention provided to patients to improve
hibit sleep onset.46 Sleep deprivation sleep and to enable them to have an ac-
worsens postconcussive manifestations tive role in their health care.60,61 The prin-
such as pain, including headache, and ciples of sleep hygiene are summarized
intellectual performance.47,48 in Table 7-7. Sleep hygiene counseling
Features of PTSD may heighten or
unmask deficits and symptoms caused Principles of Sleep
TABLE 7-7
by mild TBI. Reduction in sleep time Hygiene
may unmask subclinical neurologic def-
icits and can impair cognitive perfor- " Adapt a fixed bedtime
mance.45,47,48 Disruption of the normal
" Avoid activities that may
sleep-wake cycle can desynchronize trigger flashbacks
hormones that are synchronized with
the circadian cycle. Desynchronization " Stop watching television
1 hour before bedtime and
of circadian hormones can impair cog- engage in calming activities,
nition and attention and result in a de- eg, reading, intimacy
creased capacity to learn.47 The presence
" Sleep only when sleepy and
of headaches in the combat veterans avoid sleeping during the
could heighten deficits caused by im- day
140 paired sleep. Pain combined with sleep
" Avoid caffeinated beverages,
deprivation will compromise several as- including energy drinks
pects of cognitive performance. Even if
one considers the adverse impact of " Engage in exercise during
the day, not within 4 hours
impaired sleep on cognitive perfor- of bedtime
mance, chronic pain itself has an ad-
verse effect on cognitive performance.48 " Take a hot bath or shower
about 1 hour before bedtime
Complex interactions occur between
chronic pain and sleep. Chronic pain is " If body weight is not an issue,
eat a light snack before
often associated with impaired sleep.48–55
bedtime
In combat mTBI, sleep impairment in
association with PTSD is an important " Receive a call from or see a
clinician to reinforce sleep
determinant of persistence of pain, in-
hygiene
cluding headache.23,28,56 Impaired sleep
can also alter pain perception, which can
KEY POINT
includes the following instructions: (1) noradrenergic activity.65 (4) Our OIF/OEF
A Combining
adapt a fixed bedtime; (2) avoid activ- study group was reluctant to take med-
pharmacologic
ities that may trigger flashbacks, includ- ications that would cloud their conscious- and behavioral
ing violent/graphic video games (such as ness or alter their mood. The OIF/OEF interventions
‘‘shooter games’’ or combat simulations) study group was willing to take prazosin for sleep
and video or audio programs/movies because it does not induce sleepiness disruption in a
about combat or violent programs, par- and is not considered an agent that will combat mTBI
ticularly within 6 hours of bedtime; (3) cloud consciousness or directly alter population
stop watching television 1 hour before mood. (5) Prazosin is now being used resulted in
bedtime and engage in calming activities by active duty military personnel to treat improvement in
such as reading or engaging in intimacy nightmares associated with combat expe- sleep,
headache pain,
with your partner; (4) sleep only when riences. (6) Prazosin is not known to
and cognitive
sleepy and engage in a boring activity cause erectile dysfunction.62
function.
if not sleepy at bedtime; (5) avoid caf- The intervention of sleep hygiene
feinated beverages (veterans were coun- counseling and prazosin was well tol-
seled about beverages that contain caf- erated. Veterans showed reduction
feine, such as coffee, sodas, and ‘‘power’’ in headache pain intensity and head-
drinks), nicotine, and alcohol within 6 ache frequency and improvement in
hours of bedtime; (6) avoid sleeping dur- cognitive functioning.59 The results
ing the day; (7) engage in exercise during were very encouraging for using sleep
the day, but not within 4 hours of bed- hygiene and prazosin to improve
time; (8) take a hot bath or shower about sleep in veterans with mTBI and
1 hour before bedtime and, (9) if obesity PTSD. However, this was an obser-
is not an issue, eat a light snack before vational study and will need to be
bedtime. We felt that the most common supported by a placebo-controlled
poor habits were playing agitating video clinical trial.
games, drinking ‘‘power’’ beverages, Pain is a common problem among
and not winding down before sleep. OIF/OEF veterans with mTBI.22,66 The
The veterans were contacted every 2 presence of pain complicates rehabili-
weeks during the 9-week study period tation in several ways. (1) As stated
to reinforce sleep hygiene, with a total earlier, pain can interfere with sleep,
of five counseling sessions during the 9- which can, in turn, compromise the
week intervention period. ability of an individual to concentrate
We chose prazosin as the pharma- and engage in rehabilitation. Sleep loss
ceutic agent to improve sleep for sev- will also reduce an individual’s endur-
eral reasons. (1) Prazosin is an -adrenergic ance for multiple hours of rehabilita- 141
blocking agent that penetrates the CNS tion each day. (2) Medications that may
and is able to block nightmares associated be used to treat pain and muscle
with stress disorders.62 (2) Placebo- spasms can compromise the ability of
controlled clinical trials demonstrated an individual to participate in reha-
that prazosin reduced nightmares and bilitation, particularly cognitive rehabil-
improved sleep in veterans with PTSD46 itation. Opioid and benzodiazepine
and civilians with PTSD.63 (3) In addition medications are particularly problem-
to improving sleep, prazosin may im- atic for people undergoing rehabilita-
prove cognitive function by reducing the tion. (3) Pain will compromise cognitive
anxiety associated with PTSD. Subjects processing, including attention and
with PTSD have impaired cognitive func- concentration, independent of its dis-
tion that can be in part attributed to ruption of sleep.48 Patients in pain
anxiety.64 Prazosin may reduce anxiety are not able to concentrate for cog-
in veterans with PTSD by reducing CNS nitive rehabilitation, and pain may
" REHABILITATION
KEY POINT
directly prevent motor and balance with mTBI created by PTSD, impaired
A The challenges to
rehabilitation. sleep due to nightmares, and pain.
returning to
functional or PTSD may create an additional chal-
vocational FUNCTIONAL RETURN/ lenge by interfering with certain oc-
baseline are VOCATIONAL REHABILITATION cupations, such as law enforcement.
different for The challenges to returning as close Veterans may need to pursue other
individuals with to a premorbid state as possible are vocations until the PTSD is well con-
mTBI compared different for individuals with mTBI trolled. Postural instability associated
to those with compared to those with moderate to with mTBI is often attributed to dam-
moderate to severe TBI.67,68 Table 7-8 contrasts the age to the middle ear labyrinth system.
severe TBI. challenges to returning to work faced It may also result from subtle damage
by veterans with mild compared with to posterior fossa structures. Vestibular
moderate/severe TBI. We previously rehabilitation can be used to overcome
discussed the problems for veterans the deficits of postural instability and
dizziness associated with mild TBI.69
Visual concerns associated with mTBI
include photosensitivity and visual al-
TABLE 7-8 Comparison of
Challenges to
terations related to migraine headache.
Returning to Work Faced By Bright lights may trigger migraine at-
Veterans With Mild Traumatic tacks. Photosensitivity may decline with
Brain Injury Compared With time and can be ameliorated by using
Moderate/Severe Traumatic darkened polarizing lenses. Fatigue is a
Brain Injury common concern, but caffeine or other
‘‘energizing’’ medications should be
" Mild Traumatic Brain Injury
used with caution because these agents
Dizziness may disrupt normal sleep. After a pe-
Fatigue riod of inactivity, it can be difficult to
return to a regular work schedule, and
Headaches
patients may need to gradually increase
Pain syndromes their work time until they are able to
Posttraumatic stress disorder work through full days.
Postural instability
Mental fatigue is a common symp-
tom after mTBI. Mental fatigue refers
Sleep interrupted by to difficulty maintaining attention, dif-
nightmares
ficulty initiating an activity, or difficulty
142 Vision deficits completing a physical or intellectual
" Moderate/Severe Traumatic task that is not due to physical tired-
Brain Injury ness. Fatigue following TBI has been
Fatigue studied extensively in association with
civilian TBI, but little published infor-
Fine motor deficits
mation is available on the frequency of
Heterotopic ossification mental fatigue among military person-
Hypertonicity nel who sustained TBI. About one-third
of individuals with civilian mTBI report
Insomnia
severe mental fatigue at some point
Postural instability during the 6-month period following
Seizures the injury.70 A subset of individuals with
mTBI may have postconcussive symp-
Visual deficits
toms associated with subjective mental
fatigue that can persist for several
KEY POINT
years.71 Women are slightly more likely overcome. The residual strengths of
A Mental fatigue
to suffer from mental fatigue following each patient need to be considered in a
following TBI
mTBI.72 Mental fatigue following mTBI vocational rehabilitation program. Indi- represents a
is more common for carriers of the viduals may not be able to return to significant
APOE 4 allele.73 Otherwise, it is not their premorbid jobs, particularly if limiting factor
clear which individuals with mTBI will those jobs place physical or cognitive in functional
go on to suffer from prolonged mental demands that exceed the individual’s recovery and is
fatigue. The presence of mental fatigue current capacity. It may be necessary to often refractory
following mTBI is not correlated with modify the work environment to en- to treatment
the etiology of the mTBI or with other able an individual with moderate or and
demographic characteristics (except for severe TBI to work. Successful voca- emotionally
distressing for
sex).72 The presence of mental fatigue tional rehabilitation programs often en-
patients.
following mTBI cannot be attributed to gage employers in the process so that
coexistent depression, pain, or sleep the job demands and work environ-
deprivation. In one study, only 23% of ment can be accommodated to the
the variance in the incidence of fatigue residual skills of the patient.67,68 Seiz-
in individuals with mTBI could be ac- ures need to be optimally controlled.
counted for by the coexistence of de- An individual with posttraumatic epi-
pression, pain, and sleep problems.72 lepsy requires work environments that
The presence of mental fatigue is are consistent with the epilepsy. Driv-
associated with reduced self-perceived ing, operating heavy equipment, and
quality of life.72 Individuals with mTBI working in isolated environments are
who have mental fatigue have more usually not appropriate for individuals
problems with returning to work and with epilepsy. Spasticity can limit an in-
to their prior style of living. In partic- dividual’s motor capacity, and the med-
ular, these individuals have difficulty ications used to treat spasticity can be
performing mental tasks quickly and problematic in a work environment.
are frustrated because of their slow- Spasticity treatments that are less likely
ness. They do not perform well on to interfere with work include intrathe-
subsets of cognitive function tests that cal baclofen and botulinum toxin to
depend on speed of response, but per- reduce muscle tone in selected muscle
formance on memory and other cogni- groups. Regular movement associated
tive testing that do not depend on with working can reduce spasticity.
processing speed are usually similar to People with spasticity should have
that of individuals with mTBI who do carefully designed work environments
not have mental fatigue.71,74 The pres- that consider each person’s specific 143
ence of mental fatigue reduces the functional deficits. Postural instability
likelihood that an individual will return associated with moderate to severe TBI
to work.68 Treatment of mental fatigue often requires special seating and per-
is difficult. Pharmacologic interventions haps bracing arrangements to enable
to increase ‘‘energy levels’’ usually do an individual to maintain a proper
not help. The best strategy at present is working position. Impairment of fine
to gradually increase the amount of time motor skills, particularly rapid upper
that an individual spends each day extremity fine movements, can limit
engaging in life tasks and to strongly the types of work that an individual can
discourage prolonged mental or physi- successfully perform. Motor tests that
cal inactivity.67,68 measure agility and speed, such as the
The physical challenges of returning grooved pegboard test, can be used to
to work faced by patients with moder- assess fine motor skills in the upper
ate or severe TBI can be difficult to extremities.75 Visual deficits associated
" REHABILITATION
KEY POINT
with moderate and severe TBI include heterotopic ossification can be treated
A Physical deficits
monocular visual loss, visual field cuts, using bisphosphates, nonsteroidal anti-
such as motor
dysfunction, loss of depth perception, and visual inflammatory drugs, and in some in-
seizures, and distortions. Visual deficits need to be stances radiation to retard new bone
heterotopic individually addressed, and the work formation. Surgical excision of hetero-
ossification are environment needs to be such that topic bone can be considered in some
factors that can uncorrected visual impairment can be instances of heterotopic ossification
limit vocational tolerated. to restore functional joint movement.
outcomes in Heterotopic ossification, which usu- Disruption of the normal sleep-wake
patients with ally manifests with abnormal periartic- cycle will sometimes respond to sleep
TBI; however, ular bone formation, is associated with hygiene interventions to regulate sleep
these are seen
altered motor tone and paresis. Het- times. Fatigue may improve over time
mostly in
erotopic ossification usually develops as the individual becomes used to reg-
moderate and
severe injuries.
in areas of restricted joint movement. ular work periods.
Symptoms of heterotopic ossification
include pain, reduced joint motion, SOCIAL REINTEGRATION
redness, and heat that may be associ- Combat veterans with histories of TBI
ated with a palpable tender mass, and are often challenged when trying to
tenderness. The most frequently in- reintegrate into society and civilian
volved joints are the hips, shoulders, life36,77,78 because behavior patterns
knees, and elbows.76 Heterotopic ossi- that are useful in a combat setting, re-
fication may be prevented by maintain- ferred to as battlemind,79 are often
ing joint range of motion. Once present, inappropriate for civilian life.
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149

PATIENT MANAGEMENT PROBLEM

Dalila W. Lewis, Stephen J. Sharp
The following patient management problem was chosen to reinforce the subject matter
presented in this issue. It emphasizes decisions facing the practicing physician. At each
decision point determine how you, as the neurologist, would respond. Then answer the
questions provided. The weight or “value” indicates the relative strength or weakness
of the response as determined by the faculty. Use these values, as well as the critical
comments, to assess your own understanding and handling of the problem. A review of
all responses, not merely the ones you select, is recommended.
Learning Objective
The goals of this article are to educate the reader regarding the correct identification and
management of postconcussive symptoms, identification of risk factors for development of
postconcussive sequelae, and determination of appropriate guidance regarding resumption
of athletic and academic activities.
Case History
A 15-year-old male soccer and football player is referred to the office for evaluation
and management because of persistent symptoms of headache and disequilibrium after
he sustained a concussion approximately 1 month ago with loss of consciousness
lasting less than 5 minutes. The impact, consisting of a knee striking the unhelmeted
occiput at running speed, occurred during soccer practice. The patient was immediately
“stunned” and states he blacked out for a few minutes. He is amnestic for the events
immediately after the impact, recalling only being on a stretcher with his coach and
150 teammates looking at him. He had been taken to a local emergency department for
evaluation, where the neurologic examination was reportedly normal and noncontrast
head CT was unremarkable. He was subsequently diagnosed with a grade 2 concussion
and discharged with instructions to follow up with his primary care physician for
return-to-play recommendations. On follow-up with his primary care physician 2 days
later, the patient reported headaches and dizziness. Neurologic examination was normal.
It was ascertained that this was his first concussion of the season. He was instructed to
rest for the next 5 days and told he could return to play in 2 weeks if he were feeling
better. Three weeks later, the patient followed up with his primary care physician, again
because of continued daily headaches. He has attended two soccer practices, and with
each he had to sit out after 10 minutes because of worsened headache. He also reported
difficulty concentrating in school, noting that he had failed two examinations in the
past 2 weeks. The primary care physician prescribed ibuprofen for his headaches and
Relationship Disclosure: Drs Lewis and Sharp have nothing to disclose.

Unlabeled Use of Products/Investigational Use Disclosure: Drs Lewis and Sharp have nothing to disclose.
Copyright © 2010, American Academy of Neurology. All rights reserved.
referred him for pediatric neurology evaluation. He was informed that he may not
return to play until he is evaluated and cleared by a neurologist.
Decision Point A. Based on the clinical history, what is the patient’s diagnosis?
A1. Grade 2 concussion
A2. Complex concussion
A3. Posttraumatic stress disorder
A4. Postconcussive syndrome
A5. Vertebral artery dissection
Decision Point B. What are the most important considerations regarding

return-to-play recommendations?
B1. History of previous concussions
B2. Presence of postconcussive symptoms
B3. Grade or severity of concussion
The patient is seen in the pediatric neurology clinic 6 weeks after the initial concussion.
At the time of his evaluation, the patient reports he has a daily headache that is dull,
yet throbbing, in quality and frontal and occipital in location. He is taking 400 mg of
ibuprofen almost daily. He does not endorse significant photophobia, phonophobia,
nausea, or vision changes. He does endorse feeling off balance when he is walking,
however, although he is not falling or bumping into objects. He states he has difficulty
sleeping at night and is fatigued during the day. Prior to the concussion, he reports he
slept well most nights and had no significant daytime fatigue. He also reports that prior
to the concussion he did not have headaches and his school performance was above
average. Currently, his school performance is poor, and his most recent test scores
have been well below average. His parents report that he seems angry all the time and
he has gotten into trouble at school this week for “mouthing off” at a teacher.
Decision Point C. Based on the above, what other diagnoses should be considered?
C1. Narcolepsy
C2. Migraine headaches
C3. Medication-overuse headache syndrome
151
Decision Point D. Based on the clinical history, what is the most important next step?
D1. Detailed past medical history, including previous history of head trauma
D2. Detailed neurologic examination
D3. Polysomnography
D4. Urine toxicology screen
Past medical history is notable for attention deficit hyperactivity disorder (ADHD)
diagnosed at age 6 for which the patient takes methylphenidate (Concerta) 36 mg once
daily. He has no other history of head trauma, with the exception of taking “headers”
and tackles in the course of playing soccer and football, respectively. He has been
playing soccer for 3 years and football for 9 years. He denies a history of drug or
alcohol abuse and uses no tobacco. Neurologic examination reveals the following:
normal funduscopic, cranial nerve, motor, and sensory examinations; normal deep
tendon reflexes with flexor plantar responses bilaterally; mildly abnormal cerebellar
examination with slightly impaired tandem gait but normal rapid alternating movements
and no dysmetria; and negative Romberg sign.
Decision Point E. Based on the clinical history and the neurologic examination, which
of the following evaluations should be obtained?
E1. Neuroimaging
E2. Ears, nose, and throat consultation for vestibular testing
E3. Neuropsychological testing
A noncontrast brain MRI is normal. Vestibular testing is also normal. Neuropsychologic
testing reveals mild deficits in attention/concentration and executive function tasks. In
addition, mildly decreased processing speed and a personality index score consistent with
mild depression are noted.
Decision Point F. Based on the clinical history and the above test findings, which of
the following recommendations should be made for this patient?
F1. Individualized education plan to be developed by the school
F2. Behavioral counseling
The patient is referred for behavioral counseling. A recommendation is made to the
school to formulate an individualized education plan for the patient to include
appropriate test accommodations based on his decreased processing speed and
attentional difficulties.
Decision Point G. What medical therapy, if any, should be prescribed for this patient?
G1. Antidepressant
G2. Prophylactic headache medication
G3. Stimulant medication
G4. Sleep-inducing medication
G5. Antiepileptic medication for the purpose of seizure prophylaxis
152
WEIGHTS AND COMMENTS
EXPLANATION OF WEIGHTS:
+5 Unequivocally required for diagnosis or effective treatments, without which management
would be negligent
+3 Important for diagnosis and treatment but not immediately necessary
+1 Potentially useful for diagnosis and treatment (routine studies fall into this category)
0 Neutral impact; neither clearly helpful nor harmful under given circumstances
–1 Not harmful; but nonproductive, time-consuming, and not cost-effective
–3 Nonproductive and potentially harmful
–5 Totally inappropriate and definitely harmful; may threaten life
A1. Grade 2 concussion +1
The definition of concussion is widely accepted as a complex pathophysiologic process
affecting the brain that is induced by trauma and is manifest by rapid onset of transient
impairment of neurologic function that may or may not involve loss of consciousness.1,2
The term is often used synonymously with mild traumatic brain injury (mTBI). Variance in
the literature regarding the definition of mTBI often exists, however, with some definitions
including the qualification of normal standard brain neuroimaging.3,4 The definition of
mTBI proposed by the American Congress of Rehabilitation Medicine in 1993 included
loss of consciousness lasting less than 30 minutes, posttraumatic amnesia lasting less than
24 hours, and Glasgow Coma Scale score of 13 or greater.5 However, the most recent
update by the Centers for Disease Control and Prevention regarding concussion and
mTBI concluded that the terms may be used interchangeably. It further specifically
states the following:
An MTBI or concussion is defined as a complex pathophysiologic process affecting the
brain, induced by traumatic biomechanical forces secondary to direct or indirect forces
to the head. MTBI is caused by a blow or jolt to the head that disrupts the function of
the brain. This disturbance of brain function is typically associated with normal structural
neuroimaging findings (ie, CT scan, MRI).6
As mentioned earlier, loss of consciousness or posttraumatic amnesia is not required
for the diagnosis of concussion. Thus, the preferred term is concussion because of the
universally accepted definition as well as the potential implications of labeling someone
with brain injury. Further, a recent study highlights parental perceptions of differences in
meaning of the terms concussion, mild traumatic brain injury, and minor traumatic brain
injury, regardless of their equivalence in the medical community.7 Although consensus
on the definition of concussion exists, concussion grading and classification schemas are
controversial and not as widely accepted. A grade 2 concussion may differ depending on
which grading scheme is used. The three most widely used scales have been the Cantu,
the AAN, and the Colorado Medical Society. Per the AAN, a grade 2 concussion consists of
transient confusion lasting more than 15 minutes without a loss of consciousness; grade 3
consists of any loss of consciousness.1 According to the Cantu concussion grading scale,
a grade 2 concussion consists of a loss of consciousness less than 5 minutes with
postconcussive amnesia and/or postconcussive symptoms lasting from 15 minutes to
24 hours after injury.8 Finally, the Colorado concussion grading scale refers to a grade 2
153
concussion as one in which posttraumatic amnesia and confusion without loss of
consciousness are present; grade 3 includes any loss of consciousness.9 Thus, this patient
had a grade 2 concussion per the Cantu grading scale and a grade 3 concussion per the
AAN and Colorado Medical Society grading scales. Given these ambiguities, it has been
recommended that grading schema be abandoned.
A2. Complex concussion +1

In 2004, the participants of the 2nd International Symposia on Concussion in Sport held in
Prague reached consensus recommending that concussions be classified as either simple
or complex based on the length of postconcussive symptoms.10 A simple concussion was
defined as one in which postconcussive symptoms last less than 7 to 10 days, and a complex
concussion was defined as one in which postconcussive symptoms persist more than 7 to
10 days. However, in 2008, the consensus of the 3rd International Symposia on Concussion
in Sport held in Zurich recommended that the simple versus complex classifications also
be abandoned, citing that the terminology was not adequately descriptive.11
A3. Posttraumatic stress disorder –1

According to the Diagnostic and Statistical Manual of Mental Disorders (Fourth Edition)
(DSM-IV), posttraumatic stress disorder consists of the following symptoms: persistent
reexperiencing of the traumatic event, persistent avoidance of stimuli associated with the
traumatic event, and persistent symptoms of increased arousal to include insomnia, difficulty
focusing, irritability, and hypervigilance.12 While the patient does have some symptoms of
increased arousal, he does not meet the other criteria. Further, symptoms of posttraumatic
stress disorder tend to develop over time rather than more acutely as in this case.
A4. Postconcussion syndrome +5
Postconcussion syndrome may develop as a sequela of minor head injury and typically
encompasses symptoms of headache, dizziness, fatigue, irritability or other mood
disturbance, impaired memory and/or concentration, and/or sleep disturbance. The
reported incidence of postconcussion syndrome among persons after head injury varies
widely in the literature, between 30% and 80%.13–15 Among those with normal standard
neuroimaging, however, the incidence is reported to be roughly 40% based on the diagnostic
criteria set forth by the International Classification of Diseases.16 The symptoms may persist
weeks to months after the injury, and the grade or severity of the concussion has little
predictive value regarding length of postconcussive symptoms.13,15,17 Most persons with
postconcussive symptoms recover within 3 to 6 months; however, recent literature states
recovery in children and adolescents may be prolonged.4,18,19
A5. Vertebral artery dissection –3
Vertebral artery dissection should be a consideration in someone who has sustained
posterior head trauma and has been reported to have minor head or neck injury. Most
persons with vertebral artery dissection, however, develop focal neurologic signs referable
to brainstem or cerebellar dysfunction within days of the injury.20 This patient reportedly
has a normal neurologic examination and, other than subjective mild dizziness, does not
have other symptoms indicative of brainstem or cerebellar dysfunction. Thus, this diagnosis
is less likely, and embarking upon a workup to include potentially invasive neuroimaging
techniques to rule out vertebral artery dissection is not indicated.
B1. History of previous concussions +3
154 It has been well established that prior concussions or repeated minor head injury increases
the risk for sustaining one or more future concussions or postconcussive sequelae with
each subsequent head injury.1,2,10,11,15,21,22 Recent data suggest that even minor head
injury, such as that attained with soccer ball heading (hitting the ball with one’s head),
may in fact have a cumulative effect and be associated with prolonged recovery from
concussion as well as decreased cognitive performance.22,23 Previous concussion grading
scales have attempted to quantify the risk based on number and severity of concussions
sustained within a given sport season and have established return-to-play guidelines
accordingly. As concussion grading scales have fallen out of favor, however, these return-
to-play guidelines are becoming less heavily relied upon as recent literature places greater
emphasis on a symptom-based rather than grade-severity or number-based approach. This
is in large part because the grade of concussion has ultimately been found to have little
predictive value regarding severity or length of postconcussive symptoms.10–17 Thus, the
persistence of postconcussive symptoms regardless of grade or severity of concussion is
the most important factor regarding return-to-play recommendations. That being stated, a
history of prior concussion places one at higher risk of having a prolonged recovery with
subsequent head trauma.
B2. Presence of postconcussive symptoms +5
The persistence of postconcussive symptoms has been recognized as the rate-limiting factor
regarding return-to-play recommendations. Nearly all experts agree that return to play
should not be recommended until postconcussive symptoms have completely resolved.
Further, the symptoms must not only be absent at rest, but also absent with exertion.2,8–11
B3. Grade or severity of concussion 0
As stated previously, the grade or severity of concussion has been found to have little
predictive value regarding development of postconcussive symptoms. A symptom-based
approach is more useful in guiding return-to-play recommendations as well as guiding therapy.
C1. Narcolepsy –1
Narcolepsy is a chronic sleep disorder characterized by a classic tetrad consisting of
excessive daytime sleepiness, sleep paralysis, hypnogogic or hypnopompic hallucinations,
and cataplexy. The first symptom is typically excessive daytime sleepiness with associated
sleep paroxysms (“sleep attacks”). Onset is typically in adolescence, and patients may not
exhibit all components of the tetrad. While narcolepsy has been reported to occur after
significant brain injury, typically it is thought of as a primary sleep disorder.24 This patient
reports daytime fatigue; however, he also reports insomnia without any other features of
narcolepsy. Fifty percent of patients with narcolepsy also have disturbed nocturnal sleep.
A detailed sleep questionnaire may be a useful clinical tool in patients with sleep
problems to best identify sleep disorders and determine whether they would benefit from
polysomnography. This patient currently only has symptoms of daytime fatigue and
insomnia, which he reports were not present prior to the concussion. Clinical suspicion
for narcolepsy would be low at this time.
C2. Migraine headaches –1

Migraine headaches are characterized by moderate to severe intensity, throbbing or pulsating,
unilateral or bilateral headache with associated photophobia or phonophobia and/or nausea
or vomiting during the headache. This patient reports headaches that are throbbing in
quality, but he also reports that the headaches are dull and without photophobia,
phonophobia, or nausea. Thus, this patient’s headaches are not likely migrainous.
155
C3. Medication-overuse headache syndrome +3
Medication-overuse headache, also called analgesic rebound headache, may develop in
persons who use analgesics more than 15 times per month or more than 3 to 4 times per
week. Typically, medication-overuse headache syndrome develops over months to years.
It manifests clinically with refractory daily or near-daily headaches that are usually
described as dull and throbbing or bandlike, thus sharing many features of what is often
called tension-type headache or chronic daily headache.25 Persons with medication-overuse
headaches are often diagnosed with chronic daily headache, and prophylactic headache
therapy is prescribed. Concomitant prophylactic medications are relatively ineffective
when patients continue to consume excess amounts of analgesics. Thus, evaluation of any
person with chronic headaches must include screening for analgesic medication overuse,
and all patients should be counseled to limit analgesic or immediate-relief medication use
to less than twice per week. This patient reports taking ibuprofen almost daily and is thus
at risk for development of medication-overuse headache syndrome if this pattern continues
for several months.
D1. Detailed past medical history, including previous history of head trauma +5
Detailed past medical history is important to obtain. As discussed previously, prior
head trauma raises the risk of future development of concussion with even minor
head injury and also may increase the length of the recovery period. Furthermore,
comorbid conditions, such as ADHD or mood disorder—which may implicate
preexisting disturbance in executive function—may also portend longer recovery
from concussion.26
D2. Detailed neurologic examination +5

Detailed neurologic examination is important to rule out occult focal findings that
may prompt further investigation, in particular neuroimaging. Most persons with
mTBI/concussion have a normal neurologic examination.
D3. Polysomnography –1
The onset of sleep disturbance in this patient is postconcussive and acute rather than
premorbid or chronic and is unlikely to be representative of a primary sleep disorder.
As discussed previously, a detailed sleep questionnaire would best screen for patients
who would yield diagnostic benefit from polysomnography. Clinical suspicion for a
primary sleep disorder is minimal in this patient. Polysomnography would be of low
yield, time-consuming, and costly.
D4. Urine toxicology screen +1

Illicit drug use should always be of concern to the clinician faced with an adolescent
with behavior changes. A urine toxicology screen is a noninvasive and inexpensive
test that may provide useful information, especially if it is positive. However,
postconcussive syndrome may include mood swings and irritability, and thus a urine
toxicology screen would not be diagnostic.
E1. Neuroimaging 0
Most patients who have a loss of consciousness in the context of head injury will have
a head CT scan as part of the emergency department evaluation. Most patients with
minor head injury will have normal standard neuroimaging.27–29 In the nonacute setting,
156 if a patient has a normal neurologic examination but has persistent nonfocal
postconcussive symptoms, it is unclear whether further neuroimaging will provide
additional diagnostic benefit. Some sources recommend obtaining a brain MRI if
symptoms persist for longer than 1 month.15,19 Other studies have found that PET or
diffusion-tensor imaging may be more sensitive in identifying deficits in brain
metabolism and cerebral white matter, respectively, in both the acute and nonacute
setting in persons with mild or moderate TBI.26 – 29 However, these findings and their
significance have not been validated in large-scale studies. Certainly, neuroimaging
may be a useful adjunctive, albeit costly, tool; however, at present the guidelines are
not clear regarding neuroimaging in mTBI in the nonacute setting.
E2. Ears, nose, and throat consultation for vestibular testing +1

Vestibular testing may be useful in persons who have symptoms of dizziness if it is
unclear whether inner ear dysfunction may be either primary or comorbid. Inner ear
dysfunction may develop as a result of head injury and may be occult, as in the case
of perilymphatic fistula. Vestibular testing may identify whether inner ear dysfunction is
present and thus may guide therapy.
E3. Neuropsychological testing +3
Neuropsychological testing is somewhat controversial in mTBI with regard to
prognostic implications; however, it is indeed clear that mTBI is not uncommonly
associated with neuropsychologic deficits--specifically in tasks of memory, concentration,
and executive function.4,14–19,21–23,26 Most of the literature is in agreement with performing
neuropsychologic testing in persons with postconcussive symptoms of impaired
memory and concentration present for greater than 1 month after injury.
Neuropsychological testing may provide valuable information that can direct resources
and interventions in the academic setting.
F1. Individualized education plan to be developed by the school +1

An individualized education plan, developed in collaboration with teachers, parents, and
other members of the educational team, outlines areas of specific educational or behavioral
difficulties quantified by objective means, including neuropsychological or educational
testing and/or formal developmental assessment. Deficits that are identified as impediments
to learning or as interfering with optimal school performance are targeted so that modifications
may be made in the educational environment to improve performance and learning. For
example, decreased processing speed identified on neuropsychological testing may lead
to allocation of increased time during test taking in order to optimize test performance.30
F2. Behavioral counseling +1

Behavioral counseling may be helpful in mood disorders such as anxiety and depression.
In some cases, counseling alone may improve outcome; at a minimum, counseling or
psychotherapy can be a useful adjunct to pharmacologic therapy. Studies have shown that
the combination of behavioral therapy with pharmacologic therapy is better than either
therapy alone in many psychiatric conditions, including ADHD, depression, and anxiety.31,32
G1. Antidepressant +3
Persons with depression are more likely to have somatic symptoms such as frequent
headache and vice versa. Certain antidepressants may have the dual effect of improving
mood and decreasing headaches. Specifically, tricyclic antidepressants have proven
efficacy in chronic daily headache and may improve multiple symptoms, including 157
insomnia and irritability. Often, persons with postconcussive syndrome have multiple
symptoms, including mood disorder, sleep disturbance, and chronic headache; treating
with an antidepressant to target multiple symptoms is common practice.15,16,25
G2. Prophylactic headache medication +5

Headaches that occur more than 2 to 3 times per week, or that occur less frequently but
are associated with significant interference with activities of daily living, warrant
consideration for prophylactic therapy. Numerous medications have been studied for
headache prophylaxis, including antidepressants (eg, tricyclic antidepressants, nefazodone),
antiepileptic drugs (AEDs) (eg, topiramate, valproate, gabapentin, lamotrigine),
antihypertensives (eg, calcium channel blockers, beta-blockers, angiotensin-converting
enzyme inhibitors), and complementary medicine (eg, riboflavin, magnesium, butterbur,
feverfew).25,33 Of these, tricyclic antidepressants and AEDs are the most widely prescribed
for headache prophylaxis. Specifically, topiramate, valproate, and propanolol have a US
Food and Drug Administration (FDA) indication to include headache prophylaxis.
G3. Stimulant medication 0
Data support limited use of stimulant medications in persons with attentional difficulty
after TBI.34,35 No specific data address use of stimulant medication to treat symptoms
of decreased attention or focus in postconcussive syndrome. As stated previously,
persons with preexisting ADHD may experience more pronounced postconcussive
symptoms and have a longer recovery period. It may not be unreasonable to prescribe
stimulant therapy in persons with clear deficits in attention and focus as identified by
neuropsychologic testing or by history, especially if a preexisting diagnosis of ADHD is
present. However, most persons with postconcussion syndrome recover within a few
months without need for stimulant medication.
G4. Sleep-inducing medication +1

Insomnia, a common component of postconcussive syndrome, is often associated with
headaches, irritability, fatigue, and poor mood.14–16 It is prudent to address sleep
disturbances in persons with postconcussive syndrome. One should avoid prescribing
multiple medications for multiple symptoms, however, as they would increase the risk
for side effects and toxicity. It is often possible to treat multiple symptoms with one
medication, commonly antidepressants, in postconcussive syndrome. For example, a
side effect of tricyclic antidepressants is somnolence, which may be useful in a person
with frequent headaches and insomnia.
G5. Antiepileptic medication for the purpose of seizure prophylaxis –3

Many AEDs have indications outside of epilepsy. For example, topiramate and valproic
acid are FDA approved for migraine prophylaxis, and valproic acid has been widely
used by psychiatrists for mood stabilization. In selected cases, it may be appropriate to
use an AED to treat postconcussive symptoms; again, avoidance of polypharmacy and
unfavorable side effects must be maintained. Prescribing an AED under the auspices of
seizure prophylaxis for concussion or postconcussive syndrome would be inappropriate
as there is no indication to initiate antiepileptic therapy under these circumstances.
Conclusion
158 The patient was prescribed amitriptyline (Elavil), a tricyclic antidepressant, to be taken
nightly. It was felt that this would treat multiple symptoms without introducing
polypharmacy. Specifically, amitriptyline may be an effective medication for headache
prophylaxis as well as have the added benefit of antidepressant properties. Furthermore,
the tricyclic antidepressants often cause somnolence, which may be of benefit to this
patient who has insomnia. The patient was counseled against excessive over-the-counter
analgesic use and was instructed to limit his use to fewer than 3 times per week.
Because the patient was already taking methylphenidate, a stimulant medication, an
additional stimulant was not prescribed. However, his dose was increased from 36 mg
to 54 mg daily in attempt to improve efficacy, given the worsening of his symptoms
in the context of postconcussive syndrome. He was instructed to not return to team
play until his symptoms of headache and disequilibrium were resolved, particularly
with exertion. He was encouraged to engage in light to moderate intensity exercise
as tolerated.
On follow-up 3 months later, the patient was markedly improved. His headache
frequency was less than once per week, and the intensity was mild with no exertional
exacerbation. He reported sleeping well and no longer experienced disequilibrium. His
ability to focus was improved, and his school performance was back to baseline. While
he still was allotted additional time for tests, he felt that it often was unnecessary. His
parents reported that his behavior was improved and he did not display the mood
lability he had previously. The amitriptyline and increased dose of methylphenidate
were continued for an additional 3 months while he completed the academic year and
then were discontinued (methylphenidate was decreased to the original dose of 36 mg).
Repeat neuropsychologic testing was considered but ultimately not pursued.
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2. Aubry M, Cantu R, Dvorak J, et al; Concussion in Sport Group. Summary and agreement statement
of the First International Conference on Concussion in Sport, Vienna 2001; recommendations for
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3. Kushner D. Mild traumatic brain injury: toward understanding manifestations and treatment. Arch
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mild traumatic brain injury in children. Pediatrics 2010;125(6)e1331– e1339. http://pediatrics.
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facts for physicians about mild traumatic brain injury (MTBI). Available at www.cdc.gov/concussion/
headsup/pdf/Facts_for_Physicians_booklet-a.pdf. Accessed October 20, 2010.
7. Gordon KE, Dooley JM, Fitzpatrick EA. Concussion or mild traumatic brain injury: parents appreciate
the nuances of nosology. Pediatr Neurol 2010;43(4):253–257.
8. Cantu RC. Guidelines for return to contact sports after a cerebral concussion. Phys Sportsmed
1986;14(10):75–76,79,83.
9. Denver Medical Society. Guidelines for the management of concussion in sports. Rev. May 1991.
159
Denver: Colorado Medical Society, 1991.
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International Conference on Concussion in Sport, Prague 2004. Br J Sports Med 2005;39(4):196–204.
11. McCrory P, Meeuwisse W, Johnston K, et al. Consensus statement on concussion in sport: the 3rd
International Conference on Concussion in Sport held in Zurich, November 2008. Br J Sports Med
2009;43(suppl 1):i76 –i90.
12. American Psychiatric Association. Diagnostic and statistical manual of mental disorders, Fourth
edition. Washington, DC: American Psychiatric Association, 1994.
13. Bazarian JJ, Atabaki S. Predicting postconcussion syndrome after minor traumatic brain injury.
Acad Emerg Med 2001;8(8):788 –795.
14. Mittenberg W, Strauman S. Diagnosis of mild head injury and the postconcussion syndrome. J Head
Trauma Rehabil 2000;15(2):783 –791.
15. Ryan LM, Warden DL. Post concussion syndrome. Int Rev Psychiatry 2003;15(4):310 –316.
16. Mittenberg W, Canyock EM, Condit D, Patton C. Treatment of post-concussion syndrome following
mild head injury. J Clin Exp Neuropsychol 2001;23(6):829– 836.
17. Bleiberg J, Cernich AN, Cameron K, et al. Duration of cognitive impairment after sports concussion.
Neurosurgery 2004;54(5):1073–1078.
18. Kirkwood MW, Yeates KO, Wilson PE. Pediatric sport-related concussion: a review of the clinical
management of an oft-neglected population Pediatrics 2006;117(4):1359–1371.
19. Meehan WP 3rd, Bachur RG. Sport-related concussion. Pediatrics 2009;123(1):114 –123.
20. Stahmer SA, Raps EC, Mines DI. Carotid and vertebral artery dissections. Emerg Med Clin North Am
1997;15(3):677– 698.
21. Collins MW, Grindel SH, Lovell MR, et al. Relationship between concussion and neuropsychological
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2549–2555.
23. Witol AD, Webbe FM. Soccer heading frequency predicts neuropsychological deficits. Arch Clin
Neuropsychol 2003;18(4);397– 417.
24. Frenette E, Kushida CA. Primary hypersomnias of central origin. Semin Neurol 2009;29(4):354 –367.
25. Mathew NT. Transformed migraine, analgesic rebound, and other chronic daily headaches. Neurol
Clin1997;15(1):167–186.
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traumatic brain injury: a diffusion tensor imaging (DTI) study. Arch Clin Neuropsychol. 2007;22(5):
555–568.
27. Davis GA, Iverson GL, Guskiewicz KM, et al. Contributions of neuroimaging, balance testing,
electrophysiology and blood markers to the assessment of sport-related concussion. Br J Sports
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28. Difiori JP, Giza CC. New techniques in concussion imaging. Curr Sports Med Rep 2010;9(1):35–39.
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brain injury. J Clin Exp Neuropsychol 2001;23(6):775 –791.
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31. Asarnow JR, Emslie G, Clarke G, et al. Treatment of selective serotonin reuptake inhibitor-resistant
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2005;115(6):e749 – e757.
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traumatic brain injury in children. J Dev Behav Pediatr 2007;28(2):108 –118.
ETHICAL PERSPECTIVES IN
NEUROLOGY: SPORTS-ACQUIRED
Michael B. Russo, Kevin E. Crutchfield
The practice of neurology presents a series of ethical challenges for the clinician. These
rarely have simple or straightforward solutions, but require careful consideration by the
neurologist. This section of , written by colleagues with particular interest in
the area of bioethics, provides a case vignette that raises one or more ethical questions
related to the subject area of this issue. The discussion that follows should help the reader
understand and resolve the ethical dilemma.
Hypothetical Case
A 16-year-old boy came to the office with his parents because he may have had a concussion
during a high school football game the past weekend and needed to be cleared to play in
an important game 4 days later. He said that during the past weekend’s game he got “dinged.”
He had told his coach, who removed him from the game and sent him to the emergency
department (ED). The ED physician said that the head CT was normal, but he would not
clear the boy to play and referred him for a neurology consultation for clearance. The boy
said that he had had this kind of contact before, but this was the first time he had
experienced persistent symptoms. He had a “dizzy and spacey” feeling that resolved in a
couple of days but still had headaches, although they were better. His parents had
observed him feeling dizzy and spacey and said it appeared that his headaches worsened
if he exerted himself.
The patient’s neurologic examination was normal, with the exception of subtle ataxia,
ie, abnormal tandem gait and stance. The head CT performed the night of the concussion
was normal. With subtle but definite abnormalities on examination and persistent symptoms
of concussion, the boy and his parents were informed that he could not return to play for
at least another week. They pled for him to be cleared to play. Several college scouts 161
would be at next weekend’s game to see him play. The patient said that he had to play so
the scouts could select him for a scholarship, and his family could not afford a college
education for him otherwise. They said that their neighbor, who was a physician, told
them their son was fine and should be allowed to play. Finally, they demanded that the
neurologist not send a report to the football coach, stating that they knew that federal
privacy regulations prevented the neurologist from releasing the information to anyone
without their permission, which they refused to give.
COMMENT
Sports-related concussion has received significant public attention during the past two
years. The National Football League (NFL) has created new guidelines and in July 2010
Relationship Disclosure: Dr Russo has nothing to disclose. Dr Crutchfield has received or anticipates receiving personal compensation for acting as
an expert witness in a medical liability case.
Unlabeled Use of Products / Investigational Use Disclosure: Drs Russo and Crutchfield have nothing to disclose.
Copyright © 2010 American Academy of Neurology. All rights reserved. Continuum Lifelong Learning Neurol 2010;16(6):161–165.
ETHICAL PERSPECTIVES IN NEUROLOGY
distributed a poster for NFL locker rooms that “warns of the dangers of concussions in
much harsher language than before.”1 This topic has also been the subject of hearings
in the US Congress in 2009 and 2010.2–4 In 2007, the Centers for Disease Control and
Prevention (CDC) reported that each year between 2001 and 2005 an estimated 207,830
patients with nonfatal sports-related traumatic brain injuries were treated in US hospital
EDs, of which 10% were admitted to the hospital, meaning that 90% of patients with
sports-related head injuries were sent home.5 The highest incidence occurred among
those between the ages of 10 and 19; 70% were boys and 30% were girls. When this
report was published, the CDC also launched a national campaign called “Heads Up on
Brain Injury.”6 As of May 2010, at least three states (Oregon, Texas, and Washington)
had passed legislation that addressed concussion education and athletes’ return to play,
and more states are expected to follow suit.7 Neurologists can expect to evaluate
greater numbers of young athletes for concussion and to be asked to give their clearance
for athletes’ return to play.
This case presents several ethical dilemmas:
(1) Does the patient’s need for a college scholarship provide sufficient ethical
justification to allow him to return to play at this point?
(2) Conversely, does the need to prevent a second concussion in the short-term or
the cumulative effects of concussions in the long-term provide sufficient ethical
justification to prevent him from playing?
(3) Can the neurologist share the report with the coach despite the parents’ instructions
not to do so?
DISCUSSION
Treatment of teenagers with sports-related concussion is rarely simple or straightforward,
especially when their wish is to continue playing despite medical concerns. In the current
case, the problem is magnified because the boy’s desire to play is supported by his parents,
and the decision to keep him from playing is arguably harmful to him and his family, as
he may lose the opportunity for a college scholarship. Thus, lifelong consequences may
result if he is prevented from playing. On the other hand, with definite signs and symptoms
of a concussion, this athlete is at increased risk of sustaining a second concussion because
his reaction time is likely to be impaired. He could suffer permanent and more severe
162 brain injury or death if he were to sustain another concussion,8 as adolescents are at a
greater risk of the second-impact syndrome.
Assessment of the risks and benefits of alternative treatment decisions is inherent to
almost every decision that neurologists make in treating patients. Normally, the risks
and benefits are directly related to the patient’s health and potential outcomes. In this
case, the medical risks of returning to play are well known and substantial. A prospective
nonrandomized study of 16,624 player seasons from 1999 to 2004 found that the risk of
a second concussion was 3.8%, with 80.0% occurring within 10 days of the initial
concussion.9 Inexplicably, patients who returned to play before resolution of symptoms
had a lower rate of second concussion (0.9%); however, the authors recommend
waiting 10 days because of a window of increased vulnerability during the first 7 to 10
days after concussion. Thus, according to available guidelines and evidence, the
neurologist’s recommendation that the boy not return to play is justified on the basis of
preventing injury.
The ethical analysis is more complex, however, because the boy and his parents
assert that he will be harmed if he is kept from playing. The harm in this case is not to
his health; rather, it is a lost opportunity to win a college scholarship. Preventing him
from playing could keep him from attending college, which would have a lifelong
detrimental effect on his career and earning potential.
Is it ethically permissible for the neurologist to weigh the medical risks of returning
to play against the lost opportunity of college scholarship and future employment? The
AAN Code of Professional Conduct (1.1) indicates that the “profession of neurology exists
primarily to study, diagnose and treat disorders of the nervous system” [italics added].10 As
a general rule, neurologists may consider the financial costs of tests or treatments when
caring for patients, as long as doing so does not compromise the effectiveness of the
treatment plan—for example, using a lower-cost generic medication rather than a
name-brand medication. Neurologists may consider the financial and employment
consequences of their medical assessments and determinations when evaluating patients;
however, it would not be appropriate to give more weight to these matters than to the
medical risks, benefits, and consequences for the patient. In fact, in this case, the
consequences represent a potential conflict of interest in decision making for the patient
and his parents, and the neurologist has a duty to minimize these interests in favor of the
patient’s health and medical interests. While the AAN has no specific guidance, the
International Federation of Sports Medicine Code of Ethics states, “The physician’s duty
to the athlete must be his/her first concern and contractual and other responsibilities are of
secondary importance.”11 Only if the medical risks of a decision were minimal would it be
appropriate to allow the scholarship consideration to outweigh the medical consideration.
Thus, the best decision in this case is to keep the patient out of competition.
Despite the parents’ demands that the neurologist not send a report to the coach,
sound ethical and regulatory justification exists for the neurologist to share the report
with the patient’s coach or other health care professionals involved in his care. (1) The
National Federation of State High School Associations 2010 sports concussion guidelines
state, “Any athlete who is removed from play because of a concussion should have
medical clearance from an appropriate health care professional before being allowed to
return to play or practice.”12 The patient’s coach therefore is in need of the neurologist’s
report. (2) The legal justification for disclosing to the coach despite the parents’ objection
is less clear. State law may require a medical examination of an athlete with a suspected
concussion before the coach may allow the athlete to return to play. (3) The Health
Insurance Portability and Accountability Act (HIPAA) regulations allow, in very limited
situations, information to be carefully disclosed if “necessary to prevent or lessen a
163
serious and imminent threat to the health or safety of a person.” Because the patient’s
parents object, any disclosure of protected health information about a minor may
involve an interpretation of state law, and the HIPAA rule requires an analysis of the
factual context (ie, is the disclosure in good faith and [1] necessary to [2] prevent or
lessen a [3] serious and imminent threat to the [4] health and safety of a person). To
prevent a problem such as the one in the case, at the beginning of the evaluation the
neurologist could address with the patient and his parents the HIPAA-related issues and
the requirement to disclose the examination results to the coach regardless of the findings.
In this circumstance, however, the neurologist should seek an opinion from an attorney
familiar with HIPAA to confirm that disclosure to the coach is permissible.
CONCLUSION
The ethical choices involved in determining whether an athlete with a concussion can
return to play should be based on the patient’s current and future health, with an emphasis
ETHICAL PERSPECTIVES IN NEUROLOGY
on injury prevention. Other considerations, such as missed opportunities for college

scholarships or important games, such as championship playoffs, while important to the
athlete or others, should be secondary and should not override the treating neurologist’s
best medical judgment.
ACKNOWLEDGMENT
We thank Murray Sagsveen, JD, CAE, for his assistance with legal research for this article.
REFERENCES
1. Associated Press. League’s new poster uses stronger language about concussions. July 27, 2010.
Available at: www.nfl.com/news/story/09000d5d81952853/printable/leagues-new-poster-uses-
stronger-language-about-concussions. Accessed August 16, 2010.
2. Committee on the Judiciary, House of Representatives. Hearing on: legal issues relating to football
head injuries. Available at: www.judiciary.house.gov/hearings/hear_091028.html. Accessed August
16, 2010.
3. Committee on the Judiciary, House of Representatives. Field hearing on: legal issues relating to
football head injuries, part II. Available at: www.judiciary.house.gov/hearings/hear_100104.html.
4. Committee on the Judiciary, House of Representatives. Forum on: key issues related to the
identification and prevention of head injuries in football. Available at: www.judiciary.house.gov/
hearings/hear_100524.html. Accessed August 16, 2010.
5. Nonfatal traumatic brain injuries from sports and recreational activities—United States, 2001–2005.
Morbidity and Mortality Weekly Report. Available at: www.cdc.gov/mmwr/preview/mmwrhtml/
mm5629a2.htm. Accessed August 16, 2010.
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concussion/. Updated June 30, 2010. Accessed August 16, 2010.
164 7. Kohn LT. Concussion in high school sports: overall estimate of occurrence is not available, but key
state laws and nationwide guidelines address injury management. GAO-10-569T. US Government
Accountability Office. Available at: www.gao.gov/new.items/d10569t.pdf. May 2010. Accessed
August 16, 2010.
8. Mueller FO, Colgate R. Annual survey of football injury research. Waco, TX: American Football
Coaches Association, and Indianapolis, IN: National Collegiate Athletic Association and National
Federation of State High School Associations, 2009.
9. McCrea M, Guskiewicz K, Randolph C, et al. Effects of a symptom-free waiting period on clinical

outcome and risk of reinjury after sport-related concussion. Neurosurgery 2009;65(5):876 – 883.
10. American Academy of Neurology. Code of professional conduct. 2008. Available at: www.aan.com/
globals/axon/assets/3968.pdf. Accessed August 16, 2010.
11. International Federation of Sports Medicine. Code of ethics. Sept. 23, 1997. Available at:
www.fims.org/pages/311417173/FIMS/General/codeofethics.asp. Accessed August 16, 2010.
12. National Federation of State High School Associations. Suggested guidelines for management of
concussion in sports. Available at: www.nfhs.org/content.aspx?id=3325. 2009. Accessed
August 16, 2010.
ADDITIONAL RESOURCES
Concussion in sports. National Collegiate Athletic Association. Available at: www.ncaa.org/wps/portal/

ncaahome?WCM_GLOBAL_CONTEXT=%2Fncaa%2Fncaa%2Facademics+and+athletes%2Fpersonal+
welfare%2Fhealth+and+safety%2Fconcussion. 2010. Accessed August 16, 2010.
NCAA concussion management plan: National Collegiate Athletic Association. Available at: www.ncaa.
org/wps/wcm/connect/327bf600424d263692cdd6132e10b8df/Memo+Concussion+Managmen+04292010.
pdf?MOD=AJPERES&CACHEID=327bf600424d263692cdd6132e10b8df 2010. Accessed August 16, 2010.
O’Reilly KB. Put me in, Doc: When doctors must say no to athletes. American Medical News.
October 18, 2010. www.amednews.com. Accessed October 21, 2010.
165
PRACTICE ISSUES IN NEUROLOGY:
TRAUMATIC BRAIN INJURY:
ENHANCING OUR ABILITY TO
IMPROVE COMMUNICATION
WITH FAMILIES
Jay H. Rosenberg
In addition to the lifelong learning of new clinical and scientific knowledge, neurologists
must understand the constantly evolving environment in which they practice. Changes
occur rapidly in reimbursement and regulatory areas, in the integration of evidence-based
medicine, and in the implementation of patient safety measures into clinical practice.
This section of presents a case-based example of these issues as they
relate to the clinical topic. These vignettes are written by neurologists with particular
experience in systems-based practice and practice-based learning and improvement.
INTRODUCTION
A catastrophic traumatic brain injury is a sudden, life-changing event for both the patient
and family. Families are frequently thrust into the quagmire of the medical system, which
they neither understand nor are prepared to deal with. The vocabulary is foreign, and
frequently information is contradictory and often provided in an uncoordinated approach.
The families are anxious and may be faced with very difficult life and death decisions.
Families want to know if their loved one will survive and the anticipated quality of life.
To optimize communication, health care professionals must decide what information the
families are ready to hear and when.
The journey from the time of onset of the acute injury through recovery can be
compared to crossing from one valley to another over a winding and mountainous road.
166 This road is potentially very challenging and involves traversing many dangerous mountain
passes that may temporarily or permanently block forward progress. The four different
valleys traversed are an analogy for the four levels of care that constitute a traumatic brain
injury journey from onset to recovery: acute trauma care (Valley of the Shadow of Death),
long-term chronic care (Valley of Limbo), acute rehabilitative care (both inpatient and
outpatient) (Valley of Enlightenment), and postrehabilitative care to recovery (Valley of
Adjustment and Reconciliation). By means of a patient vignette, each level of care will be
described and the pivotal information identified. This identified data potentially can predict
the timing and progression to the next level of care. The ideal time and manner of
communication of this information to the family will be discussed.
Relationship Disclosure: Dr Rosenberg has received personal compensation from Biogen Idec; EMD Serono, Inc.; and Teva Neuroscience as a
member of their speakers’ bureaus, and from Acorda Therapeutics and Allergan, Inc., as an advisory board member. Dr Rosenberg has
received or anticipates receiving personal compensation for a professional report for plaintiff reference and serving as a defendant’s expert
witness for a multiple sclerosis case for a school district.
Unlabeled Use of Products/Investigational Use Disclosure: Dr Rosenberg has nothing to disclose.
Copyright © 2010, American Academy of Neurology. All rights reserved. Continuum Lifelong Learning Neurol 2010;16(6):166–170
ACUTE TRAUMA CARE — THE VALLEY OF THE SHADOW OF DEATH
Case
A 47-year-old physician had a cycling accident witnessed and reported by bystanders. His
helmet was cracked, with blood lining the inside surface; other injuries included a right
scapular fracture, multiple bilateral rib fractures, left orbital fracture, and a fracture of the
right zygoma. He had a Glasgow Coma Scale score of 5 (decorticate right upper extremity,
decerebrate left upper extremity) at the scene and was air evacuated to the local trauma
center. By day 6 he had some movement in most of his extremities; on day 9 his chest tube
was removed; and on day 17 his intracranial pressure was stabilized.
His wife was at his bedside almost immediately. Her initial concern was whether or not
he would survive. Most of the staff remained positive and projected relative optimism.
Later, as she turned her attention from survival to quality of life, she finally asked, “Will he
ever practice medicine again?” One of the residents answered negatively. The patient’s wife
felt that the response could have been framed in a more positive manner such as, “He is
doing well now. It is way too early to be able to predict his full level of recovery.”
Families are most connected to the patient and frequently make the first observation of
their loved one’s responsiveness. While in the “valley of the shadow of death,” two
important patient responses should be discussed with the family to help them feel they are
part of the recovery process and enlist their help: (1) arousal or eye opening and
(2) responsiveness to stimulation. The definition of coma is that period after injury when
the eyes remain closed and the patient is unconscious and not responsive to any stimuli.
Coma begins 30 minutes after loss of consciousness has occurred.1
Inform the family that between 2 and 6 weeks after coma onset, arousal occurs when
the patient opens his eyes and normal wake-sleep cycles return. The absence of specific
responses to stimulation and voluntary bodily functions defines the vegetative state (full
arousal, no responsiveness).2 Inconsistent, but definite responses to tactile, verbal,
visual, or auditory stimulation define the minimally conscious state (full arousal, partial
inconsistent responsiveness).3 A consistent response to stimulation indicates a state
of full responsiveness and arousal. This state, the lowest level of recovery, defines a time
of full consciousness yet profound dependency for all activities of daily living. There is no 167
consensus on a descriptive term.
During week 4, the patient’s eyes opened spontaneously, and he developed wake-sleep
cycles but showed no responsiveness or recognition of the staff or his wife. He was
transferred by air ambulance to a long-term care facility.
LONG-TERM CHRONIC CARE—THE VALLEY OF LIMBO
Through week 5, the patient was weaned off the ventilator and showed signs of
responsiveness. At his wife’s insistence, amantadine was instituted as this may be helpful
in improving long-term alterations of consciousness in traumatic brain injury.4 At the
beginning of week 6, he suddenly talked for the first time, clearly stating, “I woke up!”
When he saw his wife, he yelled, “No! Go away!”
PRACTICE ISSUES IN NEUROLOGY
As in this case, a patient may suddenly develop full consciousness or enter a state of
minimal consciousness, either emerging slowly to full consciousness or remaining in the
minimal conscious state.
Educating the family on the various techniques used to stimulate the patient and the
responses that are potentially significant can create helpful and accurate observers. The JFK
Coma Recovery Scale established and validated by Joseph Giacino, PhD, is very useful for
this purpose (Appendix B).5 The scale tests six modalities, including auditory, visual,
motor, oromotor/verbal function, communication, and arousal. Subscale items are hierarchically
arranged with specific items tied to existing diagnostic criteria for coma, vegetative state,
and minimally conscious state. Addressing the patient by his name is a helpful strategy
when attempting arousal through verbal stimulation. Employing a mirror to see whether
the patient follows his own image can help demonstrate visual responsiveness. Presenting
everyday objects in the visual field can validate that the patient attends, grabs, or
appropriately uses the object when directed. An inconsistent response to several trials
establishes minimal consciousness, and consistent responses in all modalities reflect
full consciousness.
During week 6, the patient started speech therapy, requiring him to label objects and
colors, but he was rebellious and threw the objects. He slept a great deal during the day
and at other times wanted to walk constantly. A “sitter” was required to assure that the
patient remained safe, but once it was deemed he could participate in therapy 3 hours a
day, he was appropriately transferred to acute rehabilitation.
ACUTE REHABILITATION— THE VALLEY OF ENLIGHTENMENT

Patients and families often come to acute rehabilitation with an expectation that patients
will walk independently out the door at the end of their stay and require no further care
or supervision and that they will remain in acute rehabilitation until this is achieved, no
matter how long this takes. On admission to acute rehabilitation, a complete evaluation by
all therapies (including but not limited to physical, occupational, and speech therapies) is
used to develop a treatment plan with appropriate goals. It is the responsibility of the team
168 to communicate this treatment plan to the patient and the family and emphasize
the achievable goals that will potentially be met by the end of the stay. If it is possible to
estimate early what resources might be needed to facilitate future discharge, this information
should be communicated in an ongoing way to the family.
During the first days of his stay, the patient was depressed, agitated, obstructive, and obstinate,
showing disgust with the entire rehabilitative process. Psychiatric consultation was obtained,
and he began to respond to psychotropic and antidepressant medications. A severe
Wernicke aphasia was diagnosed, and standard aphasia treatment sessions were modified
to be more engaging. Instead of flash cards showing pictures of unrelated objects, objects
with hospital and medical terminology, such as IV poles, a gurney, or scrubs, were used,
improving his tolerance and cooperativeness. The patient worked extensively on his
balance. The occupational therapist worked to improve his ability for self-care. With the
patient, a list of goals for self-care and mobility were created and posted in his room.
When completed, he could be discharged and transitioned to the outpatient brain
injury program.
Standard terminology for assessment and communication among the professional brain
injury providers was helped by the use of the Rancho Los Amigos Cognitive Levels of
Functions Scale (Appendix C),6 which evaluates patients from level I, which might be
considered equivalent to coma, to level VII, where the patient requires only minimal
assistance with appropriate oriented behavior. Levels II and III are equivalent to various
stages of the vegetative state, and level IV to emergence from the vegetative state on to
minimal consciousness and finally to full consciousness. Active rehabilitation involves
levels IV through VII. After level VII, the usefulness of the scale decreases by ambiguity of
the description. Since levels IV and V both require maximal assistance, the distinction between
the two is the presence or absence of agitation resulting in the inability to cooperate with
treatment efforts. Confusion is present in both levels V and VI; they are distinguished from
each other by inappropriate versus appropriate behavior and maximal assistance versus
moderate assistance. Rancho Los Amigos cognitive level VII requires only minimal assistance
with appropriate oriented behavior.
A clearer and more understandable means of communicating potential level of patient
functions to the family relies on the Functional Independence Measure (FIM) scale7 adapted
to activities of daily living (ADLs) and motor and cognitive functions. The FIM scales describe
six levels of function, from total assist, where the patient can offer no help with the activity,
to modified independent, with 100% effort of the patient. The FIM provides a clearer way
of communicating to the family the various stages of patient function.
When the patient is judged by the team to be safe at anywhere from a minimal assist
to modified independent level, a transition is made from the inpatient setting to the
outpatient setting. At this point, the direction of therapy may incorporate higher levels of
function as it pertains to achieving mastery over those tasks deemed necessary to reintegrate
and function highly in society.
POSTREHABILITATIVE CARE—THE VALLEY OF ADJUSTMENT AND RECONCILIATION

Active recovery is a continuum and ongoing for the first year after acute traumatic brain
injury. The rate of recovery is generally very rapid for the first 6 months and less rapid
over the remaining 6 months. After the first year, recovery levels out and then waxes and
wanes. In very rare cases, some improvements are still seen. 169
Eight months after the injury, the patient continued to improve. Major concerns included
decreased auditory processing speed and some hesitation with word finding. He was able
to perform all basic and intermediate levels of ADLs and was placed at the modified
independent level. He participated in some advanced ADLs in that he sat in on some
patient conferences without any direct patient input and was driving. After discharge from
inpatient rehabilitation, he began outpatient therapy in a brain injury day treatment
program 5 days per week.
This patient is on the road to excellent functional recovery with achievement of many
advanced ADLs, but at the moment no good functional outcome scale is available to help
communicate this to him and his family. Jennett and Bond developed the Glasgow
Outcome Scale8 in order to classify recovery outcomes. The scale consists of five
outcomes: (1) death, (2) persistent vegetative state, (3) severe disability, (4) moderate
disability, and (5) good recovery. This patient would be classified at the “good recovery”
PRACTICE ISSUES IN NEUROLOGY
level. This term is not able to capture meaningful differences in higher levels of function.
A more meaningful scale that describes outcomes and links them to functional descriptions
that correlate with basic, intermediate, and advanced ADLs is needed.
Patients with head injuries and their families must maintain hope and a positive
attitude couched in the reality of the situation. Communicating the key information at the
appropriate time will help facilitate travel through the valleys of recovery.
ACKNOWLEDGMENT
I thank Dawn Holman, PhD, for review and suggestions for improvement of this article.
REFERENCES
1. Posner JB, Saper CB, Schiff N, Plum F. Plum and Posner’s diagnosis of stupor and coma fourth
edition. New York: Oxford University Press, 2007.
2. Quality Standards Subcommittee of the American Academy of Neurology. Practice parameters:

Assessment and management of patients in the persistent vegetative state (Summary Statement).
Neurology 1995;45(5):1015 –1018.
3. Giacino JT, Ashwal S, Childs N, et al. The minimally conscious state: definition and diagnostic
criteria. Neurology 2002;58(3):349 –353.
4. Meythaler JM, Brunner RC, Johnson A, Novack TA. Amantadine to improve neurorecovery
in traumatic brain injury-associated diffuse axonal injury: a pilot double-blind randomized trial.
J Head Trauma Rehabil 2002;17(4):300 –313.
5. Giacino JT, Kalmar K, Whyte J. The JFK Coma Recovery Scale-Revised: measurement characteristics
and diagnostic utility. Arch Phys Med Rehabil 2004;85(12):2020 –2029.
6. Hagan C. Levels of cognitive functioning: rehabilitation of the head injured adult: comprehensive
physical management, 3rd ed, Downey California: Professional Staff Association of the Rancho
170 Los Amigos Hospital, Inc.
7. Braddom Randall L. Physical medicine and rehabilitation, e-edition: text with continually updated
online reference. 3rd ed. Philadelphia: Saunders, 2006.
8. Jennett B, Snoek J, Bond MR, Brooks N. Disability after severe head injury: observations on the use
of the Glasgow Outcome Scale. J Neurol Neurosurg Psychiatry 1981;44(4):285 –293.
CODING TABLE
Laura B. Powers, MD, FAAN, Marc R. Nuwer, MD, PhD, FAAN
Accurate coding is an important function of neurologic practice. This section

of , contributed by members of the AAN Medical Economics and
Management Committee, includes a table of helpful coding information related
to the issue topic. The table may include diagnosis coding, Evaluation and
Management (E/M) coding, procedure coding, or a combination, depending on
which is most useful for the subject area of the issue.
International Classification of Diseases, Ninth Revision, Clinical

Modification (ICD-9-CM) Codes Used in Traumatic Brain Injury
Acute Injury Codes
Note that codes in categories 800, 801, 803, 804, 851, 852, 853, and 854 require a
fifth digit as follows:
0 unspecified state of consciousness
1 with no loss of consciousness
2 with brief [less than 1 hour] loss of consciousness
3 with moderate [1–24 hours] loss of consciousness
4 with prolonged [more than 24 hours] loss of consciousness and return to
preexisting conscious level
5 with prolonged [more than 24 hours] loss of consciousness without return
to preexisting conscious level
Use fifth-digit 5 to designate when a patient is unconscious and dies before
regaining consciousness, regardless of the duration of loss of consciousness
6 with loss of consciousness of unspecified duration
7 with concussion, unspecified
Traumatic Brain Injury With Skull Fracture
800.00–800.09 Fracture of vault of skull, closed, without mention of

intracranial injury
171
800.10–800.19 Fracture of vault of skull, closed, with cerebral laceration
and contusion
800.20–800.29 Fracture of vault of skull, closed, with subarachnoid,
subdural, and extradural hemorrhage
800.30–800.39 Fracture of vault of skull, closed, with other and unspecified
intracranial hemorrhage
Dr Powers recently retired from private practice. Dr Nuwer is professor of neurology at UCLA School of
Medicine and department head, Clinical Neurophysiology, UCLA Medical Center, Los Angeles, CA.
Relationship Disclosure: Dr Powers has nothing to disclose. Dr Nuwer has received personal compensation from
SleepMed for serving as local medical director and from CortiCare for serving as medical advisor.
Unlabeled Use of Products/Investigational Use Disclosure: Drs Powers and Nuwer have nothing to disclose.
Continuum Lifelong Learning Neurol 2010;16(6):171–178 Copyright # 2010, American Academy of Neurology. All rights reserved.
" CODING TABLE
Continued
800.40–800.49 Fracture of vault of skull, closed, with intracranial injury of

other and unspecified nature
800.50–800.59 Fracture of vault of skull, open, without mention of
intracranial injury
800.60–800.69 Fracture of vault of skull, open, with cerebral laceration
and contusion
800.70–800.79 Fracture of vault of skull, open, with subarachnoid,
800.80–800.89 Fracture of vault of skull, open, with other and
unspecified intracranial hemorrhage
800.90–800.99 Fracture of vault of skull, open, with intracranial injury of
801.00–801.09 Fracture of base of skull, closed, without mention of
intracranial injury
801.10–801.19 Fracture of base of skull, closed, with cerebral laceration
and contusion
801.20–801.29 Fracture of base of skull, closed, with subarachnoid,
801.30–801.39 Fracture of base of skull, closed, with other and
801.40–801.49 Fracture of base of skull, closed, with intracranial injury of
801.50–801.59 Fracture of base of skull, open, without mention of
intracranial injury
801.60–801.69 Fracture of base of skull, open, with cerebral laceration
and contusion
801.70–801.79 Fracture of base of skull, open, with subarachnoid,
801.80–801.89 Fracture of base of skull, open, with other and unspecified
intracranial hemorrhage
172 801.90–801.99 Fracture of base of skull, open, with intracranial injury
of other and unspecified nature
803.00–803.09 Other and unqualified skull fractures, closed, without
mention of intracranial injury
803.10–803.19 Other and unqualified skull fractures, closed, with cerebral
laceration and contusion
803.20–803.29 Other and unqualified skull fractures, closed, with
subarachnoid, subdural, and extradural hemorrhage
803.30–803.39 Other and unqualified skull fractures, closed, with other
and unspecified intracranial hemorrhage
Continued
803.40–803.49 Other and unqualified skull fractures, closed, with

intracranial injury of other and unspecified nature
803.50–803.59 Other and unqualified skull fractures, open, without
mention of intracranial injury
803.60–803.69 Other and unqualified skull fractures, open, with cerebral
laceration and contusion
803.70–803.79 Other and unqualified skull fractures, open, with
subarachnoid, subdural, and extradural hemorrhage
803.80–803.89 Other and unqualified skull fractures, open, with other and
803.90–803.99 Other and unqualified skull fractures, open, with
intracranial injury of other and unspecified nature
804.00–804.09 Multiple fractures involving skull or face with other bones,
closed, without mention of intracranial injury
closed, with cerebral laceration and contusion
closed, with subarachnoid, subdural, and extradural hemorrhage
closed, with other and unspecified intracranial hemorrhage
closed, with intracranial injury of other and unspecified nature
open, without mention of intracranial injury
open, with cerebral laceration and contusion
804.70–804.79 Multiple fractures involving skull or face with other bones, open,
with subarachnoid, subdural, and extradural hemorrhage
open, with other and unspecified intracranial hemorrhage
804.90–804.99 Multiple fractures involving skull or face with other bones, 173
open, with intracranial injury of other and unspecified nature
Traumatic Brain Injury Without Skull Fracture
850.0 Concussion with no loss of consciousness

850.11 Concussion with brief loss of consciousness of 30 minutes or less
850.12 Concussion with brief loss of consciousness of 31–59 minutes
" CODING TABLE
Continued
850.2 Concussion with moderate loss of consciousness

(1–24 hours)
850.3 With prolonged loss of consciousness (more than 24 hours)
and return to preexisting conscious level (complete recovery)
850.4 Concussion with prolonged loss of consciousness without
return to preexisting conscious level
850.5 With loss of consciousness of unspecified duration
850.9 Concussion, unspecified
851.00–851.09 Cortex (cerebral) contusion without mention of open
intracranial wound
851.10–851.19 Cortex (cerebral) contusion with open intracranial wound
851.20–851.29 Cortex (cerebral) laceration without mention of open
intracranial wound
851.30–851.39 Cortex (cerebral) laceration with open intracranial wound
851.40–851.49 Cerebellar or brainstem contusion without mention of
open intracranial wound
851.50–851.59 Cerebellar or brainstem contusion with open intracranial
wound
851.60–851.69 Cerebellar or brainstem laceration without mention of
851.70–851.79 Cerebellar or brainstem laceration with open intracranial
wound
851.80–851.89 Other and unspecified cerebral laceration and contusion,
without mention of open intracranial wound
851.90–851.99 Other and unspecified cerebral laceration and contusion,
with open intracranial wound
852.00–852.09 Subarachnoid hemorrhage following injury without
mention of open intracranial wound
852.10–852.19 Subarachnoid hemorrhage following injury with open
174 intracranial wound
852.20–852.29 Subdural hemorrhage following injury without mention of
852.30–852.39 Subdural hemorrhage following injury with open
intracranial wound
852.40–852.49 Extradural hemorrhage following injury without mention
of open intracranial wound
852.50–852.59 Extradural hemorrhage following injury with open
intracranial wound
Continued
853.00–853.09 Other and unspecified intracranial hemorrhage following

injury, without mention of open intracranial wound
(This is the default code for traumatic cerebral hemorrhage)
853.10–853.19 Other and unspecified intracranial hemorrhage following
injury, with open intracranial wound
854.00–854.09 Intracranial injury of other and unspecified nature without
mention of open intracranial wound
(This is the default code for traumatic brain injury)
854.10–854.19 Intracranial injury of other and unspecified nature with
959.01 Head injury, unspecified
Manifestation Codes
Coding manifestation is encouraged since there is not one common presentation
for traumatic brain injury (TBI). The ‘‘coma’’ codes from 780.0 to 780.93 may not be
used with TBI. Likewise, memory loss, 780.93, may not be used with TBI. The
manifestation codes should be listed after the primary TBI code from the preceding
list during the acute hospitalization.
Following is a list of relatively new or little known TBI code manifestations:
310.0 Frontal lobe syndrome (due to brain damage)

310.2 Postconcussion syndrome
310.8 Other specified nonpsychotic mental disorders following
organic brain damage
Mild memory disturbance due to organic brain damage
The use of the term mental disorders here is unfortunate; yet
the classification rules make this the code that must be used.
339.20 Posttraumatic headache, unspecified
175
339.21 Acute posttraumatic headache
339.22 Chronic posttraumatic headache
These codes are new and available for use beginning October 1, 2010.
780.33 Posttraumatic seizures

Note that this code is not to be used for posttraumatic
epilepsy, where the appropriate code from category 345.xx
should be used.
" CODING TABLE
Continued
799.50 Unspecified signs and symptoms involving cognition

799.51 Attention or concentration deficit
799.52 Cognitive communication deficit
799.53 Visuospatial deficit
799.54 Psychomotor deficit
799.55 Frontal lobe and executive function deficit
Note that the code 310.0 is to be used if the manifestation is
due to brain damage.
799.59 Other signs and symptoms involving cognition
The 799-series codes (different from those mentioned above) allow providers
to code emotional/behavioral symptoms without using mental health diagnosis
codes. These codes do not replace mental health diagnosis codes. Providers should
use these codes when they observe the symptoms but a mental health diagnosis
is not established. While these codes are intended to be used for TBI symptoms,
they are not limited to TBI.
799.21 Nervousness
799.22 Irritability
799.23 Impulsiveness
799.24 Emotional lability
799.25 Demoralization and apathy
799.29 Other signs and symptoms involving emotional state
Other manifestations, such as paresis, speech and language disturbances, and

176 sleep disorders, may be found in the ICD-9-CM index and are too numerous to
list here.
Late Effects of Traumatic Brain Injury

Anytime after the acute phase, manifestations of TBI would be considered ‘‘late
effects.’’ The first-listed code becomes the manifestation (late effect), and the
second code is a ‘‘late effect code’’ appropriate to the injury as listed below:
905.0 Late effect of fracture of skull and facial bones

Late effect injury classifiable to 800–804
907.0 Late effect of intracranial injury without mention of skull fracture
Late effect of injury classifiable to 850–854
Screening for Traumatic Brain Injury
Especially in the military setting, patients may be screened for possible TBI. The
code to be used in this situation is
V80.01 Screening for traumatic brain injury
Personal History of Traumatic Brain Injury

It may be of value in some cases to add the information to a list of diagnoses that
a patient has a history of TBI, and instances may occur when no ‘‘late effect’’ is
present; this information needs to be captured. In that case, use the code
V15.52 Personal history of traumatic brain injury
This code may not be a first-listed diagnosis.
CURRENT PROCEDURAL TERMINOLOGY CODING FOR TRAUMATIC

BRAIN INJURY
Current Procedural Terminology (CPT) coding does not depend on the diag-
nosis. It depends on the work performed in the service, and more work is
needed for more serious presenting problems.
New patients with moderate to severe TBI are usually level 5 consultations CPT
99255 or level 3 admissions CPT 99223 because of the altered mental state and
risk of substantial morbidity.
When managing the patient in the intensive care unit, and when the patient is
unstable and critically ill, the correct codes are the critical care codes. These codes,
CPT 99291 and 99292, use time as the basis for setting level of service instead
of bullet points. 177
New office patients often have concussion, and the level of Evaluation and
Management (E/M) service depends on the severity of the presenting problem and
risk. For example, a level 3 office new patient visit CPT 99203 would be a high
school athlete presenting asymptomatic 4 days after a concussion, requesting
permission to return to playing on the football team next week. Symptomatic TBI
patients usually require a higher level of service when seen in the office.
The template at the end of this article is a useful reminder of all the particular
elements that must be documented in each new, consultation, or admission
note. The breakdown of bullets required for each kind of follow-up service is
beyond the scope of this summary.
" CODING TABLE
Neurology Outpatient New/Consultation/Admission Template
Date:
Consultation requested by:
Chief Concern:
History of Present Illness (4+ facts):
Past History and Medications:
Social:
Family History:
Review of Systems: Check if normal; state any abnormality
& Constitutional (fever, weight) & Respiratory & Endocrine
& Neurologic & Gastrointestinal & Hematologic/lymphatic
& Eyes & Genitourinary & Allergic/immunologic
& Ears, nose, throat & Musculoskeletal & Psychological
& Cardiovascular & Skin, breast & Neurologic
Physical Examination: Check if normal; state any abnormality
Vital signs: BP__________ HR______ Wght________
& General appearance & CN 2 & CN 12
& Cardiovascular & CN 3-4-6 & Sensation
& Orientation & CN 5 & Power
& Attention & CN 7 & Tone
& Memory & CN 8 & Coordination
& Language & CN 9 & Reflexes
& Fund of knowledge & CN 11 &Gait
& Funduscopy
Impressions and Plans:
Level of Service 5: Needs one of the following:
178
& Chronic illness with severe exacerbation/progression/side effects
& Risk of mortality or serious morbidity, eg, intracranial hemorrhage
& Abrupt neurologic change, eg, altered mental state, seizure
& High-risk medications
ACKNOWLEDGMENT
Tara A. Cozzarelli, RN, LCDR, USPHS; Defense Centers of Excellence for
Psychological Health and Traumatic Brain Injury, reviewed and made suggestions
for this coding table.
APPENDIX A
Practice Guidelines for Traumatic Brain Injury
Title Citation Month/Year Web Address Status
Update: Determining Neurology June 2010 www.aan.com/go/ Current guideline.

Brain Death in Adults 2010;74(23): practice/guidelines Endorsed by the
1911–1918 American College of
Radiology, the Association
of Organ Procurement
Organizations, the Child
Neurology Society, the
Neurocritical Care Society,
and the Radiological
Society of North America.
Antiepileptic Drug Neurology January 2003 www.aan.com/go/ Reaffirmed on 10/17/2009
Prophylaxis in 2003;60(1): practice/guidelines and 07/28/2006.
Severe Traumatic 10–16 Current guideline.
Brain Injury
The Management of Neurology March 1997 www.aan.com/go/ Update in progress.
Concussion in Sports 1997;48(3): practice/guidelines
581–585
179
APPENDIX Ba
180
w/o = without.
*Denotes minimally conscious state.
yDenotes emergence from minimally conscious state.
aThis scale should only be used in accordance with the instructions provided in the CRS-R Administration and Scoring Manual, which is
available at tbims.org/combi/crs. If interested in additional information or training resources, please contact kdecamp@solarishs.org.
Reprinted with permission from Giacino JT, Kalmar K, Whyte J. The JFK Coma Recovery Scale-Revised: measurement characteristics and diagnostic utility. Arch Phys
Med Rehabil 2004;85(12):2020–2029.
APPENDIX C
Rancho Los Amigos Scale—Revised
I. No Response
Persons at this level:
Will not respond to sounds, sights, touch, or movement.
II. Generalized Response
Will begin to respond to sounds, sights, touch, or movement.
Will respond slowly, inconsistently, or after a delay.
Will respond in the same way to what they hear, see, or feel. Responses may include chewing,
sweating, breathing faster, moaning, moving, and/or increasing blood pressure.
III. Localized Response
Will be awake on and off during the day.
Will make more movements than before.
Will react more specifically to what they see, hear, or feel. For example, they may turn toward a
sound, withdraw from pain, and attempt to watch a person move around the room.
Will react slowly and inconsistently.
Will begin to recognize family and friends.
Will follow some simple directions such as, ‘‘Look at me’’ or ‘‘Squeeze my hand.’’
Will begin to respond inconsistently to simple questions with ‘‘yes’’ or ‘‘no’’ head movements.
IV. Confused-Agitated
Will be very confused and frightened.
Will not understand what they feel or what is happening around them.
181
Will, because of confusion, overreact to what they see, hear, or feel by hitting, screaming, using
abusive language, or thrashing about.
Will be restrained so they do not hurt themselves.
Will be highly focused on their basic needs, eg, eating, relieving pain, going back to bed, going to
the bathroom, or going home.
May not understand that people are trying to help them.
Will not pay attention or be able to concentrate for a few seconds.
Will have difficulty following directions.
Will recognize family and friends some of the time.
Will, with help, be able to do simple routine activities, such as feeding themselves, dressing, or talking.
" APPENDIX C
Continued
V. Confused-Inappropriate, Nonagitated
Will be able to pay attention for only a few minutes.
Will be confused and have difficulty making sense of things outside themselves.
Will not know the date, where they are, or why they are in the hospital.
Will not be able to start or complete everyday activities, such as brushing their teeth, even when
physically able. They may need step-by-step instructions.
Will become overloaded and restless when tired or when too many people are present.
Will have a very poor memory; they will remember past events from before the accident better than
their daily routines or information they have been told since the injury.
Will try to fill in gaps in memory by making up things (confabulation).
May get stuck on an idea or activity (perseveration) and need help switching to the next part of the activity.
Will focus on basic needs, such as eating, relieving pain, going back to bed, going to the bathroom,
or going home.
VI. Confused-Appropriate
Person at this level:
Will be somewhat confused because of memory and thinking problems. They will remember the
main points from a conversation but forget and confuse the details. For example, they may remember
having visitors in the morning but forget what they talked about.
Will follow a schedule with some assistance but become confused by changes in the routine.
Will know the month and year unless a serious memory problem is present.
Will pay attention for about 30 minutes but have trouble concentrating when it is noisy or when
the activity involves many steps. For example, at an intersection, they may be unable to step off
the curb, watch for cars, watch the traffic light, walk, and talk at the same time.
Will brush their teeth, get dressed, and feed themselves with help.
Will know when they need to use the bathroom.
Will do or say things too fast without thinking first.
182 Will know that they are hospitalized because of an injury but will not understand all the problems
they are having.
Will be more aware of physical problems than thinking problems.
Will associate their problems with being in the hospital and think they will be fine as soon as they
go home.
VII. Automatic-Appropriate
Will follow a set schedule.
Will be able to do routine self-care without help, if physically able. For example, they can dress or
feed themselves independently.
Will have problems in new situations and may become frustrated or act without thinking first.
Continued
Will have problems planning, starting, and following through with activities.
Will have trouble paying attention in distracting or stressful situations, eg ,family gatherings, work,
school, church, or sports events.
Will not realize how their thinking and memory problems may affect future plans and goals. They
therefore may expect to return to their previous lifestyle or work.
Will continue to need supervision because of decreased safety awareness and judgment. They still do
not fully understand the impact of their physical or thinking problems.
Will think slower in stressful situations.
Will be inflexible or rigid and may be stubborn; however, their behaviors are related to their brain
injury.
Will be able to talk about doing something but will have problems actually doing it.
VIII. Purposeful-Appropriate
Will realize that they have a problem with their thinking and memory.
Will begin to compensate for their problems.
Will be more flexible and less rigid in their thinking. For example, they may be able to come up with
several solutions to a problem.
Will be ready for driving or job-training evaluation.
Will be able to learn new things at a slower rate.
Will still become overloaded with difficult, stressful, or emergency situations.
Will show poor judgment in new situations and may require assistance. Will need some guidance
when making decisions.
Will have thinking problems that may not be noticeable to people who did not know them before
the injury.
Modified with permission from Rancho Los Amigos Scale-Revised. Rancho Los Amigos National Rehabilitation Center, Downey, California.
183

MULTIPLE-CHOICE QUESTIONS
These items are an integral part of the issue. They are not intended as
an examination but rather as a means of stimulating thought and helping
you assess your general understanding of the material presented in this issue.
Some are designed to stimulate independent study; the comments and
references provided with the preferred responses should assist in this process.
For each item, select the single best response, marking it on the answer
form provided inside the back cover of this issue and return your completed
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subscribers are encouraged to complete the Multiple-Choice

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186
TYPE A QUESTIONS (SINGLE BEST ANSWER)
1. A 16-year-old girl has a 1-minute generalized tonic-clonic seizure
immediately after falling from her bicycle and striking her head. After
5 minutes, she is conscious and conversant but feels “dazed.” On arrival at
the emergency department, her Glasgow Coma Scale score is 15/15. Her
neurologic examination is normal, and CT head imaging is unremarkable.
She is seen 1 week later by the neurologist with a report of generalized
headache and nonspecific “wooziness.” An EEG shows mild, generalized,
intermittent slowing. Which of the following is the most appropriate next
step in management?
A. observation and reassurance
B. prolonged video EEG monitoring
C. repeat a standard EEG in 1 month
D. start carbamazepine
E. start levetiracetam
2. A 25-year-old soldier sustains a concussion due to a blast injury from
a roadside bomb that detonated next to the vehicle in front of his.
He has no structural brain damage evident on neurologic examination or
neuroimaging, but he develops headaches on the day of injury that persist.
The headaches are described as left sided with pain felt primarily behind
the eye, occurring typically once a week. They are throbbing in quality,
and on two occasions he vomited during an episode. Sleep may relieve the
headache. Medication aimed at treatment of which of the following
conditions is indicated for this patient?
A. migraine without aura
B. occipital neuralgia
C. paroxysmal hemicrania
D. posttraumatic stress disorder
E. tension-type headache
3. A 28-year-old man reports insomnia with multiple awakenings and

excessive daytime fatigue over the past 6 months after sustaining a mild
traumatic brain injury in a bicycle accident. He states that he lies in bed
staring at the ceiling for several hours each night and dreads going to bed
because he knows that he won’t be able to sleep. He reports that he feels
unrestored after the few hours of sleep he achieves and usually takes a
45-minute nap in the afternoon. He previously consumed an alcoholic
beverage to get to sleep, as well as multiple caffeinated beverages during
the day to stay awake. He has discontinued both of these practices. He denies
depressed mood or anxiety. His neurologic examination is normal. Which of
the following is the optimal next step in diagnosis or management?
A. perform polysomnography
B. prescribe a selective serotonin reuptake inhibitor
C. prescribe modafinil
D. prescribe zolpidem
E. provide cognitive-behavioral therapy
187
4. A college football player is seen in follow-up by a physician retained

by the university. He sustained a concussion 2 weeks earlier during a
practice. Initially, he had a headache and poor memory for the event, but
he felt better in 2 days. The same type of accident happened to him the
previous season. He completes a graduated exercise regimen 2 weeks
after the event and is anxious to be fit for an important upcoming game.
Which of the following is the greatest potential concern in this athlete’s
return-to-play decision?
A. additive effect of multiple concussions
B. development of exertional headaches
C. possibility of delayed intracerebral hemorrhage
D. possibility of late arterial dissection
E. posttraumatic seizures
5. A 45-year-old man presents to the physician with symptoms of chronic

fatigue and poor memory following a mild head injury 3 months ago. He
was the belted driver of a motor vehicle that was rear-ended by another
vehicle. He struck his head on the steering wheel, but no loss of consciousness
occurred. He has had chronic cervical pain without radiation since that time.
He is using 50 mg of tramadol daily for cervical pain and takes no other
medications. He denies depressed mood but notes chronic fatigue and
daytime sleepiness despite no disruptions of nighttime sleep. He has gained
15 kg (33 lb) because of inactivity, and his current body mass index is 31.
His wife reports that he snores. Mental status examination score is 30/30,
and the remainder of the neurologic examination is normal. His neck
measures 45.7 cm (18 in) in circumference. Which of the following actions
is the next most appropriate step?
A. discontinue tramadol
B. perform MRI of the brain
C. perform polysomnography
D. prescribe methylphenidate
E. prescribe prazosin
6. A 24-year-old driver is in an automobile accident during which his head hits

the steering wheel. He was not wearing a seat belt. According to his passenger,
he did not lose consciousness, but when the paramedics arrive, he is dazed
and cannot figure out what happened. He is taken to a local hospital, where
he becomes oriented to his current circumstances on arrival but cannot
recount the events of the accident. By the next day, he is fine except for a
generalized headache. Which of the following best describes his injury?
A. Glasgow Coma Scale score of 9
B. grade 2 concussion
C. moderate traumatic brain injury
D. postconcussive syndrome
E. seizure
188 7. A 15-year-old boy experiences a 3-minute episode of unconsciousness

resulting from a head injury sustained during a football tackle. He regains
consciousness and appears dazed for 10 minutes but is able to communicate
coherently and is fully oriented. He can recall the details of the game prior
to his injury but has no memory of the tackle and his injury. His neurologic
examination is normal. The patient wants to resume playing football as soon
as possible. Which of the following is the most appropriate advice to give
the patient and his parents (as supported by the AAN Practice Parameter)?
A. he may resume playing football today if a head CT scan of the brain
is normal
B. he should be hospitalized overnight for observation and return to play
after 1 asymptomatic week
C. he should be observed at home for 24 hours, then return to play
tomorrow if no symptoms occur
D. he should be withheld from play for 2 weeks
E. he should not play football anymore
8. Which of the following is the most common cause of civilian traumatic
brain injury?
A. assault
B. automobile accident
C. collision with a moving object
D. fall
E. motorcycle accident
9. A 30-year-old woman reports multiple daily episodes of “zoning out”

over the past 8 months. During these episodes she is noted to stare briefly,
stop what she is doing, and sometimes flutter her eyes or move papers on
her desk. She is amnestic for these episodes and feels exhausted afterward.
She had a generalized tonic-clonic seizure 6 months ago. One year ago, she
sustained a moderate traumatic brain injury in a motor vehicle collision. A
CT at that time revealed a right anterior temporal contusion. Currently, her
brain MRI demonstrates right anterior temporal encephalomalacia. During an
inpatient video-EEG monitoring stay, multiple episodes of her “zoning out”
spells were captured and diagnosed as seizures. The EEG during these
events showed localized onset in the right temporal area. In addition, the
inter-ictal EEG demonstrates right anterior temporal sharp waves and spikes.
Her seizures have failed to be controlled on therapeutic doses of three
anticonvulsants (levetiracetam, lamotrigine, and carbamazepine). Which of
the following is the most appropriate next step in diagnosis or management?
A. consider deep brain stimulation for treatment
B. consider vagal nerve stimulation
C. order a presurgical evaluation for right temporal lobectomy at an epilepsy
surgical center
D. start lacosamide
E. start phenytoin
10. A 25-year-old soldier develops acute headaches after minor head trauma
from a blast injury. The headaches persist, and after 3 weeks, when his unit
is removed from a combat zone, he is seen at sick call. The headaches are
described as typically unilateral and throbbing; they occur several times
per week. He has had a great deal of trouble sleeping since the traumatic 189
incident. Which of the following medications is the best choice for
headache prophylaxis in this patient?
A. amitriptyline
B. gabapentin
C. propranolol
D. tizanidine
E. topiramate
11. Which of the following brain regions is most susceptible to focal

traumatic brain injury?
A. anterior temporal lobes
B. lateral frontal cortex
C. medial temporal cortex
D. occipital lobes
E. posterior parietal cortex
12. A 23-year-old man has recurring nightmares and poor sleep after
sustaining a mild traumatic brain injury in combat 1 month ago. Prazosin
is prescribed. In discussing the use of this medication with the patient,
which of the following adverse effects is most likely to be experienced?
A. anxiety
B. daytime sleepiness
C. dizziness
D. erectile dysfunction
E. hypertension
13. A high school soccer player’s head collides with another player while
“heading” the ball. She is knocked to the ground and has a 2-minute
episode of disorientation but does not pass out and walks off the field.
Her head hurts for a few minutes, and no nausea or vomiting is present.
Which of the following conditions best defines this injury?
A. collision
B. concussion
C. exertional headache
D. seizure
E. whiplash
14. A 40-year-old man sustained a mild head injury in a motor vehicle accident
2 weeks ago. He was the belted driver of a motor vehicle struck from behind.
He thinks he struck his head on the steering wheel but does not remember the
impact. He was unconscious for 30 seconds and remembers getting out of the
car to help the other driver and inspect the damage. He did not go to hospital.
Now he notes generalized mild headache and neck pain. He has been able to
return to work as a salesman but notes that he has difficulty “keeping track.”
He needs to write down messages and sales orders immediately or he cannot
remember them 2 minutes later. Previously he had never needed to do this.
Injury to which of the following areas is most likely responsible for this
patient’s cognitive symptoms?
A. anterior thalamic nuclei
B. fornices
190 C. mamillary bodies
D. mesial temporal lobes
E. prefrontal cortex
15. A 50-year-old man is thrown off his motorcycle and sustains a closed
head injury. He is found unconscious at the scene with a Glasgow Coma
Scale score of 8/15. Fifteen minutes after the accident he has a 2-minute
generalized tonic-clonic seizure in the ambulance. In the emergency
department, he is intubated and ventilated. A CT of the head reveals a
1-cm left subdural hematoma and a small amount of subarachnoid blood
over the convexity. Which of the following is the most critical determinant
of the subsequent development of posttraumatic epilepsy in this patient?
A. occurrence of an immediate seizure following the head injury
B. patient age
C. presence of subarachnoid hemorrhage
D. presence of a subdural hematoma
E. severity of the head injury
16. A 20-year-old sailor hits his head on a pipe when his ship is in rough
seas. He sustains a laceration and needs seven stitches. He was not knocked
out and is able to recount the entire event. In evaluating his need for a brain
imaging study, which of the following is recommended for this patient?
A. contrast CT
B. noncontrast CT
C. noncontrast MRI
D. observation only
E. PET scan
17. A 40-year-old woman sustained a mild traumatic brain injury with

no loss of consciousness in a motorcycle accident 3 months ago.
She experienced some difficulty with concentration and memory retrieval,
which resolved after 2 months. She now has changed jobs and is having
difficulty learning new protocols as a computer programmer. She has
received no complaints concerning her job performance, but she worries
she is becoming demented. She denies symptoms of depression and states
she has been sleeping and exercising regularly. She scores 29/30 on mental
status examination, and the remainder of her neurologic examination is
normal. Which of the following is the most appropriate next step
in management?
A. MRI brain with contrast
B. neuropsychometric testing
C. PET scan
E. reassurance
18. A high school soccer player sustains a concussion in a game. He is

momentarily disoriented and reports a headache but starts to feel better 30
minutes later. According to several recent studies, how does recovery in the
high school age group compare with that of college-aged athletes?
191
A. delayed neurocognitive deficits are more common in college athletes
B. high school students have milder memory deficits
C. neurocognitive deficits appear more prolonged
D. no appreciable difference in the groups was found
E. subjective symptoms clear more rapidly
19. Which of the following is identified as a risk factor for the development
of chronic posttraumatic headaches?
A. male sex
B. mild head injury
C. preexisting diagnosis of depression
D. prolonged posttraumatic coma
E. structural lesion on neuroimaging
20. A high school athlete sustains a grade 3 concussion in a football

game. One week after the event, his parents feel that he is still not back
to normal. Which of the following symptoms is most closely associated with
a postconcussive syndrome?
A. diplopia
B. disinhibition
C. nightmares
D. poor concentration
E. violent outbursts
21. A 45-year-old man falls on the ice in a parking lot, strikes his head, and
passes out for several seconds. He develops an immediate headache and is
seen in an emergency department where he undergoes a head CT, which is
normal. He is given hydrocodone and told to follow up with his regular
physician. He feels better later that night. One week later, when seen in
follow-up, he still reports a moderate, dull, bilateral, and intermittent
headache that starts at the base of the skull and has no lancinating
features. He receives another prescription for hydrocodone and continues
this on a daily basis. A neurologic consultant sees the patient 2 weeks later
and confirms a normal neurologic examination. Two months after his injury,
the patient returns to the neurologist reporting a daily, unremitting headache.
Medications include hydrocodone and butalbital in addition to zolpidem for
sleep. What is the most likely headache diagnosis?
A. cervicogenic headache
B. medication-overuse headache
C. migraine
D. occipital neuralgia
22. A 20-year-old woman reports to her physician 3 days after hitting her
head while playing hockey. She was unconscious for 1 minute and then
awoke “seeing stars.” She resumed playing hockey but felt dizzy and was
taken to an emergency department immediately after the game. A CT head
192 scan was negative, and she was dismissed. Now she notes generalized
headache, poor concentration and memory, and vague lightheadedness.
She remembers the start of the hockey game and the trip to the emergency
department but does not remember striking her head. She scores 28/30
on mental status examination, and the remainder of her neurologic
examination is normal. Which of the following is the most appropriate
next step in management?
A. brain MRI
B. educate and reassure patient
C. neuropsychometric testing
D. PET scan
E. repeat CT of the head
23. A 30-year-old soldier has two generalized tonic-clonic seizures occurring
on separate days, both more than 10 days after a moderately severe traumatic
brain injury from a combat blast injury. An MRI of the brain demonstrates
resolving bifrontal contusions, and an EEG demonstrates generalized
intermittent slow-wave activity but no epileptiform discharges. Carbamazepine
is started. The patient is seen by a neurologist 3 weeks later. He has had no
further seizures and takes carbamazepine 1000 mg/d with a therapeutic drug
level. The drug has been well tolerated. He scores 28/30 on mental status
testing and has an otherwise normal neurologic examination. Assuming the
patient is seizure free, at what point can consideration be given for tapering
the anticonvulsant?
A. immediately
B. 6 months
C. 1 year
D. 2 years
E. continue the anticonvulsant indefinitely
24. A high school football player sustains a hard tackle and is slow in
getting up from the field. He arises independently after 30 seconds and is
noted by a physician’s assistant on the sidelines to be disoriented to the
current circumstances. No other focal findings are evident, and he reorients
in a few minutes. What is the best course of action regarding this athlete?
A. administer nonsteroidal anti-inflammatory drugs at the sidelines
B. bar the athlete from returning to the game
C. have the patient perform a sprint and reassess
D. observe for 10 minutes and allow the athlete to return to the game
E. send to an emergency department for a CT scan
25. A 30-year-old soldier develops headaches immediately after falling

during a training exercise and striking the back of his head. No loss
of consciousness occurs, and he resumes his duties the next day. Two
weeks later, he is seen at sick call still reporting headaches that start at the 193
base of the skull. These occur at least twice a week, last 3 to 6 hours, are
throbbing in quality, associated with nausea, and at times interfere with his
work. Neurologic examination and a CT scan of the brain are normal.
Long-acting valproic acid, 250 mg at bedtime, is started. Two weeks later,
he still has several headaches per week but reports no side effects of
valproic acid. What is the next best step in management?
A. change the medication to a long-acting opioid
B. change the medication to a tricyclic antidepressant
C. increase the valproic acid dose
D. obtain a cervical MRI scan
E. repeat the head CT scan
26. Four months after a motor vehicle accident, a 42-year-old woman comes
to the physician for evaluation of memory impairment. She was the belted
driver of a pickup truck that slid off an icy road into a ditch. She struck her
head on the steering wheel but did not lose consciousness. She felt shaken
up but was able to get out of her vehicle immediately and call for help. She
recalls the accident vividly and had no other serious injury. Since that time,
she reports poor memory and inability to function at her job as a nurse. She
details for the physician all of the many mistakes she almost made at work
and at home because of her poor memory. She has received no complaints
about her work performance, and her husband feels she is too hard on
herself. Her sleep is poor. She is not bothered by intrusive memories of the
accident. She reports diffuse muscle aches. She is tearful during the history
and examination. She scores 29/30 on mental status testing, and the remainder
of her examination is normal. Which of the following disorders is most
likely responsible for this patient’s cognitive symptoms?
A. depression
B. malingering
C. mild traumatic brain injury
D. obstructive sleep apnea
E. posttraumatic stress disorder
27. A 25-year-old woman is a passenger in a car that is hit at high speed

from behind while stopped at a traffic light. She receives a hyperextension
injury and is taken to a hospital. She is confused and combative. She is
admitted and eventually referred for inpatient rehabilitation because of several
fractures. She is treated with a sedative-hypnotic at night. Her therapists
note that she is slow to process and has difficulty following directions,
although she is motivated to be discharged home. Her head CT on admission
was normal. MRI is later performed, looking for a delayed hematoma.
Microhemorrhages are seen in the corpus callosum. Which of the following
is the most likely mechanism for this patient’s cognitive impairment?
A. axonal shear injury
B. depression
C. medication effect
194 D. subclinical seizures
E. subdural hematoma
28. How much greater is the risk of developing mild cognitive impairment
in athletes who have sustained repeated (three or more) concussions
compared to those with no history of concussions?
A. no increased risk
B. threefold
C. fivefold
D. sevenfold
E. 10-fold
29. Which of the following concerns has historically been raised about
long-term effects of repeated concussions in athletes?
A. dementia pugilistica in boxers
B. higher incidence of normal pressure hydrocephalus in former athletes
C. higher prevalence of migraine in athletes
D. higher stroke rates in athletes
E. premature atrophy in brain scans of athletes
30. A 26-year-old man sustained a mild traumatic brain injury after detonation
of a roadside improvised explosive device in Afghanistan 2 months ago. He
has recovered from his injuries well but reports excessive daytime fatigue
and sleepiness and very poor nighttime sleep. He awakens frequently from
disturbing nightmares in which he sees his friend who was killed in the
explosion. He reports depressed mood and symptoms of anxiety. There is
no suicidal ideation. His general and neurologic examinations are normal. In
addition to treatment of his depression and anxiety, which of the following
medications would be most helpful in reducing the occurrence of his
disturbing nightmares?
A. diphenhydramine
B. modafinil
C. prazosin
D. trazodone
E. zaleplon
31. A 55-year-old man comes to the physician for evaluation of dizziness

following a mild head injury sustained in a motor vehicle accident 1 week
ago. No loss of consciousness or serious injury occurred, but he struck his
head on the steering wheel and felt dazed for 1 to 2 minutes. Since that
time he has had moderate generalized headache and dizziness with 195
spinning that is worse when he bends over or turns to the left. With the
Dix-Hallpike maneuver, he develops vertigo and fatigable nystagmus when
his head is turned to the left and lowered. The remainder of the neurologic
examination is normal. Which of the following is the most appropriate next
step in management of this patient?
A. bed rest
B. canalith repositioning
C. meclizine therapy
D. MRI of the brain
E. posturography
32. Two weeks after sustaining a traumatic brain injury playing football, a
30-year-old man experiences difficulty with memory that mildly affects his
day-to-day functioning. His wife, who accompanies him, notes that while he
can remember events subsequent to the injury (such as a family barbecue),
he forgets where they occurred or exactly when. This is an example of
impairment, commonly seen following traumatic brain injury, to which
type of memory?
A. immediate memory
B. memory retrieval
C. retrospective memory
D. source memory
E. working memory
33. Which of the following is considered the most important intervention in

mild traumatic brain injury?
A. anxiolytics
B. non-narcotic analgesics
C. physical therapy
D. psychotherapy
E. removal from activity
34. A 35-year-old woman is seen in consultation 1 month after a motor

vehicle accident during which she suffered a cervical hyperextension injury.
No head trauma was reported. She had a prior history of bifrontal, mild,
nondisabling, squeezing-type headaches occurring usually toward the end of
the day, 2 days out of the week, that were rapidly relieved by ibuprofen.
After the accident, the headaches increased in frequency to 4 days per week
but were otherwise similar to her prior headaches. Neurologic examination
and MRI of the brain and cervical spine are normal. Which of the following
is the most likely diagnosis?
A. acute posttraumatic headache
B. cervical radiculopathy
C. migraine headache
196 D. occipital neuralgia
35. Which of the following steps is recommended in all cases of

sports concussion?
A. avoidance of all analgesics
B. CT done the same day
C. evaluation by a neurologist
D. fitting of hard cervical collar
E. several hours of close observation
TYPE R EXTENDED MATCHING
Match each of the following clinical scenarios with the pathophysiologic mechanism
that best describes it.
A. contrecoup injury
B. coup injury
C. diffuse axonal injury
D. hyperacute metabolic phase: acute massive depolarization of neurons
with glutamate release
E. hypometabolic phase
36. A 64-year-old man trips and falls backward down four stairs, striking his
occiput on concrete. He is unconscious for 3 minutes and then appears
dazed with a flattened affect. He has a large subgaleal hematoma over his
occiput. A noncontrast CT head scan reveals bifrontal cerebral contusions.
37. A 22-year-old soldier is injured in an improvised explosive devices

blast. He is unconscious at the scene with no visible injury. On arrival of
emergency vehicles, his Glasgow Coma Scale score is 7, and his pupils
are 4 mm and sluggishly reactive. His examination is otherwise nonlocalizing.
A noncontrast CT shows diffuse cerebral edema.
38. A 16-year-old boy falls from his bicycle and strikes his head. He is not
wearing a helmet. Immediate loss of consciousness occurs followed by a
30-second generalized tonic-clonic seizure.
39. A 4-month-old infant is brought to the emergency department unconscious.

His mother states that she found him apneic in his crib and that he had
rolled off the bed earlier in the day, striking his head. His examination
reveals weak withdrawal to pain, weak cry, and brief eye opening. He is
diffusely hypotonic. The pupils are 4 mm and reactive. Retinal hemorrhages 197
are present bilaterally. No bruising of the head is present. The anterior
fontanelle is bulging. A CT of the brain reveals diffuse cerebral edema.
40. A 22-year-old woman struck her forehead on the net post while
playing volleyball. She lost consciousness for 1 to 2 minutes and then
felt dazed. At the emergency department, her Glasgow Coma Scale score
was 15, and she had a normal neurologic examination. A noncontrast
CT head was normal. Now, 4 days later, she continues to note poor
concentration and attention.

Continuum Lifelong Learning Neurol 2010;16(6):198– 215.
PREFERRED RESPONSES
Following are the preferred responses and critiques for the multiple-choice
items in this issue. The questions and answer selections are
repeated, and the preferred response appears in bold print. In most cases,
this is followed by an explanation and a reference with which you may seek
more specific information. No score will be assigned to the answer form you
complete, since the emphasis of this program is on self-assessment. You are
encouraged to review the responses and explanations carefully to evaluate
your general understanding of the course material.
TYPE A QUESTIONS (SINGLE BEST ANSWER)

1. A 16-year-old girl has a 1-minute generalized tonic-clonic seizure
immediately after falling from her bicycle and striking her head. After
5 minutes, she is conscious and conversant but feels “dazed.” On arrival at
the emergency department, her Glasgow Coma Scale score is 15/15. Her
neurologic examination is normal, and CT head imaging is unremarkable.
She is seen 1 week later by the neurologist with a report of generalized
headache and nonspecific “wooziness.” An EEG shows mild, generalized,
intermittent slowing. Which of the following is the most appropriate next
step in management?
A. observation and reassurance
B. prolonged video EEG monitoring
C. repeat a standard EEG in 1 month
198 D. start carbamazepine
E. start levetiracetam
The correct answer is A. This patient had an immediate posttraumatic

seizure (concussive convulsion) in the setting of a mild traumatic brain
injury (TBI). She does not have a severe TBI and thus does not need 7 days
of phenytoin. In addition, she does not have posttraumatic epilepsy and
therefore should not be placed on anticonvulsants at this time. EEG has not
been shown to be helpful in predicting the development of epilepsy after
TBI. For more information, refer to the article “Epilepsy, Sleep Disturbances,
and Psychiatric Consequences.”
2. A 25-year-old soldier sustains a concussion due to a blast injury from a

roadside bomb that detonated next to the vehicle in front of his. He has no
structural brain damage evident on neurologic examination or neuroimaging,
but he develops headaches on the day of injury that persist. The headaches
are described as left sided with pain felt primarily behind the eye, occurring
typically once a week. They are throbbing in quality, and on two occasions
he vomited during an episode. Sleep may relieve the headache. Medication
aimed at treatment of which of the following conditions is indicated for
this patient?
A. migraine without aura
B. occipital neuralgia
C. paroxysmal hemicrania
D. posttraumatic stress disorder
The correct answer is A. The patient’s headaches are posttraumatic in

etiology, but per the authors of the article ”Posttraumatic Headache,”
treatment should be based on the type of primary headache that best fits
the characteristics of the presenting posttraumatic headache. In this case, the
headache description of unilateral symptoms, retro-orbital pain, and
throbbing pain at times causing vomiting are most akin to migraine without
aura. For more information, refer to the article “Posttraumatic Headache.”
3. A 28-year-old man reports insomnia with multiple awakenings and

excessive daytime fatigue over the past 6 months after sustaining a mild
traumatic brain injury in a bicycle accident. He states that he lies in bed
staring at the ceiling for several hours each night and dreads going to
bed because he knows that he won’t be able to sleep. He reports that he
feels unrestored after the few hours of sleep he achieves and usually
takes a 45-minute nap in the afternoon. He previously consumed an
alcoholic beverage to get to sleep, as well as multiple caffeinated beverages
during the day to stay awake. He has discontinued both of these practices.
He denies depressed mood or anxiety. His neurologic examination is
normal. Which of the following is the optimal next step in diagnosis
or management?
A. perform polysomnography
B. prescribe a selective serotonin reuptake inhibitor
C. prescribe modafinil
D. prescribe zolpidem
E. provide cognitive-behavioral therapy 199
The correct answer is E. Insomnia and excessive daytime sleepiness are
extremely frequent symptoms following mild traumatic brain injury. Usually
these symptoms are best addressed using cognitive-behavioral therapy to
improve sleep habits. This patient should avoid using alcohol and caffeine and
avoid daytime napping. Modafinil may improve his daytime fatigue but is not a
long-term solution for insufficient sleep. Zolpidem may help him to initiate
sleep but will not help his multiple awakenings because of its short half-life. In
the absence of other symptoms of depression, a selective serotonin reuptake
inhibitor is unlikely to be helpful. Unless complicating factors exist (eg, sleep
apnea, cataplexy, parasomnias) formal polysomnography will not be
diagnostically useful. For more information, refer to the article “Epilepsy, Sleep
Disturbances, and Psychiatric Consequences.”
4. A college football player is seen in follow-up by a physician retained by

the university. He sustained a concussion 2 weeks earlier during a practice.
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Initially, he had a headache and poor memory for the event, but he felt better
in 2 days. The same type of accident happened to him the previous season.
He completes a graduated exercise regimen 2 weeks after the event and is
anxious to be fit for an important upcoming game. Which of the following is
the greatest potential concern in this athlete’s return-to-play decision?
A. additive effect of multiple concussions
B. development of exertional headaches
C. possibility of delayed intracerebral hemorrhage
D. possibility of late arterial dissection
E. posttraumatic seizures
The correct answer is A. The authors of the article “Sports Concussion”

discuss in some detail the somewhat nebulous question of prior concussions
predisposing athletes to prolonged recovery times with future concussions
or possible permanent neurologic sequelae. Additionally, one study cited
found a higher incidence of concussion in the same season among college
football players who had sustained a previous concussion. For more
information, refer to the article “Sports Concussion.”
5. A 45-year-old man presents to the physician with symptoms of chronic

fatigue and poor memory following a mild head injury 3 months ago. He
was the belted driver of a motor vehicle that was rear-ended by another
vehicle. He struck his head on the steering wheel, but no loss of
consciousness occurred. He has had chronic cervical pain without radiation
since that time. He is using 50 mg of tramadol daily for cervical pain and
takes no other medications. He denies depressed mood but notes chronic
fatigue and daytime sleepiness despite no disruptions of nighttime sleep. He
has gained 15 kg (33 lb) because of inactivity, and his current body mass
index is 31. His wife reports that he snores. Mental status examination score
is 30/30, and the remainder of the neurologic examination is normal. His
neck measures 45.7 cm (18 in) in circumference. Which of the following
actions is the next most appropriate step?
A. discontinue tramadol
B. perform MRI of the brain
200 C. perform polysomnography
E. prescribe prazosin
The correct answer is C. This patient has fatigue following a mild traumatic
brain injury. In this case, features suggest he may have obstructive sleep
apnea (OSA), which in turn is related to a significant weight gain likely from
lack of exercise following his injury. Because OSA is a treatable cause of
fatigue, it should be further evaluated with polysomnography. Prazosin and
methylphenidate are unlikely to provide benefit. An MRI of the brain is
unlikely to yield new information. The small dose of tramadol he takes is
probably not contributing to his symptoms. For more information, refer to
the article “Rehabilitation in the Patient With Mild Traumatic Brain Injury.”
6. A 24-year-old driver is in an automobile accident during which his head hits

the steering wheel. He was not wearing a seat belt. According to his passenger,
he did not lose consciousness, but when the paramedics arrive, he is dazed
and cannot figure out what happened. He is taken to a local hospital, where
he becomes oriented to his current circumstances on arrival but cannot
recount the events of the accident. By the next day, he is fine except for a
generalized headache. Which of the following best describes his injury?
A. Glasgow Coma Scale score of 9
B. grade 2 concussion
C. moderate traumatic brain injury
D. postconcussive syndrome
E. seizure
The correct answer is B. A grade 2 concussion is characterized by altered

mental status lasting more than 15 minutes, with the possibility of
posttraumatic amnesia lasting up to 24 hours. A moderate traumatic brain
injury (TBI) is equivalent to a Glasgow Coma Scale (GCS) score of 9 to 13;
this patient has transient mild confusion without any other localizing features,
which is less severe than a moderate TBI or GCS in the midrange. His symptoms
resolved and do not indicate a postconcussive problem; no indication of
seizure is present. For more information, refer to the article “Diagnosis and
Management of Traumatic Brain Injury.”
7. A 15-year-old boy experiences a 3-minute episode of unconsciousness

resulting from a head injury sustained during a football tackle. He regains
consciousness and appears dazed for 10 minutes but is able to communicate
coherently and is fully oriented. He can recall the details of the game prior to
his injury but has no memory of the tackle and his injury. His neurologic
examination is normal. The patient wants to resume playing football as soon
as possible. Which of the following is the most appropriate advice to give the
patient and his parents (as supported by the AAN Practice Parameter)?
A. he may resume playing football today if a head CT scan of the brain is normal
B. he should be hospitalized overnight for observation and return to play
after 1 asymptomatic week
C. he should be observed at home for 24 hours, then return to play
tomorrow if no symptoms occur
D. he should be withheld from play for 2 weeks 201
E . he should not play football anymore
The correct answer is D. The AAN guidelines state that athletes experiencing
a grade 3 concussion with loss of consciousness for more than 1 minute
should be withheld from play for 2 weeks, assuming the patient has a normal
neurologic examination and all symptoms have resolved. If the loss of
consciousness is not prolonged and the patient has a normal neurologic
examination on recovery of consciousness, CT of the head and hospitalization
are not indicated. For more information, refer to the article “Memory
Impairment After Mild Traumatic Brain Injury.”
8. Which of the following is the most common cause of civilian traumatic

brain injury?
A. assault
B. automobile accident
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C. collision with a moving object

D. fall
E. motorcycle accident
The correct answer is D. Falls are the leading cause of traumatic brain injury
(TBI) (35.2%) in the civilian population, followed by traffic accidents
(17.3%), collision with a moving or stationary object (16.5%), and assaults
(10.1%). Blasts from improvised explosive devices are the leading cause of
TBI in the military population. For more information, refer to the article
“Mild Traumatic Brain Injury Update.”
9. A 30-year-old woman reports multiple daily episodes of “zoning out”

over the past 8 months. During these episodes she is noted to stare
briefly, stop what she is doing, and sometimes flutter her eyes or move
papers on her desk. She is amnestic for these episodes and feels
exhausted afterward. She had a generalized tonic-clonic seizure 6 months
ago. One year ago, she sustained a moderate traumatic brain injury in a
motor vehicle collision. A CT at that time revealed a right anterior
temporal contusion. Currently, her brain MRI demonstrates right anterior
temporal encephalomalacia. During an inpatient video-EEG monitoring
stay, multiple episodes of her “zoning out” spells were captured and
diagnosed as seizures. The EEG during these events showed localized
onset in the right temporal area. In addition, the interictal EEG
demonstrates right anterior temporal sharp waves and spikes. Her
seizures have failed to be controlled on therapeutic doses of three
anticonvulsants (levetiracetam, lamotrigine, and carbamazepine).
Which of the following is the most appropriate next step in diagnosis
or management?
A. consider deep brain stimulation for treatment
B. consider vagal nerve stimulation
C. order a presurgical evaluation for right temporal lobectomy at an
epilepsy surgical center
D. start lacosamide
E. start phenytoin
202
The correct answer is C. This patient has medically intractable
posttraumatic epilepsy likely stemming from the temporal lobe injury she
sustained 1 year ago. The chance that a fourth anticonvulsant will be
effective in controlling seizures is less than 10%. Given the fact that the
seizure focus is in a surgically accessible area, lesionectomy (right
anterior temporal lobectomy) is the most likely procedure to be effective
in controlling her seizures. A vagal nerve stimulator should be reserved
for patients who are not surgical candidates. Deep brain stimulation is not
yet approved for use outside of a clinical trial. For more information,
refer to the article “Epilepsy, Sleep Disturbances, and Psychiatric
Consequences.”
10. A 25-year-old soldier develops acute headaches after minor head trauma
from a blast injury. The headaches persist, and after 3 weeks, when his unit
is removed from a combat zone, he is seen at sick call. The headaches are
described as typically unilateral and throbbing; they occur several times per
week. He has had a great deal of trouble sleeping since the traumatic
incident. Which of the following medications is the best choice for
headache prophylaxis in this patient?
A. amitriptyline
B. gabapentin
C. propranolol
D. tizanidine
E. topiramate
The correct answer is A. Prophylactic medication in posttraumatic headaches

should be tailored both to the headache type and possible comorbid conditions.
The headaches described resemble migraine, for which several of the agents
shown are appropriate. The comorbid condition of insomnia may be helped
by the sedative properties of amitriptyline. For more information, refer to
the article “Posttraumatic Headache.”
11. Which of the following brain regions is most susceptible to focal

traumatic brain injury?
A. anterior temporal lobes
B. lateral frontal cortex
C. medial temporal cortex
D. occipital lobes
E. posterior parietal cortex
The correct answer is A. Orbitofrontal and anterior temporal lobes are most
susceptible to direct traumatic injury. Secondary injury, which is presumed
to occur from a variety of mechanisms, some of which are hypoperfusion
and hypoxia, is found commonly in vascular watershed zones or medial
temporal cortex (hippocampus). For more information, refer to the article
“Diagnosis and Management of Traumatic Brain Injury.”
12. A 23-year-old man has recurring nightmares and poor sleep after
sustaining a mild traumatic brain injury in combat 1 month ago. Prazosin is
prescribed. In discussing the use of this medication with the patient, which
of the following adverse effects is most likely to be experienced? 203
A. anxiety
B. daytime sleepiness
C. dizziness
D. erectile dysfunction
E. hypertension
The correct answer is C. Prazosin is an α-adrenergic blocker that is useful

in treating symptoms related to posttraumatic stress disorder, including
nightmares and anxiety, related to excessive CNS noradrenergic activity. It
usually produces no sedation or erectile dysfunction. Dizziness, possibly
related to mild orthostatic hypotension, occurs in approximately 10% of
patients. For more information, refer to the article “Rehabilitation in the
Patient With Mild Traumatic Brain Injury.”
13. A high school soccer player’s head collides with another player while
“heading” the ball. She is knocked to the ground and has a 2-minute
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episode of disorientation but does not pass out and walks off the field. Her
head hurts for a few minutes, and no nausea or vomiting is present. Which
of the following conditions best defines this injury?
A. collision
B. concussion
C. exertional headache
D. seizure
E. whiplash
The correct answer is B. A concussion is defined as an event where a

biomechanical force is applied to the head, causing what is typically brief
and transient neurologic dysfunction, but it does not require loss of
consciousness. The mechanics of the above injury may involve some
acceleration/deceleration, but the patient is not reporting neck pain as in
whiplash. The exertional nature of sports makes the headache more likely to
recur, although that is not what is described here. For more information, refer
to the article “Sports Concussion.”
14. A 40-year-old man sustained a mild head injury in a motor vehicle

accident 2 weeks ago. He was the belted driver of a motor vehicle struck
from behind. He thinks he struck his head on the steering wheel but does
not remember the impact. He was unconscious for 30 seconds and remembers
getting out of the car to help the other driver and inspect the damage. He
did not go to hospital. Now he notes generalized mild headache and neck
pain. He has been able to return to work as a salesman but notes that he
has difficulty “keeping track.” He needs to write down messages and sales
orders immediately or he cannot remember them 2 minutes later. Previously
he had never needed to do this. Injury to which of the following areas is
most likely responsible for this patient’s cognitive symptoms?
A. anterior thalamic nuclei
B. fornices
C. mamillary bodies
D. mesial temporal lobes
E. prefrontal cortex
204
The correct answer is E. This patient’s primary problem is difficulty with
working memory. Working memory is defined as the ability to maintain
short-term storage of information that is inaccessible in the environment and
the processes that keep memory active for later use. The prefrontal cortex
appears to be most important for normal working memory. Injury to the
other areas of brain mentioned would result in difficulties with long-term
memory. For more information, refer to the article “Memory Impairment
After Mild Traumatic Brain Injury.”
15. A 50-year-old man is thrown off his motorcycle and sustains a closed
head injury. He is found unconscious at the scene with a Glasgow Coma
Scale score of 8/15. Fifteen minutes after the accident he has a 2-minute
generalized tonic-clonic seizure in the ambulance. In the emergency department,
he is intubated and ventilated. A CT of the head reveals a 1-cm left subdural
hematoma and a small amount of subarachnoid blood over the convexity.
Which of the following is the most critical determinant of the subsequent
development of posttraumatic epilepsy in this patient?
A. occurrence of an immediate seizure following the head injury
B. patient age
C. presence of subarachnoid hemorrhage
D. presence of a subdural hematoma
E. severity of the head injury
The correct answer is E. The severity of the head injury, in this case a Glasgow
Coma Scale score of 8 at time of the accident, is the most critical determinant
of the development of posttraumatic epilepsy. The occurrence of the early
seizure and the presence of an intracranial subdural hematoma as well as the
subarachnoid hemorrhage are also independent risk factors but are not as
important as the severity of the head injury. The patient’s age is not greater
than 65 years or that would also be a risk factor. For more information, refer to
the article “Epilepsy, Sleep Disturbances, and Psychiatric Consequences.”
16. A 20-year-old sailor hits his head on a pipe when his ship is in rough seas.
He sustains a laceration and needs seven stitches. He was not knocked out
and is able to recount the entire event. In evaluating his need for a brain
imaging study, which of the following is recommended for this patient?
A. contrast CT
B. noncontrast CT
C. noncontrast MRI
D. observation only
E. PET scan
The correct answer is D. According to the authors of the article “Mild

Traumatic Brain Injury,” this patient falls into a minimal risk category and
does not require neuroimaging. For more information, refer to the article
“Diagnosis and Management of Traumatic Brain Injury.”
17. A 40-year-old woman sustained a mild traumatic brain injury with no

loss of consciousness in a motorcycle accident 3 months ago. She
experienced some difficulty with concentration and memory retrieval, which 205
resolved after 2 months. She now has changed jobs and is having difficulty
learning new protocols as a computer programmer. She has received no
complaints concerning her job performance, but she worries she is
becoming demented. She denies symptoms of depression and states she has
been sleeping and exercising regularly. She scores 29/30 on mental status
examination, and the remainder of her neurologic examination is normal.
Which of the following is the most appropriate next step in management?
A. MRI brain with contrast
B. neuropsychometric testing
C. PET scan
E. reassurance
The correct answer is E. Many patients who have sustained mild traumatic
brain injury with resolution of symptoms may experience recurrence of
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symptoms when confronted with a novel cognitive challenge. Additional

testing and medications are unlikely to be helpful at this point. The
physician should validate her concerns and reassure her. Use of memory
prostheses (eg, lists, reminders) and other behavioral strategies can also be
helpful. For more information, refer to the article “Memory Impairment After
Mild Traumatic Brain Injury.”
18. A high school soccer player sustains a concussion in a game. He is

momentarily disoriented and reports a headache but starts to feel better
30 minutes later. According to several recent studies, how does recovery in
the high school age group compare with that of college-aged athletes?
A. delayed neurocognitive deficits are more common in college athletes
B. high school students have milder memory deficits
C. neurocognitive deficits appear more prolonged
D. no appreciable difference in the groups was found
E. subjective symptoms clear more rapidly
The correct answer is C. Several recent studies have shown that when
comparing concussed high school and college students, high school
students have a more prolonged recovery period in terms of acute memory
and learning deficits than college students, even when they report
resolution of concussion symptoms. Furthermore, neurocognitive deficits
have more of a tendency to show up in a delayed fashion in high school
students after acute symptoms have resolved. For more information, refer to
the article “Sports Concussion.”
19. Which of the following is identified as a risk factor for the development
of chronic posttraumatic headaches?
A. male sex
B. mild head injury
C. preexisting diagnosis of depression
D. prolonged posttraumatic coma
E. structural lesion on neuroimaging
206 The correct answer is B. The authors of the article “Posttraumatic

Headache” note the arbitrary time period of greater than 3 months’
duration designated as the conversion point from acute to chronic
posttraumatic headaches (PTHAs). Risk factors associated with chronic
PTHAs include female sex, milder rather than more severe head injury,
and low educational and socioeconomic status. While some psychiatric
disorders or symptoms, such as depression, are suspected to contribute to
the development of chronic PTHAs, the authors state that no data are
available to prove that preexisting psychiatric disease causes chronic
PTHAs. Since severity of injury is inversely correlated with development
of chronic PTHAs, it can be inferred that structural imaging abnormalities
are less likely to be present. For more information, refer to the article
“Posttraumatic Headache.”
20. A high school athlete sustains a grade 3 concussion in a football game.

One week after the event, his parents feel that he is still not back to normal.
Which of the following symptoms is most closely associated with a
postconcussive syndrome?
A. diplopia
B. disinhibition
C. nightmares
D. poor concentration
E. violent outbursts
The correct answer is D. The mild traumatic brain injury associated with a
grade 3 concussion (loss of consciousness and/or posttraumatic amnesia
lasting less than 24 hours) may produce postconcussive symptoms such as
headache, vertigo, or poor concentration. Less likely would be a major
change in behavior or a focal neurologic syndrome. For more information,
refer to the article “Diagnosis and Management of Traumatic Brain Injury.”
21. A 45-year-old man falls on the ice in a parking lot, strikes his head, and
passes out for several seconds. He develops an immediate headache and is
seen in an emergency department where he undergoes a head CT, which is
normal. He is given hydrocodone and told to follow up with his regular
physician. He feels better later that night. One week later, when seen in
follow-up, he still reports a moderate, dull, bilateral, and intermittent
headache that starts at the base of the skull and has no lancinating features.
He receives another prescription for hydrocodone and continues this on a
daily basis. A neurologic consultant sees the patient 2 weeks later and
confirms a normal neurologic examination. Two months after his injury, the
patient returns to the neurologist reporting a daily, unremitting headache.
Medications include hydrocodone and butalbital in addition to zolpidem for
sleep. What is the most likely headache diagnosis?
A. cervicogenic headache
B. medication-overuse headache
C. migraine
The correct answer is B. The authors of the article “Posttraumatic Headache” 207
underscore the fact that medication overuse headache is a common
complication of posttraumatic headache in patients who use acute
medications on a frequent basis. In the above instance, the headache,
although starting in the cervical region, is atypical for occipital neuralgia and
has become more frequent with the regular use of narcotic analgesics. The
diagnosis can be confirmed if the headaches resolve within weeks after
discontinuing the offending analgesics. For more information, refer to the
article “Posttraumatic Headache.”
22. A 20-year-old woman reports to her physician 3 days after hitting her
head while playing hockey. She was unconscious for 1 minute and then
awoke “seeing stars.” She resumed playing hockey but felt dizzy and was
taken to an emergency department immediately after the game. A CT head
scan was negative, and she was dismissed. Now she notes generalized
headache, poor concentration and memory, and vague lightheadedness.
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She remembers the start of the hockey game and the trip to the emergency
department but does not remember striking her head. She scores 28/30
on mental status examination, and the remainder of her neurologic
examination is normal. Which of the following is the most appropriate next
step in management?
A. brain MRI
B. educate and reassure patient
C. neuropsychometric testing
D. PET scan
E. repeat CT of the head
The correct answer is B. This patient has sustained a mild traumatic brain
injury, which is commonly associated with impaired attention, slowness of
mental processing, and impaired memory retrieval. The short episode of
retrograde and anterograde memory loss is typical. Eighty-five percent to
90% of patients will recover within the first 3 months following the injury.
Neuroimaging and neuropsychometric testing are not recommended unless
the patient manifests red flags or the memory impairment persists beyond
30 days from the injury. She should be reassured that full recovery within
3 months is the expected outcome. Education to inform expectations has
been shown to positively affect clinical outcome. For more information,
refer to the article “Memory Impairment After Mild Traumatic Brain Injury.”
23. A 30-year-old soldier has two generalized tonic-clonic seizures occurring

on separate days, both more than 10 days after a moderately severe traumatic
brain injury from a combat blast injury. An MRI of the brain demonstrates
resolving bifrontal contusions, and an EEG demonstrates generalized
intermittent slow-wave activity but no epileptiform discharges. Carbamazepine
is started. The patient is seen by a neurologist 3 weeks later. He has had no
further seizures and takes carbamazepine 1000 mg/d with a therapeutic drug
level. The drug has been well tolerated. He scores 28/30 on mental status
testing and has an otherwise normal neurologic examination. Assuming the
patient is seizure free, at what point can consideration be given for tapering
the anticonvulsant?
208 A. immediately
B. 6 months
C. 1 year
D. 2 years
E. continue the anticonvulsant indefinitely
The correct answer is D. This patient by definition has posttraumatic epilepsy,

which has a remission rate of 25% to 60%. After moderate traumatic brain
injury, his risk of recurrent seizures is elevated for the next 10 years. However,
the general recommendation is that adult patients who remain seizure free for
2 years and have a normal neurologic examination and normal EEG may
attempt an anticonvulsant taper. For more information, refer to the article
“Epilepsy, Sleep Disturbances, and Psychiatric Consequences.”
24. A high school football player sustains a hard tackle and is slow in
getting up from the field. He arises independently after 30 seconds and is
noted by a physician’s assistant on the sidelines to be disoriented to the
current circumstances. No other focal findings are evident, and he reorients
in a few minutes. What is the best course of action regarding this athlete?
A. administer nonsteroidal anti-inflammatory drugs at the sidelines
B. bar the athlete from returning to the game
C. have the patient perform a sprint and reassess
D. observe for 10 minutes and allow the athlete to return to the game
E. send to an emergency department for a CT scan
The correct answer is B. The authors of the article “Sports Concussion”

remark that an athlete diagnosed during an event with a concussion should
be removed from the contest and treated basically with avoidance of
exertion or stimulation. Use of acetaminophen is suggested in the early
phase. For more information, refer to the article “Sports Concussion.”
25. A 30-year-old soldier develops headaches immediately after falling

during a training exercise and striking the back of his head. No loss of
consciousness occurs, and he resumes his duties the next day. Two weeks
later, he is seen at sick call still reporting headaches that start at the base of
the skull. These occur at least twice a week, last 3 to 6 hours, are throbbing
in quality, associated with nausea, and at times interfere with his work.
Neurologic examination and a CT scan of the brain are normal. Long-acting
valproic acid, 250 mg at bedtime, is started. Two weeks later, he still has
several headaches per week but reports no side effects of valproic acid.
What is the next best step in management?
A. change the medication to a long-acting opioid
B. change the medication to a tricyclic antidepressant
C. increase the valproic acid dose
D. obtain a cervical MRI scan
E. repeat the head CT scan
The correct answer is C. Per the article ”Posttraumatic Headache,”
posttraumatic headaches (PTHAs) may require prophylactic treatment,
similar to nontraumatic headaches, if they occur frequently (2 or more
times per week) or cause a major disruption in lifestyle. Valproic acid is
209
an appropriate choice for PTHAs with migraine features. Like any
prophylactic drug, it should be increased over time and should not be
abandoned without a titration until 6 weeks have elapsed, unless
intolerable side effects are present. For more information, refer to the
article “Posttraumatic Headache.”
26. Four months after a motor vehicle accident, a 42-year-old woman comes
to the physician for evaluation of memory impairment. She was the belted
driver of a pickup truck that slid off an icy road into a ditch. She struck her
head on the steering wheel but did not lose consciousness. She felt shaken
up but was able to get out of her vehicle immediately and call for help.
She recalls the accident vividly and had no other serious injury. Since that
time, she reports poor memory and inability to function at her job as a
nurse. She details for the physician all of the many mistakes she almost
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made at work and at home because of her poor memory. She has received
no complaints about her work performance, and her husband feels she is
too hard on herself. Her sleep is poor. She is not bothered by intrusive
memories of the accident. She reports diffuse muscle aches. She is tearful
during the history and examination. She scores 29/30 on mental status testing,
and the remainder of her examination is normal. Which of the following
disorders is most likely responsible for this patient’s cognitive symptoms?
A. depression
B. malingering
C. mild traumatic brain injury
D. obstructive sleep apnea
E. posttraumatic stress disorder
The correct answer is A. This patient most likely has somatic symptoms
related to depression. Her symptoms have a strong affective component.
The relatively trivial injury and long duration from the accident make
traumatic injury to the brain unlikely as an explanation for her ongoing
symptoms. She has no other symptoms to suggest posttraumatic stress
disorder or obstructive sleep apnea. Malingering is unlikely with the history
as given and her normal performance on cognitive testing. It is important to
diagnose and treat psychiatric disorders that may produce or aggravate
cognitive symptoms after head trauma. For more information, refer to the
article “Memory Impairment After Mild Traumatic Brain Injury.”
27. A 25-year-old woman is a passenger in a car that is hit at high speed

from behind while stopped at a traffic light. She receives a hyperextension
injury and is taken to a hospital. She is confused and combative. She is
admitted and eventually referred for inpatient rehabilitation because of
several fractures. She is treated with a sedative-hypnotic at night. Her
therapists note that she is slow to process and has difficulty following
directions, although she is motivated to be discharged home. Her head
CT on admission was normal. MRI is later performed, looking for a
delayed hematoma. Microhemorrhages are seen in the corpus callosum.
Which of the following is the most likely mechanism for this patient’s
210 cognitive impairment?
A. axonal shear injury
B. depression
C. medication effect
D. subclinical seizures
E. subdural hematoma
The correct answer is A. The patient had a clear acceleration/deceleration

injury, placing her at risk for axonal shearing in the white matter. This
may be seen on MRI in the form of microhemorrhages; however, her
scan does not otherwise demonstrate a focal lesion. Seizures are
unlikely, given both the lack of a penetrating or focal lesion. While
sedative-hypnotic medication may interfere with functioning, the patient
does not appear to have impaired consciousness or delirium. For more
information, refer to the article “Diagnosis and Management of Traumatic
Brain Injury.”
28. How much greater is the risk of developing mild cognitive impairment in
athletes who have sustained repeated (three or more) concussions compared
to those with no history of concussions?
A. no increased risk
B. threefold
C. fivefold
D. sevenfold
E. 10-fold
The correct answer is C. Guskiewicz and colleagues (2005) studied retired

professional football players and found a significant increase in risk (fivefold)
of developing mild cognitive impairment in those who had sustained three or
more concussions, and a threefold prevalence of reported significant memory
concerns. Those players who developed Alzheimer disease had an earlier
onset when compared with age-matched controls in the general population.
For more information, refer to the article “Memory Impairment After Mild
Traumatic Brain Injury.”
Guskiewicz K, McCrea M, Marshall S, et al. Cumulative effects associated with
recurrent concussion in collegiate football players: the NCAA concussion study.
JAMA 2005;290(19):2549–2555.
29. Which of the following concerns has historically been raised about
long-term effects of repeated concussions in athletes?
A. dementia pugilistica in boxers
B. higher incidence of normal pressure hydrocephalus in former athletes
C. higher prevalence of migraine in athletes
D. higher stroke rates in athletes
E. premature atrophy in brain scans of athletes
The correct answer is A. Historically, boxers have been the group most linked
with permanent changes in brain function, attributed to chronic head trauma.
More recently, concern has been raised in the United States about higher
incidences of cognitive impairment in retired professional football players,
and an entity called chronic traumatic encephalopathy has been described. 211
For more information, refer to the articles “Sports Concussion” and “Traumatic
Brain Injury Update.”
30. A 26-year-old man sustained a mild traumatic brain injury after detonation
of a roadside improvised explosive device in Afghanistan 2 months ago.
He has recovered from his injuries well but reports excessive daytime fatigue
and sleepiness and very poor nighttime sleep. He awakens frequently from
disturbing nightmares in which he sees his friend who was killed in the
explosion. He reports depressed mood and symptoms of anxiety. There is no
suicidal ideation. His general and neurologic examinations are normal.
In addition to treatment of his depression and anxiety, which of the following
medications would be most helpful in reducing the occurrence of his
disturbing nightmares?
A. diphenhydramine
B. modafinil
PREFERRED RESPONSES
C. prazosin
D. trazodone
E. zaleplon
The correct answer is C. This patient most likely has posttraumatic stress
disorder (PTSD), and this, in turn, contributes to his sleep disturbance.
Treating the associated anxiety and depression is appropriate. Prazosin, an
α-adrenergic blocking agent that penetrates the blood-brain barrier, is the
medication of choice to block nightmares and may help other symptoms of
PTSD as well. Of note, prazosin is not FDA approved for this indication but
has been reported to be of benefit. The other medications listed would not
be useful in this regard. For more information, refer to the article “Epilepsy,
Sleep Disturbances, and Psychiatric Consequences.”
31. A 55-year-old man comes to the physician for evaluation of dizziness

following a mild head injury sustained in a motor vehicle accident 1 week
ago. No loss of consciousness or serious injury occurred, but he struck his
head on the steering wheel and felt dazed for 1 to 2 minutes. Since that
time he has had moderate generalized headache and dizziness with spinning
that is worse when he bends over or turns to the left. With the Dix-Hallpike
maneuver, he develops vertigo and fatigable nystagmus when his head is
turned to the left and lowered. The remainder of the neurologic examination
is normal. Which of the following is the most appropriate next step in
management of this patient?
A. bed rest
B. canalith repositioning
C. meclizine therapy
D. MRI of the brain
E. posturography
The correct answer is B. This patient most likely has benign paroxysmal
positional vertigo, and canalith repositioning is the most appropriate therapy.
Additional testing is not required in this case. Meclizine sometimes can help
the symptoms of this disorder but does not provide definitive treatment. Bed
212 rest is of no use and actually could aggravate deconditioning, which may
follow head injury if patients are inactive. For more information, refer to the
article “Rehabilitation in the Patient With Mild Traumatic Brain Injury.”
32. Two weeks after sustaining a traumatic brain injury playing football,
a 30-year-old man experiences difficulty with memory that mildly affects his
day-to-day functioning. His wife, who accompanies him, notes that while he
can remember events subsequent to the injury (such as a family barbecue),
he forgets where they occurred or exactly when. This is an example of
impairment, commonly seen following traumatic brain injury, to which type
of memory?
A. immediate memory
B. memory retrieval
C. retrospective memory
D. source memory
E. working memory
The correct answer is D. This patient has difficulty with source memory.
Source memory is defined as the ability to accurately remember when and
where an event occurred. Persons with impairment of source memory usually
retain the ability to acquire new memories of events but may confuse the
temporal order or location ascribed to the event. For more information,
refer to the article “Memory Impairment After Mild Traumatic Brain Injury.”
33. Which of the following is considered the most important intervention in

mild traumatic brain injury?
A. anxiolytics
B. non-narcotic analgesics
C. physical therapy
D. psychotherapy
E. removal from activity
The correct answer is E. According to the authors of the article “Diagnosis

and Management of Traumatic Brain Injury,” mild traumatic brain injury may
go unrecognized. When it is diagnosed, symptomatic treatment may be
helpful, including physical therapy, nonsteroidal anti-inflammatory drug
analgesics, and reassurance. However, the authors stress that the first line
of treatment is cessation of the at-risk activity, whether it is play or work.
For more information, refer to the article “Diagnosis and Management of
Traumatic Brain Injury.”
34. A 35-year-old woman is seen in consultation 1 month after a motor vehicle

accident during which she suffered a cervical hyperextension injury. No head
trauma was reported. She had a prior history of bifrontal, mild, nondisabling,
squeezing-type headaches occurring usually toward the end of the day, 2 days
out of the week, that were rapidly relieved by ibuprofen. After the accident,
the headaches increased in frequency to 4 days per week but were otherwise
similar to her prior headaches. Neurologic examination and MRI of the brain
and cervical spine are normal. Which of the following is the most likely diagnosis?
A. acute posttraumatic headache
B. cervical radiculopathy
C. migraine headache 213
The correct answer is E. Per the authors of the article ”Posttraumatic

Headache,” headaches that exist prior to head or neck injury and modestly
increase in frequency after the injury are not classified as posttraumatic
headaches. This patient appeared to have tension-type headaches prior to her
accident, and, while these headaches may or may not have worsened as a
result of her whiplash, it is most correct to diagnose them as tension-type
headache. For more information, refer to the article “Posttraumatic Headache.”
35. Which of the following steps is recommended in all cases of

sports concussion?
A. avoidance of all analgesics
B. CT done the same day
PREFERRED RESPONSES
C. evaluation by a neurologist
D. fitting of hard cervical collar
E. several hours of close observation
The correct answer is E. Acute care after a concussion should include

assessment of airway, breathing, and circulation (ABCs) and for cervical
spine injury, although application of a hard collar is not required.
“Field-side” mental status examinations and brief physical examinations can
be performed by any trained medical personnel. CT is not required without
worsening level of consciousness or focality on examination. Analgesia may
not be required at all. After a concussion requiring cessation of the athlete’s
participation, he or she should be observed for the next 3 to 4 hours to
assess for any change in level of consciousness. For more information,
refer to the article “Sports Concussion.”
TYPE R EXTENDED MATCHING

Match each of the following clinical scenarios with the pathophysiologic
mechanism that best describes it.
A. contrecoup injury
B. coup injury
C. diffuse axonal injury
D. hyperacute metabolic phase: acute massive depolarization of neurons
with glutamate release
E. hypometabolic phase
36. A 64-year-old man trips and falls backward down four stairs, striking his
occiput on concrete. He is unconscious for 3 minutes and then appears
dazed with a flattened affect. He has a large subgaleal hematoma over his
occiput. A noncontrast CT head scan reveals bifrontal cerebral contusions.
The correct answer is A. This patient has sustained most of his brain injury
opposite to the side of the actual blow. Contrecoup-type injuries are
particularly common when a moving head strikes a stationary object. For
more information, refer to the article “Mild Traumatic Brain Injury Update.”
214
37. A 22-year-old soldier is injured in an improvised explosive devices blast.
He is unconscious at the scene with no visible injury. On arrival of
emergency vehicles, his Glasgow Coma Scale score is 7, and his pupils are
4 mm and sluggishly reactive. His examination is otherwise nonlocalizing.
A noncontrast CT shows diffuse cerebral edema.
The correct answer is C. This man most likely sustained a diffuse axonal
injury from shearing and stretching of axons caused by motion of brain
structures relative to the skull. This type of injury may result in severe
neuronal injury without visible contusions on CT and is particularly
common in blast-type injuries. For more information, refer to the article
38. A 16-year-old boy falls from his bicycle and strikes his head. He is not
wearing a helmet. Immediate loss of consciousness occurs followed by a
30-second generalized tonic-clonic seizure.
The correct answer is D. With concussive-type injuries, an immediate
massive depolarization of neurons associated with indiscriminate release of
glutamate occurs. This results in loss of consciousness and likely is
responsible for “impact” seizures. For more information, refer to the article
39. A 4-month-old infant is brought to the emergency department

unconscious. His mother states that she found him apneic in his crib and
that he had rolled off the bed earlier in the day, striking his head. His
examination reveals weak withdrawal to pain, weak cry, and brief eye
opening. He is diffusely hypotonic. The pupils are 4 mm and reactive.
Retinal hemorrhages are present bilaterally. No bruising of the head is
present. The anterior fontanelle is bulging. A CT of the brain reveals diffuse
cerebral edema.
The correct answer is C. This patient most likely suffers from shaken baby
syndrome, which produces diffuse axonal injury. Retinal hemorrhages are
particularly common. The history is immediately suspect as 4-month-old
infants do not yet possess the ability to roll over. For more information,
refer to the article “Mild Traumatic Brain Injury Update.”
40. A 22-year-old woman struck her forehead on the net post while playing
volleyball. She lost consciousness for 1 to 2 minutes and then felt dazed. At
the emergency department, her Glasgow Coma Scale score was 15, and she
had a normal neurologic examination. A noncontrast CT head was normal.
Now, 4 days later, she continues to note poor concentration and attention.
The correct answer is E. Following the acute hypermetabolic phase after

traumatic brain injury, a longer period of decreased cerebral metabolism
occurs, lasting 7 to 10 days, which may correlate with postconcussive
cognitive deficits. For more information, refer to the article “Mild Traumatic
Brain Injury Update.”
215
INDEX
for posttraumatic headache, 33, 59c, 60c
ANAM (Automated Neuropsychological Assessment
Metrics), 67t, 91t, 92
Angiotensin-converting enzyme inhibitors, for headache
Page numbers in boldface type indicate major
discussions. Letters after page numbers refer to the prophylaxis, 157
following: c = case study; f = figure; r = reference; Animal models of TBI, 26r, 52
t = table. Anticoagulation, 36
Antidepressants, tricyclic
for headache prophylaxis, 68f, 71, 157, 159
for sleep disturbances, 117, 158
Antiemetics, 68f
Antiepileptic drugs (AEDs)
A for headache prophylaxis, 68f, 71, 157
AAN (American Academy of Neurology), 18, 28, 36, 97, for seizures, 35, 113–114, 113c
153, 163 discontinuation of, 114
Acceleration/deceleration forces, 21, 30 prophylaxis, 35, 112–113, 158, 179
Acetaminophen, for headache, 35, 59c, 60c, 68f Anxiety/anxiety disorders, 32, 117–118
Acetaminophen/aspirin/caffeine, for headache, 69 in military personnel, 137
Acetaminophen/isometheptene/dichloralphenazone, for obsessive-compulsive disorder, 122, 123, 127r
headache, 69, 72c posttraumatic headache and, 66
N-Acetylaspartate (NAA), 19 posttraumatic stress disorder, 120 – 122
ACRM (American Congress of Rehabilitation Medicine), Aphasia, 168
18, 28, 37r, 153 Apnea, 30
Acupuncture, for headache, 73 Apolipoprotein E ε4 allele, 102, 109r, 143
AD (Alzheimer disease), 21, 25r, 102, 109r Art therapy, 22
Adenosine triphosphate (ATP), 19, 20f Assaults, 18, 138c
ADHD (attention-deficit hyperactivity disorder), 151, Assistive technology, 136
156, 157, 160r Ataxia, 49c
treatment of, 151, 158, 160r Athletes, concussion in, 19, 21, 27, 39r–40r, 41 – 52,
Adolescents. See also Pediatric traumatic brain injury 53r–54r. See also Sports concussion
sports concussion in, 21, 49c ATP (adenosine triphosphate), 19, 20f
patient management problem on, 150 – 159, Attention, memory and, 84–85, 85f
159r – 160r Attention-deficit hyperactivity disorder (ADHD), 151,
TBI rate in, 18, 27 156, 157, 160r
AEDs. See Antiepileptic drugs treatment of, 151, 158, 160r
Age Automated Neuropsychological Assessment Metrics
TBI rate by, 18, 27 (ANAM), 67t, 91t, 92
of TBI survivors, 28
Aggressive behavior, 123
Alcohol-related disorders, 117, 123
assessment tools for, 67t
B
posttraumatic headache and, 66 Barbiturate coma, 34
216 Alzheimer disease (AD), 21, 25r, 102, 109r Beck Depression Inventory, 67t
Amantadine, 167 Behavioral symptoms, 22
American Academy of Neurology (AAN), 18, 28, 36, 97, Behavioral therapy, 157
153, 163 for headache, 68f, 73
American Association of Neurological Surgeons, 33 Behaviorally induced insufficiency sleep syndrome, 116
American Congress of Rehabilitation Medicine (ACRM), Benign paroxysmal vertigo (BPPV), 133, 135
18, 28, 37r, 153 Benzodiazepines
American Neuropsychiatric Association, 122 impact on rehabilitation, 141
Amitriptyline, 68f, 71, 158–159 for insomnia, 117, 118c
Amnesia, posttraumatic (PTA), 17, 19–20, 32, 79–80, 80c, Beta-blockers, for headache prophylaxis, 68f, 71, 157
104r. See also Memory impairment Biofeedback, for headache, 68f, 73
anterograde or retrograde, 19, 28, 80, 80c Bipolar disorder, 117, 120
after concussion, 18, 28 Blast injuries, 24r, 26r, 29, 38r
return to play or work and, 53r, 80c cognitive assessment after, 92
duration of, 79, 80c long-term sequelae of, 99
severity of injury and, 20 in military personnel, 18, 21, 30c
period of, 80 posttraumatic amnesia after, 80c, 82c
Analgesic rebound headache, 58, 63, 76r, 77r, 155 posttraumatic epilepsy after, 111
Analgesics posttraumatic stress disorder and, 99
impact on rehabilitation, 141 pathophysiology of, 21, 31
posttraumatic headache and, 66 Cerebral vasospasm, 30c
treatment of, 72c Cerebrospinal fluid (CSF)
Blood pressure management, 33 hypocretin-1 levels in, 116, 125r
Blood-brain barrier disruption, 30 posttraumatic headache and, 66
Botulinum toxin injections, for headache, 68f, 73, 78r Cervical collar, 33
Boxers, 31, 50–51, 53r, 54r Cervicogenic headache, 62, 63, 66, 77r
BPPV (benign paroxysmal vertigo), 133, 135 treatment of, 68f
Brain Cholinesterase inhibitors, 99
edema of (See Cerebral edema) Chronic traumatic encephalopathy (CTE), 31, 38r,
herniation of, 34 50 – 51, 54r, 102, 109r, 144r
hyperosmotic saline for, 35 Circadian rhythm sleep disorders, 116 – 117, 126r
ischemic injury of, 30, 38r CISG (Concussion in Sport Group), 18
neural circuitry of memory, 83 – 88, 85f, 86f Cluster headache, 62
Brain Trauma Foundation, 33 CNS Vital Signs S7, 91t
Brief Visuospatial Memory Test-Revised (BVMT-R), 93t Coding table, 171–178
Butalbital/acetaminophen/caffeine, for headache, 69, 70 Cognitive impairment, 22
Butalbital/aspirin/caffeine, for headache, 69, 70 chronic cumulative effects of concussion, 50 – 51, 102,
BVMT-R (Brief Visuospatial Memory Test-Revised), 93t 154, 160r
chronic traumatic encephalopathy, 31, 38r, 50 – 51,
54r, 102, 109r, 144r
C correlation with neuroimaging findings, 94 – 97
CAGE questionnaire, 67t executive dysfunction, 88 – 91
Calcium channel blockers, for headache prophylaxis, management and outcomes of, 97–103, 100t, 104
71, 157 compensatory strategies, 101–102
California Verbal Learning Test-Second Edition (CVLT-II), key points, 102–103
93t, 105r in military personnel, 99–101
forced choice on, 94t for persistent postconcussive symptoms, 100
Caloric needs, 36 pharmacotherapy, 33, 98–99
Cantu guidelines, 36, 153, 159r memory impairment, 79 –104, 104r–109r
Carbamazepine, for neuralgiform headache pain, 68f, 71 neurocognitive assessment of, 22 – 23, 32, 79, 91– 94
Case studies pharmacotherapy for, targeting neurotransmitters, 99
blast injury, 30c posttraumatic headache and, 66
combat-related posttraumatic stress disorder, 137c recovery from, 135
memory impairment after TBI, 82c sleep disturbance and, 115
posttraumatic amnesia, 80c sports concussion and duration of, 40r, 160r
penetrating injury, 31c treatment of, 33
posttraumatic epilepsy, 113c Cognitive rehabilitation, 22, 26r, 135 –136, 145r
posttraumatic headache, 59c– 60c Cognitive Stability Index (CSI), 91t
treatment of, 69c, 72c Cognitive-behavioral therapy, 22
psychiatric disorders, 121c for headache, 73
recovery from TBI, 131c for insomnia, 117, 118c
sleep disturbance, 118c for posttraumatic stress disorder, 121
sports concussion, 43c Colorado Medical Society, 36, 153 217
return-to-play decisions after, 48c, 49c Coma, barbiturate, 34
Category Test, 93t Combat injuries. See Military service–related TBI
Causes of injury, 17–18, 27 Communication with families, 166 –170, 170r
CDC (Centers for Disease Control and Prevention), 18, 21, Compression stockings, 36
24r, 25r, 37r, 41, 153, 159r, 162 Computed tomography (CT), 23, 32, 38r, 94 – 96, 156
Centers for Disease Control and Prevention (CDC), 18, 21, guidelines for use of, 96
24r, 25r, 37r, 41, 153, 159r, 162 in posttraumatic epilepsy, 112
Central executive system, 89 for posttraumatic headache, 65 – 66
Central pontine myelinolysis, hypertonic saline – induced, after sports concussion, 45, 49
35 Concerta. See Methylphenidate
Central venous catheter, 35 Concussion, 17. See also Mild traumatic brain injury
Cerebral blood flow, 19, 22 in athletes, 19, 21, 27, 39r – 40r, 41– 52, 53r – 54r
Cerebral edema, 22 (See also Sports concussion)
avoiding hypo-osmotic feeds in patient with, 36 patient management problem on, 150 –159, 159r–160r
in children, 31– 32, 50, 53r chronic cumulative effects of, 50 – 51, 102, 154, 160r
hypertonic saline in management of, 35 complex, 153
in second-impact syndrome, 31– 32, 50 definition of, 18, 42, 153
timing of, 36 grading systems for, 28, 42, 153
Cerebral perfusion pressure (CPP), 34 – 35, 39r loss of consciousness and, 28, 42, 44
neurocognitive testing in, 22 – 23 Digit Span test, 93t

pathophysiology of, 19, 20f, 24r –25r Digit Symbol-Coding test, 93t
repeated, 21, 25r, 31– 32, 48, 48c, 49c, 82c, 139, 146r Diphenhydramine, for insomnia, 118c
return to play or work after, 22, 26r, 28, 33, 36, 46 – 49, Disability, Glasgow Outcome Scale and, 169, 170r
47t, 48c, 49c Disability after TBI, 28, 37r
signs and symptoms of, 44, 45t Disturbances of consciousness, 169
resolution of, 44 Dix-Hallpike maneuver, 133
simple, 153 Dizziness, 132 – 135, 143, 145r
terminology of mild TBI and, 18, 28, 153 causes of, 133t
treatment of, 22 therapy for, 135
types of brain damage from, 21– 22 Dizziness Handicap Inventory, 133, 134
Concussion in Sport Group (CISG), 18 Dopamine, 35
Concussion Symptom Inventory, 94, 107r Driving, 22
Confusion, posttraumatic, 18, 32 DSM-IV-TR (Diagnostic and Statistical Manual of
Congress of Neurological Surgeons, 33 Mental Disorders), 122, 123, 127r, 138c, 154, 159r
Continuous Performance Test (CPT), 93t DTI (diffusion tensor imaging), 49, 96, 147r
Contrecoup injuries, 21 DVBIC (Defense and Veterans Brain Injury Center), 18, 22,
Controlled Oral Word Association Test (COWAT), 93t 26r, 32, 91, 92, 99, 108r, 124r
Contusions of brain, 29 DWI (diffuse weighted imaging), 94, 107r
Cooling blankets, 35 Dynamic Visual Acuity test, 133, 134
Coup injuries, 21
COWAT (Controlled Oral Word Association Test), 93t
CPP (cerebral perfusion pressure), 34 – 35, 39r
CPT (Continuous Performance Test), 93t
E
CPT (Current Procedural Terminology) codes, 177 – 178 Early intervention after TBI, 22, 26r, 145r
Cranial neuralgias, 61, 62, 63 Economic cost of TBI, 27– 28, 37r
CSF (cerebrospinal fluid), posttraumatic headache and, 66 Educational interventions, 22, 131 – 132, 133t
CSI (Cognitive Stability Index), 91t EEG (electroencephalography), 112, 113c, 124r
CT. See Computed tomography Elavil. See Amitriptyline
CTE (chronic traumatic encephalopathy), 31, 38r, 50 – 51, Electroencephalography (EEG), 112, 113c, 124r
54r, 102, 109r, 144r Electronystagmography, 134
Current Procedural Terminology (CPT) codes, 177 – 178 Eletriptan, for migraine, 68f
CVLT-II (California Verbal Learning Test-Second Edition), Emotional symptoms, 22
93t, 105r Encephalopathy, 20, 21, 30
forced choice on, 94t chronic traumatic, 31, 48r, 50 – 51, 54r, 102, 109r, 144r
Endothelial changes, 30 – 31
Epidemiology
of posttraumatic epilepsy, 110 – 111, 124r
D of posttraumatic headache, 56 – 60
Deep brain stimulation, for epilepsy, 114 of sports concussion, 41
Deep vein thrombosis prevention, 36, 39r of TBI, 17–18, 24r, 27, 37r, 53r
Defense and Veterans Brain Injury Center (DVBIC), 18, 22, Epilepsy, posttraumatic (PTE), 110 – 114, 124r
218 26r, 32, 91, 92, 99, 108r, 124r definition of, 110
Delirium, 122 epidemiology of, 110 – 111
Dementia pugilistica, 31, 50–51 military, 111
Depression, 21, 22, 25r, 26r, 77r, 91, 117, 118 – 120, 121c, evaluation of, 112, 113c
123, 126r – 127r natural history of, 113 – 114
assessment tools for, 67t occurrence of, 111– 112
effect on recovery from TBI, 130 prophylaxis for, 35, 39r, 112 – 113, 158, 179
memory impairment and, 79, 81 risk factors for, 111, 112t
in military personnel, 119, 137 treatment of, 35, 113 – 114
monoamine deficiency hypothesis of, 119 – 120 websites for information about, 114
pathogenesis of, 119 – 120 Epworth Sleepiness Scale, 67t
posttraumatic headache and, 66 Ethical issues in management of sports concussion,
prevalence of, 66, 118 – 119 161 – 164, 164r
sleep disturbance and, 115, 116 Etiologies of injury, 29 – 31, 30c, 31c
treatment-resistant, in adolescents, 160r Excedrin. See Acetaminophen/aspirin/caffeine
Diagnostic and Statistical Manual of Mental Disorders Excessive daytime sleepiness, 115 – 116, 117, 138c, 155
(DSM-IV-TR), 122, 123, 127r, 138c, 154 Executive function, 106r – 109r
Diffuse axonal injury, 21– 22, 29, 30 central executive system, 89
Diffuse weighted imaging (DWI), 94, 107r fluid and crystallized cognitive processes, 90
Diffusion tensor imaging (DTI), 49, 96, 147r memory processing and, 88 – 91
neural correlates of, 89 classification of, 55 – 56, 57t – 58t
rehabilitation training for problems with, 102 clinical evaluation of, 64 – 67
Exercises, for vestibular deficits, 135t comorbidities, 66 – 67, 67t
history, 65
neuroimaging, 65 – 66
other diagnostic tests, 66
F physical examination, 65
Falls, 17, 27, 44 clinical features of, 61 – 63
Family education and communication, 166 – 170, 170r cranial neuralgias, 61, 62, 63
Fatigue, 115 – 116, 131c, 148r – 149r, 155 differential diagnosis of, 63 – 64, 64t
mental, 142 – 143, 148r red flags for potentially serious conditions, 64
Fever, management of, 35 – 36 due to whiplash injury, 56
FIM (Functional Independence Measure), 169 epidemiology of, 56 – 60
Finger-to-nose test, 133 in different countries, 58
Fioricet. See Butalbital/acetaminophen/caffeine impact on rehabilitation, 136
Fiorinal, Butalbital/aspirin/caffeine location of, 62
Fluid management, 34 – 35, 39r low CSF pressure, 66
fMRI (functional magnetic resonance imaging), 49, 96 – 97 migraine, 43, 43c, 56, 61, 62
Focal brain damage, 21 in military personnel, 58, 60, 136, 145r – 146r
Fukuda stepping test, 133 pathophysiology of, 60 – 61, 61f
Functional Independence Measure (FIM), 169 in pediatric patients, 56
Functional magnetic resonance imaging (fMRI), 49, 96 – 97 primary headache disorders and, 55, 58
Functional rehabilitation, 22 psychiatric disorders and, 60, 66, 67t
Functional return, 142 – 144, 142t after repeated concussion, 48c, 49c
severity of injury and, 56, 58, 60c
with sound and light sensitivity, 59c, 62, 69c
syndromes of, 55 – 56
G tension-type, 55, 62
time criteria for onset of, 56, 61
Gabapentin treatment of, 33, 59c, 60c, 67 – 73
for headache, 68f, 71, 72c abortive medications, 67 – 70, 69c
for headache prophylaxis, 157 algorithm for, 68f
Gait instability, 132, 145r injections and procedures, 73
exercises for, 135, 135t nonpharmacologic therapies, 71 – 73
tests for evaluation of, 134, 134t prevention medications, 70 – 71, 72c, 157
GCS. See Glasgow Coma Scale trigeminal autonomic cephalalgias, 62 – 63
Glasgow Coma Scale (GCS), 18 after whiplash injury, 56, 58
posttraumatic headache and, 58 HeadMinder Cognitive Stability Index (CSI), 91t
severity of injury and, 28 “Heads Up on Brain Injury” campaign, 162
Glasgow Outcome Scale, 169, 170r Health Insurance Portability and Accountability Act
Glucose metabolism, 19, 24r – 25r (HIPAA), 163
Glutamate release, 19, 20f, 24r Helmet use, 29
Green’s Word Memory Test, 94t Hematoma 219
Guidelines delayed, 30
for return to play or work, 36, 39r, 42, 153, 159r headache due to, 56
for TBI management, 33, 38r – 39r, 179 subdural, 22
“Guidelines for Management of Severe Traumatic Brain Hemicrania continua, 63
Injury,” 33 Hemicraniectomy, 34
“Guidelines for the Field Management of Combat-Related Hemorrhagic lesions, 22, 23
Head Trauma,” 33, 39r Heparin, 36
Heterotopic ossification, 144, 149r
HIPAA (Health Insurance Portability and Accountability
Act), 163
Hippocampus, role in memory, 86 – 87
H Hopkins Verbal Learning Test-Revised (HVLT-R), 93t
Headache, posttraumatic (PTHA), 22, 26r, 32, 55 – 73, HVLT-R (Hopkins Verbal Learning Test-Revised), 93t
73r – 78r, 131c Hyperchloremia, 35
acute, 56, 57t, 59c – 60c Hyperosmolar IV solutions, 34
cervicogenic, 62, 63, 66 Hyperosmotic saline, 35
chronic, 56, 57t – 58t Hypersomnia, 115, 116, 117, 129
medication-overuse headache, 58, 63, 155 Hypertonic saline, 34 – 35, 39r
risk factors for, 60 Hyperventilation, induced, 34
Hypnotics, for insomnia, 117

Hypocretin-1, 116, 125r
L
Hypoperfusion injury, 30 Lamotrigine
Hypothermia, induced, 34, 39r for headache prophylaxis, 157
Hypoxia, 29, 30 for neuralgiform headache pain, 71
avoidance of, 35 Learning disorders, 157
Levels of consciousness, 169
Light sensitivity, 22, 59c, 62
LOC. See Loss of consciousness
I Loss of consciousness (LOC), 17, 19
Ibuprofen, for headache, 59c, 68f, 69c, 72c, 150 Alzheimer disease risk and, 102
ICD (International Statistical Classification of Diseases), in mild TBI/concussion, 18, 28, 42, 44, 79, 80c
20, 21t, 25r, 119, 154 severity of TBI and, 19
codes for TBI, 171 – 177 Lumbar puncture, for posttraumatic headache, 66
ICHD-2 (International Classification of Headache
Disorders), 55, 73r
ICP. See Intracranial pressure
IEDs (improvised explosive devices). See Blast injuries M
Immediate Post-Concussion Assessment and Cognitive MACE (Military Acute Concussion Evaluation), 32, 38r, 80c,
Testing (ImPACT), 91t, 92 82c, 91, 91t
Improvised explosive devices (IEDs). See Blast injuries MAE (Military Acute Concussion Evaluation), 32, 38r,
Impulsivity, 22 80c, 82c
Incidence of TBI, 17, 27, 37r, 79 Magnetic resonance imaging (MRI), 23, 32, 94, 147r, 156
Incoordination, 132 – 133 of blast injury, 30c
Individualized education plan, 157 functional, 49, 96 – 97
Indomethacin, for headache, 68f in posttraumatic epilepsy, 113c
Infants, TBI rate in, 18 for posttraumatic headache, 66
Informational materials for patients, 22, 132 sensitivity of different sequences for, 94
Insomnia, 115 – 116, 125r, 126r, 129, 155, 158 after sports concussion, 49
International Classification of Headache Disorders of subarachnoid hemorrhage, 59f
(ICHD-2), 55, 73r Magnetic resonance spectroscopy (MRS), 19, 25r, 49
International Classification of Sleep Disorders, 115, 125r Malingering
International Statistical Classification of Diseases (ICD), categories of, 93 – 94
20, 21t, 25r, 119, 154 cognitive assessment for detection of, 93 – 94, 94t, 95c
codes for TBI, 171 – 177 Mania, 117, 120, 123
Intracranial pressure (ICP) Mannitol, 34
cerebral perfusion pressure and, 34 MAP (mean arterial pressure), 34
elevation of, 20, 22, 34 Massage therapy, for headache, 73
ideal, 34 Mean arterial pressure (MAP), 34
lowering of Mechanisms of injury, 29
barbiturate coma, 34 Medical Symptom Validity Test (MSVT), 94t
hyperosmotic saline, 35 Medication-overuse headache (MOH), 58, 63, 76r, 77r, 155
220 hypertonic saline, 34 – 35 treatment of, 68f
induced hyperventilation for, 34 Melatonin, for circadian rhythm sleep disorders, 117
surgical decompression or hemicraniectomy, 34 Memantine, for migraine prophylaxis, 68f, 77r
monitoring of, 29, 34, 36 Memory
Intubation, 33 attention and, 84 – 85, 85f
Irritability, 22 cognitive assessment of, 91 – 94, 91t, 93t
Ischemia, 30, 38r for detection of malingering, 93 – 94, 94t, 95c
Isotonic fluids, 34 episodic, 83, 87
explicit, 83 – 86, 84t, 85f, 86f
functional neuroanatomy of, 83 – 88, 85f, 86f
J implicit, 83 – 84, 84t
long-term, 83
JFK Coma Recovery Scale, 168, 180 remote, 87 – 88
semantic, 83, 87
short-term, 83
working, 83, 88 – 90, 106r
K verbal, 90
Ketorolac, 69c visuospatial, 90
Memory impairment, 22, 79 – 104, 104r – 109r. See also terminology of concussion and, 18, 28, 153
Amnesia, posttraumatic treatment of, 22, 32 – 33
comorbidities and misattribution to TBI, 79, 81, 81f, cost of, 28
82c types of brain damage in, 21– 22
executive dysfunction and, 88 – 91 Military Acute Concussion Evaluation (MACE), 32, 38r,
management and outcomes of, 97 – 103, 100t, 104 80c, 82c, 91, 91t
compensatory strategies, 101 – 102 Military service–related TBI, 26r, 79, 104r, 146r
key points, 102 – 103 adaptation to civilian life after, 139
in military personnel, 99 – 101 blast injuries, 18, 21, 30c, 92
for persistent postconcussive symptoms, 100 posttraumatic amnesia after, 80c, 82c
neuroimaging-cognitive correlation, 94 – 97 compared with civilian TBI, 136 – 137
persistent symptoms of, 81 factors affecting recovery from, 21, 136 – 141
posttraumatic amnesia, 17, 19 – 20, 32, 79 – 80, 80c guidelines for field management of, 33, 39r
source amnesia, 87 malingering and, 95c
Mental fatigue, 142 – 143, 148r management and outcomes of cognitive symptoms of,
Mental status alterations, 18, 28 99 – 101, 107r
concussion grade and, 28 memory impairment after, 82c
Mental status examination, 32 penetrating injuries, 31c
after sports concussion, 45 postdeployment cognitive assessment of, 92 – 93
Meperidine, 35 posttraumatic epilepsy and, 111
Metabolic cascade of TBI, 19, 20f, 24r – 25r, 144r posttraumatic headache and, 58, 60, 75r, 136, 140,
Methylphenidate, 99, 121c, 151, 158 – 159 145r – 146r
Metoclopramide, 68f treatment of, 72c
MicroCog, 91t posttraumatic sleep disorders and, 118c
Microvascular injuries, 22, 29, 30, 31 psychiatric disorders and, 139 – 140
Midrin. See Acetaminophen/isometheptene/ depression, 119
dichloralphenazone posttraumatic stress disorder, 99, 122, 137 – 140,
Migraine, 43, 43c, 55, 56, 61, 62, 75r – 76r, 142 137c, 146r
symptoms of, 155 repeated injuries, 139
treatment of, 68 – 69, 68f, 69c, 160r return to duty after, 22
Migraine Disability Assessment Questionnaire, 76r sleep disturbances and, 140 – 141
Mild traumatic brain injury (mTBI), 17 – 24, 24r – 26r. Minimally responsive state, 37r, 167 – 168
See also Concussion Minnesota Multiphasic Personality Inventory, Second
definition of, 18 – 19, 24r, 28, 37r, 153, 159r Edition (MMPI-2), 93t
diagnosis of, 18, 19, 32–33 Mirtazapine, for headache, 68f, 71
duration of posttraumatic amnesia after, 18, 28 MMPI-2 (Minnesota Multiphasic Personality Inventory,
executive dysfunction after, 88 – 91 Second Edition), 93t
Glasgow Coma Scale score in, 18, 28 MoCA (Montreal Cognitive Assessment), 131c, 138c
headache after, 58, 61 Modafinil, for excessive daytime sleepiness, 117, 126r
incidence of, 17, 27, 79 Moderate traumatic brain injury
level of severity of, 28 Glasgow Coma Scale score in, 28
long-term consequences of, 19 headache after, 58
loss of consciousness and, 18, 28, 42, 44, 79, 80c postconcussive syndrome after, 28 221
memory impairment after, 79 – 104, 104r – 109r treatment of, 33
in military personnel, 79 MOH (medication-overuse headache), 58, 63, 76r, 77r,
monitoring patient after, 32 155
mortality from, 17, 27 treatment of, 68f, 70
neurocognitive assessment of, 22 – 23, 32, 67t, 79, Monoamine deficiency hypothesis of depression, 119 – 120
91 – 94, 91t, 93t Montreal Cognitive Assessment (MoCA), 131c, 138c
for detection of malingering, 93 – 94, 94t, 95c Mortality from TBI, 17, 27
neuroimaging in, 18, 23, 32 second-impact syndrome, 31, 50
pathophysiology of, 19, 20f, 24r – 25r Motor sensitivity
recovery from, 17, 19 exercises for, 135, 135t
rehabilitation in, 22, 28, 128 – 144, 144r – 149r tests for evaluation of, 134t
repeated, 21, 25r, 31 – 32, 48, 48c, 49c, 82c, 139, Motor vehicle/traffic accidents, 18, 27, 30, 44
146r MRI. See Magnetic resonance imaging
seizures after, 110 – 114 MRS (magnetic resonance spectroscopy), 19, 25r, 49
sleep disturbances after, 114 – 117, 115t MST (Medical Symptom Validity Test), 94t
symptoms of, 19 – 21 mTBI. See Mild traumatic brain injury
postconcussive, 32 Multiple sleep latency test, 115
N Nutrition, 36
Nystagmus, 133
NAA (N-acetylaspartate), 19
NAB (Neuropsychological Assessment Battery), 95c
Naproxen, for headache, 68f
Narcolepsy, 116, 117, 155 O
Nasogastric tube, 36 Obsessive-compulsive disorder (OCD), 122, 123, 127r
National Comorbidity Survey Replication (NCS-R), 117, Obstructive sleep apnea, 116, 117
118, 122, 126r Occipital nerve blocks, 68f, 73, 77r
National Federation of State High School Associations, Occipital nerves, 60
163, 164r Occipital neuralgia, 61, 63
National Football League (NFL), 161–162 treatment of, 68f, 71, 77r–78r
NCS-R (National Comorbidity Survey Replication), 117, Occupational therapy, 22, 136
118, 122, 126r OCD (obsessive-compulsive disorder), 122, 123, 127r
Neck collar, 33 OIF/OEF (Operation Iraqi Freedom/Operation Enduring
Nefazodone, for headache prophylaxis, 157 Freedom), 139. See also Military service–related TBI
Neural circuitry of memory, 83 – 88, 85f, 86f Older adults, TBI rate in, 18, 27
Neurobehavioral Symptom Inventory, 67t Operation Iraqi Freedom/Operation Enduring Freedom
Neurocognitive assessment, 22 – 23, 32, 79, 91 – 94 (OIF/OEF), 139. See also Military service–related TBI
in acute phase after mild TBI, 79 Opioid analgesics
collateral information for, 23 impact on rehabilitation, 141
for detection of malingering, 93 – 94, 94t, 95c for posttraumatic headache, 70
determination of premorbid level of functioning, 22 – 23 Orogastric tube, 36
functional domains for, 23 Osteopathic manipulation therapy, for headache, 73
postdeployment, of military personnel, 92 – 93 Outcomes of TBI, 37r
tests for, 67t, 91– 92, 91t Oxygen saturation, 33
computer-based, 23 Oxygen therapy, 35
selection of, 23
Neuroimaging, 23, 32, 38r, 107r – 108r, 147r. See also
specific imaging modalities
correlation with neurocognitive symptoms, 94 – 97 P
functional, 96 – 97 Paced Auditory Serial Addition Test (PASAT), 93t
guidelines for use of, 96 PAI (Personality Assessment Inventory), 93t
indications for, 32, 33 Pain, chronic, 22, 26r, 129, 147r
in mild TBI, 18, 23, 32 impact on rehabilitation, 141–142
newer techniques for, 96 – 97 posttraumatic headache, 55 – 73, 57t – 58t
in posttraumatic epilepsy, 112, 113c prevalence of, 129
for posttraumatic headache, 65 – 66 sleep disturbances and, 140 – 141
in severe TBI, 28 – 29 Paresthesias, 43c
of sports concussion, 45, 49 – 50, 156, 160r Parkinson disease, 102
Neurologic examination, 23, 36, 151, 156 Paroxysmal hemicrania, 63
Neurologic injury, 20, 29 PASAT (Paced Auditory Serial Addition Test), 93t
222 focal, 29, 30 Pathophysiology, of concussion, 19, 20f, 24r–25r
Neurologic “soft signs,” 23 Patient education, 22, 131–132, 133t
Neurologist's role in TBI treatment, 128 – 129 Patient Health Questionnaire-9 item depression scale,
Neurometabolic cascade of TBI, 19, 20f, 24r – 25r, 144r 67t, 119
“Neuronal suicide,” 29 Patient management problem: adolescent sports
Neuropsychological assessment, 67t, 93, 93t, 157 concussion, 150 – 159, 159r–160r
Neuropsychological Assessment Battery (NAB), 95c PCS. See Postconcussion syndrome
Neuropsychological Impairment Scale (NIS), 93t Pediatric traumatic brain injury, 53r, 54r
Neuropsychological Symptom Inventory (NSI), 93t age distribution of, 18, 27
Neurosurgical decompression, 34 animal models of, 52
NFL (National Football League), 161 – 162 cerebral edema due to, 31– 32, 50, 53r
NIS (Neuropsychological Impairment Scale), 93t individualized education plan for children with, 157
Nonsteroidal anti-inflammatory drugs (NSAIDs), for nonaccidental, 27
headache, 33, 59c, 60c, 67 – 68, 68f, 131c postconcussive symptoms and, 153 – 155, 159r
Norepinephrine, 35 posttraumatic headache and, 56
Normal saline, 34, 35 second-impact syndrome and, 31, 50
Nortriptyline, for headache prophylaxis, 68f, 71 sports concussion, 51 – 52
NSAIDs (nonsteroidal anti-inflammatory drugs), for sports-related, 21
headache, 33, 59c, 60c, 67 – 68, 68f, 131c Penetrating injuries, 29, 31c
NSI (Neuropsychological Symptom Inventory), 93t Periodic limb movements of sleep, 116, 117
Personal protective equipment, 29 for return to play or work, 36, 39r, 42, 153, 159r
Personality Assessment Inventory (PAI), 93t for TBI management, 33, 38r – 39r, 179
Personality changes, 122 – 123 Practice issues: improving communication with families,
PET (positron emission tomography), 19, 49, 96 – 97, 156 166 – 170, 170r
Pharmacotherapy, 22, 37r. See also specific drugs Prazosin, for nightmares in PTSD, 138c, 141, 148r
and classes Prednisone, for headache, 68f, 70, 72c
for attention deficit hyperactivity disorder, 151, 158 Pregabalin, for headache prophylaxis, 71
for cognitive impairment, 33, 98 – 99, 108r “Prehospital Guidelines for Management of Severe
for fever, 36 Traumatic Brain Injury,” 33
for headache, 33, 59c, 60c, 67 – 71, 68f, 69c, 72c, 157 Prehospital management of TBI, 33, 39r, 44 – 45
impact on rehabilitation, 141 Primary injury phase, 29
to maintain cerebral perfusion pressure, 35 Prochlorperazine, 68f
prazosin for nightmares in PTSD, 138c, 141, 148r Prognosis, 130 – 131, 130t, 144r
for seizures, 35, 112 – 114 Promethazine, 68f, 69c
for sleep disturbances, 117, 118c, 158 Propranolol, for migraine prophylaxis, 68f, 71, 157
Phenylephrine, 35 Psychiatric disorders, 77r, 117–123, 119t, 121c,
Phenytoin, prophylaxis for seizures, 35, 39r 126r – 127r
Phonophobia, 22, 59c, 62 alcohol use disorders, 117
Photosensitivity, 22, 59c, 62, 142 alcohol-related disorders, 123
Physical examination, 23 anxiety disorders, 32, 117–118
for posttraumatic headache, 65 behavioral therapy and pharmacotherapy for, 157
after sports concussion, 45 combat TBI and, 1
Physical therapy, 22 depression, 117, 118 – 120
for headache, 73 effect on recovery from TBI, 130
Pittsburgh Sleep Quality Index, 67t mania, 117, 120
Polysomnography, 67t, 115, 125r, 155, 156 memory impairment and, 79, 81
Positron emission tomography (PET), 19, 49, 96 – 97, 156 obsessive-compulsive disorder, 122
Postconcussion syndrome (PCS), 17, 32, 130, 159r – 160r personality changes, 122 – 123
duration of, 154 posttraumatic headache and, 60, 66, 67t
in ICD-10, 20, 21t, 154 posttraumatic stress disorder, 120 – 122
incidence of, 154 combat-related, 99, 122, 137–141, 137c
after moderate TBI, 28 psychosis, 122
in pediatric patients, 154, 159r suicide, 120
recovery from, 154 Psychosis, 122, 123, 127r
symptoms of, 154 PTA. See Amnesia, posttraumatic
Postconcussive symptoms, 32, 129t PTE. See Epilepsy, posttraumatic
assessment tools for, 67t PTHA. See Headache, posttraumatic
headache, 22, 26r, 32, 55 – 73, 73r – 78r PTSD. See Posttraumatic stress disorder
management of persistent cognitive symptoms, 99 – 100 PTSD Checklist, 67t
rehabilitation for, 129 Pulmonary artery catheter, 35
return-to-play decisions and, 155 Pupil size and reactivity, 20, 34
severity of injury and, 154, 155
simple vs complex concussion and, 153 223
Postcraniotomy headache, 56
Posttraumatic stress disorder (PTSD), 105r, 108r – 109r, Q
120 – 122, 123, 127r, 146r Quetiapine, 121c
assessment tools for, 67t for migraine prophylaxis, 68f, 71, 77r
effect on recovery from TBI, 130, 137–141
malingering and, 95c
memory impairment and, 79, 81 – 83, 82c
military service–related, 99, 122, 137–141, 137c R
overlap of symptoms with features of TBI, 138f Rancho Los Amigos Cognitive Levels of Function Scale,
posttraumatic headache and, 66 169, 181–183
prevalence of, 66, 120 –122 RBANS (Repeatable Battery for the Assessment of
sleep disturbances and, 115, 140 Neuropsychological Status), 91, 91t
prazosin for nightmares, 138c, 141, 148r effort index, 94t
symptoms of, 154 Recovery from TBI, 130 –131, 130t
Postural instability, 135t, 142, 143. See also Vestibular Recreational therapy, 22
deficits Rehabilitation, 22, 28, 128 –144, 144r–149r
Posturography, 134, 134t education as focus of, 22, 131–132, 133t
Potassium ions, 19, 20f, 24r factors affecting recovery, 136 –142
Practice guidelines in civilian population, 138c
in military personnel, 137–141, 137c prophylaxis for, 35, 39r, 112 –113, 158, 179
pain, 140–142 risk factors for, 111, 112t
posttraumatic headache, 136 treatment of, 35, 113 –114
posttraumatic stress disorder, 137–141.138f, 137c websites for information about, 114
sleep disturbances, 140–141, 140t Selective serotonin reuptake inhibitors, 33, 160r
functional return/vocational rehabilitation, 142 –144, Sensory pathways, 85, 85f
142t Severe traumatic brain injury, 28–29
improving communication with families during, acute management of, 29
166 – 170, 170r Glasgow Coma Scale score in, 28
neurologic deficit–specific, 132 –136 guidelines for management of, 33
cognitive deficits, 135 –136 headache after, 58
vestibular deficits, 22, 132 –135, 133t –135t treatment of, 33 – 36, 38r
neurologist's role in, 128 –129 cost of, 28
patient referral for, 131 Severity of injury, 17, 28 – 29
prognosis and, 130 –131, 130t duration of posttraumatic amnesia and, 20
social reintegration, 144 Glasgow Coma Scale score and, 28
team approach to, 129 loss of consciousness and, 19
Reimbursement, coding table for, 171–178 postconcussive symptoms and, 154, 155
Relaxation training, 22 posttraumatic headache and, 56, 58, 60c
for headache, 73 SF-36 (36-Item Short Form Health Survey), 116
Repeatable Battery for the Assessment of Shearing injuries, 22, 30
Neuropsychological Status (RBANS), 91, 91t Shivering, 35
effort index, 94t Short-lasting, unilateral, neuralgiform headache attacks
Repeated head trauma, 21, 25r, 31 – 32, 48, 48c, 49c, 82c, with conjunctival injection and tearing (SUNCT), 63
139, 146r Single photon emission computed tomography
Responsive neurostimulation (RNS), for epilepsy, 114 (SPECT), 96
Return to play or work, 22, 26r, 28, 33, 36 SIS (second-impact syndrome), 31 – 32, 50, 53r
of athlete, 22, 36, 40r, 42, 44, 46 – 49, 47t, 48c, 49c, 159r “Sleep attacks,” 155
ethical issues related to, 160 –164 Sleep disturbances, 22, 26r, 32, 48c, 114 – 117, 115t,
patient management problem on, 150 –159 125r – 126r, 138c, 147r – 148r
baseline data and, 51 assessment tools for, 67t
guidelines for, 36, 39r, 42, 153, 159r chronic pain and, 140 – 141
postconcussive symptoms and, 155 depression and, 115, 116
posttraumatic amnesia and, 80c in military personnel, 140 – 141
second-impact syndrome and, 31–32, 50 narcolepsy, 116, 117, 155
vocational rehabilitation for, 142 –144, 142t posttraumatic headache and, 66
Rey-Osterreith Complex Figure (ROCF), 93t posttraumatic stress disorder and, 115, 140
Risperidone, 121c prazosin treatment of nightmares in, 138c, 141, 148r
Rizatriptan, for migraine, 68f prevalence of, 114, 115, 129
RNS (responsive neurostimulation), for epilepsy, 114 treatment of, 116 –117, 118c, 158
ROCF (Rey-Osterreith Complex Figure), 93t Sleep hygiene, 117, 138c, 140 –141, 140t
Rotary chair testing, 134 Social reintegration, 144, 148r
224 Sodium, serum level, 35
Sound sensitivity, 22, 59c, 62
Source amnesia, 87
S Spatial disorientation, tests for evaluation of, 134t
SAC (Standardized Assessment of Concussion), 32, 91, 91t SPECT (single photon emission computed
SCAT (Sports Concussion Assessment Tool), 46, 91t, 92 tomography), 96
SDMT (Symbol Digit Modalities Test), 93t Speech therapy, 22, 136, 168
Secondary injury phase, 29 Sports concussion, 19, 21, 27, 39r – 40r, 41 – 52, 43c,
Second-impact syndrome (SIS), 31 – 32, 50, 53r 53r – 54r
Seizures, posttraumatic, 20, 110 – 114, 124r acute assessment and management of, 26r, 44 – 46
early, 110 baseline testing and, 51
effect on TBI outcome, 110 chronic cumulative effects of, 50 – 51, 102, 154, 160r
epidemiology of, 110 –111 classification of, 42
military, 111 definition of, 18, 42
evaluation of, 112, 113c differences in athletes and general population, 42 – 44
hypertonic saline– induced, 35 duration of cognitive impairment after, 40r, 160r
immediate, 110 grading system for, 28, 42
late, 110 guidelines for management of, 37r, 39r, 179
natural history of, 113 –114 heightened awareness of, 41, 43f, 161–162
occurrence of, 111–112 incidence of, 41
management of, 24r, 25r animal models of, 26r, 52
monitoring athlete after, 45 causes of, 17– 18, 27
neuroimaging of, 45, 49 – 50 economic cost of, 27–28
patient management problem on, 150 – 159, 159r – 160r epidemiology of, 17–18, 27
in pediatric patients, 51 – 52 etiologies of, 29 – 31, 30c, 31c
personal protective equipment for mitigation of, 29 improving communication with families about,
recurrent, 21, 25r, 31, 48, 48c, 49c, 154 166 – 170, 170r
return-to-play decisions after, 22, 36, 40r, 42, 44, 46 – 49 incidence of, 17, 21, 27
ethical issues in, 161 – 164, 164r long-term consequences of, 19, 27
graduated reintroduction of physical activity, 47, 47t mechanisms of, 29
repeated concussions and, 48, 48c, 49c memory impairment after, 79 – 104, 104r – 109r
second-impact syndrome and, 31– 32, 50 mild, 17 – 24, 24r – 26r
signs and symptoms of, 44, 45t in military personnel, 18, 21
athlete’s hiding or minimization of, 44 mortality from, 17
management of, 46 primary injury phase of, 29
worsening in hours after injury, 45 prognosis for, 130 – 131, 130t
state legislation specific to, 41, 42t, 162 rehabilitation in, 22, 28, 128 –144, 144r – 149r
trends in management of, 42 repeated, 21, 25r, 31 – 32, 48, 48c, 49c, 82c, 139, 146r
Sports Concussion Assessment Tool (SCAT), 46, 91t, 92 secondary injury phase of, 29
Standardized Assessment of Concussion (SAC), 32, 91, 91t seizures after, 110 – 114
Stimulants, 99, 121c severity of, 17, 19, 28 – 29
for ADHD, 151, 158 sleep disturbances after, 114 – 117, 115t
Stress ulcer prophylaxis, 36 sports-related, 19, 21, 41 – 52, 53r – 54r (See also Sports
Stroop Color and Word Test, 93t, 106r concussion)
“Struck by/against” injuries, 18, 21, 29 symptomatology of, 19 – 21
Subarachnoid hemorrhage, 59c, 59f treatment of, 22
Subdural hematoma, 22 types of brain damage from, 21–22
Substance abuse coup and contrecoup injuries, 21
assessment tools for, 67t diffuse axonal injury, 21–22, 30
posttraumatic headache and, 66 focal injuries, 21, 30
Suicide, 120, 127r microvascular injuries, 22, 29, 30
Sumatriptan, for migraine, 68f, 69c shearing injuries, 22, 30
SUNCT (short-lasting, unilateral, neuralgiform headache Trazodone, for insomnia, 118c
attacks with conjunctival injection and tearing), 63 Treatment of TBI, 22, 29, 32 – 36, 37r – 40r
“Surgical Management of Traumatic Brain Injury,” 33 cost of, 27–28
Swan-Ganz catheter, 35 early intervention after TBI, 22, 26r, 145r
Symbol Digit Modalities Test (SDMT), 93t education as focus of, 22, 131–132, 133t
Symptoms of TBI, 19 – 21 practice guidelines for, 33, 38r – 39r, 179
concussion, 44, 45t rehabilitation, 22, 28, 128 – 144, 144r – 149r
resolution of, 44 Triazolam, for insomnia, 117
postconcussive symptoms, 32 Tricyclic antidepressants, for headache prophylaxis, 68f, 71
Trigeminal autonomic cephalalgias (TACs), 62 – 63
Trigeminal nerve, 60 225
Trigeminal neuralgia, 61
treatment of, 71
T Trigeminocervical complex, 60
TACs (trigeminal autonomic cephalalgias), 62 – 63 Triptans, for migraine, 68 – 69, 68f, 69c
TBI. See Traumatic brain injury
Temazepam, for insomnia, 117, 118c
Tension-type headache, 55, 62, 77r, 131c, 138c
treatment of, 68f
Test of Memory Malingering (TOMM), 94t U
36-Item Short Form Health Survey (SF-36), 116 Urine toxicology screen, 156
Thrombophlebitis, hypertonic saline–induced, 35
Tizanidine, for headache, 68f, 71
TOMM (Test of Memory Malingering), 94t
Topiramate
for headache prophylaxis, 157
V
for migraine prophylaxis, 68f, 71 Valproate, 121c
Trail Making Tests A and B, 93t for headache prophylaxis, 157
Traumatic brain injury (TBI) for migraine prophylaxis, 68f, 71
age distribution of, 18, 27 for seizure prophylaxis, 35, 39r
Vecuronium, 36
Vegetative state, 37r, 169, 170r
W
Venous thromboembolism prevention, 36, 39r WCST (Wisconsin Card Sorting Test), 93t
Vertigo, 132 – 135 Wechsler Adult Intelligence Scale, 93t
tests for evaluation of, 134t Wechsler Memory Scale-III, 93t
Vestibular deficits, 132 – 135, 145r Wernicke aphasia, 168
causes of dizziness, 133t Whiplash headache, 56, 58, 74r –75r
Vestibular rehabilitation, 22, 134 – 135, 135t, 142, 148r WHO (World Health Organization), 18, 130, 132
Vestibular testing, 133 – 134, 134t Wisconsin Card Sorting Test (WCST), 93t
ear, nose, and throat evaluation for, 156 Work, return to, 28, 36, 131c, 142 – 144, 142t
Veterans Administration/Department of Defense World Health Organization (WHO), 18, 130, 132
Clinical Practice Guideline for Management of
Concussion/mTBI, 94, 97 – 98
Victoria Symptom Validity Test (VSVT), 94t Z
Video/electronystagmography, 134 Zaleplon, for insomnia, 117
Visual deficits, 43c, 143 – 144 Zolmitriptan, for headache, 72c
Vocational rehabilitation, 142 – 144, 142t Zolpidem, for insomnia, 117, 118c
VSVT (Victoria Symptom Validity Test), 94t Zurich Consensus Guidelines, 36, 40r, 53r, 153, 159r
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Traumatic Brain Injury

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L I F E L O N G L E A R N I N G I N N E U R O L O G Y®

TRAUMATIC BRAIN INJURY

JACK W. TSAO, MD, DPhil, FAAN, Guest Editor

GARY M. ABRAMS, MD, FAAN

ANTHONY G. ALESSI, MD, MMM, FAAN

JAY C. ERICKSON, MD, PhD

FREDERICK G. FLYNN, DO, FAAN

JEFFREY S. KUTCHER, MD, MPH

GEOFFREY S. F. LING, MD, PhD, FAAN

KAREN LYNN PARKO, MD, FAAN

RONALD G. RIECHERS II, MD

JAY H. ROSENBERG, MD, FAAN

MICHAEL B. RUSSO, MD, FAAN

JULIE E. HAMMACK, MD, FAAN

EDITOR FOUNDING PROGRAM DIRECTOR

ASSOCIATE EDITOR OF PRACTICE AMERICAN ACADEMY OF NEUROLOGY

MISSION AND SCOPE

STATEMENT ON PEER REVIEW PROCESS

INFORMED CONSENT/ETHICS OF EXPERIMENTATION

POTENTIAL CONFLICT OF INTEREST DISCLOSURE

Copyright # 2010, American Academy of Neurology. All rights reserved.

Continuum Lifelong Learning Neurol 2010;16(6)

EPIDEMIOLOGY true incidence of mTBI is difficult to

Copyright # 2010, American Academy of Neurology. All rights reserved.

Continuum Lifelong Learning Neurol 2010;16(6)

Continuum Lifelong Learning Neurol 2010;16(6)

FIGURE 1-1 Neurometabolic cascade following traumatic injury.

Continuum Lifelong Learning Neurol 2010;16(6)

TABLE 1-1 International Statistical Classification of Diseases, Tenth A While loss of

Sports concussions have recently be- preinjury factors, such as employment

Continuum Lifelong Learning Neurol 2010;16(6)

Continuum Lifelong Learning Neurol 2010;16(6)

Continuum Lifelong Learning Neurol 2010;16(6)

4. Ling G, Bandak F, Armonda R, et al. Explosive blast neurotrauma. J Neurotrauma

6. Quality Standards Subcommittee of the American Academy of Neurology. Practice

8. Katayama Y, Becker DP, Tamura T, Hovda DA. Massive increases in extracellular

9. Kawamata T, Katayama Y, Hovda DA, et al. Administration of excitatory amino acid

Continuum Lifelong Learning Neurol 2010;16(6)

13. Vagnozzi R, Tavazzi B, Signoretti S, et al. Temporal window of metabolic brain

15. Vagnozzi R, Signoretti S, Tavazzi B, et al. Temporal window of metabolic brain

18. World Health Organization. International statistical classification of diseases and

Continuum Lifelong Learning Neurol 2010;16(6)

28. Poirier MP. Concussions: assessment, management, and recommendations for

30. Cernak I. Animal models of head trauma. NeuroRx 2005;2(3):410–422.

39. Ponsford J, Willmott C, Rothwell A, et al. Impact of early intervention on outcome

41. Tsaousides T, Gordon WA. Cognitive rehabilitation following traumatic brain

Continuum Lifelong Learning Neurol 2010;16(6)

DIAGNOSIS AND A The actual

MANAGEMENT OF traumatic brain

TRAUMATIC BRAIN cases is

INJURY may receive

INTRODUCTION many as 8 million head injuries occur

Copyright # 2010, American Academy of Neurology. All rights reserved.

Continuum Lifelong Learning Neurol 2010;16(6)

Continuum Lifelong Learning Neurol 2010;16(6)

Continuum Lifelong Learning Neurol 2010;16(6)

Case 2-2 A Second-impact

uncertain, it may play a role in cerebral consequence of this re-injury.22 Iden-

Continuum Lifelong Learning Neurol 2010;16(6)

Continuum Lifelong Learning Neurol 2010;16(6)

Continuum Lifelong Learning Neurol 2010;16(6)

Continuum Lifelong Learning Neurol 2010;16(6)

Continuum Lifelong Learning Neurol 2010;16(6)

Continuum Lifelong Learning Neurol 2010;16(6)