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Understanding Mild Traumatic BrainInjury and Postconcussion SyndromeBy Frank D. Lewis, PhD, and John Lucas, MA, LPC, LMFT

Despite having a label of "mild,"mild traumatic brain injury(MTBI) is a major publichealth problem in the United

States, according to the Centers forDisease Control and Prevention (CDC).It is estimated that up to 1.2 millionpeople sustain a MTBI each year theUnited States. MTBI accounts for morethan 1 million (or 1% of) yearly emer-gency department visits. Most MTBIsoccur to persons under the age of 24or older than age 74. Fifty percentof MTBIs result from motor vehiclecrashes, 25% from falls, 15% fromassaults, and 10% from sports inju-ries. Most fall injuries occur in thoseyounger than 5 and older than 75.'

In 2001, the CDC reported thecost of MTBI to be $16.7 billion.1 Mostof this economic cost was the resultof lost productivity. These figures donot include the indirect cost of familycaregiver expense and those who weretreated in the emergency department,released, and then received subsequentcare in other hospitals for symptomsrelated to their injury. A study byBoake and colleagues2 found thatMTBI patients had similar duration ofwork absences as did general traumapatients. In their study, work absencesresulting from MTBI ranged from 1week to 3 months. Other researchershave reported unemployment rates

Frank D. Lewis, PhD, is Director of Clinical

Outcome Services and Clinical Director at

NeuroRestorative Georgia in Augusta. John

Lucas, MA, LPC, LMFT, is in Private Practice.

of 15% 2 years from the onset of theMTBI.34 Perhaps the most importantstep in ensuring that these patientsreceive access to proper care is a thor-ough understanding of the definitionand diagnosis of MTBI.

Definition and DiagnosisFailure to properly diagnosis a MTBIcan readily lead to symptom exacer-bation and chronic emotional andphysical problems. An accurate under-standing of the disorder will help casemanagers make better decisions regard-ing the nature, frequency, and durationof treatment necessary to minimize theseverity of symptoms. However, definingand diagnosing MTBI has proven to bechallenging. Traditionally, diagnosisof MTBI relied heavily on the GlasgowComa Scale (GCS), a broad measureof neurologic functioning, rangingfrom nonresponsive-to-external-stimulito fully oriented and conversant. TheGCS emphasis on consciousness leveland depth of coma has significant valuefor directing the emergency care ofmore severe neurological injuries, yetunderestimates the presence of signifi-cant symptoms of MTBI. For example,most MTBIs are admitted to emergencydepartments with the highest GCSscore of 15, which could be erroneouslyinterpreted as normal neurologicalfunction. In response to these limita-tions, more comprehensive injury classi-fications have been developed. In 1993the America Congress of RehabilitativeMedicine defined a MTBI as onethat resulted from a blow to the head

causing any alteration of mental statuswith the following criteria: (1) loss ofconsciousness not exceeding 30 min-utes, (2) after 30 minutes an initialGCS score of 13 to 15, and (3) post-traumatic amnesia (PTA) not lastinglonger than 24 hours.' Although widely-used, this system of classification lacksthe clarity and specificity necessaryto detect characteristic symptoms ofMTBI. The symptoms that should beconsidered are presented in Table 1.

To address these limitations andimprove diagnostic accuracy, theCDC6 published a detailed operationaldefinition of MTBI in 2003. Its criteriainclude the following:• Any period of observed or self-

reported transient confusion, disori-entation, or impaired consciousness

• Any period of observed or self-reported dysfunction of memory(amnesia) around the time of injury

• Observed signs of other neurologicalor neuropsychological dysfunction,such as:

- Seizures acutely following headinjury

- Among infants and very youngchildren: irritability, lethargy, orvomiting following head injury

- Symptoms among older childrenand adults such as headache, diz-ziness, irritability, fatigue, or poorconcentration (when identifiedsoon after injury can be used tosupport the diagnosis of mild TBI,but cannot be used to diagnosis inthe absence of loss of conscious-ness or altered consciousness)

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• Any period of observed or self-reported loss of consciousness lasting30 minutes or less

Since 2003, several organizationshave published definitions of MTBI,with considerable overlap of acuteinjury characteristics. McCrea' providesa summary and review of various defini-tions. Taken together, these definitionsforge a consensus among profession-als as to the defining characteristicsof MTBI. With this understanding,research is now advancing in the areaof neuroimaging techniques with thehope of providing precise assessment ofthe structural and functional changesthat are correlated with subtle neuro-logical injury and recovery.

Neuroimaging and MTBITraditionally, head CT scans are takenin emergency departments to detectthe presence of moderate and severebrain injuries. The CT scan is effectivein detecting structural abnormalitiesand hemorrhagic lesions that requiresurgical intervention. The CT scans,however, lack the sensitivity necessaryto detect small petechial hemorrhagesand cellular dysfunction associated withMTBI. While effective in ruling out theneed for surgical intervention, relianceon CT can lead to a false assumption ofnormal brain function.

Although not foolproof, magneticresonance imaging (MRI) is more sen-sitive for detecting subtle brain abnor-malities caused by MTBI. A review ofstudies in which patients were givenboth CT and MRI scans found that theMRI detected brain abnormalities in30% of the patients that had normalCT scans. Despite the increased capa-bility to reveal brain abnormalities,MRIs have been shown to be only mini-mally effective in predicting the pres-ence of symptoms long term.

Diffusion tensor imagining (DTI),a relatively recent variation on MRI,can detect small neural abnormali-ties not seen on the traditional MRIs.9

Specifically, it is possible to observemicroscopic abnormalities of white mat-ter neural tracts using DTI. Also, DTIallows researchers to detect improve-ment in neural connectivity followingbrain injury.

When neuroimaging does identifyabnormalities after a MTBI, the injuryis considered to be a "complicatedMTBI." If the scans are normal, theinjury is classified as "uncomplicatedMTBI." Patients with complicatedMTBI—with lesions, sustained meta-bolic change, or diffuse injury—are atrisk for slow or incomplete recovery.Kashluba and colleagues10 found thatMTBI patients with identifiable lesionsexperience outcomes more similar topatients with moderate brain injuryas measured by GCS. These patientsexperienced significant symptoms 1year post-injury. Symptoms were severeenough to prevent return to work ornormal productive activity.

Mechanism of InjuryThe neurological damage caused by aMTBI was once thought to occur in thesame fashion as that of moderate andsevere injuries. Shearing or rotationalforces resulting from a blow to thehead cause tearing and misalignmentof axons and ultimately death of thecell. The damage, referred to as diffuseaxonal injury, is widespread, typicallyconcentrating at the junction betweenthe gray matter of the cerebral cortexand the white matter of ascending anddescending neurons. The ability torecover from such injuries relies pri-marily on adjacent uninjured neuronsassuming function of the damagedneurons. Concussions or MTBLs wereconsidered to be a milder form of dif-fuse axonal injury.

Recent research suggests a morehopeful model of mild injuries, whichinvolves cellular dysfunction instead ofdeath. A blow to the head of sufficientforce to cause a MTBI initiates a pro-cess of accelerated neurotransmitter

Symptoms of Mild TraumaticBrain Injury

Physical

Headache

Seizure acutely following blow tohead

Nausea

Vomiting

Dizziness

Fatigue

Hypersensitivity

Sleep disturbance

Numbness/tingling

Cognitive

Decreased attention/concentration

Short term memory deficits

Diminished capacity of workingmemory

Decreased processing speed

Decreased verbal fluency

Diminished executive functioning :planning, judgment, insight

Emotional/Behavioral

Mood changes or mood swings

Depression

Anxiety

Irritability

release, which increases cellular metab-olism and impairs the connectivity ofneurons. Giza and Hovda" refer to thisdisruption in function as a "neurologicmetabolic cascade." This disruption ofcellular function causes posttrau-matic amnesia, headache, and the r

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other cognitive symptoms of MTBI. Inuncomplicated MTBIs, neurologicalfunction typically returns to normalafter a period of days to weeks. As nor-mal neural function returns, symptomssubside. In rare cases, symptoms persistfor an indefinite period at which timethe patient may be given a diagnosis ofpostconcussion syndrome (PCS).

Postconcussion SyndromeIn medical terminology, a syndromeis defined as the presence of clinicallyrecognizable features or characteristicsthat occur together and in which thepresence of one or more features indi-cates the possibility of the presence ofothers. In the case of postconcussionsyndrome, symptoms are preceded amaximum of 4 weeks by a MTBI witha loss of consciousness. Additionally,diagnosis requires symptoms in atleast three or more of the followingcategories12:• Headache, dizziness, malaise, fatigue,

noise tolerance• Irritability, depression, anxiety,

emotional lability• Subjective concentration, memory,

or intellectual difficulties withoutneuropsychological evidence ofmarked impairment

• Insomnia• Reduced alcohol tolerance• Preoccupation with the above s

ymptoms and fear of brain damagewith hypochondriacal concern andadoption of a sick role

Other features that may be asso-ciated with PCS include changes inpersonality, apathy, lack of spontaneity,learning difficulties, and worseningacademic performance (children) oroccupational performance (adults).

As is the case with MTBI, diagnos-ing PCS can be quite problematic.Diagnosis of the syndrome is plaguedwith poor reliability.7 Many of the symp-toms are subjective and may have beenpresent, at least in part, prior to theTBI. Also, PCS symptoms are similar to

other disorders, such as fibromyalgia,chronic pain, and chronic depression.IversonlS reported that 90% of personswith depression and no TBI historywould likely meet PCS criteria. In addi-tion to symptom overlap, several demo-graphic and psychosocial factors arepredictive of PCS after a MTBI includ-ing female gender, older age, unstablerelationships, lack of social support,preexisting psychiatric problems, chem-ical dependency, and litigation. Somehave hypothesized that depression,anxiety, and stress in the weeks fol-lowing a head injury contribute to thepersistence of symptoms." Therefore,to be effective, treatment models mustaddress the underlying psychologicalfactors maintaining the symptoms.

Model for Clinical ManagementObviously initial treatment is oftengiven in the emergency department,where more serious brain injury isruled out. As indicated previously, formost cases, initial symptoms are tempo-rary, clearing by 3 to 4 weeks. Duringthis acute phase, the treating physi-cian will likely prescribe medication toalleviate symptoms of pain and anxietyand recommend lifestyle changes.Depending on the individual, thesechanges might include avoiding contactsports and situations placing one at riskfor fall or collision, bright lights, vigor-ous exercise, and prolonged time infront of computer screens. The patientwill likely be counseled to get adequaterest and sleep, while work and schoolschedules may be modified.

Following the acute phase of injury,if the symptoms have not resolved,clinical management should shift toa comprehensive multidisciplinaryapproach.7 An Internet search revealsnumerous clinics offering comprehen-sive assessment and treatment of MTBIand PCS. To be effective, these pro-grams must have rehabilitation profes-sionals with expertise in treating braininjury. Often these teams are led by a

neuropsychologist in close associationwith a physician, typically a physiatristor neurologist with a brain injury spe-cialty. The management process beginswith a thorough patient history toinclude information concerning previ-ous concussions or head injuries, devel-opmental issues (eg, learning disabilityor ADHD), psychiatric issues, and socialhistory. The physician may order addi-tional neuroimaging to determine thepresence of lesions or other neurologi-cal impairment.

Next the neuropsychologist initi-ates a neuropsychological evaluationto determine performance on a widearray of cognitive functions poten-tially affected by the brain injury. Keyamong these functions are workingmemory, attention and concentration,verbal problem solving, visuo-spatialperception, reasoning, and processingspeed. The battery should include tests(ie, MMPI-2 validity profile, Test ofMalingering) designed to detect symp-tom exaggeration and malingeringmotivated by secondary gain.

Test results are reviewed by the neu-ropsychologist and the physician. Basedon the findings, the appropriate treat-ment team is assembled and a treat-ment plan is written to address deficitsand monitor progress. Depending onthe extent of deficits, the team mayinclude all or some of the followingspecialists: psychologist/counselor,speech pathologist, physical therapist,and occupational therapist. Oftenmultiple therapists will approach thesame functional deficit from a some-what different treatment approach.Consistent communication on problemsand progress is essential for a posi-tive outcome. The psychologist plays akey role in adjustment to the changesinitiated by the brain injury. The psy-chologist is typically the team memberwho conducts patient and family braininjury education and, along with thephysician, discusses the course of treat-ment and prognosis. The psychologist

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The comprehensive studies to date suggest the team approach withsupportive counseling and education given soon after injury offers the best hope

for positive functional outcomes and minimized PCS symptoms.

also provides counseling and support,teaches coping and compensatorystrategies, and provides family counsel-ing to help loved ones adjust and reactto potential changes in behavior. Thespeech pathologist focuses on improv-ing attention and concentration, whileproviding strategies to compensate formemory loss. When necessary, physi-cal therapists improve conditioning,strength, and vestibular and balanceproblems. Occupational therapists typi-cally will address safety and judgmentin the home and work setting. Otherteam members who may be enlistedin the treatment include an educatorto facilitate a successful transition toschool and a dietitian to promote abrain healthy diet.

When injury initiates an array ofboth neurologic and non-neurologicalsymptoms, the team approach to treat-ment offers several advantages oversingle provider care including:• Detailed assessment of risk factors in

multiple domains of functioning• Behavioral management to prevent

the development of maladaptivebehavior and symptom exacerbation

• Treatment from multiple specialists inbrain injury

• Support system and education for thepatient and family

• Availability of specialized psychologi-cal and counseling services

• Consistent observation and monitor-ing of progress

• Allowance for repeated practice ofadaptive behaviors

• A positive treatment context with highexpectation for success

While additional empirical stud-ies will help to improve the efficacy of

MTBI treatments, the most comprehen-sive studies to date suggest the teamapproach with supportive counselingand education given soon after injuryoffers the best hope for positive func-tional outcomes and minimized PCSsymptoms.7 The case example that fol-lows illustrates frustrations often expe-rienced by MTBI patients. Frustrationstems not only from physical and cogni-tive symptoms, but also from the impactthey have on work performance andpersonal relationships. Unfortunately,for patients, convincing physicians andpayers that the symptoms are real maypose their greatest challenge.

Case ExampleJulia, a healthy women in her early 50s,was employed as a claims adjuster earn-ing a 6-figure salary. She had a longand positive employment history andwas highly regarded by her peers in thebusiness. W7hile on the job inspectinga roof, she was hit on the top of herhead by a large metal extension ladderwhen it became dislodged from its rails.Although dazed and disoriented, shereported no loss of consciousness. Sherefused medical treatment at the timeand continued to work. Later that dayshe complained of a severe headache.Three days later she was referred forevaluation and testing. She reportedthat her tests were unremarkable;however, she was prescribed physicaltherapy to treat neck pain and othersomatic complaints. She attended physi-cal therapy for approximately 1 month,during which time she did not work.Following therapy, she returned to herjob. After 2 months her symptoms wors-ened. As a result, she was referred for

a neurosurgery consult. Her appoint-ment with the neurosurgeon occurredapproximately 4 months after herinjury. At the time of her appointment,she reported daily headaches, inter-mittent forgetfulness, and heightenedemotionality. Other symptoms includedposterior neck pain, pain in her upperthoracic region, tingling in her righthand, and weakness in her right leg.Julia reported that her neurosurgeonwas skeptical with regard to her reportof cognitive symptoms. He believed thatbecause she was so articulate in describ-ing her difficulties, she must have beencognitively intact. According to Julia, hemade her feel that her symptoms werejust "in her head" at best, or worse, shewas faking in order to get disabilitypayments. Nonetheless, his evaluationcited cervical strain and posttraumaticheadaches with "elements to suggestpostconcussion syndrome." Ultimately,he did recommend continuing physicaltherapy and rehabilitation to addressher PCS. Insurance approval for outpa-tient treatment of PCS was not obtaineduntil almost 2 months after her neu-rosurgery appointment, or 6 monthspostinjury.

Prior to therapy, Julia received acomprehensive neuropsychologicalevaluation, which she paid for outof pocket. That evaluation showedimpaired functioning in working mem-ory, processing speed, and attention/concentration. Tests showed no evi-dence of malingering or symptom fak-ing. Julia's insurance approved physicaland speech therapies each for 1 hourper day 5 days per week. She was alsoapproved to receive counseling 3days per week. Insurance approval r

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for treatment was given weekly contin-gent on progress in the program. Juliaattended therapy sessions in the morn-ing and went to work in the afternoon.

Julia's counseling sessions were thefocal point of her treatment becauseof her emotional lability and anxietyabout changes in cognitive function-ing. Concerns regarding her abilityto return to work at pre-injury perfor-mance and income levels contributedgreatly to her anxiety and emotionality.At work she felt she was falling behind,regardless of how hard she tried.

Julia was married just a few monthsprior to her injury. She described hermarriage as a good one with highexpectations for success, but she statedthat she did not feel like herself. Sheworried her husband might think shewas not the women he married. Shedescribed herself as easily irritatedand short tempered. She reportedthat extreme fatigue greatly curtailedher evening activities; stating she onlywanted to "go home and sleep afterwork." When requested, Julia's husbandattended therapy sessions. He was verysupportive and demonstrated an under-standing that changes in Julia's moodwere largely due to her injury.

Julia put forth significant effort inher counseling and other therapy ses-sions. Each week in therapy was markedby improvements in emotional controland adjustment to her limitations. Shereported improvements in her ability tofocus and complete assignments. Whileshe still experienced headaches, theywere less frequent and less severe. Shealso reported that her cervical pain wasmore manageable.

Julia's improvements in therapy,however, only transferred minimallyto her job. Compared to her pre-injury performance, she was slow andinefficient. Anxiety made it difficultfor her to sustain attention to herduties. As Julia's therapists began tofocus on helping her utilize newlylearned coping skills while at work,

her coverage was abruptly terminated.After only 3 weeks of treatment, Juliawas discharged. Against the recom-mendations of the therapy team,she returned to work full time. For 6months she struggled. Neck pain andstress escalated, making it difficult forher to concentrate and complete herwork. Ultimately, almost 1 year fromher injury, Julia lost her job. At home,Julia's marital problems had worsened.

Julia experienced a poor outcomefrom her brain injury. During therapyshe realized some relief from symptoms,but treatment was ended prematurelyand she continued to experience diffi-culty at work and stress in her marriage.Julia's case was poorly managed fromthe beginning. Without empirical study,one cannot definitively say what her out-come would have been had she receivedtreatment sooner, but comprehensivespecialized rehabilitation given shortlyafter injury, when her symptoms wereemerging, would have likely preventedher downward spiral. An early neuropsy-chological evaluation could have ruledout malingering and facilitated propercoordination of her treatment withexperts in treating MTBI and PCS.

SummaryMost of the estimated 1.2 million per-sons who sustain a MTBI each year willexperience an excellent functionaloutcome in a relatively short period oftime. However, for approximately 15%of those cases, cognitive, emotional,and physical symptoms will persist.Symptoms are the result of both neuro-logical and non-neurological factorsthat left untreated may worsen as mal-adaptive patterns of coping develop outof a lack of understanding of symptomsand prognosis. The multidisciplinaryteam model provides an importantoption in managing complicated casesof MTBI, preventing symptoms of PCS,and achieving meaningful functionaloutcomes.

References1. Rutland-Brown W, Langlois JA, Thomas KE,Xi YL. Incidence of traumatic brain injury inthe United States, 2003. J Head Trauma RehaUl.2006;21(6):544-548.

2. Boake C, McCauley SR, Pedroza C, LevinHS, Brown SA, Brundage SI. Lost productivework time after mild to moderate traumaticbrain injury with and without hospitalization.Neurosurgeiy. 2005;56(5) :994-1003.

3. Rimel RW, Giordan! B, Earth JT, Boll TJ,Jane JA. Disability caused by minor headinjury. Neurosurgery. 1981;9(3):221-228.

4. Dikmen SS, Temkin NR, MachamerJE, Holubkov AL, Eraser RT, Winn HR.Employment following traumatic head injuries.Arch Neurolagy. 1994;51 (2):177-186.

5. Kay T, Harrington DE, Adams R. Definitionof mild traumatic brain m}Mrj.JHe.ad TraumaRehabil. 1993;8(3):8frS7.

6. Report to Congress on Mild Traumatic Braininjury in the United States: Steps to Prevent aSerious Public Health Problem. Atlanta, GA;National Center for Injun1 Prevention andControl, Centers for Disease Control andInjury Prevention; 2003.

7. McCrea MA. Mild Traumatic Brain Injuryand Postconcussion Syndrome. Oxford: OxfordUniversity Press; 2008.

8. Bazarian JJ, Blyth B, Cimpello L. Bench tobedside: evidence for brain injury after concus-sion-looking beyond the computed tomogra-phy scan. AcadEmerg Mud. 2006;13:199-214.

9. Arfanakis K, Haughton VM, Carew JD,Rogers BP, Dempsey RJ, Meyerand ME.Diffusion tensor MR imaging in diffuse axonalinjury. Am]Neuroradiol. 2002;23:794-802.

10. Kashluba S, Hanks, RA, Casey JE, MillisSR. Neurologic and functional outcome aftercomplicated mild traumatic brain injury. ArchPhys Med Rehabil. 2008;89:904-911.

11. Giza CC, Hovda DA. The neuromcta-bolic cascade of concussion. JAM Train.2001;36:228-235.

12. World Health Organization. InternationalStatistical Classification of Diseases andRelated Health Problems. 10th ed. Geneva,Switzerland: World Health Organization; 1992.

13. Iverson GL. Misdiagnosis of the persistentpostconcussion syndrome in patients withdepression. Arch CKn Neuropsychol. 2006;21:303-310.

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