Traumatic Brain Injury and VestibularPathology as a Co morbidity AfterBlast ExposureMatthew R. Scherer, Michael C. Schubert

M.R. Scherer, PT, MPT, NCS, is

CPT, US Army, Army Medical Spe­

cialist Corps, and a PhD student inthe Department of Physical Ther­

apy and Rehabilitation Science,

University of Maryland School ofMedicine, 100 Penn St, Baltimore,

MD 21201 (USA). Address all cor­

respondence to CPT Scherer at:

matthew .scherer@us.army.mil.

M.C Schubert, PT, PhD, is Assis­

tant Professor, Department of

Otolaryngology-Head and Neck

Surgery, Johns Hopkins School of

Medicine, Baltimore, Maryland.

[Scherer MR, Schubert MC Trau­

matic brain injury and vestibular

pathology as a comorbidity after

blast exposure. Phys Ther. 2009;89:980-992.]

© 2009 American Physical TherapyAssociation

Blasts or explosions are the most common mechanisms of injury in modern warfare.Traumatic brain injury (TBI) is a frequent consequence of exposure to such attacks.Although the management of orthopedic, integumentary, neurocognitive, andneurobehavioral sequelae in survivors of blasts has been described in the literature,less attention has been paid to the physical therapist examination and care of peoplewith dizziness and blast-induced TBI (BITBI). Dizziness is a common clinical findingin people with BITBI;however, many US military service members who have beenexposed to blasts and who are returning from Iraq and Mghanistan also complain ofvertigo, gaze instability, motion intolerance, and other symptoms consistent withperipheral vestibular pathology. To date, few studies have addressed such "vestibu­lar" complaints in service members injured by blasts. Given the demonstrated efficacyof treating the signs and symptoms associated with vestibular pathology, vestibularrehabilitation may have important implications for the successful care of servicemembers who have been injured by blasts and who are complaining of vertigo orother symptoms consistent with vestibular pathology. In addition, there is a greatneed to build consensus on the clinical best practices for the assessment andmanagement of BITBI and blast-related dizziness. The purpose of this review is tosummarize the findings of clinicians and scientists conducting research on the effectsof blasts with the aims of defining the scope of the problem, describing and char­acterizing the effects of blasts, reviewing relevant patients' characteristics and sen­sorimotor deficits associated with BITBI,and suggesting clinical best practices for therehabilitation of BITBIand blast-related dizziness.

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980 II Physical Therapy Volume 89 Number 9 September 2009

TBI and Vestibular Pathology After Blast Exposure

he risk of blast exposure to de­ployed US military servicemembers is significant. Injury

tternsin survivors of blasts are typ­Uy complex and characterized byItisystem involvement and vari-degrees of severity. 1 Such pat­s may include orthopedic

lima, limb loss, visual impair­ats, burns, and posttraumatic

ess disorder.2-s Improvements indy armor, vehicle-hardening mea­Ires, and advances in battlefielddicinehave led to dramatic reduc­as in mortality rates for servicembers.5.9.10As a result, servicembers are surviving injuries thatuldhave been fatal a decade ago.nversely, many service membersmrn home with multisystem pa­logy (ie, polytrauma) and signifi-

at rehabilitation needs.

plosive attacks account for aerpercentage of casualties in cur­tconflicts than in other recent USntlicts.9 Traumatic brain injury,I),which often results from blastposure, has been described as thegnature injury" of the wars in Iraqd Afghanistan.s-ll The Depart­nt of Defense (DOD) and the De­se Veterans Brain Injury Centerimate that as many as two thirdsmedicalevacuations from Iraq and.Ighanistan can be attributed tostexposure. 10Neurologic pathol­; as a result of blast exposure ismmon; 32% of service members

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wounded in war and evacuated tothe Walter Reed Army Medical Cen­ter since January 2003 have been di­agnosed with TBI.12 The DefenseVeterans Brain Injury Center has pro­vided care for nearly 8,000 servicemembers with TBI in support of Op­eration Iraqi Freedom (Iraq) andOperation Enduring Freedom (Af­ghanistan); however, this figure rep­resents only service members whosustained trauma significant enoughto require medical evacuation anddoes not reflect service members

who were exposed to blasts butwere able to return to duty. Despiterecent advances in the battlefielddiagnosis of TBI, mild TBI (mTBI)is difficult to diagnose in the warzone, and the condition likely isunderreported.1o,13

Although the multiple effects associ­ated with blast injuries may inflict awide range of pathologies, impair­ments, functional limitations, anddisabilities in injured survivors, dizzi­ness and vertigo are common symp­toms in patients with blast-inducedTBI (BITBl). The medical literatureincludes several perspective pieces,case studies, and epidemiologicalstudies documenting "vestibular"symptoms in patients who havebeen exposed to blasts. In additionto nonspecific complaints of dizzi­ness or unsteadiness, complaints ofvertigo and oscillopsia, typically rec­ognized as being more specific tovestibular pathology, have been re­ported.5,14-24Given the complexitiesof treating patients with polytrauma,it is essential that any vestibular com­plaints be assessed and managed inan efficient manner with the goal ofproviding an optimal return to activ­ities of daily living, quality of life, andreturn to dUty.25,26

From this point forward, we con­sider "dizziness" to be an impreciseterm indicating light-headedness or afeeling that one is going to fall; it isnot necessarily specific to vestibular

involvement. Vertigo is consideredto be an illusion of movement, typi­cally perceived as spinning, andcommonly indicates vestibular pa­thology. Oscillopsia is the percep­tion that objects known to be sta­tionary are moving in the visualenvironment. Oscillopsia occurs dur­ing head movement in people withvestibular hypofunction, indicatinginadequate gaze stabilization by thevestibulo-ocular reflex.27 The term"blast-induced traumatic brain in­jury" describes head injury sustainedduring an explosion as a result of 1or more of the following effects ofthe blast: primary, secondary, or ter­tiary. This term encompasses the the­oretical effects of the primary over­pressure wave (primary blast effects)as well as the documented effectsassociated with blunt head traumafrom flying debris (secondary blasteffects) or from displacement of theindividual (tertiary blast effects). Fur­thermore, it conforms to clinicalmanagement patterns in DOD andVeterans Health Administration facil­ities, where the majority of survivorsof blasts with moderate to severe TBI

receive acute care and subsequentrehabilitation.

The topic of blast injury assessmentand management is timely given theconflicts in Iraq and Afghanistan;however, it is not without contro­versy. According to the USArmy Sur­geon General's Task Force on TBI,there is no objective evidence in hu­mans to support the hypothesis thata primary overpressure wave from ablast causes neuronal damage andsubsequent brain injury.28 It is ex­pected that current research in ani­mal models and clinical work withsurvivors of blasts will yield impor­tant evidence in support of neuro­trauma after blast injuries.

Clinicians serving in war zones, theDOD, and the Veterans Health Ad­ministration have contributed to thebody of knowledge about blast inju-

"

y

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TBI and Vestibular Pathology A.fter Blast Exposure

ries and polytrauma in the currentconflicts.3-5,23.29-33However, thereremains a paucity of research relatedto the assessment and managementof dizziness and vestibular sequelaein BITBl. With renewed attention toand education about EITBI, the reha­bilitation community has an oppor­tunity to contribute to the growingbody of knowledge and to help in­vestigate mechanisms of injury andeffective recovery strategies.

The purpose of this review is to sum­marize the findings of clinicians andscientists conducting research onthe effects of blasts with the aims ofdefining the scope of the problem,describing and characterizing the ef­fects of blasts, reviewing relevant pa­tients' characteristics and sensorimo­tor deficits associated with BITBI,and suggesting clinical best practicesfor the rehabilitation of BITBI andblast-related dizziness.

Epidemiology of BITBIAccording to the Defense VeteransBrain Injury Center, blast injurieshave been responsible for over 65%of the casualties in the ongoing con­flicts in Iraq and Afghanistan. 12,32In arecent study of injury patterns asso­ciated with Operation Iraqi Free­dom, improvised explosive devicesand mortars accounted for 78% ofbattle wounds treated at clinical fa­cilities in Iraq.33 It is estimated thatas many as 16,000 service membershave sustained blast-induced trau­ma.12Unfortunately, the actual num­ber of service members who havebeen wounded likely is larger giventhe difficulties associated with mon­itoring blast exposure in a war zoneand the failure of service members to

report mild concussive injuries, par­ticularly when there are no concom­itant orthopedic or soft-tissue inju­ries. Recent findings for a brigadecombat team (N=3,973) returningfrom Iraq after a year-long deploy­ment indicated that 22.8% of servicemembers had at least one TBI con-

firmed by a clinician and that 88% ofthese were caused by blasts. In ad­dition, the rates of comorbid dizzi­ness (59.3%) and balance problems(25.9%) after the blasts were amongthe top 3 complaints of service mem­bers (headache was first), suggestingthat the prevalence of blast-relateddizziness (and potential vestibular in­volvement) may be greater than pre­viously reported.34

Much of what has been learnedabout the effects of blasts in the cur­rent conflicts has been obtainedfrom the characterization of servicemembers whose injuries weretreated in polytrauma centers, suchas the Walter Reed Army MedicalCenter and the Veterans Health Ad­ministration. Although much hasbeen reported regarding the neuro­psychiatric and orthopedic sequelaeassociated with blasts, considerablyless attention has been paid to ves­tibular deficits. The incidences ofdizziness, vestibular pathology, andTBI secondary to blast-induced baro­trauma are unknown. In the litera­ture on blunt (nonblast) TBI, the in­cidence of dizziness in patients withTBI has been reported to be as highas 80%, with the incidence of spe­cific vestibular pathology ranging be­tween 30% and 65%.35-42The char­acterization of blast-related dizzinessis further complicated by the incred­ible physical and psychologicalstresses associated with injuries in awar zone.10,43A survivor of a blast

may have sustained not only a widearray of physical injuries but also of­ten intense psychological traumathat can further complicate the re­covery process.

There is an ongoing debate aboutwhether the symptoms associatedwith mTBI, collectively referred to aspostconcussion syndrome (PCS),originate from a pathophysiologicalprocess or are psychosomatic in na­ture. Proponents of a pathophysio­logic etiology suggest that PCS is a

manifestation of the delayed effectsof diffuse axonal injury.44 Othershave maintained that PCS may bemore strongly associated with pre- orpostinjury psychological factors.45Rutherford46 hypothesized that thedelayed onset ofPCS (days to weeks)often coincides with patients' returnto daily activities. Although plausi­ble, such an explanation does notaccount for the immediate onset ofsymptoms, such as headaches, dizzi­ness, and nausea, in patients whohave been exposed to blasts andhave mTBp4,47 Although the occur­rence of dizziness in conjunctionwith other PCS-like symptoms hasbeen documented in patients whohave psychiatric disorders andchronic pain but do not have braininjuries, several studies have demon­strated that somatic and cognitivesymptoms are more likely to be as­sociated with head trauma and lossof consciousness, whereas behav­ioral symptoms are more likely to berelated to psychological distress.46-50

In summary, the extent of blast­related dizziness and BITBI may bedifficult to assess. Even by the mostconservative estimates of vestibu­lopathy in BITBI,it is likely that thou­sands of people have vestibular

. pathology but that only a small per­centage have been formally assessedor treated.

Blast EffectsA blast results when solids or liquidsare rapidly converted into a gas. Inthis state, the gas molecules becomeheated and highly pressurized. Theheated gas expands into the sur­rounding air at speeds higher thanthat at which light travels, com­pressing the air and creating a peakoverpressure wave or shock waveradiating from the point of detona­tion.14,17.18.51Closely following theshock wave is a blast wind that alsoradiates from the point of detona­tion. As the gas expands, the pres­sure drops and creates a vacuum or

982 • Physical Therapy Volume 89 Number 9 September 2009

Injuries from projectiles (eg, shrapnel or debris)

Injuries from displacement of the individual by blast wind

Other injuries

ITBI=traumatic brain injury.

Types of Injuries

Injuries from impact or shearing from overpressure wave

•

In 2006, Taber et al52reviewed thelimited clinical findings in humansand animals exposed to a primaryblast. Neuropathological changes inhumans included small hemorrhageswithin white matter, chromatolyticchanges in neurons (degeneration ofNissl bodies, an indication of neuro­nal damage), diffuse brain injury, andsubdural hemorrhage. 52 Mott60 de­scribed a few cases in which a pri­mary blast was the proposed causeof death as a result of perivascularspace enlargement, subpial hemor­rhages, venous engorgement, whitematter hemorrhages into the myelinsheath and perivascular spaces, andchromatolysis. Recent mTBl re­search in animal models suggestedthat the degree of injury may bemore extensive than previouslybelieved. The absence of focal ax­onal swelling (a neuropathologicalmarker that is used to gauge the se­verity of head injury) in severe TBlmay be one reason that the magni­tude of mTBl is underestimated.61Other findings obtained in animalmodels of blast injury included wide­spread microglial activation (indica­tive of neural degeneration) in thecerebellar and cerebral cortices, pi­neal gland involvement, and func­tional deficits in coordination, bal­ance, and strength (force-generatingcapacity) testing.62-64 These dataprovide evidence of the insidiousand potentially devastating cellularand functional effects of blasts. 52

Patterns of Injuries"

Brain (TBI),17 viscera, lungs (pulmonary emboli),54 tympanic

membrane rupture or inner ear patholpgy (vestibular,cochlear, or both)9, 17,18,21,53

Fractures, limb loss, TBI, soft-tissue injuriesS2,53

TBI, limb loss, fractu res17,53

Burns, crush injuries, asphyxia, exposure to toxic substances,exacerbation of chronic illness'7,53

1BI and Vestibular Pathology After Blast Exposure

The most common forms of closed

head injury (CHI) related to blast ex­posure are diffuse axonal injury, con­tusion, and subdural hemorrhage. Ofthese, diffuse axonal injury is mostfrequently associated with mTBl andcharacterizes the vast majority ofblast injuries sustained by servicemembers. 52Diffuse axonal injury oc­curs when shearing, stretching, ortraction on small nerves leads to im­

paired axonal transport, focal axonalswelling, and possible axonal discon­nection.55.56 This pathophysiologicprocess is not unique to BlTBI.BluntTBIand mixed TBl (blunt trauma andbarotrauma) may further contributeto comorbid dizziness and vestibular

pathology in cases of secondary andtertiary effects of blasts. Temporalbone fractures, labyrinthine concus­sion, benign paroxysmal positionalvertigo (BPPV), perilymphatic fistu­lae, and vascular or central lesionsare commonly implicated as causesof vestibular pathology after headtrauma. 18.36,41.42,57-59

mon among survivors of blast inju­ries in the current conflicts; 15% to40% complain of dizziness or verti­gO.14,21Blast injuries to the eye canrupture the globe and cause blind­ness.17 Primary blast injuries alsomay cause coup-contrecoup braindamage, pulmonary emboli, gastroin­testinal tract rupture, or internalbleeding, 17

Secondary

Tertiary

Quaternary

Category

Primary

Mechanisms of InjuryThe effects of blasts are typicallyconcomitant and not mutually exclu­sive. They are categorized as pri­mary, secondary, tertiary, and qua­ternary (Tab. 1).53 Primary blastinjuriesare caused by barotrauma at­tributable to either overpressuriza­lion or underpressurization relativeto atmospheric pressure.17 Primaryblast injuries commonly affect thehollow organs in the chest, abdo­men, and middle ear as well as thegreat vessels in the neck, the innerear, and possibly the brain.17.18.53.54Given the relative exposure of theheadand neck during a blast, middleand inner ear trauma is common.The ear traditionally has been con­sidered a sensitive indicator of blast

exposure, with 35% to 50% of survi­vors experiencing conductive, sen­sorineural, or mixed hearing loss.14Vestibular complaints are also com-

negative-pressure wave. Extremepressurechanges occur as the stressandshear waves of the blast hit the

~ody.52The effects of the primaryoverpressurewave are nonlinear and~omplex.Although the damage pro­ducedby the overpressure wave typ­icallydecreases exponentially from'theblast epicenter, if the explosion~ detonated within an enclosed

~paceor if the blast waves travel in­sjdea vehicle, then the effects of theblastwaves become additive as thewaves reflect off walls, floor, andreiling.17

September 2009 Volume 89 Number 9 Physical Therapy • 983

TBI and Vestibular Pathology Aft.er Blast Exposure

Table 2.Clinical and Laboratory Tests for Vestibular Pathology in Subjects Exposed to Blasts

Structures, Pathways, orTestsProcess AssessedApplicationsAbnormal FindingsInterpretation

Head impulse test65

Horizontal semicircular canals,High-acceleration, moderate-Corrective saccade to targetAbnormal angular vestibulo-(clinical)

superior branch ofvelocity, low-amplitudeafter head rotationocular reflex (aVOR)vestibular nerve

head rotation with subject attributable to peripheralmaintaining gaze on fixed

vestibular hypofunctiontarget

Electro ny stag mog ra phy66

Extraocular muscles,Exposure to aural and visualAbnormal nystagmus,Abnormal 8th cranial nerve;(laboratory)

horizontal semicircularstimulation (eg, calorics,abnormal eyeabnormal smooth pursuitcanals, superior branch of

moving targets)movementsor saccades attributable

vestibular nerve, vestibularto pathology within

and oculomotor pathwaysperipheral or central

within central nervousvestibular pathways,

systemoculomotor pathways, or

bothRotary chair test66

Horizontal semicircular canals,Sinusoidal rotation atAbnormal nystagmus,Abnormal aVOR gain or(laboratory)

superior branch offrequencies of 0.01-0.64abnormal eyephase attributable tovestibular nerve

Hz; clockwise andmovementspathology withincounterclockwise rotation

peripheral or centralat 600/s and 2400/s

vestibular or oculomotor

pathwaysPositional test66,6?

Semicircular canalsMovement of involved canalPatient-reported complaintsAbnormal presence of(clinical or laboratory)

into gravity-dependentof vertigo and pathologicotoconia in semicircular

positionnystagmuscanal (ie, benign

paroxysmal positionalvertigo)Dynamic visual acuity

Horizontal semicircular canals,Active or passive headInability to identify targetAbnormal aVOR attributable

test66,68 (clinical)

vestibular nervemovement whileduring head movementto peripheral vestibular

visualizing optotypehypofunction;

directionuncompensated aVOR

Computerized dynamic

Integration of multisensoryChallenge of balance withSOT: inappropriateSOT: age- and height-posturography,69

input for balanceequipment and softwareresponses to inaccuratereferenced responses tosensory organization

under different conditionssensory inputs; MCT:sway in sagittal plane;test (SOT), motor

delayed motor responsesMCT: balance dysfunctioncontrol test (MCT)

to unpredictableand impaired reactive(clinical or laboratory)

perturbationslatencies

Balance Manager

Horizontal semicircular canals,Head movement whileAbnormal oculometricBehavioral measure

Dynamic inVision

vestibular nerve, vestibularvisualizing letters; trackingfeatures compared withsuggesting cerebellarSystem,?" gaze

and oculomotor pathwaysof moving targetsthose of subjects whodysfunction; damage to

stability, perceptionwere healthy andcentral oculomotor

time, targetmatched for agepathways, vestibular

acquisition, targetpathways, or both

tracking (clinical)a

a The Balance Manager Dynamic inVision System (NeuroCom International Inc, 9570 SE Lawnfield Rd, Clackamas, OR 97015) provides oculomotor and

vestibular testing not available in other NeuroCom systems. Novel assessments include perception time, target acquisition, and target tracking. Gaze stabilitytesting is provided in commercially available models such as the SMART Equi-Test System (NeuroCom Internationallnc). Visual testing typically is performedin a darkened room with a viewing distance of 390 cm (13ft). Perception time is measured by calculating the time (in milliseconds) that a randomlypresented target must be on the screen before accurate recognition by a subject. Target acquisition is the time (in milliseconds) required to make a saccadefrom the center of the screen to the new optotype position. Target tracking is the speed (in degrees per second) at which a subject can accurately track asymbol. Gaze stabilization is the speed (in degrees per second) at which a subject can move his or her head and accurately hold a target in view'?"

Patients' Characteristicsand Sensorimotor Deficitsin BITBITo date, few reports have character­ized vestibular findings in detail, anda definitive incidence of blast-relatedvestibular pathology has not beenestablished. 51 Table 2 summarizes

common clinical and laboratory mea­sures, the structures that they assess,and how the tests should be applied.Additionally, abnormal test findingsand guidelines on how such findingsshould be interpreted are included.For a more-detailed review of vestib­ular testing techniques, see Schubert

and Minor27 as well as the referencescited in Table 2.65-70

In a retrospective review and casestudy, Scherer et aFl reported dizzi­ness (39%), vertigo (24%), and oscil­lopsia (27%) in the days or weeksafter blast exposure and the persis-

984 II Physical Therapy Volume 89 Number 9 September 2009

TBI and Vestibular Pathology After Blast Exposure

enceof some symptoms months af­er the injury. Shupak et aF2 de­cribed symptoms and objectivelearingand vestibular findings in 5sraelisoldiers exposed to a blast.'atient-reported complaints in­:ludedvertigo (60%), hearing loss80%), tinnitus (80%), and otalgia20%). Tympanic membrane perfora­ionoccurred at a rate of 80% (8 ofhe 10 assessed ears). None of theDldiers had head trauma, loss of:onsciousness, or amnesia. Clinicalnd laboratory assessments werelerformed for all soldiers within 1feek of the incident and includedrmpanometry; pure-tone andpeech audiometry (the auditoryIrainstem response was tested in 1latient); a sinusoidal rotary chairest;electronystagmography (ENG),nc1udingmeasures of spontaneous,laze-evoked, positional, and posi­ioningnystagmus; and bithermal ca­orictesting. Three of the 5 patients60%) were diagnosed with unilat­:ralvestibular hypofunction, and 1latient was diagnosed with BPPV.Uthoughall of the subjects reportedheresolution of symptoms by their[·monthfollow-up, 2 of the 3 diag­losedwith unilateral vestibular hy­lofunctionwere shown to have per­nanent damage to the peripheral·estibularsystem. That study22 washefirst to document vestibular pa­hologyindependent of a TBI diag­losisin soldiers exposed to a blast.

nasingle-subject study, Sylviaet apolocumented vestibular and balancelelicitsin an active-duty Marine ex­losed to the backblast from a

houlder-launched missile system.Uthoughthe Marine experienced aIriefloss of consciousness and con­usionat the scene, the full effects ofheblast were reportedly mitigatedI)'a Kevlar* helmet and hearing pro­ection and by the fact that the Ma­inewas not directly facing the ex-

E.I. du Pont de Nemours & Co, 1007 MarketI, Wilmington, DE 19898.

plosion. On subsequent evaluation,he reported an intense frontal head­ache, photophobia, nausea, tinnitus,dizziness, oscillopsia, and abnormal­ity of gait. The results of a clinicalneurological examination and a braincomputed tomography examinationand the integrity of the tympanicmembranes were all normal. The ser­vice member was discharged 11 daysafter the blast exposure with a med­ical diagnosis of mTBI. At a I-monthfollow-up, he reported dizziness,headaches, and fatigue as well as dif­ficulty sleeping and increased irrita­bility. Cognitive testing revealed def­icits in attention, concentration,processing speed, and memory. At 6weeks after the insult, the subjectundelwent a comprehensive vestib­ular examination (he continued toreport oscillopsia and imbalance).The audiometry results were normal;however, the subject had abnormallylow vestibulo-ocular reflex gains atfrequencies of 0.02, 0.08, 0.32, and0.64 Hz in a sinusoidal rotary chairassessment, refixating saccades withleftward head impulse testing, andleft lateropulsion during gait testing.In aggregate, the authors reportedthat the findings were consistentwith a chronic left peripheral vestib­ular lesion that was uncompensatedfor both dynamic vestibulospinal re­flexes and the vestibulo-ocular re­flex. When the Marine returned toduty, he continued to reportbalance-related difficulties at night,suggesting possible performance im­pairments that could jeopardize hissafety or the safety of his team mem­bers. Interestingly, the authors re­ported that the results of a vestibularexamination at a 4-month follow-upwere normal, suggesting transientperipheral vestibular hypofunctionof several months' duration. Thevestibulo-ocular reflex phase (a mea­sure of eye position relative to headposition during rotary chair testingand a more persistent indicator ofchronic pathology) was notreported.2o

In a study examining the effects of ablast in a confined space, Cohen etaP5 documented a 1994 bus bomb­ing that resulted in 22 people beingkilled, 48 people being injured, and23 people being hospitalized. Seven­teen patients were monitored for 6months in an outpatient otolaryngol­ogy clinic. Vestibular testing in­cluded ENG and computerized dy­namic posturography (CDP). A totalof 41% of survivors of the blast re­ported dizziness, 35% had deficits inpostural stability, and 12% com­plained of positional vertigo. TheENG testing did not reveal abnormal­ities in the 13 people who weretested. A total of 71%of the survivorswith initial complaints of dizzinesscontinued to be symptomatic at the6-month follow-up.

Van Campen et al performed thelargest systematic evaluation of sur­vivors of a blast to date in a 2-paperseries after the Oklahoma City bomb­ing; the first report focused on au­diologic sequelae,71 and the secondreport documented vestibular se­quelae.25 In the latter study, investi­gators evaluated 30 subjects withcomplaints of dizziness, vertigo, orimbalance over the course of 1 yearusing a questionnaire, ENG, and CDP.The onset of symptoms in this groupwas variable; 48% of subjects re­ported the immediate onset of dizzi­ness on the day of the blast, and 63%reported that this symptom occurredwithin 48 hours afterward. Sixteenof the 24 subjects evaluated 1 yearlater (67%) reported troubling symp­toms. The ENG findings indicatedthat 30% of subjects had positionalnystagmus, 11% had BPPV, 7% hadbithermal caloric weakness, 4% hadabnormal smooth pursuit, and 4%had gaze-evoked nystagmus. TheCDP results were mixed; 68% of sub­jects had normal function, 15%showed a vestibular pattern (diffi­culty standing with eyes closed/mov­ing platform and difficulty standingwith moving surround/moving plat-

II

·eptember 2009 Volume 89 Number 9 Physical Therapy III 985

TBI and Vestibular Pathology After Blast Exposure

form), 13% had surface-dependentdeficits (difficulty standing on a mov­ing platform), and 4% had physiolog­ically inconsistent results.24

In a recent abstract, Hoffer et aF2compared dizziness in service mem­bers exposed to a blast with dizzi­ness in service members not ex­

posed to a blast. The investigatorsreported on 34 patients who had ex­perienced a CHIwithout a blast com­ponent (CHI group) and 21 patientswho had experienced a blast injuryonly (blast group). Each group pro­vided a detailed history and under­went audiologic and vestibular test­ing. In the CHI group, 59% (20/34)were classified as having posttrau­matic migraine-associated dizziness,6% (2/34) were classified as havingposttraumatic exercise-induced diz­ziness, and 35% (12/34) were classi­fied as having posttraumatic spatialdisorientation. The investigators de­scribed 2 subgroups within the blastgroup-a group with vertigo and agroup without vertigo. Headachesand chronic unsteadiness were com­

mon in both subgroups. Another dif­ference between the CHI and blastgroups was the report of headachesand dizziness beginning during ex­ercise in the blast group but the re­port of the onset of dizziness afterexercise in the CHI group. Finally,the blast group had significantlymore people with hearing loss andneurocognitive disorders. These datasuggest that there are pathophysio­logic differences between BITBIandblunt trauma-induced TBL

In summary, the current body of lit­erature describing the vestibular-likesymptoms attributable to a blast ex­posure consists primarily of casestudies and single-subject reports.Nonetheless, these studies and re­ports consistently described patientswith persistent symptoms (eg, pos­tural instability and oscillopsia) andphysiologic findings characteristic ofvestibular pathology (eg, positional

nystagmus and asymmetry on ENGtesting). Although the current bodyof literature on the effects of blastexposure seems to support correla­tions among blast exposure, vestibu­lar pathology, and TBI, the smallamount of evidence in these studies

precludes inferences of causality. Todate, the absence of a gold standardor at least agreement about diagnos­tic measures for blast-related dizzi­ness has made definitive links amongblast exposure, vestibular pathology,and TBI elusive. The rehabilitation

community has an opportunity tocontribute data toward a consensuson optimal diagnostic and treatmentpractices.

Toward a Consensus onClinical Best PracticesIt is important to use evidence-baseddiagnostic and rehabilitation strate­gies in the management of servicemembers with BITBIY In recentyears, clinicians across disciplines inthe DOD and the Veterans Health

Administration have significantly ad­vanced knowledge about blast se­quelae with the publication of policyreports, systems-of-care reports,editorials, and clinical case re­portS.4,5,20,21,30,73-76Additionally, se-lected studies of the characterizationand treatment of dizziness after con­

cussive injuries in personnel on ac­tive duty and in the literature onsports-related trauma and braininjury may be relevant to the man­agement of head trauma from sec­ondary and tertiary blast ef­fects.26,27,77-82Despite this growingbody of literature describing the pre­sentation of BITBI and blast-relateddizziness, there is no official consen­sus on how to assess blast injuries oron how to conduct the clinicalexamination.

The American Physical Therapy As­sociation's Guide to Physical Thera­pist Practice83 emphasizes clinicalmanagement based on a frameworkfor assessing the level of pathology

(eg, asymmetric peripheral vestibu­lar function), impairment (eg, gazeor gait instability), functional limita­tions (eg, ability to perform job­related tasks), and disability (eg, in­ability to function in one's chosenvocation). For the care of patientswith polytrauma attributable to blasteffects, this model provides arehabilitation-focused complementto traditional medical (diagnosis­driven) or mechanism-of-injury­driven models of clinical manage­ment.84 The application of the WorldHealth Organization's InternationalClassification of Functioning, Dis­ability and Health (ICF)85expandstraditional concepts of the physicaltherapy plan of care through an eval­uation of the impact of identified def­icits relative to a service member'sunique social and vocational con­texts. Clinical integration of the ICFmodel into the assessment of dizzi­ness in service members who havebeen exposed to a blast can aid re­habilitation providers in their effortsto articulate how even subtle disrup­tions in body structure and functioncan dramatically affect participationand disability.

Physical TherapyAssessment of BITBI and

Vestibular PathologyHistory and Physical ExaminationFor clinicians caring for servicemembers who have been injured,tools such as the Military Acute Con­cussion Evaluation13 and the WalterReed Army Medical Center Blast In­jury Questionnaire21 may be usefulin directing the initial screening andcharacterization of patients withblast exposure and suspected TBI orvestibular pathology. Other self­report measures, such as the Dizzi­ness Handicap Inventory86 and theActivities-specific Balance Confi­dence Scale,87provide insight into apatient's self-perceived limitations,which may have deleterious effectson rehabilitation or social function-

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TBI and Vestibular Pathology After Blast Exposure

Ig. These measures are ideally ad­rinistered initially and duringJllow-upvisits. Pierce and HanksHHtported that participation in activi­esof daily living is one of the bestI[edictorsof quality of life in peoplerithTBl.

hephysical examination should be~rected toward an assessment ofunction implicated in the historyndsystems review.20.21The clinicalssessment of symptomatic blast­xposed personnel should includeaeasures of vestibulo-ocular reflexunction,positional testing, and mea­ures of posture and gait stability.'roviders at the DOD have advo­~tedthe screening of service mem­lerswho have been exposed to aIlastwith a series of questionnaires,aldiologymeasures, and clinical ves­ibular tests (eg, noncomputerizedlassive dynamic visual acuity testm.dhead impulse test) (Figure).21[heFigure is adapted from a DODagorithm detailing the process forhe care of people with TBJ.H9Itlighlightscritical management prac­icesfor personnel with blast injuries'romthe time of the injury (combat'One)to the eventual discharge from·ehabilitation. The Figure informs!ecisionsabout patient care by guid­ng appropriate provider referrals,lighlighting the specific capabilities)f interdisciplinary team members,lighlighting commonly used assess­Illentsfor testing people who havebeenexposed to blasts, and present­il:J.gmanagement options for blast­related dizziness. In aggregate, thealgorithmillustrates the importanceofinterdisciplinary cooperation foroptimal diagnostic, prognostic, andtherapeutic practices and outcomes.

Computerized behavioral measuresmchas the dynamic visual acuity testandCDP are widely used in rehabil­itation settings to assess gaze andpostural stability, respectively, in pa­tientswith blast exposure, dizziness,or TBI.15.24,25,70Vestibular function

testing (eg, rotary chair test andENG) is also advisable in this patientpopulation.27,66 The sensitivity ofclinical gait analysis to vestibular def­icits may be enhanced by the admin­istration of a standardized measure,such as the Dynamic Gait Index90 orthe Functional Gait Assessment.91For people with suspected mTBI andcognitive deficits (in addition to diz­ziness), therapists should considerdual tasking in balance and gait ac­tivities to identify processing and re­action time impairments.79-H2.92

Because some clinicians caring forservice members who have been ex­

posed to a blast are reporting associ­ations between physical exertion(eg, running) and the onset of symp­toms (eg, headache and vertigo), cur­rent DOD guidelines recommend ex­ertional testing in patients with TBIbefore a return to full dUty.91A ser­vice member's successful (ie, asymp­tomatic) completion of such testingmay offer reasonable assurance thatsymptoms will not recur with phys­ical stress, gauge readiness to returnto work, and serve as a long-termrehabilitation goal guiding dischargefrom physical therapy.

Table 3 provides a concise review ofvestibular impairments associatedwith TBl. Because the underlying pa­thology associated with blast-relateddizziness has not been causally estab­lished in prospective studies, Table 3shows an impairment-based ap­proach to assessment; references forboth blast-related TBI and non- blast­related TEl are cited as the founda­tion for current best-practiceguidelines.

Impairments to ParticipationPatients who have been exposed to ablast and are symptomatic may havesignificant barriers to participation intheir unique social context. For ser­vice members with blast injuries,persistent dizziness and TBI maycontribute to disability by limiting

their ability to serve in a prior capac­ity on active duty. In the context ofthe ICF model, it is conceivable thata patient with severe neurologic pa­thology (eg, spinal cord injury or ce­rebrovascular accident) may havesignificant impairments (eg, paralysisor hemiparesis) but not necessarilyhave barriers at the level of partici­pation given sufficient time and suc­cess with rehabilitation. The con­verse is equally conceivable for aservice member with subtle impair­ments in the demanding context ofmilitary service. For instance, an in­dividual who requires a high degreeof gaze stability to function as anaviator or sniper may be effectivelydisabled by even a minor vestibulardeficit. Similarly, a service memberwho demonstrates little objective im­pairment during vestibular testingbut who continues to complain ofmotion intolerance may be ineffec­tive or, worse, detrimental to mis­sion performance in an operationalenvironment.

Physical TherapyManagement of BITBI andVestibular PathologyIndividualized vestibular physicaltherapy has been shown to be ben­eficial for survivors of blasts withvestibular symptoms. Recently,Gottshall70 reported that servicemembers with blast-related balance

problems demonstrated significantimprovement in gaze and gait stabil­ity after 16 weeks of vestibular phys­ical therapy. Dynamic visual acuity,target acquisition, and target track­ing improved after 4 weeks. In addi­tion, horizontal gaze stabilizationtest scores improved significantly af­ter 12 weeks, and vertical gaze stabi­lization test scores improved signifi­cantly between 12 and 16 weeks­coinciding with patients' self-reportsof resolving dizziness while running.The Dynamic Gait Index showed sig­nificant improvement at week 8 andcontinued improvement at week 12.

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TBI and Vestibular Pathology·After Blast Exposure

Comprehensive Neurological Examination(Triage MD)

Imaging studies PRN (MRI or CT scan)Neurobehavioral/neurocognitive evaluations

Patient Evaluated by M D (PRN)

Patient complaints of symptoms and signsconsistent with blast-induced dizziness

Headaches OscillopsiaDizziness Hearing lossVertigo Spatial disorientationHearing loss Postural instabilityAltered gait

(central or peripheral vestibular etiologysuspected)

NO I Return to duty or patient mayfollow up PRN with delayed­onset symptoms

Medical managementLimited duty/profile x 2 weeks+

YES I Follow up with MD (PRN)Appropriate referral generation

PT Diagnosis: blast-induced dizziness of centraland/or peripheral etiology (VH) with or without TBI I YES

Vestibular Laboratory Testing (ENT / Audiology)Clinical evaluation (ENT)AudiogramTympanogram/otoscopyDistortion product oto-acoustical emission testingElectronystagmogram

(central/peripheral vestibular oculomotor function)Rotary chair testing

(sinusoidal and velocity steps)Vestibular evoked myogenic potentials

(otolith function tests)

YES (+) clinical/laboratory findings consistent withvestibular pathology (peripheral or central)

YES

Physical Therapy (Clinical Examination)Patient self-report measures administered

Dizziness Handicap InventoryActivities-specific Balance Confidence QuestionnaireWRAMC Blast Injury Questionnaire

History and systems reviewTests and measures:

Gait analysisClinical gait analysis for gross function and symmetryDynamic Gait Index/functional gait assessment

Neuro-musculoskeletal examinationCerebellar tests

Rapid alternating movementsFinger to nose/past pointing

Oculomotor examination (assess CN integrity and aVOR)Cranial nerve III, IV, VI, VIIISmooth pursuitaVOR cancellation

Positional nystagmus testingHead impulse testingHead-shaking nystagmus test (administered with Frenzel lenses)Positional testingDynamic visual acuity testingGaze stabilization test

Computerized dynamic posturographySensory organization testHead-shaking sensory organization testMotor control test

Romberg/Sharpened Romberg test

NO

YES (+) red flags

Evaluate for 12 Red Flags Guidance (91)1. Progressively declining level of consciousness2. Progressively declining neurological examination3. Pupillary asymmetry4. Seizures

5. Repeated vomiting6. Double vision

7. Worsening headache8. Cannot recognize people or disoriented to place9. Behaves unusually or seems confused and irritable10. Slurred speech11. Unsteady on feet12. Weakness or numbness in arms/legs

Plan of Care/PT Management-I nitiate vestibular PT

Canalith repositioning techniquesGaze and gait stability exercisesStatic and dynamic postural stability trainingHabituation training

-Vocational/military specific skills trainingFire Arms Training SimulatorComputer-assisted rehabilitation environmentFormal physical fitness testing

-Management of comorbid deficits in body structureand function, barriers to participation

Exertional Testing Protocol (91)

1. 65%-85% THR (nO-age) using push up, step aerobic, treadmill, orupper body ergometer2. Assess for symptoms (HA, vertigo, photophobia, balance, dizziness,nausea, tinnitus, visual changes, response to bright light/loud noise)3. This test should be administered prior to RTD to ensure fitness inoperational environments among otherwise well-compensated SMs

Figure.Integrated rehabilitation management of blast-related dizziness. LOC=loss of consciousness; PRN=as needed/indicated by provider;RTD=return to duty; MRI=magnetic resonance imaging; CT=computed tomography; ENT=ear, nose, and throat (otolaryngologyMD); PT=physical therapy; PCM=primary care provider; VH=vestibular hypofunction; ED=emergency department; SM=servicemember; TBI=traumatic brain injury; THR=target heart rate; WRAMC=Walter Reed Army Medical Center; CN=cranial nerve;aVOR=angular vestibulo-ocular reflex.

988 11'1 Physical Therapy Volume 89 Number 9 September 2009

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TBI and Vestibular Pathology After Blast Exposure

Table 3.Clinical Presentation of Common Vestibular Symptoms and Findings Associated With Traumatic Brain Injury (TBI)O

ImpairmentRecommended TesUbEvidencec

Increased motion sensitivity

Clinical examination, Motion Sensitivity Quotient,Abnormal posturography77(motion sickness)

clinical test of sensory integration of balance

Oscillopsia or gaze instability

Clinical examination, computerized dynamicAbnormal computerized dynamic visual acuity in

visual acuity

patients with acute-stage mTBI,78 significant

dizziness-related disability relative to that insubjects without mTBI'8Vertigo

Clinical examination, positional test (Dix-Isolated BPPV in absence of documented head

Halipike), electronystagmography

injury (PBI),",18,51 blast-induced BPPV

secondary to head trauma, d,15 BPPV in 15% ofpatients with TBI,92 BPPV secondary toprimary overpressure wave (PBI),",22non positional vertigo in 5/5 service memberslocated within 300 cm (10ft) of blastepicenter,d,23 abnormal Dix-Halipike testresults (positional testing)25Posttraumatic migraine-

Clinical examination, computerized dynamicAbnormal aVOR gain, phase, symmetry inassociated dizziness

posturography, rotary chair testsinusoidal rotary chair test,25,26 abnormal

high-frequency aVOR gain,2s,26 normal CDPfindings25,26Spatial disorientation

Clinical examination, computerized dynamicAbnormal CDP findings,25,26 abnormaliy low

posturography, rotary chair test,

vestibulo-ocular reflex gains and abnormal

videonystagmography

phase shifts during midfrequency (0.32 and

0.64 Hz) sinusoidal rotary chair test,25,26 visualfixation abnormalities duringvideonystag mog raphy2S,26Gait deficits

Clinical examination, motion capture test (gaitLower gait speed (acute), subnormal gait speed

laboratory)

(chronic), conservative gait strategy with dual

tasking," abnormality of gait, d,20 significantlyreduced gait speed and stride length in.subjects with TBI'2Postural instability

Clinical examination, computerized dynamicSignificantly lower composite CDP scores in

posturography

subjects with mTBI than in control subjects

who were healthy,92 15% of subjects whowere exposed to blasts demonstrated a"vestibular pattern" of postural instability, thatis, abnormal on conditions 5 and 6 (ie,moving force plate with eyes closed [sensoryorganization test condition 5] and deficitswith moving force plate and moving surround(sensory organization test condition 6)d,24Vestibular hypofunction

Clinical examination, caloric examination80% incidence of vestibular pathology in

(electronystagmography), rotary chair test,

patients with TBI per caloric assessment: 7/10

computerized dynamic visual acuity

had unilateral vestibular hypofunction and 1/

10 had bilateral vestibular hypofunction92

a Data include vestibular pathology secondary to blast exposure and TBI.b Clinical examination included cervical range of motion, vertebral artery test, oculomotor examination, head impulse test, passive dynamic visual acuity test(noncomputerized), and Dix·Halipike test.e mTBI=mild traumatic brain injury, BPPV=benign paroxysmal positional vertigo, PBI=primary blast injury, aVOR=angular vestibulo-ocular reflex,CDP=computerized dynamic posturography.d Testing was performed for patients exposed to blasts.

er;

gyice

ve;

Preliminary data suggested that thisbattery of tests may be a sensitivemeasure of behavioral vestibularfunction in patients with blast­induced head injuries.7°

Vestibular physical therapy interven­tions commonly include gaze stabil-

ity exercises to facilitate central an­gular vestibulo-ocular reflex gainadaptation93; substitution exercises,which are believed to increase therecruitment of compensatory sac­cades to help with gaze stability93.94;habituation techniques (eg, the Mo­tion Sensitivity Quotient) to mitigate

the hypersensitivity to head move­ments that is characteristic of motion

intolerance95,96; and static and dy­namic balance and gait exercises toaddress postural instability.97 Benignparoxysmal positional vertigo ismanaged with the canalith reposi­tioning maneuver.98,99Current reha-

')09

r

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TBI and Vestibular Pathology After Blast Exposure

bilitation practices at medical cen­ters (such as the Walter Reed ArmyMedical Center) include trainingwith therapeutic technologies thatchallenge survivors of blasts by ex­posing them to virtual reality stimuli.Although training devices such asthe Computer-Assisted Rehabilita­tion Environment and the Fire ArmsTraining Simulator have been used tomitigate complaints of increased mo­tion sensitivity, they are particularlyeffective at addressing barriers toparticipation because of their utilityin simulating military tasks.

ConclusionLittle is known about the specificpathophysiology of blast injuries andthe resultant effects on the periph­eral or central vestibular system. It isnot known how these processes mayaffect the cortical and subcorticalstructures responsible for motionperception, spatial orientation, equi­librium, and gaze stability. Cliniciansand researchers working with pa­tients exposed to blasts must de­velop sensitive screening and assess­ment measures to identify vestibularpathology in this patient population,quantify the degree of impairmentattributable to a blast, and formulateappropriate treatment strategies toensure optimal participation andminimal disability.

Both authors provided concept/idea/projectdesign and writing. Dr Schubert providedproject management, facilities/equipment,institutional liaisons, and consultation (in­cluding review of manuscript beforesubmission).

This article was received November 3, 2008,and was accepted May 6, 2009.

DOl: 10.2522/ptj.20080353

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992 • Physical Therapy Volume 89 Number 9 September 2009