MAA

Oo(rSnpeSgRtmsdltttfCwdlqatSaptot2

F

S

P

R

0

C

d

5

anagement of posttraumatic vertigoRNE ERNST, MD, PHD, DIETMAR BASTA, PHD, RAINER O. SEIDL, MD, INGO TODT, MD, HANS SCHERER, MD, and

NDREW CLARKE, PHD, Berlin, Germany

Bjtoabnnceqcpvmafics

M

c1twgTnIpNMnWiftppwhfiwcdo

BJECTIVE: To evaluate patients after blunt traumaf the head, neck, and craniocervical junctionwithout fractures) with vertigo and to report theesults of treatment after extensive diagnostics.TUDY DESIGN: Prospective study of consecutiveew cases with vertigo after trauma at differenteriods of onset. During 2000-2002, 63 patients werexamined and treated.ETTING: Regional trauma medical center for thereater Berlin Area, tertiary referral unit.ESULTS: The primary disorders included labyrin-

hine concussion (18), rupture of the round windowembrane (6), and cervicogenic vertigo (12). The

econdary disorders included otolith disorders (5),elayed endolymphatic hydrops (12), and canalo-

ithiasis (9). The patients were free of vertigo symp-oms (except cervicogenic and otolith disorder) af-er treatment, which consisted of habituationraining, medical and surgical therapy options. Theollow-up was 1 year.ONCLUSION: Posttraumatic vertigo can be treatedith a high success rate once the underlying disor-er has been identified. The extent of the neuroto-

ogical test battery determines the precision anduality of diagnostics. Surgical measures should ben integral part of treatment modalities if conserva-

ive treatment is not effective.IGNIFICANCE: Minor trauma of the head, neck,nd craniocervical junction can have major im-act on the vestibular system at different sites. Pa-

ients need to be carefully diagnosed, even if thenset of vertigo occurs a few weeks or months after

he initial trauma. (Otolaryngol Head Neck Surg005;132:554-558.)

rom the Department of Otolaryngology at ukb Medical Center (Drs Ernst,

Basta, Seidl, and Todt) and the Department of Otolaryngology, Vestibular

Research Labs at University Hospital Berlin (Charité), Benjamin Franklin

Medical Center, (Drs Scherer and Clarke) Berlin, Germany.

upported by a grant from the Sonnenfeld Foundation, Berlin, Germany.

resented at the Annual Meeting of the American Academy of Otolaryngolo-

gy–Head and Neck Surgery, Orlando, FL, September 21-24, 2003.

eprint requests: Prof. Arne Ernst, Department of Otolaryngology at ukb,

Warener Str. 7, D-12683 Berlin, Germany; e-mail, ArneborgE@ukb.de.

194-5998/$30.00

opyright © 2005 by the American Academy of Otolaryngology–Head and

Neck Surgery Foundation, Inc.

moi:10.1016/j.otohns.2004.09.034

54

lunt trauma of the head, neck, and craniocervicalunction can result from injuries such as falls, whiplash-ype injuries, contact injuries after impact with a solidbject, among others. The trauma mechanisms can varys well as the impact forces. The vestibular system cane impaired at different sites despite the fact that scan-ing (by MRI, CT) usually reveals no evident intracra-ial pathological changes, skull base fractures, orhanges of the craniocervical junction. There are sev-ral reports in the literature about neurotological se-uelae of a blunt trauma of the head, neck, and cranio-ervical junction.1-5 One of the most commonathologies described is benign paroxysmal positionalertigo (BPPV), which can be treated by repositioninganeuvers with a high success rate.6 It is, therefore, the

im of the present paper to summarize the vestibularndings of a larger sample of trauma patients whoomplained of dizziness and to outline managementtrategies.

ATERIALS AND METHODSIn a prospective study, 63 consecutive patients who

omplained of vertigo (52 female, 11 male; age range7-59 years with a mean of 27.5 years) after bluntrauma of the head, neck, and craniocervical junctionere included (from 2000 through 2002). The patientsave their informed consent to participate in the study.he pathomechanisms of the trauma, the related diag-oses, and the gender ratio are summarized in Table 1.n all cases, primary care and further diagnostics wereerformed by the Departments of Trauma Surgery,eurology, and Radiology. After clinical examination,RI or CT scanning was performed of the neurocra-

ium, the skull base, and the craniocervical junction.hen no evident pathology (e.g., fractures, wounds,

ntracranial pathology, or neurological deficits) wasound, the patients were asked to describe any addi-ional symptoms or health problems. If they com-lained of vertigo (“dizziness”, “unsteadiness”, “slip-ing away”, “rotational or positional vertigo”), theyere transferred to our department. This is denotedere as “primary disorder”, i.e., occurrence within therst 24 hours after the trauma. In the other cases inhich any such symptoms were reported during a later

onsultation, they were referred to “secondary disor-er” (3 weeks to 3 months after the trauma). Auditoryr other sensory deficits (e.g., blurred vision or anos-

ia) are not dealt with in the present study, although a

pttjwwtohrtOpmoa(eKa

ipbot

esT

ghln

R

nct

w

Tnb

n

Otolaryngology–Head and Neck SurgeryVolume 132 Number 4 ERNST et al 555

ure-tone audiogram (PTA) was obtained from all pa-ients. On referral, the case history of each patient wasaken (trauma mechanism, date, initial complaints, sub-ective typing of vertigo); an otoscopic examinationas carried out and the following neurotological testsere performed: vestibulospinal tests (Romberg, Un-

erberger test); videooculographic testing of spontane-us, positional nystagmus, random horizontal or fixedorizontal saccades; caloric irrigation (VOR testing);otational chair testing (sinusoidal harmonic accelera-ion testing of low-frequency VOR gain and phase; GNtometrics, Neckartenzlingen, Germany); dynamicosturography testing [sensory organization test (SOT),otor control test (MCT); Neurocom, Clakamas, OR7];

tolith testing [saccular testing by VEMP recordingsnd utricular testing using subjective visual verticalSVV) and/or otolith-ocular response (OOR) duringccentric rotation; VIKING V, Nicolet Biomedical,ornwestheim, Germany; for methodology see Refs. 8

nd 9]; electrocochleography (optional, only performedn cases of suspected delayed, posttraumatic, endolym-hatic hydrops10; trunk sway measures of postural sta-ility by Sway Star (optional, only performed in casesf suspected cervicogenic vertigo; Balance Int Innova-ions, Basle, Switzerland11,12).

After diagnosing the different neurotological diseasentities (Table 1), they were subject to a managementcheme according to the underlying disease (Table 2).he follow-up period of the patients was 1 year.

The patients’ test results were compared to age- andender-related control subjects without a history ofead and neck trauma. A statistically significant corre-ation between the trauma mechanisms and the type of

able 1. Pathomechanisms involved in blunt traumaeurotological disorders involved in the 63 patientse observed simultaneously or successively.

Trauma mechanisms

Brain concussion (i.e. falling from different heights on the ground)

Brain concussion with cervical compression (i.e. falling from a horse o

Anteretroflexion of the cervical spine (classical “whiplash” mechanism

Anteretroflexion of the cervical spine with contact trauma the head hits

to the head restraint)

Other mechanisms (i.e. the head is hit by another solid item, e.g., a do

Neurotological disorders

Perilymphatic fistula (round-window rupture)

Benign paroxysmal positional vertigo

Labyrinthine concussion

Central vestibular disorder

Delayed endolymphatic hydrops (posttraumatic)

Otolith disorder(saccular or utricular dysfunction)

Cervicogenic vertigo (vestibulospinal postural instability)

, number of patients in each subgroup; f, female; m, male.

eurotological disorder could not be found.

ESULTSThe different trauma mechanisms led to a variety of

eurotological disorders (Table 1) although no signifi-ant correlation was found between mechanism andypes of disorder.

The primary disorders that affected the patientsithin the first 24 hours after trauma included:

● BPPV (n � 36), which reoccurred in 9 patients.Primary treatment consisted of repositioningmaneuver6,13 repeated up to 3 times if required.After reoccurrence, 2 patients were surgicallytreated by occlusion of the posterior semicircularcanal.14 A positional, torsional nystagmus uponDix-Hallpike’s maneuver was taken as confir-mation of the diagnosis.

● Labyrinthine concussion (n � 12) had normal-ized over the first 5 days with drug treatment(sedatives, antemetics) on average. The occur-rence of spontaneous nystagmus, initial unilat-eral hyporesponsiveness upon caloric irrigation,pathological rotational chair test result (periph-eral lesion), and deviation upon vestibulospinaltesting was taken as confirmation of the diagno-sis.

● Perilymphatic fistulae (n � 3) led to a suddenonset of dizziness in combination with sensori-neural hearing loss (SNHL) of varying degree.These patients were treated surgically by patch-ing the round and oval window niches withconnective tissue and fibrin glue. The occur-rence of spontaneous nystagmus, initial unilat-eral hyporesponsiveness upon caloric irrigation,

e head, neck, and craniocervical junction andthat in some patients 2 or more disorders could

Number of patients

n � 12 (9 f, 3 m)

ad) n � 8 (3 f, 5 m)

n � 23 (22 f, 1 m)

parts of the car, in addition n � 16 (16 f)

nt instrument, a soccer ball) n � 4 (2 f, 2 m)

n �3 (1 f, 2 m)

n � 36 (33 f, 3 m)

n � 12 (11 f, 1 m)

n � 3 (3 f)

n � 12 (10 f, 2 m)

n � 16 (10 f, 6 m)

n � 17 (16 f, 1 m)

of th. Note

n the he

)

interior

or, a blu

pathological rotational chair test result (periph-

aa

t(ptc

The

Otolaryngology–Head and Neck Surgery

556 ERNST et al April 2005

eral lesion), deviation upon vestibulospinal test-ing, a sensorineural hearing loss of differentextent (in 50 % more than 40 dB over all fre-quencies) with/without tinnitus was taken asconfirmation of the diagnosis.

● Central vestibular disorder (n � 3) had a mixedpathology with the leading symptom of “tum-bling”. The patients were instructed to rest, theywere treated by drugs (sedatives, antemetics)and 2 of them had fully recovered within the first5 days. One patient was additionally given anindividualized home training. Different types ofnystagmus (vertical nystagmus, skew deviation,ocular torsion), horizontal body rotations uponvestibulospinal tests, pathological SOT over allconditions (I-VI) was taken as confirmation ofthe diagnosis.

The following secondary disorders were diagnosedt a later date (3 weeks to 3 months, 6 weeks on averagefter the trauma):

● Delayed endolymphatic hydrops (n � 12). Thepatients reported classical Mènière-like type ofvertigo with attacks, but without hearing loss ortinnitus. EcoG was used to confirm the presenceof hydrops. 8 patients were free of vertigo under(betahistine) drug treatment, 4 patients were op-erated on by endolymphatic sac surgery (saccusexposure) and were free of vertigo after theoperation.

● Cervicogenic vertigo (n � 17) occurred widely,but not only after a “whiplash-type” of injury.The diagnosis was confirmed by Sway Star test-ing (pathological), by exclusion of other disor-ders and by pathological SOT (conditions 5 and6, visual preference with unilateral stance imbal-ance7,12). These patients gave mixed symptomsthat were reinforced when the neck pain and thelimitation of cervical spine mobility was maxi-

able 2. Neurotological disorders, their leading cliniours after the trauma, or secondary, with a certaiach disorder (for details see “Results”)

Neurotological disorder Clinical symptoms/tim

Perilymphatic fistula Dizziness, hearing loss (prima

BPPV Positional vertigo (primary, bu

Labyrinthine concussion Dizziness, lateropulsion vomit

Central vestibular disorder Mixed, “tumbling” (primary)

Delayed endolymphatic hydrops Attacks of rotational vertigo (M

(secondary)

Otolith disorder Unsteadiness, stumbling (secon

Cervicogenic vertigo “Tumbling”, “feeling drunk” (

(secondary)

mal. In general, the extent and expression of v

vertigo varied in dependence of the physicalcondition of the patient. The patients were pri-marily treated by physiotherapy (e.g., osteopa-thy, exercises), analgesics and antirheumaticsand by platform training on the BalanceMaster(Neurocom, Clakamas, OR) to give them bettercontrol of their increase in sway in the roll andpitch plane. These patients produced widelyscattered results; only 12 patients were definitelyfree of vertigo after 1 year. 5 patients com-plained, to varying degrees, but continuously,about vertiginous episodes after 1 year.

● Otolith disorders (n � 16) were determined byVEMP testing (saccular) or eccentric rotation(utricular). A combination of saccular and andutricular dysfunction was usually found,whereas in 2 cases an isolated utricular dys-function was found. The patients with otolithdisorders generally presented after a longerperiod of time (usually after approximately 10weeks) because 85 % did not consider their“unsteadiness” as a specific symptom, butrather as common sequelae of the trauma.These patients were provided with individual-ized training routines on a tilting platform.The success of such a habituation training canonly be determined after a 12- to 24-monthperiod. After 12 months, 35% of the patientsreported partial improvement of their symp-toms. The remaining patients had not yetfound the habituation training to be effective.

Of the 63 patients, 29 (46%) manifested a combina-ion of 2 different types of neurotological disorderse.g., initially BPPV, followed by a delayed endolym-hatic hydrops); whereas 7 patients (11 %) had morehan 2 neurotological disorders (e.g., labyrinthine con-ussion, followed by otolith disorder and cervicogenic

mptoms, time-of-onset (i.e. primary, within 24-lag, and the management schemes applied in

nset Therapeutic management

Tympanoscopy (patching the RW)

rring) Repositioning maneuver, posterior canal occlusion

ary) Drugs (sedatives, antemetics)

Drugs (sedatives, antemetics) habituation training

like) Drugs (betahistidine), surgery (endolymphatic sac

exposure)

Habituation training (platform training)

d to pain) Physiotherapy, analgesics, habituation training

cal syn time

e-of-o

ry)

t reoccu

ing (prim

énière-

dary)

correlate

ertigo; Table 3).

D

ortctotpoIpothfiPotsbisavchafnpp

ctcmeltauloTmtrsea(ttbtnaciut

lalp

R

Td

B

d

Otolaryngology–Head and Neck SurgeryVolume 132 Number 4 ERNST et al 557

ISCUSSIONThe present study is intended to evaluate the impact

f acceleration or forces applied to the head, neckegion, and to the craniocervical junction (bluntrauma). The 2 most interesting findings are the lack oforrelation between the trauma mechanism and a par-icular neurotological disorder; and the variety of dis-rders found concomitantly or successively in some ofhe patients. We did not systematically work up theatients’ subjective complaints or the impact of vertigon the quality of life (e.g., by the Dizziness Handicapnventory15) in this study; this requires the long-termerspective and is therefore still in progress. A majorityf the patients (76%) also reported temporary subjec-ive hearing loss, although we only found substantialearing losses in the subpopulation with perilymphaticstula (a SNHL could be evidenced in all cases byTA). However, we could report recently on the impactf blunt head trauma on the central auditory processinghat can be significantly impaired.16 There is a long-tanding controversy in the literature as to whetherlunt trauma to the head and neck, “whiplash” type ofnjury, or other types of injury can affect the vestibularystem (see Refs. 1-3, 5 and the comments on thisrticle). In our series, the patients with cervicogenicertigo had undergone various trauma mechanisms (in-luding brain concussion with cervical compression,aving the head and craniocervical junction hit bynother solid item, apart from “whiplash”) and wererequently affected by another or even 2 other types ofeurotological disorders (Table 3). The majority of ouratients were female, which is due to the fact that the

ABLE 3. Parallel or subsequent occurrence ofifferent neurotological disorders

Type of disordersNumber

of patients

Labyrinthine concussion, BPPV (parallel) 8

Labyrinthine concussion, central vestibular

disorder (parallel)

1

Labyrinthine concussion, cervicogenic vertigo

(subsequent)

1

BPPV, delayed el hydrops (subsequent) 9

Otolith disorder, cervicogenic vertigo (subsequent) 7

Perilymphatic fistula, otolith disorder (subsequent) 3

Labyrinthine concussion, otolith disorder,

cervicogenic vertigo (subsequent)

1

BPPV, otolith disorder, cervicogenic vertigo

(subsequent)

4

BPPV, delayed el hydrops, cervicogenic vertigo

(subsequent)

2

PPV, benign paroxysmal positional vertigo; el hydrops, endolymphatic hy-

rops.

revailing trauma mechanisms (ante/retroflexion of the

ervical spine, Table 1) affected young women withoutrained musculoskeletal system (frequently on diet,ontraceptive intake, in smaller cars) with no adequateuscular resistance against a sudden impact (e.g. rear-

nd collision) (see below). This female prevalence is inine with the literature, the Quebec Task Force in par-icular17 and our recent paper on auditory symptomsfter blunt head trauma.16 When considering the medi-m-term prognosis (1 year) of each type of neuroto-ogical disorder, the primary disorders had the bestutcome. This is in line with other reports (13, 14, 18).he poorest outcome was observed in the (largely fe-ale) subpopulation of patients with cervicogenic ver-

igo and otolith disorder. The first is presumed to be theesult of the interindividual variation in the musculo-keletal system (and the ability to develop coping strat-gies by habituation/training7,12,19) and the highly vari-ble conditions of the cervical spine and the soft tissuemuscles, ligaments, joints) in the largely female pa-ients (pain episodes, pre-trauma conditions, contracep-ive intake, etc.). Otolithic vertigo could likewise onlye treated with very limited success in the medium-erm perspective. This seems to be based on the specificature (gravity sensor) of this type of receptor20and itsncient phylogenetic origin, which makes it and theentral vestibular correlates quite resistant to externalnfluences, including training and habituation. Vestib-lar (inferior branch) neurectomy could be an alterna-ive treatment option in the long-term perspective.21

In essence, posttraumatic vertigo can become a chal-enge for the otolaryngologist because of the variabilitynd the late onset of symptoms. An extended neuroto-ogical test battery is required to reliably assess thoseatients.

EFERENCES

1. Fitzgerald DC. Head trauma: hearing loss and dizziness.J Trauma 1996;40:488-96.

2. Guyot JP, Liard P, Thielen K, et al. Isolated vestibular areflexiaafter blunt head trauma. Ann Otol Rhinol Laryngol 2001;110:562-5.

3. Vibert D, Hausler R. Acute vestibular deficits after whiplashinjuries. Ann Otol Rhinol Laryngol 2003;112:246-51.

4. Basford JR, Chou LS, Kaufmann KR, et al. An assessment ofgait and balance deficits after traumatic brain injury. Arch PhysMed Rehabil 2003;84:343-9.

5. Rubin AM, Wooley SM, Dailey DV, et al. Postural stabilityfollowing mild head or whiplash injury. Am J Otol 1995;16:216-21.

6. Parnes LS, Price-Jones RG. Particle repositioning manoeuver forBPPV. Ann Otol Rhinol Otol 1993;102:325-31.

7. Allum JHJ, Shepard NT. An overview of the clinical use ofdynamic posturography in the differential diagnosis of balancedisorders. J Vest Res 1999;9:223-52.

8. Colebatch JG, Halmagyi GM, Skuse NF. Myogenic potentialsgenerated by a click-evoked vestibulocollic reflex. J NeurolNeurosurg Psychiatry 1994;57:190-7.

9. Clarke AH, Engelhorn A. Unilateral testing of utricular function.

Exp Brain Res 1998;121:457-64.

1

1

1

1

1

1

1

1

1

1

2

2

Otolaryngology–Head and Neck Surgery

558 ERNST et al April 2005

0. Ge X, Shea JJ. Transtympanic electrocochleography: a 10-yearexperience. Otol Neurotol 2001;22:465-70.

1. Allum JHJ, Aitkin AL, Ernst A. Differences between trunk swaycharacteristics on a foam support surface and on the Equitestankle-sway-referenced support surface. Gait Posture 2002;16:264-70.

2. Sjostrom H, Allum JHJ, Carpenter MG, et al. Trunk swaymeasures of postural stability during clinical balance tests inpatients with chronic whiplash injury symptoms. Spine 2003;28:1725-34.

3. Epley JM. Particle repositioning for BPPV. Otolaryngol ClinNorth Am 1996;29:323-31.

4. Parnes LS, McClure JA. Posterior semicircular canal occlusionin the normal hearing ear. Otolaryngol Head Neck Surg 1991;104:52-7.

5. Jacobson GP, Newman CW. The development of the Dizziness

6. Nölle C, Todt I, Ernst A. Pathophysiological changes of thecentral auditory pathway after blunt trauma of the head. J Neu-rotrauma 2004;21:251-8.

7. Spitzer WO, Skovron ML, Salmi LR, et al. Scientific mono-graph of the Quebec Task Force on Whiplash-AssociatedDisorders: redefining whiplash and ist management. Spine1995;20(Suppl 8):1S-73S.

8. Shea JJ, Xianxi G, Orchik DJ. Traumatic endolymphatic hy-drops. Am J Otol 1995;16:235-40.

9. Allum JHJ, Bloem BR, Carpenter MG, et al. Differentialdiagnosis of proprioceptive and vestibular deficits using dy-namic support-surface posturography. Gait Posture 2001;14:217-26.

0. Clarke A, Schonfeld U, Helling K. Unilateral examination ofutricle and saccule function. J Vest Res 2003;13:215-25.

1. Sanna M, Ylikoski J. Vestibular neurectomy for dizziness

Handicap Inventory. Arch Otolaryngol Head Neck Surg 1990;116:424-7.

after head trauma. ORL J Otorhinolaryngol Relat Spec 1983;45:216-25.