Vestibular Disorder

7/29/2019 Vestibular Disorder

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Vestibular Disorder (updated 09/06)

1. List important information that should be illicited on taking a history in a dizzypatient. ALCharacterize the dizziness vertiginous, disequilibrium, oscillopsia (inability to focus onobjects with motion, such as reading a sign while walking, seen with bilateral or centralvestibular loss), lightheadedness, physiologic dizziness (motion sickness, height

vertigo), multisensory dizziness (diabetes, aging)-associated otologic factors (hearing loss, aural fullness, tinnitus)-Intensity and fatigability-precipitation factors (head movement or motion, stress, diet)-systemic complaints (nausea, vomiting)-central symptoms (numbness, weakness, diplopia, blurred vision)

Onset and duration of symptoms: sec to min (BPPV, VBI, migraine associated vertigoepilepsy, arrhythmia), hours (Menieres, migraine), days (vestibular neuronitis,labyrinthitis), or constant (central), frequency and time of day, initial and last spell

Contributing factors: medications (neuroleptics, antihypertensives, ototoxic medications,

sedatives)-medical history: HTN, cardiac arrhythmias, ischemia, DM, hypothyroid, vasculardisease, otologic problems, depression, neurologic disease, migraines,premenstrual syndrome-recent head trauma-loud noise exposure-flying, diving, heavy lifting-new glasses-fam h/o hearing loss

Associated Sx: falls, confusion, weakness, weight loss, nervousness, headache

2. What are the differences on physical exam between central and peripheral

vertigo? ALPeripheral: Central:

Intensity severe mildFatigability fatigues, adaptation does not fatigueAssoc Sx nausea, hearing loss, sweating weakness, numbness, fallsEye closure worse better w eyes closedNystagmus horizontal, rotatory vertical, bilateralOcular Fix suppresses nystagmus no effect or enhancesnystagmus

3. Describe the classic presentation of Menieres Disease. CB4. Discuss the role of diagnostic studies in the work up of Menieres disease. CB 5. What is the suspected pathophysiology of Menieres disease? CB6. Provide us with an algorithm for the treatment of Menieres disease. CB7. You and (you otologist) are SCUBA diving. During descent, he/she becomesacutely dizzy. What are you worried about and how would you treat him/her? TT 8. You suspect BPPV in a dizzy patient. Discuss the work up and treatment ofthis disorder. What will you tell your patient about recurrence? AL


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DiagnosisHistory

The patient with BPPVexperiences severe vertigo associated with change in head position.The most frequently cited occurrence of this symptom follows rolling over or getting into bedand assuming a supine position. Frequently a specific side is identified as being associated

with symptom onset (e.g., the dizziness comes when I roll over to my right side but not tothe left). Patients also will experience similar symptoms on arising from a bending position,looking up to take an object off a shelf, tilting the head back to shave, positioning the headin the hairdresser's chair, or turning rapidly.Symptoms occur suddenly and last on the order of seconds but never in excess of aminute.

[35]The subjective impression of attack reported by the patient frequently is longer.

Episodes of vertigo frequently are clustered in time and separated by remissions lastingmonths or more. The patient also may report that periods of active disease may beassociated with constant feelings of lightheadedness, worsened by head movement.

[38]

These chronic balance problems may be worse on awakening.In most cases ofBPPV, no specific etiologic disorder can be identified. In a large survey byBaloh and colleagues, no cause was identified in 48% of cases.[35]The most commonknown cause was closed head injury, followed by vestibular neuritis. In our experience,BPPVwill eventually develop in nearly 15% of patients suffering from vestibular neuritis.Other cited predisposing events include infections and certain surgical procedures, includingstapedectomy

[35]and insertion of a cochlear implant.

[39]Prolonged bed rest and Meniere's

disease also are predisposing factors.Findings on Examination

The diagnosis ofBPPVis made by observing the classic eye movements in association withthe Dix-Hallpike maneuver, combined with a suggestive history. The Dix-Hallpike maneuveris carried out as follows (Fig. 165-1). The patient is positioned supine on an examinationtable with the head extending over the edge. The patient is lowered with the head supportedand turned 45 degrees to one side. The eyes are carefully observed. If no abnormal eyemovements are seen, the patient is returned to the upright position. The maneuver isrepeated with the head turned in the opposite direction and finally with the head extendedsupine.

[40]The pattern of response consists of the following: (1) The nystagmus is a combined verticalup-beating and rotary (torsional) component beating toward the downward eye (the superiorpoles of the eyes beat toward the downward ear). Pure vertical nystagmus is notBPPV.

[35]

(2) A latency of onset of nystagmus (seconds) is common. (3) Duration of nystagmus isshort (less than 1 minute). (4) Vertiginous symptoms are invariably associated. (5) Thenystagmus disappears with repeated testing (i.e., it is fatigable). (6) Symptoms often recurwith the nystagmus in the opposite direction on return of the head to the upright position.

[38]Canalithiasis of the posterior semicircular canal is the most frequent cause ofBPPV.Posterior canal BPPVrarely may be bilateral.

[41]If the head is not positioned correctly during

testing (i.e., not positioned with the head in the plane of the posterior canal during testing ofthe unaffected side), debris on the affected side may come to rest against the cupula,simulating an excitatory nystagmus from the unaffected ear.

[42]The lateral semicircular

canal has been identified as the affected structure in approximately 12% of cases, with asignificant fraction of these being induced by the repositioning maneuver for posterior canalBPPV.

[43]Lateral canal BPPVcan be detected by a variation of the Dix-Hallpike maneuver:

The patient is first brought to the supine position with the head resting on (not
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hyperextended below) the examining table. The head is then turned rapidly to the right sothat the patient's right ear rests on the table. Eye movements are monitored with Frenzellenses for 30 seconds. The patient is then returned to the supine position (looking upward)and the head is turned rapidly to the left so that the left ear rests on the table. Eyemovements are again monitored.

The nystagmus with lateral canal BPPVis horizontal and may beat toward (geotropic) oraway from (ageotropic) the downward ear. It often begins with a shorter latency, increasesin magnitude while maintaining the test position, and is less susceptible to fatigue withrepetitive testing than the vertical torsional nystagmus of posterior canal BPPV. Theincreased amplitude and duration of the horizontal nystagmus may reflect action of thecentral velocity storage mechanisms (which perseverate signals from the vestibularperiphery, especially those arising from the lateral canal). Cupulolithiasis, arising eitherindependently or in combination with canalithiasis, is more likely to be involved in theetiology of lateral canal BPPVthan is the case for posterior canal BPPV. Cupulolithiasis canbe differentiated from canalithiasis by minimal or absent latency to the onset of nystagmus.Cupulolithiaisis also can persist for minutes or even as long as the patient remains in theprovocative position.

[44]If the nystagmus is geotropic, the particles are likely to be in the long

arm of the lateral canal relatively far from the ampulla. If the nystagmus is ageotropic, theparticles may be in the long arm relatively close to the ampulla or on the opposite side of the

cupula, either floating within the endolymph or embedded in the cupula.The superior semicircular canal is affected in only 2% of cases ofBPPV.

[45]The nystagmus

expected in cases of superior canal BPPVwould be downbeat and torsional. Such anystagmus can be elicited by standard Dix-Hallpike positioning testing. The right posteriorcanal lies in roughly the same plane as that of the left superior canal, and vice versa.Placement of the head into the right Dix-Hallpike position will therefore bring the left superiorand right posterior canals into the plane of gravity. A nystagmus resulting from the leftsuperior canal BPPVwould, in this position, be expected to be downbeat, with a torsionalcomponent directed such that the superior part of each eye beats toward the upward ear.Note that this nystagmus is opposite in vertical and torsional direction from that resultingfrom right posterior canal BPPV.

Test Results

The bedside Dix-Hallpike test[21]

combined with an appropriate history is key to making thediagnosis. Standard electro-oculography (EOG) and the many videonystagmographydevices do not record the torsional eye movements associated withBPPV. The eyemovement tracings obtained with these standard devices used for clinical testing reflectsolely the associated vertical and horizontal components of the eye movements. Theobservation of these patterns may be facilitated by the use of Frenzel lenses.

Treatment with Reposition ing

First-line therapy for BPPVis organized around repositioning maneuvers that, in cases ofcanalithiasis, use gravity to move canalith debris out of the affected semicircular canal and

into the vestibule. For posterior canal BPPV, the maneuver developed by Epley[26]

isparticularly effective (Fig. 165-2). The maneuver begins with placement of the head into theDix-Hallpike position, to evoke vertigo. The posterior canal on the affected side is in theearth-vertical plane with the head in this position. After the initial nystagmus subsides, a180-degree roll of the head (in two 90-degree increments, stopping in each position untilany nystagmus resolves) to the position in which the offending ear is up (i.e., the nose ispointed at a 45-degree angle toward the ground in this position) is performed. The patient isthen brought to the sitting upright position. The maneuver is likely to be successful whennystagmus of the same direction continues to be elicited in each of the new positions (as
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the debris continues to move away from the cupula). The maneuver is repeated until nonystagmus is elicited. In our experience, when administered in this way, the Epleymaneuver is effective in more than 90% of cases in eliminating BPPV. Medications are notusually given, but a low dose of meclizine or a benzodiazepine 1 hour before may beappropriate if the patient is unusually anxious or susceptible to nausea and vomiting withvestibular stimulation.

The Semont maneuver also is effective for posterior canalBPPV[46]but is more difficult toperform and is less effective than the simpler, more comfortable Epley maneuver.

[47]The

patient is moved quickly into the position that provokes the vertigo and remains in thatposition for 4 minutes. The patient is then turned rapidly to the opposite side, ear down, andremains in this second position before slowly sitting up.For both Epley and Semont maneuvers, gravity is the stimulus that moves the particleswithin the canal, so turning the head on the body is unnecessary. En bloc movement of thehead and body to the extent possible is the preferred treatment pattern. Some physiciansalso use a small handheld vibrator over the mastoid and claim slightly better results,although the results do not seem significantly different.

[48]Mastoid vibration should be

avoided in patients who have had retinal detachment or who may be susceptible to such adetachment because of high myopia. Some investigators recommend having the patient

sleep with the head elevated for 1 to 2 days after the maneuver, but this has not beenshown to have a significant effect.

[49]The following observations support the effectiveness of these maneuvers for treatment ofposterior canal BPPV: (1) Patients who have been symptomatic for years can be cured; (2)BPPVinvolving one canal can convert to BPPVinvolving another canal as a result oftreatment; (3) patients in whom the wrong side was treated and post-treatment instructionswere given show no improvement; and (4) randomized trials have shown the effectivenessof the treatment maneuvers. Because BPPVcommonly resolves in a few weeks to a month,a repositioning maneuver may seem to be no better than placebo in an unselected group ofpatients with BPPVin whom spontaneous recovery is common. In more intractable cases,however, the treatment will almost certainly be determined to be effective.

Treatment maneuvers also have been suggested for the lateral canal variant ofBPPV. Incases that involve geotropic nystagmus, lying on one side with the affected ear up for 12hours has been reported to be effective in the vast majority of cases.

[50]Treatment maneuvers for superior canalBPPVshould follow the same principles. The headinitially should be moved into a dependent position wherein the ampulla is superior, thenrotated by 180 degrees, and then brought back to its initial position. Data on treatment ofsuperior canal BPPVhave not been reported, no doubt owing to its relative rarity.

[51]Some events that can occur during repositioning maneuvers are worthy of discussion.Posterior canal BPPVcan be converted to lateral canal BPPVduring the Epley maneuver.

The lateral canalBPPVusually resolves in several days. Posterior canalBPPVcanoccasionally be converted into a presumed anterior canal BPPV(i.e., symptoms worsen

when the offending ear is up). An obstruction of canalith material may occur at the commoncrus during the Epley maneuver, resulting in a sustained pure torsional nystagmus (both thesuperior and posterior canals are excited simultaneously, so the opposing verticalcomponents cancel and the torsional components add).

Surgical Treatment

The vast majority of patients with BPPVwill be cured by respositioning maneuvers, butsurgical therapy remains an option for the rare patient with disabling persistent disease.
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Singular neurectomy to treat refractoryBPPVwas proposed by Gacek.[25]

During the threedecades since it was described, the procedure has been performed at least 342 times, ofwhich 252 were by Gacek himself.

[52]Although the procedure generally is effective, it is

technically difficult and the risk of hearing loss from the procedure may be as high as41%.

[53]Posterior semicircular canal occlusion was introduced as a treatment forBPPVin 1990.

[54]

This technique blocks the canal lumen so that it becomes unresponsive to angularacceleration. At total of 97 cases have been reported in the literature. Although theprocedure was associated with brief postoperative vertigo, 94 of the 97 patients were curedof their BPPV.

[55]The procedure is associated with a postoperative hearing loss that usually

recovers over several weeks.9. What is Cogans syndrome? ALCogan's Syndrome

Cogan's syndrome was first described in 1945 and is characterized by interstitial keratitis,low-frequency unilateral hearing loss, and vestibular symptoms as well as nonreactivetests for syphilis.

[183]The syndrome was later divided into typical and atypical forms on the

basis of specific ocular findings.

[184]

The typical form includes interstitial keratitis, whereasthe atypical form has ocular features of scleritis, episcleritis, papilledema, and retinaldetachment.

[185]Ten percent of patients with Cogan's syndrome have the atypical form.

Multisystem involvement, including CNS manifestations and inflammatory vascular disease,is a feature ofCogan's disease. Of the two forms, systemic features are noted morecommonly in atypical Cogan's disease. In the typical form, the heart and lungs are the usualsite of systemic involvement, including aortitis, pleuritis, pericardial effusion, coronaryarteritis, and myocardial infarction. In atypical Cogan's disease, systemic features arisefrom a systemic vasculitis (e.g., polyarteritis nodosa, arthritis, glomerulonephritis,gastrointestinal problems).Ocular and inner ear changes appear concurrently or within 6 months of each other. Ocularcomplaints include photophobia, blurred vision, lacrimation, and pain. These symptoms andsigns may be unilateral or bilateral. Onset usually is sudden, and resolution is gradual.Recurrences over years are not uncommon. Ocular pathologic changes include infiltration ofthe cornea with lymphocytes and plasma cells as well as corneal neovascularization.Balance-related symptoms are similar to those of Meniere's disease and consist of suddenattacks of true vertigo with ataxia and vegetative symptoms. Progression to the completeabsence of vestibular function, manifested by ataxia and oscillopsia, is common.Hearing loss is sensorineural in type and is bilateral in 44% of patients.

[186]The loss is

progressive without spontaneous improvement, frequently becoming profound. In bilateralcases, hearing loss frequently begins on one side.Cogan's syndrome is thought to be of autoimmune basis. This suspected etiology is basedon lymphocyte transformation tests, migration inhibition to inner ear tissues, the associationwith rheumatologic diseases, and presence of lymphocytes and plasma cells in the ear andeye, as well as the clinical response to systemic steroids.Clinically, patients often report having had an upper respiratory infection within 7 to 10 daysof initial onset ofCogan's syndrome.

[184]Raised IgG and IgM titers to Chlamydia are

reported in association with activeCogan's syndrome. Furthermore, antibody titers arenoted to decrease with remission of disease. For this reason, it has been suggested that anacute infection, perhaps with Chlamydia, promotes sensitization of the immune system toself and leads to immune-mediated disease.

[184]
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Systemic corticosteroids are the accepted treatment. An initial dose of 1 mg/kg per day ofprednisone usually is recommended, followed by a slow taper. The probability of hearingimprovement is thought to be better the sooner the steroids are started.

[185]In addition,

cyclophosphamide and methotrexate have been recommended by some authorities ifsystemic vasculitis is present.
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Vestibular Disorder