Peripheral Vestibular Vertigo (Week 3--Cha) Flashcards Preview

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3 most common peripheral vestibular disorders

1) Benign paroxysmal positional vertigo (BPPV)

2) Vestibular neuritis

3) Endolymphatic hydrops (Meniere Disease)


History to take

Episodic vs. chronic

Duration: actual spell vs. aftereffect

Triggers: head movement triggered vs. body position triggered vs. situational

Associated features: auditory or neurologic



Where does the posterior canal project to?

Ipsilateral superior oblique (down and in)

Contralateral inferior rectus (down and out)


BPPV pathophysiology

Otolith particles trapped in semicircular canals (usually posterior canal because of geometry)

Abnormal metabolism of otolith particles (?)


BPPV clinical syndrome

Brief episodes of vertigo (10 sec) when head is moved in plane of canal (vertical or torsional for posterior semicircular canal)

Vertigo stops when head is still

Always worse in transitions to/from recumbency because otolith movement is gravity dependent

No hearing loss

Gait is normal

No neurological deficits


BPPV risk factors

Age (common after 50; and after 75 about a quarter of people get it)

Head trauma

Prior inner ear injury

Prolonged recumbency

Migraine with aura


BPPV diagnosis

Dix-Hallpike Maneuver

Goal is to move the head in the plane of the affected canal in order to move the otoliths and stimulate nystagmus


Nystagmus of BPPV

Delayed onset

<1 minute (usually only 10-15 seconds)

Direction consistent with canal affected (90% torsional upbeat from posterior canal; 10% horizontal from horizontal canal; 1% torsional downbeat from anterior canal)

Fatigue with repeated maneuvers


BPPV--right posterior canal

Torsional upbeat nystagmus

In right posterior canal involvement, the nystagmus will beat counterclockwise toward top of head


BPPV treatment

Canalith repositioning maneuver

(Modified Epley Maneuver)

The idea is th get the otolith particles back to the utricle where they can redissolve back into the endolymph fluid


BPPV post-treatment care

Avoid prolonged head hanging

No need to sleep sitting up

Complication is causing horizontal canal variant (10%) and patient will hate you for making their vertigo worse...

Sleep with good ear down

Specific liberatory maneuvers for horizontal variant available


Vestibular neuritis pathophysiology

Inflammation of vestibular nerve secondary to viral reactivation


Vestibular neuritis clinical syndrome

Severe isolated vertigo and nausea lasting days

No hearing loss

Gradual improvement over weeks--generally ambulatory within a week

Caloric paresis (partial weakness) or plegia (complete weakness) on vestibular function testing

Excellent functional recovery with vestibular rehab


Vestibular neuritis diagnosis

Spontaneous mixed horizontal torsional nystagmus beating toward intact ear

Nystagmus is suppressed by visual fixation

Positive head impulse test showing delayed correction of eye movement for head movement (do this because cerebellar infarct is possible and with that the head impulse test is negative)


Head impulse test

The function of the vestibulo-ocular reflex (VOR) is to compensate eye movements for head movements

If VOR is dysfunctional due to peripheral lesion, then this reflex will be slowed and eyes will move temporarily with the head and will have to make a "catch up" or corrective movement to look straight back at the examiner

This "catch up" saccade does not happen with central lesions


Vestibular neuritis treatment

If symptomatic: anti-nausea (meclizine, promethazine, benzodiazepines, etc) as needed

Do not over treat with vestibular suppressants because that impairs recovery

Steroids improve testing outcomes, not necessarily symptoms but are generally given if no contraindications

Early vestibular rehabilitation is key

Extremely low risk of recurrence


Endolymphatic hydrops (Meniere Disease) pathophysiology

Abnormal fluid balance in inner ear causing dilated endolymphatic space

Likely end-stage response due to various insults (vascular, autoimmune, metabolic, etc)


Endolymphatic hydrops clinical syndrome

Episodes of vertigo and auditory symptoms (unilateral hearing loss, tinnitus, ear fullness lasting hours)

Gradual loss of hearing in the low frequencies first but can ultimately be of any frequency

Gradual loss of vestibular function


1995 AAO-HNS criteria definite endolymphatic hydrops

At least 2 episodes of vertigo >20 min

Audiometrically confirmed hearing loss

Tinnitus or fullness


Endolymphatic hydrops treatment

Medical: diuretics, salt restriction <2g per day, stress reduction

Surgical: labyrinthectomy if no useful hearing left, vestibular nerve cut if useful hearing left, intratympanic gentamycin injection (toxic to vestibular system, not hearing!), intratympanic steroid injection


Occlusive ophthalmoscopy

Removes fixation to unmask spontaneous nystagmus

Look at patient's optic disc while occluding the other eye

Note: since you're looking at the back of the eyeball, the direction of optic disc movement will be the opposite of cornea movement


Peripheral nystagmus


Torsional with vertical or horizontal component

In plane with canal affected

Inhibit with fixation (smooth pursuit system)

Fast compensation for stable lesions

Normal ocular control

Normal neurological exam

Usually due to damage to Scarpa's ganglion, semicircular canal, vestibular nerve


Central nystagmus

Direction changing

Direction incompatible with any inner ear structure--pure vertical or pure torsional

No inhibition with fixation

No compensation

Usually other ocular control problems, especially smooth pursuit

Abnormal neurological exam

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