Peripheral Vestibular Vertigo (Week 3--Cha) Flashcards
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
Quality
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
Unidirectional
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
