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