Flashcards in Dizziness, Vertigo and Syncope Deck (19):
Why doesn't vertigo occur with ototoxic drugs or with acoustic neuromas?
ototoxic drugs will affect the vestibular system in both ears, so you don't have the imbalance necessary to cause vertigo
acoustic neuromas can affect only one ear or both, but they grow so slowly that the vestibular system adapts
It is helpful to determine if the vertigo is central or peripheral. What are some associated features of peripheral vertigo?
tinnitus or hearing loss
usually nausea and vomiting are more associated with peripheral, but can be both
What are some associated features of central vertigo?
other brainstem dysfunction like diplopia, dysarthria, dysphagia, etc.
impaired ability to walk or maintain posture is more likely with central, but can be both
How can the nature of the nystagmus help you determine peripheral vs. central vertigo?
vertical and direction-changing gaze-evoked nystagmus suggest central
unidirectional nystagmus can arise from either
What should be on the differential for vertigo?
1. vestibular neuronitis (acute unilateral peripheral vestibulopathy)
2. Layrinthine concussion
3. Vestibular migraine
4. Infarction of the labyrinth, brainstem or cerebellum (wil have additional neurological findins)
5. meniere disease
6. perilymph fistula
7. benign positional paroxysmal vertigo
True or false: there isn't actually any inflammation involved in vestibular neuronitis.
true - it's a misnomer
What is the time course for vestibular neuronitis?
gradually worsens over minutes to hours and symptoms peak within 24 hours and then improve gradually over several days or weeks. complete recovery may not occur fo rmonths
True or false: labyrinthine concussion requires a skull fracture.
false - can occur from head injury irrespective of whether there is an associated skull fracture
Blood supply to the central and peripheral vestibular appratus is via what system?
vertebrobasilar system (posterior and anterior inferior cerebellar arteries and the superior cerebellar artery)
Describe a typical presentation of meniere's.
episodic vertigo with n/v, fluctuating and progressive hearing loss (requires audiology for diagnosis), tinnitus and a sensation of fullness or pressure in the ear
What is the cause of meniere's?
an intermittent increase in endolymphatic volume (probably a sodium channel issue)
Describe the presentation for a perilymph fistula.
patients typically hear a "pop" at the time of a sudden increase in middle ear pressure with sneezing, nose-blowing, coughing, or straining, followed by an abrupt onset of vertigo
Describe the typical presentation for benign positional paroxysmal vertigo.
intermittent attacks of vertigo lasting seconds to minutes, starting after a few seconds' latency following position changes like turning over in bed or looking upward
nausea and vomiting may occur
attacks typically occur in clusters with patients remaining asymptomatic for months or years in between
BPPV results from freely moving crystals of calcium carbonate within the semicircular canals. Which canal do they usually settle in?
How do you diagnose BPPV?
Dix-Hallpike test: patient's head is turned 45 degrees to one side and then extended 30 degrees over the back of the bed. physician then looks for a rotary and vertical nystagmus
the offending ear will be facing the ground when the test is positive
How can BPPV be treated acutely?
the Epley maneuver: put them in the ending position of the Dix-Hallpike test with the offending ear pointing down (45%). Then have them turn their head 90% degrees towrad the opposite side. Then rotate their hips toward that side so their head rotates an additional 90 degrees. then sit them up.
There are many causes of syncope - in general, what are the two neurologically-mediated causes?
neurogenic syncope (reflexive syncope)
Neurogenic syncope is mediated through what nerve?
the vagus nerve
it's an acute hemodynamic reaction produced by a sudden change in the activity of the autonomic nervous system with a reflex triggered by excessive afferent discharges from the aterial or visceral mechanoreceptors with afferent impulses via the vagus nerve leading to cardioinhibition and vasodepression