oto vestibular and balance disorders Flashcards

1
Q

What is the differential diagnosis of Ménière

disease.

A

Perilymphatic fistula, vestibular migraine, Cogan syndrome, autoimmune hearing loss, syphilis, mumps, Mondini mal-
formation

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2
Q

What percentage of patients with Ménière disease

will develop bilateral involvement?

A

Approximately 30%

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3
Q

What medical treatments are most commonly
used for symptomatic treatment of active Ménière
disease?

A

● Vestibular suppressants (e.g., benzodiazepines promethazine)
● Rest
● Potentially corticosteroids

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4
Q

What are the two most commonly used surgical

approaches for vestibular neurectomy?

A

● Middle fossa or the retrosigmoid approach
● Retrolabyrinthine and transmeatal approaches have also
been used.

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5
Q

How does the efficacy of endolymphatic shunt placement compare with endolymphatic sac decompression for treatment of Ménière disease?

A

No trials have clearly demonstrated superior results in one

treatment over the other.

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6
Q

Review the clinical presentation of Ménière

disease.

A

Low-frequency sensorineural hearing loss (SNHL, fluctuating and progressive), roaring tinnitus, aural fullness, and episodic vertigo generally lasting for hours

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7
Q

Describe Lermoyez syndrome.

A

Tinnitus and hearing loss that remit after an attack of vertigo

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8
Q

Define possible, probable, definite and certain

Ménière disease.

A

● Possible: Episodic vertigo without documented hearing
loss or SNHL (fluctuating or fixed) with dysequilibrium
but without definitive vertigo episodes; other causes
excluded

● Probable: One definitive episode of vertigo, audiometri-
cally documented hearing loss on at least one occasion,

tinnitus or aural fullness in the treated ear; other causes
excluded
● Definite: Two or more definitive spontaneous episodes of
vertigo lasting 20 minutes or longer, audiometrically
documented hearing loss on at least one occasion,
tinnitus or aural fullness in the treated ear, other causes
excluded
● Certain: Definite Ménière disease plus histopathologic
confirmation

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9
Q

Describe diet modifications for treatment of

Ménière disease.

A

● Avoidance of alcohol, caffeine, tobacco and monosodium
glutamate
● Adherence to a low-sodium diet (less than 1 to 2 g/day)

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10
Q

How is electrocochleography used in the diagnosis

of Ménière disease?

A

If the ratio of the summating potential, generated by the
organ of Corti, and the action potential, generated by the
auditory nerve, is elevated, diagnosis is indicated. A value
of 0.5 or greater is considered suggestive of Ménière
disease.

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11
Q

How is electrocochleography performed?

A

Neural responses to presented sounds are recorded
through an electrode in the middle ear (transtympanic
needle electrode), on the tympanic membrane, or on a gold
foil-wrapped earplug.

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12
Q

What is the role of intratympanic injections of

gentamicin in the treatment of Ménière disease?

A

● Selectively vestibulotoxic ablative treatment for unilateral
Ménière disease, often pursued after failure of more
conservative measures such as low-salt diet, caffeine
avoidance, diuretic therapy, and intratympanic steroid
injection
● Carries a 5 to 20% chance of significant SNHL

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13
Q

What is the role of intratympanic injections of corticosteroids in the treatment of Ménière dis-
ease?

A

These injections are onsidered a nonablative adjunct to
medical therapy that carries little risk of inducing hearing
loss. Subjects may experience a brief episode of vertigo
with injection if the steroid is not body temperature
and a low risk for persistent tympanic membrane
perforation.

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14
Q

When is a patient considered a candidate for

endolymphatic sac surgery?

A

Frequent vertiginous spells despite conservative treatment
in patients who are not candidates for ablative procedures
(bilateral disease, good residual hearing, contralateral
vestibular hypofunction)

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15
Q

What is the Donaldson line?

A

The Donaldson line is an imaginary line running parallel to
the plane of the lateral semicircular canal, extending
posteriorly and inferiorly through the center of the
posterior semicircular canal. The endolymphatic sac lies just
inferior to this line on the posterior fossa dura.

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16
Q

What pure tone audiometric findings can be seen in patients with superior semicircular canal dehiscence?

A

Conductive hyperacusis is sometimes seen, with bone
conductive thresholds occasionally less than 0-dB hearing
loss. This can lead to an air-bone gap even when air
conductive thresholds are within the normal range.

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17
Q

Describe the third window phenomenon.

A

The third window refers to a third opening in the inner ear,
in addition to the round and oval windows, that permits
pathological movement of perilymph within the labyrinth,
which may induce vertigo.

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18
Q

Describe the clinical presentation of superior

semicircular canal dehiscence syndrome.

A

Aural fullness, autophony, hearing loss (generally with an
air-bone gap and often supranormal bone conduction), and
dizziness often associated with loud sounds, exertion or
straining

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19
Q

How can one differentiate otosclerosis from superior semicircular canal dehiscence syndrome?

A
Patients with otosclerosis often have type AS tympanograms, diphasic or absent stapedial reflexes, and elevated to absent cervical vestibular evoked myogenic potentials.
Patients with superior semicircular canal dehiscence will usually have normal stapedial reflexes, type A tympano-
grams, and diminished vestibular evoked myogenic poten-
tial thresholds (often < 70 dB).
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20
Q

How do you perform and interpret the Dix-

Hallpike test?

A

With the patient sitting, rotate the patient’s head by
approximately 45 degrees to the left or the right. The
patient then lies flat with the head slightly extended (~ 20
degrees). The eyes are then observed for ~ 45 seconds
looking for rotary nystagmus. If rotatory nystagmus occurs,
the test is positive. The direction of the fast phase reveals
the side that is affected.

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21
Q

Describe the clinical manifestation of benign

paroxysmal positional vertigo?

A

Short-lived (less than 60 seconds), room-spinning vertigo

provoked by head turn

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22
Q

Which semicircular canal is most commonly

involved in benign paroxysmal positional vertigo?

A

Posterior canal. Five percent involve the horizontal canal

and the superior canal is the least common.

23
Q

What anatomical structure is the source of

otoconia in benign paroxysmal positional vertigo?

A

The utricle

24
Q

What are risk factors for the development of

benign paroxysmal positional vertigo?

A

● Advanced age, head trauma, surgery, migraine
● Most patients do not have an identifiable cause (idio-
pathic).

25
Describe the mechanism of singular neurectomy in the treatment of benign paroxysmal positional vertigo.
The singular nerve innervates the posterior semicircular canal, which is the most commonly affected canal in benign paroxysmal positional vertigo. Division of this nerve may lead to symptom relief in refractory disease.
26
What conservative treatment options are available | for benign paroxysmal positional vertigo?
● Reassurance and education about the nature of the condition ● No effective pharmacologic therapy is available ● Canalith repositioning maneuvers involve taking a patient through a series of positions that are designed to return dislodged otoconia to the vestibule and are the most effective nonsurgical treatment.
27
``` What test(s) should be ordered when vertebro- basilar insufficiency is suspected? ```
● MRI and magnetic resonance angiography (MRA) provide the best information regarding acute and chronic infarcts, as well as the location and severity of vascular occlusions in the head and neck. ● Patients who cannot undergo MRI should be evaluated with CT and CT angiography (CTA). ● Duplex ultrasound can also provide information regarding proximal vertebral arteries.
28
What symptoms may accompany episodic vertigo | associated with vertebrobasilar insufficiency?
Diplopia, decrease in visual acuity, ataxia, dysarthria, | dysphagia, and other focal neurologic symptoms
29
Describe the symptoms of Wallenberg syndrome.
● Loss of pain and temperature sensation on the ipsilateral face and contralateral body, dysphagia, dysarthria, ataxia, vertigo, Horner syndrome, diplopia ● Caused by a lateral medullary infarct supplied by the posterior inferior cerebellar artery
30
What are typical initial symptoms of vestibular | neuronitis?
● Sudden onset of severe vertigo, nausea, and vomiting lasting days to weeks, often preceded by a viral upper respiratory tract infection ● Unlike labyrinthitis, hearing should remain stable.
31
What are the mainstays of treatment for vestibular | neuronitis?
High-dose corticosteroids, vestibular suppressants in the | acute period, antiemetics, and bed rest as needed
32
What are the diagnostic criteria for chronic | subjective dizziness?
● Subjective unsteadiness or nonvertiginous dizziness that is present for 3 + months and is present most days ● Hypersensitivity to one's own motion and to the move- ment of objects in the environment ● Visual dizziness marked by exacerbation of symptoms in settings with complex visual stimuli (grocery stores) or when performing precision visual tasks (reading or working on the computer)
33
What are the treatment options for chronic | subjective dizziness?
First-line pharmacologic therapy includes selective seroto- nin reuptake inhibitors. For patients with concurrent migraine, selective serotonin norepinephrine reuptake inhibitors or tricyclic antidepressants may be used. Behavioral intervention and psychoeducation serve as comple- menting therapies.
34
Describe the typical presentation of mal de débarquement syndrome.
The sensation of rocking or swaying back and forth without vertigo, difficulty concentrating, and fatigue. It most commonly occurs in middle-aged women after a week-long cruise. The mean duration of symptoms is 3.5 years.
35
What is the mechanism of motion sickness?
Disagreement between vestibular cues and visual and | somatosensory input
36
Excluding benign paroxysmal positional vertigo, what is the most common cause of vertigo in the general population?
Vestibular migraine, or migraine-associated vertigo, is estimated to have a prevalence of ~ 1% in the general population.
37
What are the diagnostic criteria for vestibular | migraine?
Definite vestibular migraine ● Recurrent episodic vestibular symptoms of at least moderate severity ● Current or previous history of migraine ● Migrainous symptoms during ≥ 2 vertiginous attacks ● Other causes ruled out by appropriate investigations Probable vestibular migraine ● Recurrent episodic vestibular symptoms of at least moderate severity ● One of the following: ○ Current or previous history of migraine ○ Migrainous symptoms during ≥ 2 attacks of vertigo ○ Migraine precipitants before vertigo in more than 50% of attacks ○ Response to migraine medications in more than 50% of attacks ○ Other causes are ruled out by appropriate investiga- tions.
38
Describe the relationship between vestibular mi- | graine and Ménière disease.
There is substantial overlap between groups. Approximately one-fourth of patients with Ménière disease also fulfill diagnostic criteria for vestibular migraine.
39
Describe the clinical features of basilar migraine.
● Similar symptoms to vertebrobasilar insufficiency with headache ● Most patients experience dizziness but may also experi- ence ataxia, hearing loss, tinnitus, dysarthria, diplopia, and syncope. ● It most commonly involves young females.
40
Describe the common neurotologic examination | findings in patients with multiple sclerosis.
Abnormalities of smooth pursuit (96%), saccadic eye movements (76%), optokinetic nystagmus (53%), and defective visual suppression of nystagmus (43%)
41
What is the Charcot triad?
Nystagmus, scanning speech, and intention tremor; asso- | ciated symptoms of multiple sclerosis
42
Define balance retraining therapy.
Specialized form of physical therapy focusing on the improvement of static and dynamic balance and gait, and promoting central vestibular compensation by taking advantage of the inherent plasticity of central balance pathways
43
What are the two phases of vestibular recovery | after an acute vestibular insult?
● Static recovery (initial phase) occurs through a central adaptive process that rebalances tonic neural activity between vestibular nuclei ● Dynamic recovery (second phase) involves recalibrating brain and cerebellar reflex pathways in response to sensory conflicts occurring with head and eye move- ments.
44
Describe the clinical findings during static compensation and dynamic compensation.
During static compensation, patients will often have marked spontaneous nystagmus and vertigo lasting from days to weeks. During dynamic compensation, patients may experience general imbalance and unsteadiness with quick head turn.
45
With regard to vestibular rehabilitation, describe | the strategy of adaptation.
Exercises aimed at improving vestibule-ocular response (VOR) gain. Initially, the patient is asked to view a stationary object while moving the head back and forth. The same exercise can be repeated but with the object moving in the opposite direction of head turn. This will strengthen gaze stability through improvement of the VOR response.
46
With regard to vestibular rehabilitation, describe | the strategy of habituation.
Patients may be exposed to repetitive visual, vestibular, or motor exercises that are designed to provoke episodes of imbalance. With repetitive exposure, there is an attenuation or modification of the response.
47
With regard to vestibular rehabilitation, describe | the strategy of substitution.
``` Exercises designed to take advantage of alternate intact balance mechanisms (remaining vestibular function, visual input, somatosensory input) to compensate for specific balance system deficits ```
48
Describe the ideal candidate for vestibular rehabilitation.
Patient with stable unilateral vestibular hypofunction who continues to feel general imbalance that is worsened by quick head movements
49
What patients are not good candidates for | vestibular rehabilitation?
Central compensation requires consistent and predictable peripheral vestibular input; therefore, patients with un- stable vestibular deficits (e.g., active Ménière disease, acute viral labyrinthitis) should not enter vestibular rehabilitation until their condition has stabilized.
50
Name several conditions that negatively influence | the outcome of vestibular rehabilitation.
Coexisting conditions that affect balance may result in less optimal outcomes than in patients with isolated stable vestibular hypofunction. Examples include central nervous system disorders (stroke, multiple sclerosis, Parkinson disease), sensory neuropathy (diabetes, peripheral vascular disease), motor dysfunction, and patients with vestibular migraine, to name a few.
51
Which medications potentially retard progress | during vestibular rehabilitation?
Anticonvulsants and sedating medications may prolong vestibular rehabilitation. Additionally, vestibular suppressive medications hinder initial static compensation.
52
To what does presbystasis refer?
Presbystasis refers to the general balance difficulties of elderly patients that is related to cumulative age-related decline in vestibular response, visual acuity, proprioception, and motor control.
53
What diagnosis must be considered with hearing evaluation with low frequency conductive loss with stapedius reflexes present?
Superior Semicircular Canal Dehiscence