DISEASES OF THE INNER EAR 1.1 (AB) Flashcards

1
Q

What are the two main divisions of ear diseases?

A

Vestibular diseases (main symptom: dizziness) and auditory diseases (main symptom: hearing loss).

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2
Q

Why can vestibular and auditory symptoms co-exist?

A

Because the membranous and bony structures of the ear are connected.

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3
Q

What is the primary function of the vestibular system?

A

To sense motion and position of the head in space and convert sensory stimuli into neural signals carried to the CNS.

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4
Q

What structures sense rotation in the vestibular system?

A

Three pairs of semicircular canals.

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5
Q

What structures sense linear acceleration and translation?

A

Otolith organs located in the utricle and saccule.

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6
Q

What reflex stabilizes gaze during head movement?

A

The vestibulo-ocular reflex (VOR).

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7
Q

How many vestibular afferents project from each labyrinth to the brainstem?

A

Almost 30,000.

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8
Q

What happens to afferent discharge rates during head movement?

A

The discharge rate increases with rotation or linear acceleration in one direction and decreases in the other.

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9
Q

What happens if one vestibular side is activated?

A

The opposite side is deactivated.

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10
Q

At rest, how do afferent fibers fire?

A

There is a balance or equal firing rate of afferent fibers going to the brain.

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11
Q

What happens to vestibular afferents during movement?

A

Excitation occurs on the side of movement, while the opposite side is inhibited.

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12
Q

What is the functional pair of the right anterior semicircular canal?

A

The left posterior semicircular canal.

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13
Q

What happens when the head moves in terms of fluid movement?

A

The fluid in the semicircular canals moves, causing hair cell deflection.

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14
Q

What occurs when stereocilia move toward the kinocilium?

A

Excitation.

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15
Q

What occurs when stereocilia move away from the kinocilium?

A

Inhibition.

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16
Q

Why does movement on one side of the ear affect the other?

A

The paired arrangement ensures an increase in firing rate on one side and a decrease on the other.

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17
Q

Why do otolith organs not respond exclusively to one direction?

A

They are curved rather than planar, allowing response to multiple acceleration directions.

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18
Q

What is the difference between roll tilt and interaural translation?

A

Both cause identical otolith afferent activity, but result in different compensatory eye movements.

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19
Q

How is the inner ear assessed clinically?

A

Through evaluation of eye movements driven by the VOR and imaging studies.

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20
Q

What are the two phases of VOR-driven eye movement?

A

Slow phase (keeps eyes on target) and quick phase (resets eye position).

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21
Q

What are the characteristics of nystagmus?

A

Can be horizontal, vertical, or torsional and consists of both slow and quick phases.

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22
Q

What is the purpose of Frenzel glasses?

A

To magnify and better observe eye movements in nystagmus.

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23
Q

How does nystagmus help diagnose vestibular dysfunction?

A

The direction of eye movement can indicate which semicircular canal is affected.

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24
Q

What eye movement is expected if the right semicircular canal is affected?

A

Horizontal eye movement.

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25
Q

What eye movement is expected if the superior semicircular canal is affected?

A

Vertical and torsional eye movement.

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26
Q

Which semicircular canal is most commonly affected in BPPV?

A

The posterior semicircular canal.

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27
Q

What is the expected slow-phase eye movement direction in BPPV?

A

Toward the axis of the affected canal.

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28
Q

What is the purpose of the Head Impulse Test?

A

To isolate the site of pathology in vestibular dysfunction.

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29
Q

How is the Head Impulse Test performed?

A

The examiner turns the patient’s head quickly while the patient maintains gaze forward.

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30
Q

What does a positive Head Impulse Test indicate?

A

A vestibular deficit on the side toward which the head was turned.

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31
Q

What is the main finding in a patient with left unilateral horizontal canal hypofunction during the Head Impulse Test?

A

A delayed catch-up saccade when turning the head to the left.

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32
Q

What type of hearing loss is associated with vestibular loss in Ménière’s disease?

A

Sensorineural hearing loss.

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33
Q

What test helps identify malingering in hearing loss?

A

Stenger test.

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34
Q

What type of hearing loss suggests superior canal dehiscence?

A

Conductive hearing loss or a suprathreshold bone line.

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35
Q

What imaging modality is preferred for evaluating temporal bone pathology?

A

High-resolution temporal bone CT.

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36
Q

What is the recommended CT slice thickness for temporal bone evaluation?

A

0.5-1 mm.

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37
Q

What imaging modality is used for detailed soft tissue assessment of the inner ear?

A

Magnetic Resonance Imaging (MRI).

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38
Q

What is the main problem in vestibular diseases?

A

Dizziness

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39
Q

What type of dizziness is characteristic of vestibular diseases?

A

Vertigo (rotatory dizziness)

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40
Q

What are the key features of central vertigo?

A

Severe imbalance, frequent neurologic symptoms, nystagmus changes direction with lateral gaze and does not change with fixation, rare hearing loss, variable nausea, slow recovery

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41
Q

What are the key features of peripheral vertigo?

A

Mild to moderate imbalance, rare neurologic symptoms, unidirectional nystagmus that decreases with fixation, frequent hearing loss, severe nausea, rapid recovery

42
Q

What is the prevalence of vertigo in individuals over 40 years old?

A

0.07400000000000001

43
Q

What percentage of individuals with an unknown cause of falls have vestibular impairment?

44
Q

What percentage of individuals with vestibular impairment complain of vertigo?

45
Q

What is BPPV and what are its characteristics?

A

Benign Paroxysmal Positional Vertigo; brief spells of severe vertigo after specific head movements, more common in women, increases with age, caused by loose otoconia from the utricle

46
Q

What is the mechanism behind PC-BPPV?

A

Canalithiasis

47
Q

What are the characteristics of PC-BPPV nystagmus?

A

Vertical and torsional nystagmus, fatigability, short duration

48
Q

What is the classic finding in the Dix-Hallpike maneuver?

A

Combined upbeating and torsional nystagmus with latency of a few seconds, lasting less than one minute, fatigable

49
Q

What treatment is used for BPPV?

A

Epley maneuver (repositioning otoconia using gravity), 80% success rate

50
Q

What medications can be used to suppress vestibular symptoms?

A

H1 receptor agonists, antihistamines, dopamine receptor antagonists, anticholinergics, benzodiazepines

51
Q

What are the key features of vestibular neuritis?

A

Vertigo lasting days to weeks without hearing loss, follows URTI, affects vestibular nuclei or nerve

52
Q

What test can help diagnose vestibular neuritis?

A

Head thrust test (positive in the direction of the affected side), caloric test (warm water = same side, cold water = opposite side)

53
Q

What imaging is used for vestibular neuritis?

A

MRI with gadolinium enhancement

54
Q

What is the treatment for vestibular neuritis?

A

Supportive and symptomatic treatment for vertigo and vegetative symptoms

55
Q

What are the key symptoms of Ménière’s disease?

A

Episodic vertigo (lasting minutes to hours), fluctuating low-frequency sensorineural hearing loss, tinnitus, aural fullness

56
Q

What is the pathology behind Ménière’s disease?

A

Endolymphatic hydrops (overaccumulation of endolymph, compressing the perilymphatic space)

57
Q

What dietary modification is recommended for Ménière’s disease?

A

Very low salt diet to reduce fluid retention

58
Q

What are the diagnostic criteria for definite Ménière’s disease?

A

Two or more episodes of vertigo lasting at least 20 min, audiometrically documented hearing loss at least once, tinnitus or aural fullness, exclusion of other causes

59
Q

What is superior semicircular canal dehiscence syndrome (SSCD)?

A

A condition where the superior semicircular canal has a hole in the membranous labyrinth, causing sound to exit and leading to dizziness/vertigo

60
Q

What are the symptoms of SSCD?

A

Dizziness/vertigo triggered by straining, heavy lifting, loud sounds (typically low frequency), autophony, sensorineural hearing loss

61
Q

What physical exam signs are associated with SSCD?

A

Hennebert’s sign (vertigo/nystagmus induced by pressure), Tullio phenomenon (vertigo/nystagmus caused by loud noise)

62
Q

What is the treatment for SSCD?

A

Supportive management or superior canal plugging via middle cranial fossa approach

63
Q

What imaging is used to diagnose SSCD?

A

High-resolution CT of the temporal bone

64
Q

Which aminoglycosides are vestibulotoxic?

A

Gentamicin and Streptomycin

65
Q

What is the general effect of aminoglycosides on the ear?

A

Ototoxicity (nausea and/or hearing loss)

66
Q

What type of toxicity do gentamicin and streptomycin cause?

A

Vestibulotoxicity

67
Q

What type of toxicity do other aminoglycosides cause?

A

Cochleotoxicity

68
Q

Which drug causes vertigo and dysequilibrium by damaging vestibular hair cells?

A

Aminoglycosides, cisplatin

69
Q

Which drug causes intoxication-related dizziness via CNS depression?

A

Tranquilizers

70
Q

Which drug causes dysequilibrium due to cerebellar toxicity?

A

Antiepileptics

71
Q

Which drug causes near syncope due to postural hypotension and reduced cerebral blood flow?

A

Antihypertensives, diuretics

72
Q

Which drug causes dysequilibrium and oscillopsia by an unknown mechanism?

A

Amiodarone

73
Q

Which drug causes intoxication, disequilibrium, and positional vertigo by CNS depression, cerebellar toxicity, and altering cupular and endolymphatic specific gravity?

74
Q

Which drug causes dysequilibrium due to brainstem and cerebellar toxicity?

A

Methotrexate

75
Q

Which drug causes vertigo due to hemorrhage into the inner ear or brain?

A

Anticoagulants

76
Q

What are the key symptoms of Cogan syndrome?

A

Interstitial keratitis, Ménière-like hearing loss, vestibular symptoms

77
Q

How is Cogan syndrome treated?

A

Systemic corticosteroids (prednisone 1 mg/kg/day with slow taper), infliximab

78
Q

What are the key features of otosyphilis?

A

Dizziness and/or hearing loss, occurs in 30% of congenital syphilis and 80% of symptomatic neurosyphilis cases

79
Q

How does early otosyphilis present?

A

Sudden hearing loss

80
Q

How does late otosyphilis present?

A

Similar to Ménière’s disease with episodes of vertigo, progressive hearing loss, and tinnitus

81
Q

What are the diagnostic tests for otosyphilis?

A

Positive VDRL and rapid plasma reagin (nontreponemal tests)

82
Q

What is the treatment for otosyphilis?

A

Penicillin + Steroids + IDS management

83
Q

What is a perilymph fistula?

A

An abnormal communication between the labyrinth and surrounding structures

84
Q

What are the three main causes of perilymph fistula?

A
  1. Leakage of perilymph due to trauma, 2. Disruption of the bony labyrinth (e.g., cholesteatoma), 3. Idiopathic bony dehiscence (e.g., superior semicircular canal dehiscence)
85
Q

What are two clinical signs of perilymph fistula?

A

Hennebert phenomenon (vertigo/nystagmus induced by pressure), Tullio phenomenon (vertigo/nystagmus caused by loud noise)

86
Q

What imaging finding suggests a perilymph fistula?

A

Pneumolabyrinth on CT

87
Q

What is the treatment for perilymph fistula?

A

Conservative management or surgical patching with a tissue graft (by an otosurgeon)

88
Q

What is labyrinthine concussion?

A

A labyrinth injury due to blunt trauma that does not violate the otic capsule or intralabyrinthine membranes

89
Q

What is the typical nystagmus pattern in labyrinthine concussion?

A

Initially beats toward the lesion acutely, then contralateral beating nystagmus

90
Q

What hearing loss pattern is associated with labyrinthine concussion?

A

Similar to noise-induced hearing loss, with loss most apparent at 4 kHz

91
Q

What percentage of blast trauma patients experience dizziness?

92
Q

What is the nystagmus pattern in penetrating trauma?

A

Beats toward the healthy ear due to acute loss on the affected side

93
Q

What are the symptoms of penetrating trauma?

A

Nystagmus, vertigo, vegetative symptoms (nausea, vomiting), gradual resolution over days to weeks

94
Q

What is the cause of enlarged vestibular aqueduct?

A

Dilation of the endolymphatic duct during embryogenesis

95
Q

When does hearing loss occur in patients with enlarged vestibular aqueduct?

A

Early childhood, often progressive with minor head trauma

96
Q

When do vestibular symptoms appear in enlarged vestibular aqueduct?

A

Often delayed until adulthood

97
Q

What is the risk of BPPV in patients with enlarged vestibular aqueduct?

A

Higher than normal

98
Q

What is the key CT finding in enlarged vestibular aqueduct?

A

Vestibular aqueduct > 1.5 mm at the midpoint (same width as horizontal semicircular canal)

99
Q

What is the management for enlarged vestibular aqueduct?

A

Symptomatic and supportive management

100
Q

What are the three main types of central vestibular disorders?

A

Vestibular migraine, vascular disorders, neoplasms

101
Q

What dietary restrictions help with vestibular migraine?

A

Low-tyramine diet (avoid cold cuts, banana, avocado, grapes, dairy products)

102
Q

What is the essential non-dietary treatment for vestibular migraine?

A

Quality sleep to allow fluid balance recovery