Chapter 23 - Vestibular disease Flashcards

1
Q

What are the mechanisms leading to the activation of the vestibular component of the vestibulocochlear nerve (CN VIII)?

A

Endolymph movement within the peripheral vestibular organs (the utricle, saccule, and three semi- circular canals) within the bony and membranous labyrinths of the inner ear causes deflection of specialized hair cells, leading to activation of the vestibular component of the vestibulochoclear nerve.

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2
Q

The vestibular nuclei send projections to the spinal cord, brainstem, and cerebellum. What do these projections control?

A
  1. The spinal cord projections modulate extensor and flexor tone and allow for co-ordination of the limbs, neck, and trunk.
  2. The brainstem projections of the vestibular system regulate and coordinate eye movements, provide input to the vomiting center, and allow for conscious perception of balance.
  3. The cerebellar projections of the vestibular system co-ordinate the eyes, neck, trunk, and limbs.
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3
Q

What are the differences between peripheral and central vestibular disease?

A

Peripheral: normal mentation, falling towards the lesion, circling and alligator rolling towards the lesion, horizontal or rotatory nystagmus, fast phase of the nystagmus away from the lesion, possible ipsilateral CN VII (facial nerve) paralysis or ipsilateral Horner’s syndrome, normal strength and postural reactions.

Central: often decreased levels of consciousness, possible head tilt towards the lesion, leaning and circling towards the lesion, possible cerebellar ataxia (hypermetria), possible intentional tremors, possible ipsilateral hemiparesis, horizontal/rotatory/vertical/or positional nystagmus, possible CN V-XII paralysis, often ipsilateral postural reaction deficit, often ipsilateral hemiparesis

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4
Q

What is paradoxical vestibular disease?

A

Paradoxical vestibular disease, caused by a lesion impacting on the cerebellopontine angle, is a subset of central vestibular disease. Because the cerebellum’s influence on the vestibular system is largely inhibitory, lesions in this location cause vestibular release that is interpreted as a contralateral deficit. This results in clinical signs that are consistent with a lesion on the opposite side

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5
Q

What is the gait/posture of a patient with bilateral peripheral vestibular disease?

A

Patients with bilateral peripheral vestibular disease typically appear crouched and remain close to the ground. The ataxia is more symmetrical and patients may fall and list to either side. Patients often exhibit characteristic wide head excursions from side to side.

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6
Q

T/F: a patient with bilateral peripheral vestibular disease does not have a head tilt nor pathological nystagmus

A

T (due to complete loss of vestibular function)

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7
Q

How long should systemic antibiotics be given for, for otitis media and interna?

A

6-8 weeks

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8
Q

Give examples of ototoxic drugs

A

aminoglycosides, cisplatin, loop diuretics, chlorhexidine, erythromycin, chloramphenicol, and minocycline

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9
Q

What endocrine disease can present with clinical signs of peripheral or central vestibular disease?

A

Hypothyroidism

This syndrome is poorly understood, but clinical signs may be secondary to myxomatous compression of the nerves.

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10
Q

What is the median age of canine patients with idiopathic vestibular disease?

A

Dogs: 12.5 years

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11
Q

When is the higher incidence of feline idiopathic vestibular disease?

A

Idiopathic vestibular disease in cats is seen
most frequently in outdoor cats, and is not restricted to geriatric animals. There is a higher incidence of feline idiopathic vestibular disease in the late summer and early fall.

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12
Q

How long does it typically take for a patient with idiopathic vestibular disease to improve and recover?

A

After 3–5 days, most patients will begin to show signs of improvement, with resolution occurring over 2–4 weeks.

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13
Q

How long do the clinical signs last in patients suffering from a central vestibular disease secondary to a vascular event?

A

This is caused by a temporary vascular disruption and result in short-term neurological signs (less than 24 hours).

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