Vestibular Disease

Question 1

Define the direction of nystagmus and the control of the fast and slow phase

Answer 1

The direction of the fast phase defines the direction of nystagmus, so if the head is turned to the left the fast phase will also be to the left. The fast phase is under control of the brainstem and the slow phase is under vestibular control.

Question 2

Differentiate physiologic nystagmus from the oculocephalic reflex

Answer 2

Physiologic nystagmus is the normal movement of the eye (controlled by the motor nuclei of CNIII, CNIV and CNVI) when the head moves; also called vestibular-ocular nystagmus.
The oculocephalic reflex is independent of vision and associated with rapid manipulation of the head. If you cannot elicit this reflex disease is either bilateral or involves damage to the medial longitudinal fasciculus and hence extensive brainstem damage.

Question 3

Describe the anatomic association of the facial and vestibular nerves

Answer 3

The facial nerve emerges from the lateral medulla ventral to the vestibulocochlear nerve at the level of the trapezoid body. The two nerves are associated closely with the petrous temporal bone and enter the internal auditory meatus together. After this the facial nerve separates and courses through the facial canal of the petrosal bone and exits through the stylomastoid foramen.

Question 4

List the clinical signs of peripheral vestibular system dysfunction

Answer 4

• Head tilt
• Horizontal nystagmus (fast phase directed away from the lesion)
• Head tilt (poll toward the lesion)
• Falling and or circling (lean or circle towards the lesion)
• Reluctance to move (if forced may take short uncoordinated steps)
• Asymmetric ataxia (with preservation of strength)
• Loss of hearing
• Note: if bilateral, ataxia is often symmetric and you may not see nystagmus, head tilt or circling and the oculocephalic reflex cannot be induced. Head may sway with wide excursions.

Question 5

Why do you see asymmetric ataxia with peripheral vestibular disease?

Answer 5

Asymmetric ataxia (with preservation of strength) occurs due to extensor hypotonia ipsilateral (due to loss of faciliatory neurons of the vestibulospinal tract to ipsilateral extensor muscles), and mild extensor hypertonia and hypereflexia contralateral (due to loss of inhibitory neurons and unopposed extensor tone of the contralateral vestibulospinal tract).

Question 6

List the clinical signs of central vestibular disease and how you would differentiate from peripheral disease

Answer 6

• Head tilt
• Nystagmus that can be horizontal, vertical or rotatory (you only see vertical or rotatory with central Dz). Fast phase is away from the lesion - in rotatory the direction is defined by the movement of the limbus from the 12O’clock position during the fast phase. Compensation is slower with central compared to peripheral Dz.
• Falling and circling towards the lesion
• Proprioceptive deficits (only see this with central Dz) due to damage within the brainstem of the descending UMN tracts of the limbs - if there is damage to the spinocerebellar tracts or caudal cerebellar peduncles you get abnormal unconscious proprioception and hypermetria.
• Obtundation (differentiates central from peripheral Dz.)
• Involvement of other cranial nerves (differentiates central from peripheral Dz)
• Evidence of cerebellar disease
• Note: if bilateral, ataxia is often symmetric and you may not see nystagmus, head tilt or circling and the oculocephalic reflex cannot be induced. Head may sway with wide excursions.

Question 7

Define paradoxic vestibular disease or cerebellar-vestibular disease.

Answer 7

The eyes are maintained centrally because the vestibulo-ocular pathways are opposed in an equal and opposite manner. If disease is unilateral this upsets the balance resulting in slow deviation of both eyes towards the lesion.

Question 8

List differentials for vestibular signs

Answer 8

• Inflammatory brain disease/inflammation of the CNS
• Space occupying lesions (Strep equi equi abscess, fungal granuloma eg Aspergillus or Cryptococcus neoformans, cholesterol granuloma). Less common neoplasms include lymphoma, ependymoma, meningeal melanoma and melanotic hamartoma.
• EPM and rabies depending on geography
• Polyneuritis equi (although caudal equina signs predominante)
• EHV myelitis (primarily spinal ataxia but may be a vestibular component)
• Togaviruses (EEEV, WEEV, VEEV - primarily depression and seizures but cranial nerve deficits may include vestibular signs)
• WNV (may have a component of vestibular disease among other CN dysfunctions)
• Aberrant parasite migration (usually quite varied neurological signs)