2.4 Principles of Vestibular Disease Flashcards
What does the vestibular system do?
- it is the sensory system that maintains the animal’s balance
- it is responsible for maintaining eye, neck, trunk and limb position appropriate to the current head position and movement
- it detects head motion and regulates lower motor neurons innervating muscles throughout the neck and body
How does the vestibular system function?
via the 2 maculae (utricle and saccule), and the 3 crista ampullares (one for each semicircular canal)
the maculae detect head position and linear acceleration
- large, crystalline statoconia (otoliths) sit on the hair cells
the crista ampullares detect angular acceleration (head rotation)
- three, at right angles to each other
- gel-like cupula
it is IPSILATERAL: when you rotate your head to one side, you will ACTIVATE the cells on that side of the head, and INHIBIT those on the opposing side, producing unequal CNVIII signals
What does CNVIII do?
carries afferent information from hair cells to vestibular nuclei in the brainstem (medulla oblongata)
- neuronal cell bodies are located in the VESTIBULAR GANGLION in the petrous temporal bone
- joins with axons from the cochlea (that carry auditory information) to form the vestibulocochlear nerve
- enters the cranium via the INTERNAL ACOUSTIC MEATUS
- axons enter the medulla oblongata and synapse on the vestibular nuclei
What are the vestibular nuclei?
- exist in the medula oblongata of the brainstem
- four pairs:
rostral, medial, lateral, caudal
What are the 5 efferent outputs of the vestibular system?
- UMN spinal cord: lateral and medial vestibulospinal tracts (increases ipsilateral and decreases contralateral extentor tone to support change in posture: look left, increased left tone)
- motor nuclei of CNIII, IV, and VI (enables coordinated conjugate eye movement)
- cerebellum: enter flocculonodular lobe via cerebellar peduncle - if either damaged = paraxodical vestibular (inhibitory to vestibular nuclei via GABA, therefore opposite signs)
- forebrain (signal travels to contralateral vestibular cortex in forebrain: allows conscious perception of balance)
- vomiting center in the reticular formation (basis of motion sickness)
What is the basis of vestibular dysfunction?
at rest there is equal tonic input from left and right vestibular nuclei
unequal input - whether from actual head movement or from a lesion - is perceived as HEAD MOVEMENT
vestibular system is ipsilateral: understand this when noting the side of symptoms
How would a lesion in the right vestibular apparatus present, including eye movement?
- lesion in the right vestibular apparatus
- right vestibular nuclei (medulla oblongata) recieve decreased input
- percieved as increased input to the LEFT: animal believes the head has moved to the left
- neck, trunk, and limb extensor tone increase on left, decrease on right
- leads to head tilt (different from head turn: look at eye level), leaning, and falling to the right
- eye jerk to the left (innapropriate vestibulo-ocular reflex): pathological nystagmus
note: the eye jerk is toward the percieved head movement, which is AWAY from the true lesion
What are the clinical signs of vestibular disease?
- head tilt: toward side of lesion (extensor tone reduced on this side)
- vestibular ataxia: leaning/falling/rolling to the side of lesion for same reason
- tight circling: toward side of lesion (same reason)
- pathological nystagmus: away from lesion (eyes look where the think the body is moving)
- abnormal vestibulo-ocular reflex: may be absent toward lesion
- positional strabismus: ventrolateral deviation of eye on affected side when tilting head up
- ipsilateral loss of extensor muscle tone
- nausea
What is the difference between the peripheral vs central portion of vestibular system?
peripheral = hair cell receptors and CNVIII
central = vestibular nuclei in the brainstem
- important to distinguish for prognosis and possible cause
- any lesion can compromise surrounding structures: can distinguish based on which other structures are affected
What other structures may be compromised in a peripheral vestibular lesion?
- could compromise CN VII
- sympathetic innervation to the eye (horner’s syndrome)
(both run in close proximity to the tympanic bulla)
What other structures may be compromised in a central vestibular lesion?
- could disrupt other cranial nerve nuclei (eg. IX, X, XI causing dysphagia and dysphonia)
- adjacent ascending proprioceptive tracts from the spinal cord (causing proprioceptive ataxia)
- descending UMN tracts (causing tetraparesis)
- ascending reticular activating system (causing abnormal mentation)
LOOK FOR EVIDENCE OF BRAINSTEM DYSFUNCTION
Horners can be central but this is rare
What are common causes of vestibular disease?
- idiopathic (no known cause)
- otitis media/interna
- ototoxic drugs (aminoglycosides)
- thiamine deficiency
- cerebellar lesion (flocculonoddular lobe or cerebellar peduncle)
- MUA (meningioencephalitis of unknown origin: most common in small young to middle-aged female dogs)
What is paradoxical vestibular disease?
caused by a lesion of the cerebellum, at either the:
- flocculonodular lobe
- cerebellar peduncle
the cerebellum is inhibitory to the vestibular apparatus (ipsilateral - decussates twice)
- on the side of the lesion there is less inhibition of the vestibular nuclei
- therefore, effectively there is more activity in vestibular nuclei on side of the lesion → the brain perceives this as the animal turning towards the side of the lesion
- increased extensor tone on the lesion side
- head tilt and leaning/falling/rolling is to the side opposite to the lesion
- fast phase of the nystagmus is towards the lesion
- Hence the clinical signs are PARADOXICAL
