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Vestibular and Balance disorders
Terms in this set (24)
Vestibular end organs
Otolith organs (utricle and saccule) and semicircular canals.
SCCs are activated during rotational movements and the otolith organs during linear movements.
SCCs are paired with the horizontal canals being paired with each other bilaterally. The superior canal on the left is functionally paired with the posterior canal on the right and vice versa.
Eye movements are produced in the plane of the canal being stimulated.
The otolith organs play the greatest role in the maintenance of an upright posture through the detection of body or head tilt. SCCs play a role in the vestibular-ocular reflex.
Function of the SCCs
With rotational head movement, one of the pair of canals will increase firing rate and the other will decrease firing rate.
The differential rate of firing will signal a head movement in the plane of that SCCa.
The difference of firing rates is the signal received by the CNS. In the case of sudden pathologic loss of function of one side, the firing from that side goes to 0. The CNS interprets that as being rotated towards the unaffected ear. The vestibuloocular reflex produces a slow phase eye movement in the direction of the bad side and a fast phase movement towards good ear.
Types of hair cells in the vestibular system
Type I: Flask-shaped, surrounded by afferent nerve terminals at its base. High amount of tonic and stimulatory activity.
Type 2: Cylindrical, surrounded by multiple terminals, predominantly inhibitory.
Each hair cell contains 50-100 stereocilia and one kinocilia that project into the gelatinous matrix of the cupula or macula
Second order neurons within the vestibular nucleu
1. Superior (Bechterew nucleus): Relay station for conjugate eye reflexes mediated by the SCCs.
2. Lateral (Deiters nucleus): control of ipsilateral vestibulospinal (righting) reflex
3. Medial (Schwalbe nucleus): coordination of eye, head, and neck movements with connections to the medial longitudinal faciculus
4. Descending (spinal vestibular nucleus): Integration of signals from the vestibular nuclei, cerebellum, and reticular formation
This is responsible for conjugate eye movements, smooth pursuit, compensation for unilateral vestibular loss
Head shake test
Presence of post head shake nystagmus correlates well with increasing right/left excitability difference on caloric testing.
Fast phase is usually directed away from the involved ear (but not always).
Loss of visible lines on Snellen or LogMAR chart with rapid horizontal head shaking.
Suggests bilateral vestibular loss.
Cardinal sign for a vestibular disorder.
The slow phase is in the direction of flow of the endolymph. The quick phase is centrally-generated compensatory mechanism.
The slow-phase velocity of nystagmus increases when the eyes look in the direction of the fast phase (commonly observed in peripheral lesions).
1st: Present only when looking in the direction of the fast phase.
2nd: Present when gazing in the direction of the fast component and with straight gaze
3rd: Present in all 3 directions.
Electronystagmography and videonystagmography (ENG and VNG)
ENG = horizontal and vertical eye movements are recorded indirectly using electrodes measuring changes in corneoretinal potential.
VNG = eye movement recorded directly using infrared video cameras and digital video
ENG and VNG interpretations
Findings of central pathology:
Spontaneous/positional nystagmus with normal calorics.
Direction-changing nystagmus with failure of fixation suppression.
Bilateral reduced or absent calorics.
Hyperactive caloric response
Findings of peripheral pathology:
Unilateral caloric weakness
Bilateral caloric weakness
Fatiguing positional nystagmus
COWS = cold opposite, warm same.
Cool water/air -> decreased endolymphatic fluid -> ampulofugal flow in the horizontal SCCa -> inhibition of involved side -> slow drift of eyes towards involved side and fast phase in the opposite.
Warm water/air -> fluid rises -> flow in horizontal canal -> excitation of involved side -> slow phase opposite and compensatory fast phase towards.
Rotational chair testing
High frequency and more physiologic conditions than calorics. Can test both sides simultaneously.
Useful for identifying residual function in patients with no calorics and for monitoring progress over time.
Measure phase, gain, and symmetry.
Phase = leading/lagging of maximum chair velocity vs maximum slow-phase velocity.
Gain = ratio of max eye velocity to max chair velocity.
Symmetry = compares left and right peak slow-wave velocity. Cannot be used alone to localize lesion.
Video head impulse test (vHIT)
Goggles with high-speed camera for capturing eye movements.
Used to evaluate vestibuloocular reflex during head thrust maneuver.
Reduced gain values when head is rotated towards impaired side.
Detects overt and covert saccades. Covert means you can't see with naked eye. Implies compensated lesion.
Magnetic scleral search coil
Silicone annulus with embedded copper wire contacts the globe of the eye.
Detects changes in orientation relative to magnetic field.
Gold-standard for measuring eye movement.
Vestibular Evoked Myogenic Potentials (VEMPs)
Brief, loud tone bursts evoke short latency myogenic potentials.
Evaluate utricle and saccule function.
Acute unilateral peripheral vs bilateral peripheral loss vs central vestibular loss
Acute unilateral peripheral: Mixed horizontal torsional nystagmus, + suppression with fixation, normal smooth pursuits and saccades, unilateral loss of calorics, severe symptoms.
Bilateral peripheral loss: No nystagmus, normal smooth pursuits, bilateral loss on calorics, oscillopsia, imbalance, gait ataxia. NO VERTIGO.
Central vestibular loss: Mixed or pure torsional or vertical nystagmus, no suppression with fixation, saccadic smooth pursuits, CNS symptoms often present. Vertigo is not as severe as unilateral peripheral.
Posterior SCC most often involved.
RF = trauma, history of neuronitis, ear surgery.
Latency is seconds, lasts <1min, fatigues with repeat testing.
Surgical treatment: PSCC occlusion, vestibular neurectomy, labyrinthectomy (recalcitrant or deafened ear)
Dysfunction of endolymph reabsorption. Most commonly seen in cochlea and saccule.
Bowing and rupture of Reissner membrane leads to leakage of endolymph into perilymph and interference with action potential.
Recurrent vertigo, tinnitus, aural fullness, and SNHL.
Otolithic crisis = unexpected falls without LOC or vertigo.
Audiogram shows low frequency SNHL.
ECoG shows increased SP/AP ratio (>0.35)
ENG/VNG shows unilateral weakness.
Autoimmune. Interstitial keratitis, bilateral rapidly progressive audiovestibular dysfunction, and multisystem vasculitis.
Progressive loss of bilateral vestibular function.
Bilateral and progressive HL.
Tx = high dose steroids.
Dramatic, sudden onset vertigo. Gradual symptom improvement over days to weeks. No HL.
Fast phase is away from the bad side and hypofunction on caloric responses.
Traumatic perilymphatic fistula
Episodic vertigo (like Meniere), motion intolerance. Dysequilibrium after increased CSF pressure like with Valsalva, Tullio phenomenon (vertigo with loud noise).
Increased SP/AP ratio on ECoG
Superior SCC dehiscence
Third window with abnormal endolymphatic flow.
Sound and pressure evoked nystagmus, hyperacusis, gaze-evoked tinnitus, disequilibrium.
Cerebellar ataxia with bilateral vestibulopathy and cerebellar ataxia with neuropathy and bilateral vestibular areflexia syndrome
Progressive imbalance from cerebellar atrophy and bilateral vestibular loss.
Suspected late-onset recessive disorder with cerebellar degeneration of anterior and dorsal vermis, sensory peripheral neuropathy.
Progressive gait ataxia, oscillopsia.
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