Lecture 4: Vestibular Function - Getting the balance right

Question 1

What are the three semicircular canals and their arrangement?

Answer 1

Horizontal canal
Anterior canal
Posterior canal
Arranged roughly at right angles to detect angular acceleration in 3D

Question 2

Where are the hair cells of the semicircular canals located and what structure do they contact?

Answer 2

In the ampulla of each canal
Hair-cell cilia (one kinocilium + multiple stereocilia) project into the cupula (gelatinous ridge spanning the ampulla)

Question 3

What stimulus do the semicircular canals detect?

Answer 3

Rotational (angular) acceleration of the head

Question 4

Describe the basic mechanism of cupula deflection leading to a neural signal.

Answer 4

Skull and ampulla move with the head; endolymph initially lags due to inertia producing relative flow
Shear on the cupula bends hair-cell cilia
Bending toward kinocilium depolarises the hair cell → increased firing in ipsilateral vestibular nerve
Bending away hyperpolarises → decreased firing

Question 5

Why do semicircular canals respond to acceleration but not constant rotation?

Answer 5

At constant velocity endolymph catches up with the canal causing the cupula to return to baseline
They detect changes in velocity (dynamic detection) not steady rotation

Question 6

What causes the transient false sensation of rotation when a rotating person stops suddenly?

Answer 6

Endolymph momentum continues to move and deflects the cupula after the head stops → transient sensation of rotation (dizziness)

Question 7

How do paired canals provide directional information?

Answer 7

Left and right homologous canals produce push–pull signals (increased firing on one side with decreased firing on the other)
Comparison of bilateral signals encodes direction and timing of head rotation

Question 8

What are the maculae and where are they located?

Answer 8

Sensory epithelia in the utricle (macula horizontal) and saccule (macula vertical)

Question 9

What structures embed the hair-cell cilia in the maculae?

Answer 9

Otolith membrane studded with calcium carbonate crystals (otoliths)

Question 10

What stimuli do the utricle and saccule each detect?

Answer 10

Utricle: head tilt and horizontal linear acceleration
Saccule: vertical linear acceleration and head orientation when supine

Question 11

Describe the transduction mechanism in the otolith organs.

Answer 11

Gravity or linear acceleration shifts otoliths relative to endolymph causing shear in the otolith membrane
Cilia bend toward kinocilium → depolarisation and ↑ AP rate; bend away → hyperpolarisation and ↓ AP rate
Spatial pattern of hair-cell activation encodes tilt angle and linear acceleration direction

Question 12

List the major sensory inputs that contribute to body-space perception.

Answer 12

Vestibular afferents (semicircular canals + otolith organs) via CN VIII
Visual input (retina → visual cortex and gaze centres)
Proprioceptors (muscle spindles, Golgi tendon organs, joint receptors)
Tactile cutaneous receptors from support surfaces
Cerebellar integration (flocculonodular lobe) and vestibular nuclei distribution

Question 13

What is the primary purpose of the vestibulo-ocular reflex (VOR)?

Answer 13

Stabilise gaze during head movement so the visual scene remains steady on the retina

Question 14

Outline the basic VOR pathway.

Answer 14

Semicircular canal afferents → vestibular nuclei → extraocular motor nuclei (III, IV, VI) → extraocular muscles to generate slow-phase eye movement opposite to head rotation and fast corrective saccade

Question 15

What are tonic labyrinthine reflexes?

Answer 15

Reflexes that help maintain head–body axis and postural tone using maculae and neck proprioceptors to adjust muscle activity

Question 16

What are dynamic righting reflexes?

Answer 16

Rapid whole-body postural adjustments after perturbation coordinated by vestibulospinal outputs to prevent falling

Question 17

What do vestibulospinal pathways mediate?

Answer 17

Postural muscle tone and limb extensor activity with both ipsilateral and contralateral projections to support balance and posture

Question 18

What is the role of cerebellum in vestibular function?

Answer 18

Receives direct vestibular input for adaptive modification and compensation of reflexes (especially archicerebellum/flocculonodular lobe)
Facilitates long-term recalibration of VOR and balance

Question 19

Define vestibular nystagmus and how its phases are named.

Answer 19

Repetitive eye movements with a slow phase driven by the VOR (opposite head rotation) followed by a fast corrective saccade
Nystagmus is named for the direction of the fast phase (e.g., right-beating = fast phase to the right)

Question 20

What is physiological nystagmus?

Answer 20

Nystagmus that occurs during sustained rotation or optokinetic stimulation as a normal response

Question 21

Explain the caloric test and the COWS mnemonic.

Answer 21

Irrigation of the external ear with warm (~44°C) or cold (~30°C) fluid to induce convection currents in horizontal canal
Warm irrigation produces nystagmus toward the irrigated ear (Warm Same)
Cold irrigation produces nystagmus away from the irrigated ear (Cold Opposite)
Mnemonic: COWS (Cold Opposite, Warm Same)

Question 22

What clinical information does the caloric test provide?

Answer 22

Assesses unilateral horizontal semicircular canal/vestibular nerve function and detects unilateral vestibular hypofunction

Question 23

How does peripheral vestibular nystagmus differ from central nystagmus?

Answer 23

Peripheral lesions: usually unidirectional horizontal nystagmus that increases when gazing toward the fast phase and is suppressed by visual fixation
Central lesions: may cause direction-changing or vertical nystagmus that is less suppressed by fixation

Question 24

What causes motion sickness (kinetosis)?

Answer 24

Sensory conflict between visual and vestibular inputs (mismatch of expected vs actual motion cues) triggering cerebellar/hypothalamic pathways and autonomic symptoms

Question 25

Describe labyrinthitis and its key clinical features.

Answer 25

Infectious or inflammatory peripheral vestibular dysfunction Acute severe vertigo, spontaneous nystagmus, nausea, balance loss May include hearing symptoms if cochlea involved

Question 26

What are the classic features of Ménière’s disease?

Answer 26

Episodic vertigo Tinnitus Fluctuating hearing loss Associated with endolymphatic hydrops (increased endolymph volume/pressure)

Question 27

What are clinical consequences of unilateral vestibular hypofunction?

Answer 27

Acute unilateral loss: spontaneous vertigo and nystagmus Chronic unilateral loss: central compensation via cerebellar and visual strategies reducing symptoms over time

Question 28

What are consequences of bilateral vestibular loss?

Answer 28

Imbalance, oscillopsia (visual blurring during head movement), difficulty walking in low light due to visual dependence, impaired dynamic visual stability

Question 29

What types of lesions produce nystagmus at rest and impaired compensation?

Answer 29

Brainstem or cerebellar lesions produce resting or direction-changing nystagmus, impaired central compensation, and often associated cranial nerve or limb ataxia

Question 30

Name common damaging factors to the vestibular system.

Answer 30

Ototoxic drugs Head trauma Ischemia Infection Neural degeneration

Question 31

What is vestibular compensation and what facilitates it?

Answer 31

Central adaptive plasticity (mainly cerebellum and visual/proprioceptive re-weighting) that reduces symptoms after unilateral vestibular loss Facilitated by intact vision and physical rehabilitation

Question 32

Why can chronic vestibular deficits be worse in the dark?

Answer 32

Compensation relies on visual input; absence of visual cues in low light removes a major compensatory input leading to imbalance

Question 33

What are clinical uses and cautions for antiemetics in vestibular disease?

Answer 33

Antiemetics (e.g., domperidone) help control nausea but choice must consider central vs peripheral action and side-effect profiles Overuse of vestibular suppressants can delay central compensation

Question 34

What diagnostic features suggest a peripheral vestibular cause rather than a central cause?

Answer 34

Unidirectional horizontal nystagmus that suppresses with fixation, severe vertigo with sudden onset, hearing symptoms (cochlear involvement), and clear peripheral triggers

Question 35

What diagnostic features suggest a central vestibular cause?

Answer 35

Direction-changing or vertical nystagmus, poor suppression with fixation, associated neurological signs (limb ataxia, cranial nerve deficits), and gradual or constant symptoms

Question 36

What is oscillopsia and when does it occur?

Answer 36

Perception that the visual world is bouncing during head movement due to impaired VOR; commonly occurs with bilateral vestibular loss

Question 37

What is the role of visual and proprioceptive inputs in vestibular rehabilitation?

Answer 37

They provide alternative cues for balance and spatial orientation; exercises aim to enhance substitution and recalibration to improve stability and reduce symptoms

Question 38

Give a clinical pearl about chronic vestibular deficits and compensation.

Answer 38

Chronic vestibular deficits often become well compensated by cerebellar plasticity and sensory substitution, but compensation fails when visual input is unavailable or in cerebellar disease