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What is the main function of the vestibulo-ocular reflex (VOR)?
The VOR stabilizes gaze during head movement by producing compensatory eye movements in the opposite direction of head motion.
During what type of movement is the VOR most important?
The VOR is most important for brief, transient head rotations and translations, such as during walking.
What kind of eye movement system does the VOR belong to?
The VOR is a gaze-holding/stabilizing eye movement system that keeps visual targets fixed on the retina during head motion.
Where is the vestibular apparatus located, and what major sensory structure is it associated with?
It is located in the inner ear and is adjacent to/continuous with the cochlea (the auditory end organ).
What is the basic structural makeup of the vestibular apparatus?
It is a membranous structure filled with viscous endolymph.
What are the main components of the vestibular apparatus, and what type of motion does each detect?
3 semicircular canals → detect rotational (angular) acceleration
Otolith organs → detect linear acceleration, often including gravity
Which part of the vestibular apparatus detects head rotation vs. linear movement?
Semicircular canals detect head rotation
Otolith organs detect linear movement and gravitational forces
How does endolymph move in the semicircular canals during head rotation?
Endolymph flows in the direction opposite to head rotation, helping signal rotational movement.
Where is endolymph flow detected in the semicircular canals?
It is detected in the ampulla, the thickened region on each semicircular canal.
What structure detects endolymph flow in the ampulla of the semicircular canals?
The crista ampullaris, a collection of sensory hair cells, detects endolymph flow.
What is the cupula, and what role does it play in the semicircular canals?
The cupula is a gelatinous structure that contains the cilia of hair cells; it is the mechanical trigger for canal signaling.
What are the key ciliary structures on vestibular hair cells in the semicircular canals?
Each hair cell has multiple stereocilia of variable length and one kinocilium located at one edge of the ciliary bundle.
What happens when stereocilia bend toward the kinocilium?
Bending toward the kinocilium causes depolarization of the hair cell and increases firing of the associated nerve fiber.
What happens when stereocilia bend away from the kinocilium?
Bending away from the kinocilium causes hyperpolarization of the hair cell and decreases firing of the associated nerve fiber.
Why is vestibular hair cell signaling directional?
Hair cell response depends on the direction of stereocilia deflection relative to the kinocilium:
Toward kinocilium = excitatory
Away from kinocilium = inhibitory
What type of head movement do the horizontal semicircular canals detect in rotational VOR?
When the cupula is deflected toward the utricle, the hair cells depolarize and increase firing = stimulation.
What happens to the horizontal canals during a rightward head turn?
A right head turn:
Stimulates the right horizontal canal
Inhibits the left horizontal canal
During a rightward head turn, which yoked extraocular muscle pair moves the eyes appropriately?
The eyes must move left to maintain fixation, so the active yoked pair is:
Right medial rectus
Left lateral rectus
This is ipsilateral medial rectus + contralateral lateral rectus relative to the stimulated canal.
What happens to the horizontal semicircular canals during a leftward head turn?
Left horizontal canal is stimulated
Right horizontal canal is inhibited
How are the vertical semicircular canals stimulated, and how does this differ from the horizontal canals?
Vertical canals are stimulated when the cupula is deflected away from the utricle, which is the opposite of the horizontal canals.
What is the general rule for activating the vertical canals during head tilt?
Vertical canals are stimulated when the head is tilted in the “direction” of the canals.
What happens to the vertical canals when the head is tilted forward (down)?
Anterior canals are stimulated
Posterior canals are inhibited
What happens to the vertical canals when the head is tilted backward (up)?
Posterior canals are stimulated
Anterior canals are inhibited
What is the basic rule linking semicircular canals to extraocular muscles (EOMs)?
Canals and eye muscles with parallel action planes are linked together.
Which extraocular muscle groups are linked to the anterior vs posterior vertical canals?
Anterior canals → ipsilateral recti + contralateral obliques
Posterior canals → ipsilateral obliques + contralateral recti
When are the anterior canals stimulated, and what eye movement do they produce?
Anterior canals are stimulated when the head tilts forward and they act to rotate the eyes upward.
What are the yoked muscle pairs for the anterior canal?
Ipsilateral superior rectus
Contralateral inferior oblique
What are the yoked muscle pairs for the posterior canal?
Ipsilateral superior oblique
Contralateral inferior rectus
In the diagnostic action field example, what happens when the head is rotated to the left?
The eyes move to the right due to stimulation of the left horizontal canal and inhibition of the right horizontal canal.
After the head is rotated left and the eyes move right, which muscle groups are acting most purely in the vertical plane?
The right recti and left obliques are most purely vertically acting.
In right gaze, which muscles are tested when the patient looks up vs down?
Right gaze + look up → Right superior rectus (RSR) + Left inferior oblique (LIO)
Right gaze + look down → Right inferior rectus (RIR) + Left superior oblique (LSO)
After rotating the head left, what happens when the head is then rotated forward (down)?
The eyes need to go up. This:
Stimulates the right anterior canal → ↑ RSR, ↑ LIO
Inhibits the left posterior canal → ↓ RIR, ↓ LSO
What is the core action of the horizontal canal in the rotational VOR?
Head turn to the ipsilateral side stimulates the horizontal canal, causing the eyes to move to the contralateral side via:
Ipsilateral medial rectus (MR)
Contralateral lateral rectus (LR)
What is the core action of the anterior vertical canal in the rotational VOR?
Head tilt forward (down) stimulates the anterior vertical canal, causing the eyes to move up via:
Ipsilateral superior rectus (SR)
Contralateral inferior oblique (IO)
What is the core action of the posterior vertical canal in the rotational VOR?
Head tilt backward (up) stimulates the posterior vertical canal, causing the eyes to move down via:
Ipsilateral superior oblique (SO)
Contralateral inferior rectus (IR)
What is the high-yield summary of R-VOR canal actions and yoked muscle pairs?
Horizontal canal: head turns ipsilateral → eyes move contralateral → ipsi MR + contra LR
Anterior vertical canal: head tilts forward/down → eyes move up → ipsi SR + contra IO
Posterior vertical canal: head tilts back/up → eyes move down → ipsi SO + contra IR
What is a key timing feature of the rotational vestibulo-ocular reflex (R-VOR)?
The R-VOR responds very quickly, allowing rapid stabilization of gaze during head movement.
What is the approximate latency of the rotational VOR?
The latency is about 16 ms.
What happens if a vestibular canal is constantly stimulated or constantly suppressed?
It can produce continuous nystagmus because the vestibular system behaves as though the head is persistently moving.
What type of nystagmus occurs if the left horizontal canal is constantly stimulated?
Left-beating jerk nystagmus occurs, meaning the fast phase is to the left.
What happens if the left horizontal canal is suppressed instead of stimulated?
You get the opposite effect: right-beating nystagmus.
What is the rule for vestibular lesions affecting a horizontal canal?
Constant stimulation of a canal → nystagmus toward that side
Suppression/inhibition of a canal → nystagmus away from that side
What vestibular change occurs in Ménière’s disease?
A change in the viscosity of endolymph (hyper- or hypoviscous), which can alter canal/cupula mechanics.
How does altered endolymph viscosity cause vestibular symptoms in this model?
It creates “heavy” bubbles/debris in the endolymph that can become stuck against the cupula, producing abnormal vestibular signaling.
Why can nystagmus be position-dependent in Ménière’s disease?
Turning the head in the direction of the affected canal increases the chance that the “heavy” material gets stuck against the cupula, so nystagmus may depend on head position.
What is the high-yield mechanism linking altered endolymph properties to nystagmus?
Abnormal endolymph/cupula mechanics → inappropriate canal stimulation or inhibition → position-dependent nystagmus.
What is benign paroxysmal positional vertigo (BPPV)?
Benign = not malignant/life-threatening
Paroxysmal = sudden attacks
Positional = triggered by changes in head position
It is the most common vestibular disorder.
What causes BPPV?
BPPV is caused by calcium carbonate crystals breaking free from the utricle and entering a semicircular canal. These crystals are called otoconia.
Which canal is most commonly affected in BPPV, and what are common age-related associations?
Posterior vertical canal is most commonly affected
Under age 50: often associated with head injury
Over age 50: usually idiopathic
What is the difference between canalithiasis and cupulolithiasis in BPPV?
Canalithiasis = free-floating otoconia in the canal
Cupulolithiasis = otoconia stuck to the cupula
In BPPV, when is nystagmus/vertigo most likely to occur?
Symptoms are more likely when the head is moved in the orientation of the affected canal, which increases abnormal canal stimulation.
Why are symptoms in BPPV considered positional?
Because specific head positions and movements trigger nystagmus, dizziness, and vertigo.
What are classic movements that can trigger BPPV symptoms?
Looking up
Rolling out of bed
Brief, position-triggered vertigo/nystagmus that occurs when the head moves into the plane of the affected semicircular canal.
What is the key vestibular effect of vestibular neuritis?
It causes hypostimulation (reduced vestibular input) from the affected side/canal.
What are possible causes/associations listed for vestibular neuritis?
Viral infection, stroke, tumor, aneurysm, ischemia, and MS as potential causes/associations.
How do symptoms of vestibular neuritis change with head movement?
Symptoms may be worse when turning the head toward the affected canal. If multiple/all canals are affected, symptoms may occur with head turning in any direction.
What type of nystagmus occurs with right-sided hypostimulation?
Right hypostimulation causes left-beating nystagmus (fast phase beats away from the hypoactive side).
Why can vestibular illness cause dizziness/oscillopsia due to a mismatch between proprioception and VOR signals?
The neck/proprioceptive system may signal one amount of head movement, while the VOR signals a different amount (e.g., proprioception says 20°, VOR says 15°), creating a sensory mismatch that causes dizziness/oscillopsia.
Why can vestibular illness cause oscillopsia from a mismatch between vision and proprioception?
If proprioception says the head moved more than the eyes actually compensated for (e.g., head moved 20°, eyes compensate only 10°), the retinal image shifts, so the person feels like either the world or they are moving.
Why might a patient with vestibular illness say they “can’t see while walking”?
Because impaired vestibular function disrupts gaze stabilization during head movement, so vision becomes unstable while walking, producing oscillopsia/blurring with motion.
What is caloric stimulation, and what is it used for?
Caloric stimulation induces vestibular nystagmus using heat convection in the lateral semicircular canal and helps determine whether a canal/labyrinth is hyperactive or hypoactive.
How is the lateral semicircular canal positioned for caloric testing?
The lateral canal normally sits about 30° up from horizontal. Tilting the head back about 60° makes the lateral canal vertical, which allows caloric convection to work effectively.
What happens with warm air/water during caloric testing?
Warm air/water rises in the vertical lateral canal, deflects the cupula toward the utricle, and produces nystagmus.
Example: warm left ear → left-beating nystagmus (slow phase right).
What is the mnemonic for predicting the fast phase of caloric nystagmus?
COWS = Cold Opposite, Warm Same
(refers to the fast phase direction)
Warm right ear → right-beating nystagmus
Cold right ear → left-beating nystagmus
What reduces the amplitude of caloric-induced nystagmus?
Visual fixation reduces the amplitude of the induced nystagmus.
How is VOR gain and phase usually tested?
It is usually tested with sinusoidal stimulation by rotating the head back and forth, often with the eyes closed.
What is VOR gain?
VOR gain = output velocity / input velocity
= eye velocity / head velocity
What does VOR gain represent, and what is the ideal value?
It represents how well eye velocity matches head velocity.
Perfect gain = 1.0
What is VOR phase?
Phase is the difference in position between the eye and head during movement.
What does it mean if the eye is 5° left while the head is 5° right?
The eye and head are 180° out of phase, which is the normal compensatory relationship for the VOR.
What does a Bode plot show for the VOR?
A Bode plot shows the relationship between frequency of head rotation and:
Gain
Phase
It is made of 2 plots: gain vs frequency and phase vs frequency.
What are the normal VOR gain and phase at frequencies of natural head rotation?
At about 0.5–5.0 cycles/sec,
Gain ≈ 1.0
Phase ≈ 180°
This means eye movement cancels head movement well.
What happens to VOR gain and phase at very low frequencies of head rotation?
At < 0.01 cycles/sec,
Gain falls
Phase deviates more from the ideal 180°
So the eyes move less effectively and more slowly relative to the head.
What is the interpretation of the VOR at low vs natural frequencies?
Natural frequencies (0.5–5 Hz): VOR works well → gain near 1, phase near 180°
Very low frequencies: VOR works less well → reduced gain and worse phase relationship