Timothy C. Hain, MD • Page last modified: March 12, 2021
This material is partially abstracted and expanded from a longer chapter found here.
The Vestibulo-Ocular Reflex
The VOR normally acts to maintain stable vision during head motion. This means that the eye must precisely counter-rotate to compensate for the head, and keep the eye stable in space.
We live in a world where we can both rotate and translate (i.e. move along a line), along 3 axes. Thus the VOR has two components, angular and linear.
The angular VOR.
The angular VOR, mediated by the semicircular canals, compensates for rotation. The angular VOR is primarily responsible for gaze stabilization. The linear VOR is most important in situations where near targets are being viewed and the head is being moved at relatively high frequencies.
Effects of head rotation on the canals. (A) The direction from which hair cells are deflected determines whether or not hair-cell discharge frequency increases or decreases. (B) Cross-section of the membranous labyrinth illustrating endolymph flow and cupular deflection in response to head motion. Adapted from (Bach-Y-Rita et al., 1971)
1. When the head turns to the right, endolymphatic flow deflects the cupulae to the left (see Figure).
2. The discharge rate from hair cells in the right crista increases in proportion to the velocity of the head motion, while the discharge rate from hair cells in the left lateral crista decreases (see Fig).
3. These changes in firing rate are transmitted along the vestibular nerve and influence the discharge of the neurons of the medial and superior vestibular nuclei and cerebellum.
4. Excitatory impulses are transmitted via white matter tracts in the brainstem to the oculomotor nuclei which activate the right (ipsilateral) medial rectus and the left (contralateral) lateral rectus. Inhibitory impulses are also transmitted to their antagonists.
5. Simultaneous contraction of the left lateral rectus and right medial rectus muscles, and relaxation of the left medial rectus and right lateral rectus occurs, resulting in lateral compensatory eye movements toward the left.
6. If the eye velocity is not adequate for the given head velocity and retina image motion is >2°per second, the cerebellar projection to the vestibular nuclei will modify the firing rate of the neurons within the vestibular nuclei to reduce the error.
The linear VOR
The linear VOR, mediated by the otoliths, compensates for translation and acceleration in a linear direction (which is basically the same thing). The linear VOR is most important in situations where near targets are being viewed and the head is being moved at relatively high frequencies.
The linear VOR scales with the point of regard. There is a far greater demand for eye movement for a near target than for a distant target (Viirre et al, 1986). This means that viewing something like your cell-phone in a car is a lot more demanding on the linear VOR than looking out the window.
The Vestibulospinal Reflex
The purpose of the VSR is to stabilize the body. The VSR actually consists of an assemblage of several reflexes named according to the timing (dynamic vs. static or tonic) and sensory input (canal vs. otolith). As an example of a vestibulospinal reflex, let us examine the sequence of events involved in generating a labyrinthine reflex.
1. When the head is tilted to one side, both the canals and otoliths are stimulated. Endolymphatic flow deflects the cupula and shear force deflects hair cells within the otoliths.
2. The vestibular nerve and vestibular nucleus are activated.
3. Impulses are transmitted via the lateral and medial vestibulospinal tracts to the spinal cord.
4. Extensor activity is induced on the side to which the head is inclined, and flexor activity is induced on the opposite side. The head movement opposes the movement registered by the vestibular system.
The Vestibulocollic Reflex -- this is not a ocular reflex but a neck reflex.
The vestibulocollic reflex (VCR) acts on the neck musculature to stabilize the head. The reflex head movement produced counters the movement sensed by the otolithic or semicircular canal organs. The precise pathways mediating this reflex have yet to be detailed. The VCR can be measured with the VEMP test.
If someone loses 90% of their vestibular system, they would need a 10X increase in VOR gain to recover for this. Thats a lot -- is this really possible? What does the data say ?
Demer et al (1989) stated that "The upper limit of human VOR gain is not known". Nevertheless, the data that they presented suggested that there is far less than a 10X capability. These authors noted that while relative increases in VOR gain can be attained by combined visual/vestibular experience, experimental data at that point from Gonshor and Melville Jones (1976) documented a VOR gain relative increase of 70% after wearing 2.1x telescopic spectacles for 5 days. Obviously, this is not even 2X. Furthermore, Istel-Lentz et al (1985) reported "complete adaptation" of human VOR gain after 5 days of continuous wearing of 2X telescopic spectacles, but only at 3 hz. When prediction was excluded, fully adapted subjects "failed to exhibit full adaptation at any point over the frequency range examined (0.5-5 Hz)".
Practically, clinical data where there is a complete unilateral vestibular loss usually documents recovery towards the "good ear" for high frequencies (e.g. VHIT test). If we assume that the VOR is driven half by each ear, this would require plasticity of 2X. However, equal push-pull contribution of the VOR is only true at low frequencies, and the VOR gain is generally much less in this situation at lower frequencies (i.e. suggesting less plasticity).
So it appears from available data that the upper limit of human VOR gain is probably about 2.0, and furthermore that this is mainly apparent at high frequencies. We would like to know if more adaptation is possible for longer periods of adaptation, but we would think not, given that patients with substantial bilateral vestibular loss, do recover even after decades of adaptation.