Normal Vestibulo-ocular Reflex
Normal activities of daily life (such as running) can be associated with head velocities of up to 550 degrees per second (deg/sec), head accelerations of up to 6,000 deg/sec2, and frequency content of head motion from 1 to 20 Hz.1,2 Only the vestibular system can detect head motion over this range of velocities, accelerations, and frequencies. Additionally, the latency of the vestibulo-ocular reflex (VOR) has been reported to be as short as 5 to 7 msec.3,4 In contrast, ocular following mechanisms, such as smooth pursuit, generate slower eye velocities (∼60 deg/sec), have relatively long latencies (up to 100 msec),5,6 and fail at frequencies exceeding 1 Hz.7 For subjects with vestibular loss that has not been compensated adequately, head movements can significantly limit participation in activities of daily life.
Abnormal Vestibulo-ocular Reflex
People who sustain vestibular damage typically experience vertigo, disequilibrium, head motion–induced oscillopsia, spontaneous nystagmus, and postural instability.8–11 In particular, when a subject with loss of vestibular function makes rapid head rotations in the direction of the damaged labyrinth, the eyes do not remain fixated on a visual target, reflecting a deficient VOR. As a result, visual acuity during head rotation is degraded.12,13 As a form of compensation, the brain can generate surrogate eye rotations that compensate for the VOR.14,15
Individuals with vestibular loss use different compensatory strategies to improve their ability to see clearly during a head rotation.16 Compensatory mechanisms include substitution or modification of a saccade, increased gain of the cervico-ocular reflex (COR), the use of a centrally preprogrammed eye movement, and, perhaps, enhancement of the smooth pursuit system.
The substitution of a saccade in the direction of the deficient VOR (compensatory saccades [CS]), also known as covert saccade because of their occurrence during the head rotation and thus not visible to the clinician's eye during ipsilesional whole-body and head-only rotations, has been identified in persons with loss of vestibular function.14,15 Recently, it has been reported that these saccades are unique in that they occur with reduced latencies of 50 to 150 msec from the onset of a head rotation (Fig. 9.1),15,17 occur during both predictable and unpredictable head movements,14,17 and have been hypothesized to be of vestibular origin.14
Compensatory (preprogrammed) saccades vs. normal vestibular-ocular reflex (VOR) in a person with unilateral vestibular hypofunction (UVH). Dark traces reflect head velocity, and lighter traces eye velocity. The vertical line marks the onset of the head rotation. (A) The slow eye velocity is deficient in relation to the head velocity (low VOR gain), and compensatory saccades (CS) are recruited. Note that the direction of the CS is the same as that of the ...
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