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Bone-conducted vibration of the forehead, in the midline at the hairline (Fz) causes linear acceleration stimulation of both mastoids and results in an ocular vestibular-evoked myogenic potential (oVEMP), recorded by surface electromyogram (EMG) electrodes just beneath the eyes. The early n10 component of the oVEMP is symmetrical in healthy subjects, absent in patients with bilateral vestibular loss, and in patients after unilateral vestibular loss (uVL) n10 is small or absent on the side contralateral to the uVL, but of normal amplitude on the side contralateral to the healthy ear. The n10 component probably reflects mainly otolithic function, since in the guinea pig, primary otolith irregular neurons are selectively activated by bone-conducted vibration (BCV) at low intensities (0.1 g), whereas semicircular canal primary afferents are not activated even at high intensities (10 g).

Research into vestibular responses to sound has evolved in four stages. The first, largely the work of Tullio in the 1920s, involved inspection of the eye, head, and postural responses to sound of alert animals with surgical fenestrae into various parts of the bony labyrinth. The second, begun in 1964 by Bickford and his group and continued by our group and then by others in the last 10 years, involves the measurement of evoked myogenic potentials to air-conducted and bone-conducted clicks and tones in normal humans. The third, begun by Mikaelian at about the same time as Bickford and continued by McCue, our group, and others, involves electrophysiological recordings of primary vestibular afferent neuron responses to sound in anesthetized animals. The fourth involves measurements of vestibulo-ocular responses to sound in humans with the Tullio phenomenon. It was begun by Minor and his group in 1998 with the observation that sound-induced nystagmus in humans, the Tullio phenomenon, aligned with the rotation axis of the superior semicircular canal. They then showed a defect in the temporal bone between the apex of the superior semicircular canal and the middle cranial fossa, which was the cause of most, if not all, cases of sound-induced nystagmus. Here some of the key observations made in each of these four stages are reviewed.

We studied the compensatory eye movements made by subjects with unilateral vestibular deficits in response to passive (unpredictable, manually generated) and active (predictable, self-generated) head impulses. A typical head impulse is a brief, low-amplitude (15-20 degrees ), high-velocity (150-350 degrees /s), high-acceleration (4000-6000 degrees /s(2)), yaw head-on-trunk rotation. In the initial 75 ms of the response, the vestibulo-ocular reflex gain was significantly higher during active head impulses to both ipsilesional and contralesional sides, than during passive impulses. Mean gains were 0.15 (ipsilesional passive), 0.44 (ipsilesional active), 0.5 (contralesional passive), and 0.76 (contralesional active). Differences between active and passive head impulses were present from near the onset of head rotation. The mechanism for producing this behavior is unclear, but the findings could be related to enhanced sensitivity of second-order neurons during active head impulses. However, even with active movements, there is still a large and statistically significant asymmetry in the eye-movement responses for ipsilesional as opposed to contralesional head rotations. After 75 ms, rapid corrective eye movements often were generated to reduce any remaining gaze error.

Sudden, spontaneous, unilateral loss of vestibular function without simultaneous hearing loss or brain stem signs is generally attributed to a viral infection involving the vestibular nerve and is called acute vestibular neuritis. The clinical hallmarks of acute vestibular neuritis are vertigo, spontaneous nystagmus, and unilateral loss of lateral semicircular function as shown by impulsive and caloric testing. In some patients with vestibular neuritis the process appears to involve only anterior and lateral semicircular function, and these patients are considered to have selective superior vestibular neuritis. Here we report on two patients with acute vertigo, normal lateral semicircular canal function as shown by both impulsive and caloric testing, but selective loss of posterior semicircular canal function as shown by impulsive testing and of saccular function as shown by vestibular evoked myogenic potential testing. We suggest that these patients had selective inferior vestibular neuritis and that contrary to conventional teaching, in a patient with acute spontaneous vertigo, unilateral loss of lateral semicircular canal function is not essential for a diagnosis of acute vestibular neuritis.

In order to test the human angular vestibulo-ocular reflex in the dynamic range of normal head movements, we measured 3-dimensional compensatory eye-movement responses to low-amplitude (10-12 degrees), high-acceleration (3000-4000 degrees/s/s), passive, manually delivered head rotations (head "impulses") in the three planes of the semicircular canals in normal subjects, in subjects who had recovered from surgical unilateral vestibular deafferentation, and in patients after acute unilateral peripheral vestibulopathy, that is, from vestibular "neuritis." We found that canal-plane head impulses away from an intact semicircular canal, that is, toward a lesioned semicircular canal, invariably produce a vestibulo-ocular reflex with permanently low gain, typically less that 0.4 if the lesion is complete. These results are a necessary consequence of primary semicircular canal afferents being driven into inhibitory saturation by rapid angular accelerations. With practice, clinicians can learn to recognize the telltale compensatory saccades that patients with unilateral loss of semicircular canal function will make if asked to look at an earth-fixed target during head impulses in any one of the three semicircular canal planes.

To test a hypothesis about how otoliths resolve roll-tilts from translations, we measured human ocular torsion position [ocular counterrolling (OCR)] to maintained linear acceleration stimuli. All subjects (n = 8) were tested in two conditions where the same magnitude of shear along an interaural axis was generated in one of two ways: either by roll-tilt on a tilt-chair in a 1-g environment, or by centripetal linear acceleration during constant velocity rotation 1 m from the axis of rotation on a fixed-chair human centrifuge. The interaural shear to the otoliths was the same for these two conditions, but the dorsoventral shear was different and for all eight subjects the OCR on the centrifuge was significantly greater than the torsion on the tilt-chair, although the resultant angle was in fact smaller on the centrifuge than on the tilt-chair. The results confirm that dorsoventral shear is important for determining OCR. The otoliths may resolve potential stimulus ambiguities between tilts and translations by virtue of the different patterns of interaural and dorsoventral shear that these stimuli generate.

To establish a link between otolith anatomy and function it is necessary to know the regions of the utricular and saccular maculae, which are stimulated by any arbitrary linear acceleration stimulus. That requires accurate information about the location and orientation of the spatially extended maculae in head-fixed coordinates and referred to head-fixed landmarks (such as Reid's line). New data showing the location of the otolithic maculae in the guinea pig with respect to head-fixed stereotaxic coordinates are presented. Guinea pigs were perfused with Karnovsky's fixative and the maculae were exposed while the head was held in a guinea pig stereotaxic device. An electrolytically sharpened fine wire held in a calibrated micromanipulator was touched to points all over the surface of each macula under visual observation with the aid of a high-power operating microscope. The x, y, z coordinates of these points were plotted using a three-dimensional plotting program. Both maculae have pronounced curvature so that dorsoventral shear forces will stimulate regions of both the utricular and saccular maculae.

The subjective visual horizontal and vestibular-evoked myogenic potentials are simple, robust, and reproducible tests of otolith dysfunction that can prove clinically useful diagnostic information in patients with vertigo and other balance disorders. While they appear to have high specificity for unilateral otolith dysfunction, further clinical research will be required to establish their sensitivity.