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The head impulse test (HIT) is a useful bedside test to identify peripheral vestibular deficits. However, such a deficit of the vestibulo-ocular reflex (VOR) may not be diagnosed because corrective saccades cannot always be detected by simple observation. The scleral search coil technique is the gold standard for HIT measurements, but it is not practical for routine testing or for acute patients, because they are required to wear an uncomfortable contact lens.

Parenteral antibiotic therapy with gentamicin, even in accepted therapeutic doses, can occasionally cause bilateral vestibular loss (BVL) due to hair cell toxicity.

Electrical vestibular stimulation is believed to directly activate the vestibular afferents to mediate an electrically evoked vestibulo-ocular reflex (eVOR). Gentamicin, an aminoglycoside antibiotic, induces vestibulotoxicity by hair cell damage and death.

Quantitative head impulse test (HIT) measures the gain of the angular vestibulo-ocular reflex (VOR) during head rotation as the ratio of eye to head acceleration. Bedside HIT identifies subsequent catch-up saccades after the head rotation as indirect signs of VOR deficit.

An enlarged, low-threshold click-evoked vestibulo-ocular reflex (VOR) can be averaged from the vertical electro-oculogram in a superior canal dehiscence (SCD), a temporal bone defect between the superior semicircular canal and middle cranial fossa.

To describe the spatial and temporal characteristics of benign positional nystagmus (BPN) subtypes in benign positional vertigo (BPV) due to vestibular lithiasis affecting one or more semicircular canals (SCCs).

That disease or dysfunction of vestibular end organs in human patients will reduce or eliminate the contribution of the affected end organs to the total eye-movement response to DC surface galvanic vestibular stimulation (GVS).

Of the more than 40 genetically defined dominantly inherited hearing loss syndromes, only a few are associated with bilateral vestibulopathy. No genetic mutations have been identified in families with bilateral vestibulopathy and normal hearing.

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°), high‐velocity (150‐350°/s), high‐acceleration (4000‐6000°/s2), 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.

The effects of unilateral vestibular deafferentation (UVD) on the linear vestibulo-ocular reflex (LVOR) were studied by measuring three-dimensional eye movements in seven UVD subjects evoked by impulsive eccentric roll rotation while viewing an earth-fixed target at 200, 300, or 600 mm and comparing their responses to 11 normal subjects. The stimulus, a whole-body roll of approximately 1°, with the eye positioned 815 mm eccentric to the rotation axis, produced an inter-aural linear acceleration of approximately 0.5gand a roll acceleration of approximately 360°/s2. The responses generated by the LVOR comprise horizontal eye rotations. Horizontal eye velocity at 100 ms from stimulus onset in UVD subjects was significantly lower than in normal subjects for all viewing distances, with no significant difference between ipsilesional and contralesional responses. LVOR acceleration gain, defined as the slope of actual horizontal eye velocity divided by the slope of ideal horizontal eye velocity during a 30-ms period starting 70 ms from stimulus onset, was bilaterally significantly reduced in UVD subjects at all viewing distances. Acceleration gain from all viewing distances was 1.04 ± 0.28 in normal subjects, and in UVD subjects was 0.49 ± 0.23 for ipsilesional and 0.63 ± 0.27 for contralesional acceleration. LVOR enhancement in the first 100 ms by near viewing was still present in UVD subjects. LVOR latency in UVD subjects (approximately 39 ms) was not significantly different from normal subjects (approximately 36 ms). After UVD, LVOR is bilaterally and largely symmetrically reduced, but latency remains unchanged and modulation by viewing distance is still present.

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 superiorvestibular 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 inferiorvestibular 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°), high-acceleration (3000-4000°ss), 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 examine the concept of selective superior and inferior vestibular nerve involvement in vestibular neuritis by studying the distribution of semicircular canal (SCC) involvement in such patients.

A patient with a postoperative fistula of the left posterior semicircular canal is presented. Negative pressure in the external ear canal produced upbeat-torsional nystagmus, which was recorded in three dimensions using binocular scleral search coils. The nystagmus was conjugate, without skew deviation, and its trajectory corresponded to the anatomic axis of the left posterior canal. The current study helps validate Ewald’s first law in humans the axis of nystagmus should match the anatomic axis of the semicircular canal that generated it. This law is clinically useful in diagnosing pathology of the vestibular end-organ, such as benign paroxysmal positional vertigo or the superior semicircular canal dehiscence syndrome.

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, zcoordinates 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.

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 (n8) 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.

The ability of 33 patients to perceive the direction, relative to the body long axis, of a linear acceleration vector acting in the coronal plane, rolltilt perception, was studied at various times, before and from 1 week to 6 months after unilateral, selective vestibular neurectomy for Meniere's disease, acoustic neuroma or intractable paroxysmal vertigo. The results of these patients were compared with the results of 31 normal subjects and two control patients who had both vestibular nerves surgically sectioned. Rotating on a fixed-chair centrifuge in an otherwise darkened room, each observer was required to indicate his perception of the direction of the resultant gravito-inertial vector by setting a small, motor-driven, illuminated bar, attached to the chair but rotatable in the frontoparallel plane, to the perceived gravitational horizontal. Normal subjects accurately align the bar with respect to the gravito-inertial resultant vector which, in the dark, they assume to be the gravitational vertical. This percept has been called the oculogravic illusion. Accurate roll-tilt perception is due to vestibular (probably mainly otolithic) sensory information since patients with bilateral vestibular neurectomies do not perceive the resultant vector accurately. Whereas normal subjects perceive resultant vectors directed to the right and to the left equally accurately, roll-tilt perception was invariably asymmetrical one week after unilateral vestibular neurectomy. Even at rest there was an asymmetry in the baseline settings, so that patients set the bar down on the side of the operated ear, in order for it to appear gravitationally horizontal: if a patient had a right vestibular nerve section then he set the bar clockwise (from the patient's view) below the true gravitational horizontal. With increasing gravitoinertial resultant angles there was an increasing asymmetry of roll-tilt perception due both to decreased sensitivity to roll-tilt stimuli directed towards the operated ear and to transiently increased sensitivity to roll-tilt stimuli directed towards the intact ear. A progressive decrease in both perceptual asymmetries followed, rapidly in the first 3 weeks, more slowly in the next 6 months. Based on these results, which are consistent with what is known about the responses of primary and secondary otolithic neurons to linear acceleration, we propose: (1) that the asymmetric roll-tilt perceptual response following unilateral vestibular neurectomy is an otolithic analogue of Ewald's second law; (2) that the perceptual asymmetries may be due to decreased spontaneous activity in the deafferented lateral vestibular nucleus; (3) that the progressive recovery of roll-tilt perceptual symmetry after vestibular neurectomy may be part of the otolithic component of the total recovery phenomenon known as vestibular compensation; (4) that ocular torsion caused by the unilateral vestibular neurectomy is a major factor contributing to the systematic errors in baseline settings to the gravitational horizontal one week after operation.

The static ocular torsional position of both eyes of 23 patients was measured by means of fundus photographs one day before and one week after unilateral vestibular neurectomy for the treatment of acoustic neuroma, Ménière's disease or paroxysmal vertigo. The results showed that in all patients the vestibular neurectomy caused both eyes to tort (i.e. to roll around the visual axis) toward the side of the neurectomy when measured one week after operation. The extent of this torsion was an average of 9.5° one week after operation and there was no statistically significant difference in the average magnitude of the torsion in the two eyes. In 8 of these patients, additional measurements were made at intervals up to one year after operation and it was found that in these patients there is a significant reduction in torsion over time from an average of 10.2° one week after operation to an average of 2.8° by 16 weeks after operation. The change in torsional eye position following the neurectomy was accompanied by a change in the perceived visual orientation of a small (9.5° visual angle) illuminated horizontal line at a straight ahead eye level position in an otherwise completely darkened room. One week after operation when asked to adjust the line to the perceived gravitational horizontal by rotating it in roll (i.e. around an X axis), patients who had had a right vestibular neurectomy consistently set the line so that the right side of the line (from the patient's point of view) was below the true gravitational horizontal. Similarly patients after a left neurectomy consistently set the line so that the left side of the line was below the true gravitational horizontal. There is a high correlation (r = 0.95) between the direction and magnitude of the change in torsional eye position and the direction and magnitude of the change in the perceived visual horizontal one week after operation. It appears that this change in static ocular torsional position (and its accompanying change in visual perception) is another oculomotor symptom of vestibular deafferentation and the progressive decrease of torsion is another manifestation of vestibular compensation.

We studied 4 patients with tonic contraversive ocular tilt reactions due to unilateral, paramedian, meso-diencephalic lesions. This is in contrast to the only 2 previously reported patients with ocular tilt reactions due to unilateral meso-diencephalic lesions, each of whom had a paroxysmal ipsiversive ocular tilt reaction. This new finding is considered in the context of previous clinical and experimental data on the various types of ocular tilt reactions that follow stimulation or destruction of the peripheral and central vestibular system. Otolithic inputs to the interstitial nucleus of Cajal from the contralateral vestibular nucleus and motor outputs from the interstitial nucleus of Cajal to cervical and ocular motoneurons could be involved in the ocular tilt reaction. We propose that in patients with unilateral meso-diencephalic lesions, a tonic contraversive ocular tilt reaction could be due to persistently decreased resting activity of ipsilateral interstitial nucleus neurons, whereas a paroxysmal ipsiversive ocular tilt reaction could be due to transiently increased activity of the same interstitial nucleus neurons. Cases of ocular tilt reaction due to unilateral meso-diencephalic lesion point to the existence of a crossed graviceptive pathway between the vestibular nucleus and the contralateral interstitial nucleus of Cajal.

Abstract:  We tested the hypothesis that the reason some patients compensate well after unilateral vestibular deafferentation (uVD) and others do not could be due to differences in eye-head coordination or in blink characteristics during natural, active head movements. Patients with well-compensated uVDs do not report distressing postural unsteadiness or an aversive sensation of apparent motion of a visual scene (oscillopsia) or ”visual confusion” upon rapid head rotation as do those patients with poorly compensated uVDs. It has been suggested that well-compensated subjects eliminate the subjective sensations associated with retinal slip, which must occur as a result of an inadequate vestibuloocular reflex (VOR), either by restricting head movement to the lesioned side or by blinking during head turns. To test this, subjects stood at the curbside of a busy road with a 180o view of regular, fast-moving traffic, which they scanned in preparation of crossing the road, and their eye and head movements and blinks were measured in this natural situation. Both normals and uVDs generated similar ranges of head position, head velocity and gaze magnitude, and all subjects performed a blink during the gaze saccade. Contrary to the hypothesis, no systematic differences were found between normals and either group of uVDs.

Abstract:  Dual search coils were used to record horizontal, vertical and torsional eye movement components of one eye during nystagmus caused by off-center yaw rotation (yaw centrifugation). Both normal healthy human subjects (n=7) and patients with only one functioning labyrinth (n=12) were studied in order to clarify how the concomitant linear acceleration affected the nystagmus response. Each subject was seated with head erect on the arm of a fixed-chair human centrifuge, 1 m away from the center of the rotation, and positioned to be facing along a radius; either towards (facing-in) or away from (facing-out) the center of rotation. Both yaw right and yaw left angular accelerations of 10°s–2 from 0 to 200°/s were studied. During rotation a centripetal linear acceleration (increasing from 0 to 1.24×g units) was directed along the subject’s naso-occipital axis resulting in a shift of the resultant angle of the gravitoinertial acceleration (GIA) of 51° in the subject’s pitch plane and an increase in the total GIA magnitude from 1.0 to 1.59×g. In normal subjects during the angular acceleration off-center there were, in addition to the horizontal eye velocity components, torsional and vertical eye velocities present. The magnitude of these additional components, although small, was larger than observed during similar experiments with on-center angular acceleration (Haslwanter et al. 1996), and the change in these components is attributed to the additional effect of the linear acceleration stimulation. In the pitch plane the average size of the shift of the axis of eye velocity (AEV) during the acceleration was about 8° for a 51° shift of the GIA (around 16% of the GIA shift) so that the AEV-GIA alignment was inadequate. There was a very marked difference in the size of the AEV shift depending on whether the person was facing-in [AEV shift forward (i.e. non-compensatory) of about 4°] or facing-out [AEV shift forward (i.e. compensatory) of around 12°]. The linear acceleration decreased the time constant of decay of the horizontal component of the post-rotatory nystagmus: from an average of 24.8°/s facing-in to an average of 11.3°/s facing-out. The linear acceleration dumps torsional eye velocity in an manner analogous to, but independent of, the dumping of horizontal eye velocity. Patients with UVD had dramatically reduced torsional eye velocities for both facing-in and facing-out headings, and there was little if any shift of the AEV in UVD patients. The relatively small effects of linear acceleration on human canal-induced nystagmus found here confirms other recent studies in humans (Fetter et al. 1996) in contrast to evidence from monkeys and emphasizes the large and important differences between humans and monkeys in otolith-canal interaction. Our results confirm the vestibular control of the axis of eye velocity of humans is essentially head-referenced whereas in monkeys that control is essentially space-referenced.

We recorded three-dimensional eye movements during angular acceleration steps from 0 to 250°/s at 20°/s2 about an earth-vertical axis. Experiments were performed on 27 normal subjects and on 19 patients who had recovered well from unilateral vestibular deafferentation on the right or left side. In addition to compensatory horizontal eye movements, significant vertical and torsional eye movement components were elicited. These vertical and torsional eye velocity traces led to a shift of the axis of eye velocity away from the axis of head velocity. Horizontal, vertical, and torsional velocity components showed clear differences between normals and patients with unilateral vestibular deafferentation. In normals, the axis of eye velocity tilted backward and slightly away from the axis of head velocity. Patients showed similar, but more pronounced, shifts during rotations toward the intact ear and shifts in the opposite direction for rotations toward the operated ear. Eye velocity traces were analyzed with special consideration given to the orientation of the axis of eye velocity. We speculate that the vertical and torsional velocity components may be due to the effects of Listing's plane, as well as the contributions of the otolith signals.

The vestibulo-ocular reflex (VOR) was studied in nine human subjects 2–15 months after permanent surgical occlusion of one posterior semicircular canal. The stimuli used were rapid, passive, unpredictable, low-amplitude (10–20°), high-acceleration (3000–4000°/s2) head rotations in pitch and yaw planes. The responses measured were vertical and horizontal eye rotations, and the results were compared with those from 19 normal subjects. After unilateral occlusion of the posterior semi-circular canal, the gain of the head-up pitch vertical VOR — the vertical VOR generated by excitation from only one and disfacilitation from two vertical semicircular canals — was reduced to 0.61±0.06 (normal 0.92±0.06) at a head velocity of 200°/s. In contrast the gain of the head-down pitch vertical VOR — the VOR still generated by excitation from two, but disfacilitation from only one vertical semicircular canal — was within normal limits: 0.86±0.11 (normal 0.96±0.04). The gain of the horizontal VOR in response to yaw head rotations — ipsilesion 0.81±0.06 (normal 0.88±0.05) and contralesion 0.80±0.11 (normal 0.92±0.11) — was within normal limits in both directions (group means ± two-tailed 95% confidence intervals given in each case). These results show that occlusion of just one vertical semicircular canal produces a permanent deficit of about 30% in the vertical VOR gain in response to rapid pitch head rotations in the excitatory direction of the occluded canal. This observation indicates that, in response to a stimulus in the higher dynamic range, compensation of the human VOR for the loss of excitatory input from even one vertical semicircular canal is incomplete.

Rapid, passive, unpredictable, low-amplitude (10–20°), high-acceleration (3000–000°/s2) head rota tions were used to study the vertical vestibulo-ocular reflex in the pitch plane (pitch-vVOR) after unilateral vestibular deafferentation. The results from 23 human subjects who had undergone therapeutic unilateral vestibular deafferentation were compared with those from 19 normals. All subjects were tested while seated in the upright position. Group means and two-tailed 95% confidence intervals are reported for the pitch-vVOR gains in normal and unilateral vestibular deafferented subjects. In normal subjects, at a head velocity of 125°/s the pitch-vVOR gains were: upward 0.89±0.06, down ward 0.91±0.04. At a head velocity of 200°/s, the pitchvVOR gains were: upward 0.92±0.06, downward 0.96±0.04. There was no significant up-down asymme try. In the 15 unilateral vestibular deafferented subjects who were studied more than 1 year after unilateral vestibular deafferentation, the pitch-vVOR was signifi cantly impaired. At a head velocity of 125°/s the pitchvVOR gains were: upward 0.67±0.11, downward 0.63 ± 0.07. At a head velocity of 200°/s, the pitch-vVOR gains were: upward 0.67±0.07, downward 0.58±0.06. There was no significant up-down asymmetry. The pitch-vVOR gain in unilateral vestibular deafferented subjects was significantly lower (P<0.05) than the pitch-vVOR gain in normal subjects at the same head velocities. These results show that total, permanent uni lateral loss of vestibular function produces a permanent symmetrical 30% (approximately) decrease in pitchv-VOR gain. This pitch-vVOR deficit is still present more than 1 year after deafferentation despite retinal slip velocities greater than 30°/s in response to head accelerations in the physiological range, indicating that compensation of pitch-vVOR function following unilat eral vestibular deafferention remains incomplete.

A new model of otolithic stimulation by linear acceleration is presented and compared to previous models, based upon anatomical evidence and on the ability of normal subjects to sense the direction of a linear acceleration vector acting in the coronal plane (roll-tilt perception). There are two basic methods of generating roll-tilt stimuli: 1) tilt-chairs either inside or outside a centrifuge and 2) fixed-chair centrifuges. The present model is based on consideration of the probable otoconial displacement produced by these two different methods of stimulation and the model incorporates a major role for the elastic restoring force of the otolith membrane. When this force is taken into account, and most previous models have ignored it, the model predicts that different patterns of otoconial displacement will be produced in tilt-chair and in fixed-chair centrifuge experiments. The different roll-tilt perception produced by these two methods may be caused by the different otoconial displacement patterns. It is suggested that the elastic restoring force of the otoconial membrane may contribute to space motion sickness.

1. The kinematics of the human angular vestibuloocular reflex (VOR) in three dimensions was investigated in 12 normal subjects during high-acceleration head rotations (head "impulses"). A head impulse is a passive, unpredictable, high-acceleration (3,000-4,000 degrees/s2) head rotation of approximately 10-20 degrees in roll, pitch, or yaw, delivered with the subject in the upright position and focusing on a fixation target. Head and eye rotations were measured with dual search coils and expressed as rotation vectors. The first of these two papers describes a vector analysis of the three-dimensional input-output kinematics of the VOR as two indexes in the time domain: magnitude and direction. 2. Magnitude is expressed as speed gain (G) and direction as misalignment angle (delta). G is defined as the ratio of eye velocity magnitude (eye speed) to head velocity magnitude (head speed). delta is defined as the instantaneous angle by which the eye rotation axis deviates from perfect alignment with the head rotation axis in three dimensions. When the eye rotation axis aligns perfectly with the head rotation axis and when eye velocity is in a direction opposite to head velocity, delta = 0. The orientation of misalignment between the head and the eye rotation axes is characterized by two spatial misalignment angles, which are the projections of delta onto two orthogonal coordinate planes that intersect at the head rotation axis. 3. Time series of G were calculated for head impulses in roll, pitch, and yaw. At 80 ms after the onset of an impulse (i.e., near peak head velocity), values of G were 0.72 +/- 0.07 (counterclockwise) and 0.75 +/- 0.07 (clockwise) for roll impulses, 0.97 +/- 0.05 (up) and 1.10 +/- 0.09 (down) for pitch impulses, and 0.95 +/- 0.06 (right) and 1.01 +/- 0.07 (left) for yaw impulses (mean +/- 95% confidence intervals). 4. The eye rotation axis was well aligned with head rotation axis during roll, pitch, and yaw impulses: delta remained almost constant at approximately 5-10 degrees, so that the spatial misalignment angles were < or = 5 degrees. delta was 9.6 +/- 3.1 (counterclockwise) and 9.0 +/- 2.6 (clockwise) for roll impulses, 5.7 +/- 1.6 (up) and 6.1 +/- 1.9 (down) for pitch impulses, and 6.2 +/- 2.2 (right) and 7.9 +/- 1.5 (left) for yaw impulses (mean +/- 95% confidence intervals). 5. VOR gain (gamma) is the product of G and cos(delta). Because delta is small in normal subjects, gamma is not significantly different from G. At 80 ms after the onset of an impulse, gamma was 0.70 +/- 0.08 (counterclockwise) and 0.74 +/- 0.07 (clockwise) for roll impulses, 0.97 +/- 0.05 (up) and 1.09 +/- 0.09 (down) for pitch impulses, and 0.94 +/- 0.06 (right) and 1.00 +/- 0.07 (left) for yaw impulses (mean +/- 95% confidence intervals). 6. VOR latencies, estimated with a latency shift method, were 10.3 +/- 1.9 (SD) ms for roll impulses, 7.6 +/- 2.8 (SD) ms for pitch impulses, and 7.5 +/- 2.9 (SD) ms for yaw impulses. 7. We conclude that the normal VOR produces eye rotations that are almost perfectly compensatory in direction as well as in speed, but only during yaw and pitch impulses. During roll impulses, eye rotations are well aligned in direction, but are approximately 30% slower in speed.

1. We studied the three-dimensional input-output human vestibuloocular reflex (VOR) kinematics after selective loss of semicircular canal (SCC) function either through total unilateral vestibular deafferentation (uVD) or through single posterior SCC occlusion (uPCO), and showed large deficits in magnitude and direction in response to high-acceleration head rotations (head "impulses"). 2. A head impulse is a passive, unpredictable, high-acceleration (3,000-4,000 degrees/s2) head rotation through an amplitude of 10-20 degrees in roll, pitch, or yaw. The subjects were tested while seated in the upright position and focusing on a fixation target. Head and eye rotations were measured with the use of dual search coils, and were expressed as rotation vectors. A three-dimensional vector analysis was performed on the input-output VOR kinematics after uVD, to produce two indexes in the time domain: magnitude and direction. Magnitude is expressed as speed gain (G) and direction as misalignment angle (delta). 3. G. after uVD, was significantly lower than normal in both directions of head rotation during roll, pitch, and yaw impulses, and were much lower during ipsilesional than during contralesional roll and yaw impulses. At 80 ms from the onset of an impulse (i.e., near peak head velocity), G was 0.23 +/- 0.08 (SE) (ipsilesional) and 0.56 +/- 0.08 (contralesional) for roll impulses, 0.61 +/- 0.09 (up) and 0.72 +/- 0.10 (down) for pitch impulses, and 0.36 +/- 0.06 (ipsilesional) and 0.76 +/- 0.09 (contralesional) for yaw impulses (mean +/- 95% confidence intervals). 4. delta, after uVD, was significantly different from normal during ipsilesional roll and yaw impulses and during pitch-up and pitch-down impulses. delta was normal during contralesional roll and yaw impulses. At 80 ms from the onset of the impulse, delta was 30.6 +/- 4.5 (ipsilesional) and 13.4 +/- 5.0 (contralesional) for roll impulses, 23.7 +/- 3.7 (up) and 31.6 +/- 4.4 (down) for pitch impulses, and 68.7 +/- 13.2 (ipsilesional) and 11.0 +/- 3.3 (contralesional) for yaw impulses (mean +/- 95% confidence intervals). 5. VOR gain (gamma), after uVD, were significantly lower than normal for both directions of roll, pitch, and yaw impulses and much lower during ipsilesional than during contralesional roll and yaw impulses. At 80 ms from the onset of the head impulse, the gamma was 0.22 +/- 0.08 (ipsilesional) and 0.54 +/- 0.09 (contralesional) for roll impulses, 0.55 +/- 0.09 (up) and 0.61 +/- 0.09 (down) for pitch impulses, and 0.14 +/- 0.10 (ipsilesional) and 0.74 +/- 0.06 (contralesional) for yaw impulses (mean +/- 95% confidence intervals). Because gamma is equal to [G*cos (delta)], it is significantly different from its corresponding G during ipsilesional roll and yaw, and during all pitch impulses, but not during contralesional roll and yaw impulses. 6. After uPCO, pitch-vertical gamma during pitch-up impulses was reduced to the same extent as after uVD; roll-torsional gamma during ipsilesional roll impulses was significantly lower than normal but significantly higher than after uVD. At 80 ms from the onset of the head impulse, gamma was 0.32 +/- 0.13 (ipsilesional) and 0.55 +/- 0.16 (contralesional) for roll impulses, 0.51 +/- 0.12 (up) and 0.91 +/- 0.14 (down) for pitch impulses, and 0.76 +/- 0.06 (ipsilesional) and 0.73 +/- 0.09 (contralesional) for yaw impulses (mean +/- 95% confidence intervals). 7. The eye rotation axis, after uVD, deviates in the yaw plane, away from the normal interaural axis, toward the nasooccipital axis, during all pitch impulses. After uPCO, the eye rotation axis deviates in same direction as after uVD during pitch-up impulses, but is well aligned with the head rotation axis during pitch-down impulses.

Patients were tested 1 day before and 1 week after therapeutic unilateral vestibular neurectomy (UVN) on vestibular tests which are likely determined primarily by otolithic function. UVN causes a maintained ocular torsion: fundus photographs showed that both eyes of every patient were rolled such that the upper pole of both eyes was tonically deviated towards the operated side, and there is a corresponding change in the perceived gravitational horizontal: patients set a small bar of LEDs bar down on the same side as their operation. One week after UVN, patients showed an asymmetrical sensitivity to linear acceleration vectors directed along their interaural axis in comparison to their preoperative settings for the same stimuli.

Taps to the forehead on the midline, at the hairline (Fz), with a reflex hammer or powerful bone conduction vibrator caused short-latency surface potentials from beneath both eyes in all healthy subjects. The earliest negative responses were invariably absent from the eye contralateral to the side of a previous vestibular nerve section but were preserved despite sensorineural hearing loss. These responses probably reflect vestibular function via crossed otolith–ocular pathways.

We describe two immunocompetent patients with tuberculous cranial pachymeningitis. Both patients underwent biopsy after focal dural thickening was identified on MRI. Histopathologic examination of tissue revealed necrotizing granulomatous inflammation. PCR for Mycobacterium tuberculosisDNA was negative on CSF but positive on tissue. Both patients responded to antituberculous therapy. Although uncommon as a cause of cranial pachymeningitis, tuberculosis should be considered, since it responds well to treatment.

Using dual torsion scleral search coils we have recorded 3-dimensional eye position during yaw angular accelerations of 20°/s2 about an earth vertical axis in healthy subjects and in patients with unilateral vestibular deafferentation (UVD). These experiments produced two interesting results: i) even in healthy subjects, the axis of eye velocity did not coincide with the (earth vertical) stimulus axis during centred rotation; ii) Patients with UVD had torsional eye velocity components that were systematically different from those in normal subjects. While in normals the direction of the torsional component of the eye velocity depended on the direction of rotation and was on average approximately symmetric for CW and CCW yaw rotation, there was a clear asymmetry in patients, which was distinctly different for left and right UVD.

The responses to rapid, passive. unpredictable, low amplitude (10-20°), high acceleration (3,000-4,000°/s2) head rotations were used to study the human vestibulo-ocular reflex (VOR) in pitch and yaw plane after unilateral posterior semicircular canal occlusion (uPCO) in 10 subjects. The results from these 10 uPCO subjects were compared with those from 18 normal subjects. The VOR gains at a head velocity of 200°/s in the uPCO subjects were: pitch upward = 0.62 ± 0.06, pitch downward = 0.87 ± 0.11, yaw ipsilesion = 0.78 ± 0.06, yaw contralesion = 0.79 ± 0.10 and in normal subjects were: pitch upward = 0.92 ± 0.06, pitch downward = 0.96 ± 0.04. yaw right = 0.88 ± 0.05, yaw left = 0.91 ± 0.12 (group means ± two-tailed 95% confidence intervals). The results showed that the pitch-vVOR gain was significantly (p <0.05) decreased in response to upward head impulses whereas in response to downward, ipsilesion and contralesion head impulses were not significantly different (p > 0.05) from the normals. This study shows that there is 30% permanent residual deficit of the upward pitch-vVOR with an up-down asymmetry in pitch-vVOR gain following inactivation of a single posterior semicircular canal and that compensation of pitch-vVOR function is incomplete.

We studied vestibular evoked myogenic potentials in 6 patients after unilateral vestibular neurectomy and in 22 patients after unilateral vestibular neuritis and unilateral absent caloric responses. We found that the ipsilesional vestibular evoked potentials were abolished in every patient after unilateral vestibular neurectomy. In vestibular neuritis patients we found that the ipsilesional vestibular evoked potentials were absent in some but not in all cases. These findings confirm that the p13-n23 potential is of vestibular origin and also show that it is not of lateral canal origin.

A case of the rigid form of Huntington's chorea is described. Treatment with levodopa provided negligible benefit, and led to severe psychiatric deterioration.

Anti-GQ1b antibodies are typically found in patients with the Miller Fisher syndrome, all of whom will have, by definition, acute ophthalmoplegia. The authors describe three patients with chronic ophthalmoplegia in the presence of persistently high titers of immunoglobulin G anti-GQ1b antibody detected in an ELISA, one of whom improved with immunotherapy. Anti-GQ1b antibodies may be associated with some cases of chronic ophthalmoplegia of unknown cause.

We investigated the use of skull taps with a modified clinical reflex hammer as a method of vestibular activation.Using recently described EMG techniques to measure vestibulocollic reflexes in response to clicks, we were able to show analogous short-latency potentials to taps. The earliest responses were invariably absent on the side of a previous vestibular nerve section but were preserved in profound sensorineural or conductive hearing loss. We propose that the taps activated the vestibular apparatus directly by a bone-conducted vibration wave.