Optic chiasm involvement on MRI with ethambutol-induced bitemporal hemianopia.

While ethambutol optic neuropathy usually causes central or cecocentral scotomas, bitemporal visual field defects also have been reported. The pathogenesis of the bitemporal hemianopia has not been established. This article describes magnetic resonance imaging abnormalities involving the optic chiasm in a patient with bitemporal visual field loss. To our knowledge, these neuroimaging findings have not been previously described in association with ethambutol therapy.

Effects of Nesting Material and Housing Parameters on Feed Wastage Behavior in Female Swiss Webster Mice.

Feed wastage in laboratory mice, also known as chewing or grinding behavior, is problematic for program management and animal welfare. The destruction of pelleted feed without consumption produces a powder accumulation on the cage floor called orts. Ort accumulation disrupts the cage microenvironment and can clog Lixits resulting in flooding. Moreover, added labor adds cost, and cage disruption increases animal stress. Published studies examining the behavior and ways to mitigate it have had inconsistent results, and the cause or causes have not yet been fully identified. The purpose of this study was to identify methods to reduce the development of chewing behavior in laboratory mice. Female Swiss Webster (Tac:SW) mice (n = 144) were randomly assigned to one of 8 groups (12 cages per group) with 2 housing densities (single and pair) and 4 nesting material paradigms. Mice were housed on clean bedding for 8 wk and then soiled bedding for the next 8 wk. Chewing behavior was evaluated by feed weight, cage weight, and feed scores. The addition of a Diamond Twist significantly increased ort production, while nest transfer decreased it but not significantly. Pair housing increased overall orts but not when adjusted for animal number. These results identified potential contributing factors to chewing behavior. However, further research is needed to elucidate the exact causes and solutions.

Ocular torsion and vertical misalignment.

PURPOSE: This article considers vertical misalignment and torsion of the eyes that arise from disorders of vestibulo-ocular reflex (VOR) pathways. RECENT FINDINGS: Infarction of the nodulus is one of the causes of skew deviation, a vertical strabismus accompanied by torsion of the eyes and tilt of the subjective visual vertical. Vertical components of childhood strabismus may arise from dysgenesis of vestibular projections in the brainstem. If vertical misalignment decreases greatly in the supine position compared to the erect poison one may conclude that skew deviation rather than a fourth nerve palsy is responsible for the strabismus. Impairment of the horizontal translational VOR in patients with skew has provided further evidence that imbalance in the otolith-ocular pathway, caused by disruption of projections from the utricle to motor neurons, is the mechanism of skew deviation. Bedside examination showing a normal horizontal head impulse test, direction-changing nystagmus in eccentric gaze, or skew deviation is sensitive and specific for stroke. Skew deviation can identify stroke when an abnormal head impulse test falsely suggests a peripheral vestiblular lesion. Reduction in gain and failure of adaptation to vision of the torsional angular VOR in head positions away from the erect signify fundamental differences in the central organization of convergence of semicircular canal and otolith signals, when compared to the horizontal and vertical angular VORs. SUMMARY: The effects of head position and of lesions of the nodulus are assuming increasing importance in analysis and differential diagnosis of vertical misalignment and torsion of the eyes.

Posterior reversible encephalopathy syndrome presenting as Balint syndrome.

Balint syndrome is a disorder of inaccurate visually guided saccades, optic ataxia, and simultanagnosia that typically results from bilateral parieto-occipital lesions. Visual perception disturbances in the posterior reversible encephalopathy syndrome (PRES) include hemianopia, visual neglect, and cerebral blindness, but Balint syndrome had not been recognized. We report Balint syndrome associated with PRES in a 37-year-old woman with acute hypertension and systemic lupus erythematosus. Balint syndrome can be an initial presentation of PRES.

The cerebellar dysplasia of Chiari II malformation as revealed by eye movements.

INTRODUCTION: Chiari type II malformation (CII) is a developmental deformity of the hindbrain. We have previously reported that many patients with CII have impaired smooth pursuit, while few make inaccurate saccades or have an abnormal vestibuloocular reflex. In contrast, saccadic adaptation and visual fixation are normal. In this report, we correlate results from several eye movement studies with neuroimaging in CII. We present a model for structural changes within the cerebellum in CII. METHODS: Saccades, smooth pursuit, the vestibulo-ocular reflex, and visual fixation were recorded in 21 patients with CII, aged 8-19 years and 39 age-matched controls, using an infrared eye tracker. Qualitative and quantitative MRI data were correlated with eye movements in 19 CII patients and 28 controls. RESULTS: Nine patients with CII had abnormal eye movements. Smooth pursuit gain was subnormal in eight, saccadic accuracy abnormal in four, and vestibulo-ocular reflex gain abnormal in three. None had fixation instability. Patients with CII had a significantly smaller cerebellar volume than controls, and those with normal eye motion had an expanded midsagittal vermis compared to controls. However, patients with abnormal eye movements had a smaller (non-expanded) midsagittal vermis area, posterior fossa area and medial cerebellar volumes than CII patients with normal eye movements. CONCLUSIONS: The deformity of CII affects the structure and function of the cerebellum selectively and differently in those with abnormal eye movements. We propose that the vermis can expand when compressed within a small posterior fossa in some CII patients, thus sparing its ocular motor functions.

Adaptive neural mechanism for Listing's law revealed in patients with skew deviation caused by brainstem or cerebellar lesion.

PURPOSE: Skew deviation is a vertical strabismus caused by damage to the otolithic-ocular reflex pathway and is associated with abnormal ocular torsion. This study was conducted to determine whether patients with skew deviation show the normal pattern of three-dimensional eye control called Listing's law, which specifies the eye's torsional angle as a function of its horizontal and vertical position. METHODS: Ten patients with skew deviation caused by brain stem or cerebellar lesions and nine normal control subjects were studied. Patients with diplopia and neurologic symptoms less than 1 month in duration were designated as acute (n = 4) and those with longer duration were classified as chronic (n = 10). Serial recordings were made in the four patients with acute skew deviation. With the head immobile, subjects made saccades to a target that moved between straight ahead and eight eccentric positions, while wearing search coils. At each target position, fixation was maintained for 3 seconds before the next saccade. From the eye position data, the plane of best fit, referred to as Listing's plane, was fitted. Violations of Listing's law were quantified by computing the "thickness" of this plane, defined as the SD of the distances to the plane from the data points. RESULTS: Both the hypertropic and hypotropic eyes in patients with acute skew deviation violated Listing's and Donders' laws-that is, the eyes did not show one consistent angle of torsion in any given gaze direction, but rather an abnormally wide range of torsional angles. In contrast, each eye in patients with chronic skew deviation obeyed the laws. However, in chronic skew deviation, Listing's planes in both eyes had abnormal orientations. CONCLUSIONS: Patients with acute skew deviation violated Listing's law, whereas those with chronic skew deviation obeyed it, indicating that despite brain lesions, neural adaptation can restore Listing's law so that the neural linkage between horizontal, vertical, and torsional eye position remains intact. Violation of Listing's and Donders' laws during fixation arises primarily from torsional drifts, indicating that patients with acute skew deviation have unstable torsional gaze holding that is independent of their horizontal-vertical eye positions.

Neurophysiology and neuroanatomy of smooth pursuit: lesion studies.

Smooth pursuit impairment is recognized clinically by the presence of saccadic tracking of a small object and quantified by reduction in pursuit gain, the ratio of smooth eye movement velocity to the velocity of a foveal target. Correlation of the site of brain lesions, identified by imaging or neuropathological examination, with defective smooth pursuit determines brain structures that are necessary for smooth pursuit. Paretic, low gain, pursuit occurs toward the side of lesions at the junction of the parietal, occipital and temporal lobes (area V5), the frontal eye field and their subcortical projections, including the posterior limb of the internal capsule, the midbrain and the basal pontine nuclei. Paresis of ipsiversive pursuit also results from damage to the ventral paraflocculus and caudal vermis of the cerebellum. Paresis of contraversive pursuit is a feature of damage to the lateral medulla. Retinotopic pursuit paresis consists of low gain pursuit in the visual hemifield contralateral to damage to the optic radiation, striate cortex or area V5. Craniotopic paresis of smooth pursuit consists of impaired smooth eye movement generation contralateral to the orbital midposition after acute unilateral frontal or parietal lobe damage. Omnidirectional saccadic pursuit is a most sensitive sign of bilateral or diffuse cerebral, cerebellar or brainstem disease. The anatomical and physiological bases of defective smooth pursuit are discussed here in the context of the effects of lesion in the human brain.

The vestibulo-ocular reflex during active head motion in Chiari II malformation.

BACKGROUND: Chiari type II malformation (CII) is a developmental anomaly of the cerebellum and brainstem, which are important structures for processing the vestibulo-ocular reflex (VOR). We investigated the effects of the deformity of CII on the angular VOR during active head motion. METHODS: Eye and head movements were recorded using an infrared eye tracker and magnetic head tracker in 20 participants with CII [11 males, age range 8-19 years, mean (SD) 14.4 (3.2) years]. Thirty-eight age-matched healthy children and adolescents (21 males) constituted the control group. Participants were instructed to 'look' in darkness at the position of their thumb, placed 25 cm away, while they made horizontal and vertical sinusoidal head rotations at frequencies of about 0.5 Hz and 2 Hz. Parametric and non-parametric tests were used to compare the two groups. RESULTS: The VOR gains, the ratio of eye to head velocities, were abnormally low in two participants with CII and abnormally high in one participant with CII. CONCLUSION: The majority of participants with CII had normal VOR performance in this investigation. However, the deformity of CII can impair the active angular VOR in some patients with CII. Low gain is attributed to brainstem damage and high gain to cerebellar dysfunction.

Square wave jerks in children and adolescents.

Square wave jerks are involuntary, horizontal, saccadic intrusions that interrupt fixation. Each square wave jerk consists of an initial saccade that moves the fovea away from the intended position of fixation, followed by a second saccade in the opposite direction, which refoveates the fixation position. Square wave jerks reportedly occur in 24-60% of healthy adults. No previous study of square wave jerks in children and adolescents is available. We recorded eye movements using an infrared eye tracker in 38 participants aged 8-19 years while they fixated on a visual target for 1 minute. The frequency of square wave jerks, and the durations, amplitudes, and peak velocities of their saccades, were calculated and correlated with age. Ninety percent of participants had square wave jerks. Their median frequency was 3 per minute (range, 1-18), median duration was 249 milliseconds, the median amplitude of their saccades was 0.81 degrees, and the median peak velocity was 60 degrees/second. No parameter of square wave jerks correlated with age. The prevalence of square wave jerks is high in children and adolescents. This finding may be a feature of the less mature brain, and may reflect an inability to suppress unwanted supranuclear triggers for saccades.

Dissociated palsy of vertical saccades: loss of voluntary and visually guided saccades with preservation of reflexive vestibular quick phases.

A patient with a diencephalic infarct displayed a persistent palsy of voluntary and visually guided vertical saccades with preserved vertical quick phases of vestibular nystagmus on magnetic search coil oculography. Vertical smooth pursuit had very low velocity in both directions without catch-up saccades. Vertical and torsional vestibulo-ocular reflex gains were normal. Preservation of vertical and torsional quick phases signifies integrity of the rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF). This case is the first to provide evidence that disruption of descending cerebral corticofugal pathways to the riMLF with preserved ascending projections from the paramedian pontine reticular formation to the riMLF can cause a dissociated palsy of vertical fast eye movements.

Saccades in children.

Saccades are necessary for optimal vision. Little is known about saccades in children. We recorded saccades using an infrared eye tracker in 39 children, aged 8-19 years. Participants made saccades to visual targets that stepped 10 degrees or 15 degrees horizontally and 5 degrees or 10 degrees vertically at unpredictable time intervals. Saccadic latency decreased significantly with increasing age, while saccadic gain and peak velocity did not vary with age. Saccadic gains and peak velocities in children are similar to reported adult values. This implies maturity of the neural circuits responsible for making saccades accurate and fast. Saccade latency decreases as the brain matures.

Saccadic adaptation in children.

Saccades are fast-orienting eye movements. Saccadic adaptation, a form of motor learning, is a corrective change in the amplitude of saccades in response to error. The aim of the study was to ascertain whether saccadic adaptation occurs in typically developing children. We recorded saccades with an infrared eye tracker in 39 children, aged 8 to 19 years, at baseline to 12-degree horizontal target steps and after an adaptive task. During the adaptive task, a saccadic hypometric error was induced. This task consisted of 200 12-degree target steps that stepped backward 3 degrees during the initial saccade and without the participants' awareness. The initial saccade triggered the back-step. This paradigm required a corrective reduction of the amplitude of the initial saccades in response to the induced error. Saccadic adaptation was achieved in 26 participants, whose mean saccadic amplitudes decreased by 13% (P < .05). Saccadic adaptation was not influenced by age. We conclude that children as young as 8 years old have established functions of the neural circuits responsible for the motor learning required for saccadic adaptation.

Saccadic adaptation in Chiari type II malformation.

BACKGROUND: Saccadic adaptation corrects errors in saccadic amplitude. Experimentally-induced saccadic adaptation provides a method for studying motor learning. The cerebellum is a major participant in saccadic adaptation. Chiari type II malformation (CII) is a developmental deformity of the cerebellum and brainstem that is associated with spina bifida. We investigated the effects of CII on saccadic adaptation. METHOD: We measured eye movements using an infrared eye tracker in 21 subjects with CII (CII group) and 39 typically developing children (control group), aged 8-19 years. Saccadic adaptation was induced experimentally using targets that stepped horizontally 120 to the right and then stepped backward 3 degrees during saccades. RESULTS: Saccadic adaptation was achieved at the end of the adaptation phase in participants in each group. Saccadic amplitude gain decreased by 6.9% in the CII group and 9.3% in the control group. The groups did not differ significantly (p = 0.27). Amplitude gain reduction was significantly less in the CII participants who had multiple shunt revisions. Regression analyses revealed no effects of spinal lesion level, presence of nystagmus, or cerebellar vermis dysmorphology on saccadic adaptation. CONCLUSION: The neural circuits involved in saccadic adaptation appear to be functionally intact in CII.

Recovery of peripheral versus central nerves identified by saccadic velocity after abducens neuropathy.

The abducens is the motor nerve with the most substantial course, both within and outside the brain and it innervates only one muscle. Sixth nerve palsy affords an opportunity to compare recovery after central versus peripheral nerve damage by assessing the dynamics of abduction. Horizontal saccade peak velocities and durations in 14 patients with unilateral peripheral sixth nerve palsies (5 acute, 9 chronic) are compared with those in 5 patients with central sixth nerve palsies (2 acute, 3 chronic) and with those in 10 normal subjects. Acutely, abducting saccades in the paretic eye were slow in both central and peripheral palsies, as anticipated from weakness of the lateral rectus muscle. In chronic central palsies, abducting saccadic velocities remained reduced, but in chronic peripheral palsies, they increased to normal within the limited range of excursion. The chronically damaged peripheral nerve behaves like a high-pass filter in transmitting phasic velocity commands, whereas tonic position commands remain defective, accounting for limited abduction but normal velocities within the range of duction. In chronic central (fascicular) palsies, saccade velocities remain reduced. Impaired conduction from damage to central myelin or axons is more persistent in central palsies, consistent with limited regeneration within the brain. Recording of saccade velocities may aid the distinction of fascicular from peripheral palsies. Saccade speed is repaired in peripheral palsies, probably by remyelination, and perhaps also by central monocular adaptation of innervation selectively to the paretic eye in order to drive both eyes rapidly and simultaneously to a target in the paretic field of motion.

Adaptations and deficits in the vestibulo-ocular reflex after sixth nerve palsy.

PURPOSE: The effects of paralytic strabismus on the vestibulo-ocular reflex (VOR) have not been systematically investigated in humans. The purpose of this study was to analyze the VOR in patients with unilateral peripheral sixth nerve palsy. METHODS: Twenty-one patients with unilateral peripheral sixth nerve palsy (6 severe, 7 moderate, 8 mild) and 15 normal subjects were studied. Subjects made sinusoidal +/-10 degrees head-on-body rotations in yaw and pitch at approximately 0.5 and 2 Hz, and in roll at approximately 0.5, 1, and 2 Hz. Eye movement recordings were obtained using magnetic scleral search coils in each eye in darkness and during monocular viewing in light. Static torsional VOR gains, defined as change in torsional eye position divided by change in head position during sustained head roll, were also measured. RESULTS: In all patients, horizontal VOR gains in darkness were decreased in the paretic eye in both abduction and adduction, but remained normal in the nonparetic eye in both directions. In light, horizontal visually enhanced VOR (VVOR) gains were normal in both eyes in moderate and mild palsy. In severe palsy, horizontal VVOR gains remained low in the paretic eye during viewing with either eye, whereas those in the nonparetic eye were higher than normal when the paretic eye viewed. Vertical VOR and VVOR were normal, but dynamic and static torsional VOR and VVOR gains were reduced in both eyes in all patients. CONCLUSIONS: In darkness, horizontal VOR gains were reduced during abduction of the paretic eye in all patients, as anticipated in sixth nerve palsy. Gains were also reduced during adduction of the paretic eye, suggesting that innervation to the medial rectus has changed. After severe palsy, vision did not increase abducting or adducting horizontal VVOR gains to normal in the paretic eye, but caused secondary increase in VVOR gains to values above unity in the nonparetic eye, when the paretic eye fixated. In mild and moderate palsy, vision enhanced the VOR in the paretic eye but caused no change in the nonparetic eye, suggesting a monocular readjustment of innervation selectively to the paretic eye. Vertical VOR and VVOR gains were normal, indicating that the lateral rectus did not have significant vertical actions through the excursions that we tested (+/-10 degrees ). Reduced torsional VOR gains in the paretic eye can be explained by the esotropia in sixth nerve palsy. Torsional VOR gain normally varies with vergence. We attribute the reduced torsional gains in the paretic eye to the mechanism that normally lowers it during convergence. The low torsional gains in the nonparetic eye may be an adaptation to reduce torsional disparity between the two eyes.

Adaptive neural mechanism for Listing's law revealed in patients with sixth nerve palsy.

PURPOSE: During fixation and saccades, human eye movements obey Listing's law, which specifies the torsional eye position for each combination of horizontal and vertical eye positions. To study the mechanisms that implement Listing's law, the authors measured whether the law was violated in peripheral and central unilateral sixth nerve palsy. METHODS: Twenty patients with peripheral (13 chronic, 7 acute) sixth nerve palsy, 7 patients with central sixth nerve palsy caused by brainstem lesions, and 10 normal subjects were studied with scleral search coils. With the head immobile, subjects made saccades to a target that moved between straight ahead and eight eccentric positions. At each target position, fixation was maintained for 3 seconds before the next saccade. To quantify violations of Listing's law, we measured ocular torsion during fixation and during saccades, and compared it with the torsion predicted by the law. The SD of the differences between the predicted and measured torsion was called Listing deviation. RESULTS: Patients with central sixth nerve palsy had abnormal ocular torsion in both the paretic and nonparetic eyes, which violated Listing's law. During fixation, Listing deviation averaged 2.4 degrees in the paretic eye and 1.7 degrees in the nonparetic eye, compared with 0.8 degrees in normal control subjects (P < 0.05). During saccades, the Listing deviation averaged 2.7 degrees in the paretic eye, and 1.6 degrees in the nonparetic eye, compared with 0.8 degrees in normal control eyes (P < 0.05). Donders' law was also violated in both eyes of patients with central sixth nerve palsy. They showed an abnormally wide range of ocular torsion in any given gaze direction. In contrast, patients with acute peripheral palsy had abnormal ocular torsion only in the paretic eye. Listing deviation of the paretic eye averaged 2.3 degrees during fixation and 3.2 degrees during saccades (P < 0.05). Donders' law was obeyed in acute peripheral palsy. Patients with chronic peripheral sixth nerve palsy obeyed Listing's and Donders' laws during both fixation and saccades. CONCLUSIONS: Patients with central unilateral sixth nerve palsy have abnormal ocular torsion in both eyes, demonstrating that brainstem circuits normally participate in the maintenance of Listing's law. Eye movements in patients with acute peripheral sixth nerve palsy violate Listing's law, whereas those in patients with chronic peripheral palsy obey it, indicating that neural adaptation can restore Listing's law, even when the eye muscle remains abnormal.

Adaptive neural mechanism for listing's law revealed in patients with fourth nerve palsy.

PURPOSE: During fixation and saccades, human eye movements obey Listing's law, which specifies the eye's torsional angle as a function of its horizontal and vertical position. Torsion of the eye is in part controlled by the fourth nerve. This study investigates whether the brain adapts to defective torsional control after fourth nerve palsy. METHODS: Thirteen patients with fourth nerve palsy (11 chronic, 2 acute), and 10 normal subjects were studied with scleral search coils. With the head immobile, subjects made saccades to a target that moved between straight ahead and eight eccentric positions. At each target position, fixation was maintained for 3 seconds before the next saccade. From the eye position data, we computed the plane of best fit, referred to as Listing's plane. Violations of Listing's law were quantified by computing the "thickness" of this plane, defined as the SD of the distances to the plane from the data points. RESULTS: Both the paretic and nonparetic eyes in patients with chronic fourth nerve palsy obeyed Listing's law during fixation and saccades. However, Listing's planes in both eyes had abnormal orientations, being rotated temporally, meaning the eye excyclotorted during downgaze and incyclotorted during upgaze. In contrast, the paretic eye of patients with acute fourth nerve palsy violated Listing's law during saccades. During downward saccades, transient torsional deviations moved the paretic eye out of Listing's plane. Torsional drifts returned the paretic eye to Listing's plane during subsequent fixation. CONCLUSIONS: During saccades, acute fourth nerve palsy violates Listing's law, whereas chronic palsy obeys it, indicating that neural adaptation can restore Listing's law by adjusting the innervations to the remaining extraocular muscles, even when one eye muscle remains paretic. The transient torsional deviations during downward saccades in acute palsy are attributed to pulse-step mismatch, as a result of lesions in the trochlear nerve that lead to an imbalance of phasic and tonic signals reaching the muscles.

Adaptations and deficits in the vestibulo-ocular reflex after third nerve palsy.

OBJECTIVE: To analyze the vestibulo-ocular reflex (VOR) in patients with unilateral peripheral third nerve palsy. PARTICIPANTS AND METHODS: Ten patients and 15 healthy subjects were studied using magnetic search coils. Subjects made sinusoidal +/-10 degrees head-on-body rotations in yaw, pitch, and roll in darkness and during monocular viewing in light. RESULTS: Horizontal VOR and visually enhanced VOR (VVOR) gains of the paretic eye were decreased during both abduction and adduction. Vertical VOR and VVOR gains of the paretic eye were decreased during both elevation and depression. Dynamic and static torsional VOR and VVOR gains of the paretic eye were reduced during both excyclotorsion and incyclotorsion. Horizontal, vertical, and torsional VOR and VVOR gains were normal in the nonparetic eye. CONCLUSIONS: Adducting VOR gains were reduced as anticipated from medial rectus palsy. Abducting gains were also reduced; the reduction is attributed to an adaptive decrease in innervation to the lateral rectus to achieve symmetry of the horizontal VOR in the paretic eye. Torsional VOR gains were reduced during excyclotorsion from palsy of the inferior oblique muscle. Gains were also reduced during incyclotorsion, which can be explained by an adaptive decrease in innervation to the superior oblique to restore symmetry of the torsional VOR in the paretic eye. CLINICAL RELEVANCE: Monocular adaptation in the VOR of the paretic eye reduces asymmetrical movement of retinal images during head motion, prevents nystagmus, and reduces retinal image disparity.

Midbrain disorders of vertical gaze: a quantitative re-evaluation.

The mesodiencephalic junction is the site of the prenuclear control of vertical eye motion. We measured vertical saccades, smooth pursuit (SP), the vertical vestibulo-ocular reflex (VOR), and its interactions with vision during active head motion in 21 patients with midbrain lesions causing palsy of vertical saccades, upward, downward, or in both directions. Most patients with limited slow or slowed saccades in one direction on clinical examination had slowed saccades in the opposed direction. SP gain was decreased in both directions in most patients, and decreased upward or downward in few. VOR gain was subnormal in both directions in many patients, and upward only in one; phase lead of the VOR was recorded in 33% of them. Subnormal SP and VOR gains were often dissociated. Visually enhanced VOR gains were subnormal in both directions in many patients. Cancellation of the VOR was impaired in many patients, both upward and downward in most and upward in few patients. Gaze (eye plus head) tracking gain was subnormal in 29% of patients. Defective SP and defective cancellation of the VOR during head free tracking were often dissociated. We conclude that VOR and SP gains are usually subnormal in patients with paresis of vertical saccades. Impairment of pursuit and the VOR are often dissociated. Phase lead of the VOR implicates damage to velocity-to-position neural integrator for vertical eye motion. These associations and dissociations of impaired vertical eye motion signify discrete structural and functional effects of supranuclear midbrain damage that are undetected by examination of saccades.

Adaptations and deficits in the vestibulo-ocular reflex after peripheral ocular motor palsies.

Palsy of a nerve might be expected to lower vestibulo-ocular reflex (VOR) responses in its fields of motion, but effects of peripheral neuromuscular disease were unknown. We recorded the VOR during sinusoidal head rotations in yaw, pitch, and roll at 0.5-2 Hz and static torsional gain in 43 patients with unilateral nerve palsies. Sixth nerve palsy (n = 21) reduced both abduction and adduction VOR gains in darkness. In light, horizontal visually enhanced VOR (VVOR) gains were normal in moderate and mild palsy. In severe palsy, horizontal VVOR gains remained low in the paretic eye when it was fixating, whereas gains in the nonparetic eye became higher than normal. Third nerve palsy (n = 10) decreased VOR and VVOR gains during abduction, adduction, elevation, depression, extorsion, and intorsion. Fourth nerve palsy (n = 13) reduced VOR gains of the paretic eye during intorsion, extorsion, elevation, depression, abduction, and adduction, but in light vertical and horizontal VVOR gains were normal. In the nonparetic eye, all gains were normal. Reduced VOR gains in the direction of paretic muscles and also in the direction of their antagonists, together with normal gains in the nonparetic eye, indicate a selective adjustment to the antagonists of paretic muscles. Increase of VVOR gains to normal in the paretic eye, when used for fixation, without conjugate increase in gains in the occluded nonparetic eye, provides further evidence of selective adaptation for the paretic eye. Motions of the eyes after nerve palsies indicate monocular VOR adaptation in three dimensions.