Abstract We conducted a double‐blind crossover trial comparing gabapentin (up to 900 mg/day) to baclofen (up to 30 mg/day) as therapy for acquired nystagmus in 21 patients. We measured visual acuity and the nystagmus before, and at the end of, 2 weeks on each medication. For a group of 15 patients with acquired pendular nystagmus (APN), visual acuity improved significantly with gabapentin, but not with baclofen. Gabapentin significantly reduced APN median eye speed in all three planes, but baclofen did so only in the vertical plane. In 10 patients with APN, the reduction of nystagmus with gabapentin was substantial and 8 of these elected to continue taking the drug. In 6 patients with downbeat or torsional downbeat nystagmus, changes in median slow‐phase eye speed were less consistent with both drugs, either increasing or decreasing, and being dependent on viewing conditions. Only 1 patient showed consistent reduction of median eye speed, and this was achieved by either drug. Our findings suggest that gabapentin may be an effective treatment for many patients with APN and that occasional patients with downbeat nystagmus will respond to gabapentin or baclofen.
1. Measurements were made in four normal human subjects of the accuracy of saccades to remembered locations of targets that were flashed on a 20 x 30 deg random dot display that was either stationary or moving horizontally and sinusoidally at +/-9 deg at 0.3 Hz. During the interval between the target flash and the memory-guided saccade, the “memory period” (1.4 s), subjects either fixated a stationary spot or pursued a spot moving vertically sinusoidally at +/-9 deg at 0.3 Hz. 2. When saccades were made toward the location of targets previously flashed on a stationary background as subjects fixated the stationary spot, median saccadic error was 0.93 deg horizontally and 1.1 deg vertically. These errors were greater than for saccades to visible targets, which had median values of 0.59 deg horizontally and 0.60 deg vertically. 3. When targets were flashed as subjects smoothly pursued a spot that moved vertically across the stationary background, median saccadic error was 1.1 deg horizontally and 1.2 deg vertically, thus being of similar accuracy to when targets were flashed during fixation. In addition, the vertical component of the memory-guided saccade was much more closely correlated with the “spatial error” than with the “retinal error” this indicated that, when programming the saccade, the brain had taken into account eye movements that occurred during the memory period. 4. When saccades were made to targets flashed during attempted fixation of a stationary spot on a horizontally moving background, a condition that produces a weak Duncker-type illusion of horizontal movement of the primary target, median saccadic error increased horizontally to 3.2 deg but was 1.1 deg vertically. 5. When targets were flashed as subjects smoothly pursued a spot that moved vertically on the horizontally moving background, a condition that induces a strong illusion of diagonal target motion, median saccadic error was 4.0 deg horizontally and 1.5 deg vertically; thus the horizontal error was greater than under any other experimental condition. 6. In most trials, the initial saccade to the remembered target was followed by additional saccades while the subject was still in darkness. These secondary saccades, which were executed in the absence of visual feedback, brought the eye closer to the target location. During paradigms involving horizontal background movement, these corrections were more prominent horizontally than vertically. 7. Further measurements were made in two subjects to determine whether inaccuracy of memory-guided saccades, in the horizontal plane, was due to mislocalization at the time that the target flashed, misrepresentation of the trajectory of the pursuit eye movement during the memory period, or both. 8. The magnitude of the saccadic error, both with and without corrections made in darkness, was mislocalized by approximately 30% of the displacement of the background at the time that the target flashed. The magnitude of the saccadic error also was influenced by net movement of the background during the memory period, corresponding to approximately 25% of net background movement for the initial saccade and approximately 13% for the final eye position achieved in darkness. 9. We formulated simple linear models to test specific hypotheses about which combinations of signals best describe the observed saccadic amplitudes. We tested the possibilities that the brain made an accurate memory of target location and a reliable representation of the eye movement during the memory period, or that one or both of these was corrupted by the illusory visual stimulus. Our data were best accounted for by a model in which both the working memory of target location and the internal representation of the horizontal eye movements were corrupted by the illusory visual stimulus. We conclude that extraretinal signals played only a minor role, in comparison with visual estimates of the direction of gaze, in planning eye movements to remembered targ
Abstract We studied dynamic properties of horizontal, vertical, and oblique eye movements in 23 patients with the following parkinsonian syndromes: idiopathie parkinsonism (PD), multiple system atrophy (MSA), pure akinesia (PA), progressive supranuclear palsy (PSP), and cortical‐basal ganglionic degeneration (CBGD). Compared with age‐matched controls, only PSP patients showed slowing of saccades. Patients in all groups showed saccadic hypometria that was most marked vertically. The trajectories of saccades made to diagonal target jumps were deviated toward the horizonal plane, due to the vertical hypometria; this was most marked in PA and PSP groups. Saccade latency was only increased in the CBGD group. Sinusoidai smooth pursuit did not differentiate between controls and patients; however, with step‐ramp stimuli, pursuit eye acceleration was impaired in all patient groups compared with controls. The vestibulo‐ocular reflex, with or without visual enhancement, was similar in patients and controls. These findings indicate that (1) in parkinsonian syndromes apart from PSP, the saccade‐generating brainstem burst neurons are probably spared, but the signals that they receive, specifying the size and direction of saccades, are flawed; and (2) measurements of the gain and trajectory of oblique saccades, and initiation of smooth pursuit, may aid in diagnosing these different types of parkinsonism.
Dynamic overshoot (DO) of saccades was investigated in 17 normal subjects and 24 patients with central nervous lesions affecting the cerebellum and its connecting pathways, in order to detect and to define a pathological pattern of DO. Eye movements were recorded binocu-larly with the infrared reflection method. Normal subjects showed a high incidence of DO (average: 86% of all saccades) with an average amplitude of 0.16 deg (range of individual averages 0.08 to 0.41 deg). In 52% of all saccades DO occurred in both eyes and in 34% in one eye only. As in normals, the incidence of DO was too variable in patients to be used as a diagnostic tool. Six patients (out of 24) were considered to have pathological DO: their DO amplitudes (range of averages 0.57-0.99 deg) and/or left-right asymmetries exceeded the range of normal subjects. Three had multiple sclerosis, one a hereditary ataxia, one Friedreich's ataxia and one Wallenberg's syndrome.DO is considered to result from an alteration in the saccade braking (deceleration) pulse of immediate premotor structures in the brainstem. Recent experimental evidence suggests that the deceleration of saccades is also under the influence of the cerebellum (more specifically the fastigial nucleus and vermis). A comparison of saccadic dysmetria, often a pathological feature in cerebellar patients, with DO shows that they are not specifically interrelated to saccadic dysmetria. We suggest that pathological DO is probably not related to cerebellar dysfunction.
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