Experimental studies in monkeys have demonstrated that injection of gamma-aminobutyric acid (GABA) agonists into the superior colliculus restricts saccadic eye movements, while injection of GABA antagonists leads to square-wave jerks (SWJ). To investigate the role of GABA in saccadic interruptions of fixation, we treated five patients who had SWJ and square-wave oscillations (SWO) with valproic acid (VPA) (2000 mg/d), which has been shown to increase brain GABA levels. VPA effectively reduced the SWJ/SWO in three patients, abolished them in one patient, but was ineffective in the fifth, who had a localized lesion in the cerebellar vermis. VPA effects may have been due to the restoration of the GABAergic tonic inhibitory action from the substantia nigra pars reticulata to the superior colliculus.
In Wilson's disease neurological manifestations result from the damage in the basal ganglia, even if a widespread degeneration of the brain occurs. The few studies performed using evoked potentials with the aim of identifying subclinical dysfunction in the three major sensory pathways have never shown abnormalities in patients without neurological manifestations. To verify this observation we studied 12 patients suffering from Wilson's disease in a pre-neurological stage by using pattern visual evoked potentials (VEPs), somatosensory evoked potentials (SEPs) to median nerve stimulation and brainstem auditory evoked potentials (BAEPs). Four of these patients had not yet been treated with penicillamine or trientine (triethylenetetramine dihydrochloride), while the remaining 8 patients were on treatment for at least 1 year. In 3 patients of this second group and in 1 patient of the first group we observed a significant (3 SD over the mean) increase in P100 wave latency, while SEPs and BAEPs were found to be abnormal in only 1 patient, respectively.
Infrared oculographic recordings of saccades evoked by auditory or visual targets in four patients with hemianopia due to an occipital lesion showed that these patients employed a different strategy to find visual and auditory targets in each hemifield. In the seeing hemifield, the patients acquired auditory targets with both monosaccadic and multiple saccadic refixations. The first saccade, the largest, brought the eyes toward the target; the following smaller saccades completed the search as in normal subjects. Saccades to visual targets consisted of one orthometric saccade or two saccades. By contrast, in the blind hemifield the patients acquired auditory targets by a staircase strategy consisting of stepwise saccadic search movements similar to those used for visual targets in the same hemifield. The similarity of strategy to auditory and visual targets suggests a common motor program controlled by the visual input. The latency, accuracy, and velocities of visual and acoustic responses were equal in both hemifields.
A boy with a left-hemispheric cerebellar astrocytoma had upbeat nystagmus exhibiting increasing-velocity slow phases. The nystagmus improved after excision of the tumour.
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