Five patients with clinical and EEG primary generalized or multifocal uncontrollable seizures underwent stereotaxic implantation of electrodes in both centromedian thalamic nuclei (CM). Each electrode consisted of a semiflexible array of three platinum-iridium wires, isolated except at their tips, which were separated by 4 mm. Bipolar, biphasic rectangular pulses were delivered in trains of 1 min every 5 min, alternating right and left side for sessions 2 h/day. Patients were followed for 3 months with charting of clinical seizures, daily 4-h EEG recordings from scalp and depth for 5 days and weekly thereafter. Baseline and 3-month evaluation of psychological performance through selected Beta R, Wechsler memory scale, visual discrimination, MMPI, and Zung's rated depression scale. Tests were evaluated for significant changes by the parametric student's t test and Mann Whitney nonparametric test. Clinical seizures were significantly reduced by electrical stimulation (ES), as were EEG interictal spikes and EEG slow waves. Psychological performance improved beyond that expected by reduction in seizure activity. ESCM induced a local afterdischarge (AD) that progressively developed in time and intensity, and the beneficial effects outlasted ES for periods of weeks to months, suggesting that a state of hyperexcitability of stimulated tissue, similar to "kindling," was created by chronic ES.
Stereotactic lesions for the treatment of tremor and rigidity in patients with Parkinson's disease are occasionally followed by neglect of the use of contralateral extremities for spontaneous movement when there are no specific sensory or motor deficits. A group of patients with neglected extremities was compared with a group of patients in which thalamotomy did not produce neglect. Neglect was shown by changes in motor performance, somatosensory evoked potentials (SEP) and electroencephalographic frequency induced by the lesion, as well as radiological evidence of brain atrophy and place and extension of lesions. Reaction time to both auditory and somatosensory stimuli was significantly increased only in the extremities contralateral to the lesion of patients with neglect; tremor decreased equally in both groups, and other motor abilities remained unchanged. P-200 component of SEP decreased in amplitude and increased in latency only in cases with neglect, particularly ipsilateral to the lesion; early components and mean electroencephalographic frequency remained unchanged. Brain atrophy was significant in patients with neglect, particularly for the posterior portion of the 3rd ventricle. No differences in size and location of the lesions were found between the groups. Results indicate that this type of neglect is not secondary to lesions in specific sensory of motor pathways, but to lesions of structures coupling sensorimotor functions and the process of attention and that midline thalamic nuclei atrophy precipitates the neglect, perhaps by critically decreasing the amount of reticulothalamocortical projections engaged in selective attention.
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