Stimulation of the thalamus and internal capsule with Medtronic® deep brain stimulation electrodes produced improvement in pain, hemiparesis, dystonia, torticollis, tremor, speech impairment and epilepsy. Stimulation at voltages above or below clinically effective levels (e.g., 6 V, 0.3 ms, 74 Hz) resulted in a loss of clinical efficacy. Somatosensory evoked responses (short and long latency) and depth electrode recordings were helpful in localisation and ‘biocalibration’ of electrical stimulation.
Data are presented for the first 50 patients with cerebral palsy who underwent chronic cerebellar stimulation for symptom alleviation. We observed significant shorter and longer term improvement in spasticity as well as athetosis, speech, and functional status. Continuing increments in improvement were noted as a function of time on stimulation. In many instances, psychometric test scores and behavior also were improved. There was one death in this series. There were no neurologic complications due to cerebellar stimulation. The results of this study warrant the judicious use of cerebellar stimulation for symptomatic and functional relief in cerebral palsy.
Six human subjects (5 male, 1 female, age 23.7 + 5.7 years) with incapacitating partial seizure disorders intractable to medical therapy have been treated by ongoing pulsed electrical stimulation of anterior nucleus of the thalamus. Four of the six patients have demonstrated statistically significant clinical control of the seizure disorder. One patient (D.L.) has been seizure-free for the last two years. In two of these six patients, it was possible to study not only electrophysiological activity of the brain, but also regional cerebral glucose metabolism by the (18F) 2-fluoro-2-deoxy-D-glucose method, blood cortisol levels, and blood levels of valproic acid, diphenylhydantoin, and carbamazepine. Significant changes were seen during periods of stimulation compared with control periods without stimulation. These results imply that stimulation of the principal thalamic relay nucleus of the limbic system causes clinical, behavioral, cerebral metabolic, electroencephalographic, endocrinologic, and pharmacokinetic responses.
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