Stationary potential of the brain: Part II. Clinical studies.
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Biomedical subjects
Publications and source records attributed to Y Mayanagi.
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Stereotactic intervention into the posterior hypothalamus gives satisfactory results for controlling both aggressive, violent behavioral disorders and intractable pain. From the endocrinological point of view, this procedure activates the hypothalamic-hypophyseal axis only temporarily, without causing any serious dysfunctions.
In 12 rhesus monkeys, made epileptic by injection of alumina cream into the temporal lobe structures, the changes of spike frequency were studied in wakefulness and natural sleep on 78 occasions. Five monkeys had a focus in the lateral surface of the temporal lobe and seven had a focus in the mediotemporal structures. Basic cortical and subcortical EEG patterns, recorded through chronic indwelling electrodes, showed fairly consistent changes in the course of natural sleep, allowing a classification of the sleep into stages. During slow wave sleep, the focal spikes increased in all 12 cases. The increase was more prominent during the light stage of slow wave sleep in the neocortical foci and during deep stage in the mediotemporal foci. During REM sleep, the mediotemporal foci showed a marked decrease of spiking, whereas changes in the neocortical foci were inconsistent.
Thalamic somatosensory evoked potentials (ThSEPs) were recorded by averaging technique from various thalamic structures during 59 stereotactic operations. From 372 records, response patterns and latency characteristics were analysed in relation to the intrathalamic localization. The findings can be summarized as follows. In N. ventro-caudalis (VC) and ventro caudalis parvocellularis (Vcpc) ThSEPs showed the most definite (and exclusively contralateral) responses characterized by a single positive (P1) deflection. The latency was shortest in VC (mean value, 17.5 msec) and in Vcpc (15.6 msec). Responses from N. centrum medianum (CM), parafascicularis (Pf) and limitans (Lim) were composed of early P1-N1 and of later P2-N2 components. The P1 latency was relatively consistent, with a mean value of 28.2 msec. Pulvinar responses showed a pattern similar to CM, with a mean P1 latency at 30.5 msec. Responses of N. dorsalis medialis (DM) were small, variable and longest, with a mean P1 latency of 54.2 msec. To ipsilateral stimulation, CM, Pul, DM and N. ventro-lateralis (VL) showed comparable wave forms. The possible role of the CM-Pf-Lim complex and of Pulvinar in the "extra-lemniscal" sensory system was considered. The usefulness of ThSEP recording to identify electrode locations in the thalamus is thus confirmed.
In 12 rhesus monkeys the injection of alumina cream into the temporal cortex, amygdala or hippocampus induced seizures after a latent period of six weeks to three months. Clinically the attacks are characterized by an arrest of movement, staring, unresponsiveness to most stimuli, wandering conjugate eye movements, automatisms, twitching of the contraleteral ear and less commonly commonly vocalization, chewing, hiccoughing, vomiting, adversive head movements and twitching of the face. The spiking from the amygdala and hippocampus, which usually fire together, propagates to the temporal cortex and multiple subcortical structures including the hypothalamus, anterior perforated space, anteromedial thalamus, cingulate gyrus, putamen, globus pallidus, subthalamus and mesencephalic reticular formation; from the temporal cortex to the amygdala and hippocampus, and secondarily to the diencephalic centers. There is a fairly consistent sequence of preferential propagation. Although there are some differences in the occurrences of clinical manifestations depending upon the sites of the focus, no specific structural correlation with clinical manifestations could be established. This experimental condition may provide a proper model for the study of clinical psychomotor epilipsy.
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In 8 monkeys, made epileptic by alum or penicillin injection into temporal lobe structures, 40 seizures were studied by both DC cortical potential and subcortical EEG recordings. Eighteen seizures of lateral temporal origin had an abrupt negative DC potential shift of 0.5 to 2.0 mV in and around the focus. The frontal, parietal and occipital cortices did not develop DC potential changes, perhaps due to the limited propagation of the neocortical seizures. Twenty-two seizures of medial temporal origin showed a negative shift of the anterior, inferior or lateral temporal cortex in 85% of seizures. The other 15% had a positive or no shift. In hippocampal seizures, a positive displacement was sometimes seen prior to the main negative shift in the lateral temporal cortex. The remote cortex developed only a minimal positive shift in 30% of the mediotemporal seizures. A marked negative shift in the frontocentral cortex was the first sign of impending generalization, which may result from a series of chain reactions with seizure propagation, involving more and more structures of the brain. Registration of DC potentials in temporal lobe seizures may give insight into the nature of abnormal EEG activities and to some extent into the origin of seizures.
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