Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038220 (status epilepticus)
 7,272 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In prior work, we developed a model of self-sustaining limbic status epilepticus (SSLSE) induced by continuous hippocampal stimulation (CHS). Previous electrographic studies showed that SSLSE was synchronized between the cerebral hemispheres. On the basis of this initial work, we postulated that hippocampal commissures were critical for the initiation and maintenance of SSLSE. In the current experiments, we tested this hypothesis by applying CHS in animals with (CMX) or without (-CMX) hippocampal commissurotomies. In the -CMX group, electrographic SSLSE was synchronized between the stimulated and contralateral sides. In the CMX group, SSLSE developed only on the stimulated sides. Regional cerebral glucose utilization (RCGU) was also studied acutely (1 hour) after CHS using 2-deoxyglucose autoradiography. In the -CMX group, there was symmetrically increased RCGU in the hippocampus, retrohippocampal structures, and associated limbic and subcortical nonlimbic regions. In the CMX group, a similar pattern was found, but confined to the side of stimulation. CMX alone did not change RCGU values from those in control (-CMX, nonstimulated) brain in any of the regions studied. Areas of bilateral neocortical hypometabolism were found in both (CMX and -CMX) SSLSE groups. These results lead to rejection of the hypothesis that hippocampal commissures play an essential role in the initiation and maintenance of SSLSE. Instead, a feedback circuit involving the hippocampus and its adjacent structures seems to be the critical anatomic substrate for SSLSE. The presence of neocortical hypometabolism after CMX indicates that the structures other than the hippocampal commissure (eg, the thalamus or other forebrain commissures) mediate this effect.
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PMID:Self-sustaining limbic status epilepticus. II. Role of hippocampal commissures in metabolic responses. 174 55