The effects of insulin-induced hypoglycemia on the human AEP (Auditory Evoked Potential) and EEG
Ito, Yoshinobu The University of Tokushima
Kawamura, Ichiro The University of Tokushima
Okura, Masao The University of Tokushima
Ikuta, Takumi The University of Tokushima
Tomotake, Masahito The University of Tokushima Tokushima University Educator and Researcher Directory KAKEN Search Researchers
auditory evoked potentials
The effects of insulin-induced hypoglycemia on the central nervous system were studied by auditory evoked potential (AEP), with 8 schizophrenic patients (31~47 y.o.), during the 'kleine Insulinbehandlung'. In the three experimental session on different days, human regular insulin was injected subcutaneously to each patient, whose consciousness level was lowered to the stage of somnolence and recovered by intake of a glucose solution (100 g). EEG containig AEPs evoked by click simuli was derived from the two derivations (3rd ch : Cz→A1+2, 6th ch : Cz→T5). In the experimental session, EEG containing AEPs was recorded before and 20, 40, 60, 80, 100 and 120 min after the injection of insulin, and 20 min after intake of glucose. Consecutive changes of group mean AEP were studied. Individual AEPs were subjected to the component analysis, and to the statistical assessment together with EEG power %.
As a result, the middle latency components of AEP significantly reduced in latency and significantly increased in amplitude in the early stage after the injection of insulin, but significantly prolonged in latency in the latter stage. On the other hand, the long latency components of AEP significantly prolonged in latency and significantly decreased in amplitude throughout hypoglycemia. EEG power % significantly decreased in δ power% in the early stage, but significantly increased in δ and θ power % and significantly decreased in α and β power % in the latter stage. These results were attributed to the inhibitory effects of insulin-induced hypoglycemia on the cerebral cortex, and to the activation of the noradrenergic neurons responding to the hypoglycemia in the early stage. The results also indicate that the activated noradrenergic neurons are gradually declined during prolonged hypoglycemia.
Shikoku Acta Medica
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