The effects of hyperventilation on the human SEP (Somatosensory Evoked Potential), VEP (Visual Evoked Potential) and AEP (Auditory Evoked Potential)

The effects of HV (hyperventilation) on the human SEP (Somatosensory Evoked Potential), VEP (Visual Evoked Potential) and AEP (Auditory Evoked Potential) were studied with healthy 64 male and 99 female subjects. SEP, VEP and AEP were recorded simultaneously, with 1024 msec of analysis time, together with EEG, before and after HV for 3 min. The following results were obtained. 1. After HV, interpeak amplitudes of SEP, VEP and of AEP almost increased significantly, and the latencies of components of VEP increased significantly in both male and female subjects. But the latencies of the components of SEP and AEP changed differently between males and females. From these results, it was considered that brain activities increased after HV, rebounding from inhibition during HV. And it is suggested that the influence of hypoxia occured during HV is prolonged in VEP than in SEP and AEP. Besides, it is considered that the recovery from the influence of HV is delayed in males than in females. 2. As for the recording of Evoked Potentials together with EEG, it is appropriate that Evoked Potentials are recorded before HV

The effects of insulin-induced hypoglycemia on the human SEP (Somatosensory Evoked Potential) and EEG

The effects of insulin-induced hypoglycemia on the central nervous system were studied by somatosensory evoked potential (SEP), with 8 schizophrenic patients (31~47 y. o.), during the 'kleine Insulinbehandlung'. In each of three experimental session on different days, human regular insulin was injected subcutaneously to the patients, whose consciousness level was lowered to the stage of somnolence, and recovered by intake of a glucose solution (100 g). EEG containig SEPs evoked by electric simuli was derived from the two derivations (1 st ch: C3'→A1+2, 4 th ch: C3'→F3'). In the experimental session, EEG containing SEPs 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 SEP were studied. Individual SEPs were subjected to the component analysis, and to the statistical assessment together with EEG power%. As a result, the middle and long latency components of SEP significantly prolonged in latency and significantly decreased in amplitude 60 min after the injection of insulin. On the other hand, the short latency components of SEP significantly prolonged in latency 100~120 min after the injection of insulin. These results suggested that the activity of cerebral cortex was inhibited, but subcortex was not affected to hypoglycemia in the early stage. In the results of the present study with SEP, the noradrenergic activities in the early stage of hypoglycemia, observed with AEP previously reported, were not confirmed