The effects of electroconvulsive shock on the short-latency somatosensory evoked potential in the rat.
The effects of electroconvulsive shock (ECS) were examined on the short-latency somatosensory evoked potential (SEP) in the awake rat. Immediately after the induction of generalized seizure activity (GSA), the primary cortical response was lost although the preceding far field thalamic component appeared to be preserved basically intact. Within 1 minute the cortical potential had begun to reemerge, albeit with an attenuated amplitude and a prolonged latency. Recordings made at 2 and 3 minutes revealed evidence of a slight postictal enhancement of the cortical potential. Within 6 minutes, a near normal waveform had been restored. It is concluded that the principal site of impact of ECS resides at the cortical level and that the somatosensory impulse is, therefore, able to traverse the central pathways unimpeded by GSA until it is finally blocked at the primary sensory cortex. The present findings are compared to previous attempts to record cortical SEPs from patients undergoing electroconvulsive therapy (ECT). It is presumed that the failure of ECT to abolish the SEP in these circumstances was due either to the protective role played by concurrent medication or because of a post-ECS delay in restarting the recordings. The relevance of the findings to an understanding of the physiology of electrical stunning is discussed.
Shaw
N A
NA
Department of Physiology, School of Medicine, University of Auckland, New Zealand.
D000818:Animals; D004558:Electric Stimulation; D004597:Electroshock; D005073:Evoked Potentials, Somatosensory / Q000502:physiology*; D008297:Male; D051381:Rats; D012640:Seizures / Q000503:physiopathology*; D013003:Somatosensory Cortex / Q000503:physiopathology; D013788:Thalamus / Q000503:physiopathology