Somatosensory evoked potentials after experimental head injury in the awake rat.
Experimental acceleration concussion was induced in 30 male rats who were immobilized with curare, artificially ventilated but not anaesthetised. Serial recordings of cortical somatosensory evoked potentials (SEPs) were made from the onset of concussion and for the following 30 min. Immediately after the head blow the initial three components of the SEP (P1, N1 and P2) were all either absent or markedly increased in latency. The late negative component (N2) was always abolished. All components reappeared and returned to approximately pre-concussion latencies within 5-6 min. The most persisting abnormality was in N2 whose post-concussion amplitude stabilized and remained depressed at only 50% of baseline value. The results suggest that experimental head injury produces a significant abnormality in every component of the evoked potential. The findings are therefore inconsistent with the theory that concussion differentially affects the diffuse nonspecific pathways whose activity is mediated by the reticular formation while leaving the lemniscal system comparatively intact. It is also shown that the morphology of the post-concussion SEP waveform can be quite accurately simulated by recording SEPs from normal animals at high rates of stimulation (50/s). This implies that the pathophysiology of concussion involves a temporary dysfunction in synaptic transmission although the level at which this is occurring has yet to be determined.
D000344:Afferent Pathways / Q000503:physiopathology; D000818:Animals; D001924:Brain Concussion / Q000503:physiopathology*; D002540:Cerebral Cortex / Q000503:physiopathology; D004195:Disease Models, Animal; D005073:Evoked Potentials, Somatosensory; D008297:Male; D009420:Nervous System / Q000503:physiopathology*; D051381:Rats; D011930:Reaction Time / Q000502:physiology; D012154:Reticular Formation / Q000502:physiology; D009435:Synaptic Transmission