Abstract
A previous report showed that following spinal cord transaction well below the C7 level in cats, later components of the cortical somatic evoked potential (SEP) (40 msec or longer) produced in response to median or radial nerve stimulation were abnormal (Katz et al., 1977). Evidence presented here shows that early components of the radial nerve SEP are also altered following spinal cord transection. Latencies of both early and late components were increased as higher functional transections of the spinal cord were made. This monotonic increase in latency of the primary components supports the hypothesis that the results may be due to increasing loss of excitatory input. Correlation of latency change with level of injury may serve as a useful diagnostic tool.
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