Abstract
T HE study of focal cortical epilepsy has led us to the belief that epileptic neurons are partially deafferentY The validity of this hypothesis has been demonstrated in the cat spinal cord where rhizotomy or hemi-cordotomy result in neuronal firing patterns that are similar to those seen in an epileptic focus. 1 Other work in our laboratories has shown that certain epileptogenic agents, when injected into the spinal cord of the cat, can produce unusual sensory states suggestive of pain and the neuronal firing patterns typical of epilepsy? It is our hypothesis that many of the central pain states that occur after nerve or spinal cord injury may be due to chronic deafferentation and subsequent hyperactivity at the segmental level. This report describes a paraplegic patient whose spinal cord neuronal activity was sampled.
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