LITTLE is known abut the pathological alterations that cause intermittent seizures in human epilepsy. Among possible mechanisms, the partial chronic deafferentation of cortical neurons has been incriminated on the basis of experimental studies on spike foci.1 This hypothesis appears to be in agreement with the widely held belief that denervation supersensitivity, known to increase the sensitivity of denervated peripheral structures to various chemical stimuli and to nervous impulses, also occurs in the deafferented cortex and leads to the development of intermittent seizures. These hypotheses are supported mainly by studies on the chronically isolated cortex which shows increased sensitivity to topical application of acetylcholine (ACh)2 and to local epicortical electrical stimulation.3,4
However, the roles of deafferentation and of denervation supersensitivity in cortical epileptogenesis have not yet been clarified. This is, at least in part, due to the fact that previous experimental models have not permitted distinction between
Spehlmann R, Chang CM, Daniels JC. Excitability of Partially Deafferented Cortex: I. Macroelectrode Studies. Arch Neurol. 1970;22(6):504–509. doi:10.1001/archneur.1970.00480240024004
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