SUCCESSFUL TREATMENT OF PAINFUL TRAUMATIC MONONEUROPATHY WITH CARBAMAZEPINE - INSIGHTS INTO A POSSIBLE MOLECULAR PAIN MECHANISM

The delayed onset of painful paresthesias following trauma to a periph eral nerve is a well recognized but poorly understood phenomenon. This report describes an illustrative case of painful paresthesias in the territory of the ilioinguinal nerve, 3 to 6 weeks after an otherwise r outine herniorraphy, which subsequently responded dramatically to carb amazepine. The case is considered in light of recent studies which hav e determined molecular changes which occur in dorsal root ganglion (DR G) neurons following axotomy and neuroma formation. Voltage-dependent sodium (Na+) channels in DRG neurons undergo a change following axotom y, in which there is significant up-and down-regulation of different s ubpopulations of Na+ channels over a time frame measured in days to we eks. Such changes may render the DRG neurons hyperexcitable, thus cont ributing to a neuropathic pain syndrome, yet susceptible to treatment with a sodium channel blocker such as carbamazepine. (C) 1997 Elsevier Science B.V.