Human epilepsies result from a number of neuronal dysfunctions, leading to recurrent ictal hyperexcitability. The physiopathological mechanisms underlying different seizure types are certainly different, depending on genetic determinants, structural abnormalities, etc. However, many experimental studies demonstrated that both interictal and ictal epileptic events depend on the concurrent presence of cellular hyperexcitability and of "permissive" local circuitry, capable of generating highly synchronous discharges. This condition typically takes place in cortical structures, while the rhythmic repetition of epileptic events may derive from the pacing activity of subcortical nuclei. At the cellular level, elementary epileptic discharges can result from every condition disrupting the equilibrium between depolarizing and hyperpolarizing mechanisms. Pathological changes in inhibitory or excitatory synaptic transmission as well as minimal changes in intrinsic control of cell firing are all capable of generating the typical "epileptic" behavior, consisting of sustained depolarizations and aberrant burst discharges. This hyperexcitable behavior shares many features with that observed in models of neuropathic pain and, in spite of obvious discrepancies, suggests an interesting connection between these two apparently disparate pathological conditions, opening a window to better understand the efficacy of many drugs on both epilepsy and neuropathic pain.
|Issue number||4 SUPPL.|
|Publication status||Published - 2000|
ASJC Scopus subject areas
- Clinical Neurology