Referenced in: none

Automatically associated channels: Kir2.3

Title: [Epilepsy--an ongoing challenge]

Authors: Danilo Hodoba

Journal, date & volume: , 2005 , 59, 31-9

PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/15813353

Abstract
Epilepsy is a sequel of depolarizing neuronal event with recurrent seizures. Neuronal membrane disorder is the main cause of epileptogenesis. The epileptic process is initiated and progressing due to the membrane inability to maintain balanced changing of the electrochemical gradient, which is physiologically necessary for intracerebral signal transfer. Membrane ion channels are deranged, which may be congenital or acquired. To date, only a few specific genetically caused ion channel aberrations in some less common epileptic syndromes have been identified, however, the main pathophysiologic sequence of events at the cellular level remains obscure. Synaptic dysregulation of epileptic neuronal groups with unbalanced inter-relationship of excitatory and inhibitory complements within the epileptic focus has been only partly elucidated. Therefore, the treatment of epilepsy remains fortuitous to a great extent because idopathic epileptogenesis is stochastically unpredictable. We do not yet know why, how and when the epileptic process begins, and vice versa, why the process may occasionally be completely silent in a continuously overstrained interaction system. What link in the excitation neuronal system is weakest: membrane instability, neurotransmitter incoordination, or something else? Yet, in two thirds of the individuals prone to epilepsy, monotherapy with so-called channel antiepileptics with selective action on membrane ion exchange and/or antiepileptics with neurotransmitter modulation will stop the manifestation of epilepsy but not the longterm proneness to epileptogenesis. In the remaining one third of sufferers the epilepsy is refractory to any therapeutic attempts. Therefore, antiepileptic treatment is a highly complex, individualized procedure in which only the observational predictors have been positively defined to date, i.e. clinical manifestation and electroencephalography specificity. They make the basis for balanced evaluation of the real extent of action of the antiepileptics available.