[Questions of epileptogenesis and prevention in symptomatic epilepsies].
Symptomatic epilepsies usually report themselves after a longer period of time after brain injury, after the so-called latent period. During this period progressive functional and structural changes occur which finally cause an increased excitatory condition. The process of epileptogenesis may be examined in animal models, such as in the kindling, status epilepticus, hypoxicischaemic models. Data gained from such sources support the hypothesis that the first injury results in a lower seizure threshold, but genetical and environmental factors also contribute to the development of epilepsy and most probably further insults may be needed. The development of epilepsy can be traced back to several reasons. In spite of this, the latent period provides opportunity for the prevention of epilepsy or for the influence of epileptogenesis in such a manner that later treatment can become more successful. Prevention should be an aim in clinical practice, as well. Medication used presently are more like to have anticonvulsive properties and their antiepileptogenic effect is questionable. Due to this fact, development of new drugs is necessary with new theoretical background. The most important influence on the incidence of epilepsy in recent years has been provided by the improvement in neonatal care. This highlights the fact that such optimal medical care should be provided in the acute period of brain injury which can terminate or lessen the risk of epilepsy.
Nikl
János
J
Zala Megyei Kórház, Neurológiai Osztály, Zalaegerszeg. niklj7@axelero.hu
D000818:Animals; D000927:Anticonvulsants / Q000627:therapeutic use; D001930:Brain Injuries / Q000150:complications; D002545:Brain Ischemia / Q000150:complications / Q000209:etiology; D001932:Brain Neoplasms / Q000150:complications; D002493:Central Nervous System Diseases / Q000150:complications* / Q000503:physiopathology; D004195:Disease Models, Animal; D004569:Electroencephalography; D004827:Epilepsy / Q000188:drug therapy / Q000209:etiology* / Q000503:physiopathology / Q000517:prevention & control*; D006801:Humans; D000860:Hypoxia / Q000150:complications; D007231:Infant, Newborn; D007696:Kindling, Neurologic; D012307:Risk Factors; D003294:Seizures, Febrile / Q000209:etiology / Q000517:prevention & control; D013226:Status Epilepticus / Q000209:etiology / Q000517:prevention & control; D020521:Stroke / Q000150:complications
D000927:Anticonvulsants