Excitotoxicity and epileptic brain damage.
The two forms of epileptic brain damage, that found in patients with chronic epilepsy (post-mortem or in an anterior temporal lobectomy specimen) and that occurring acutely after status epilepticus, have much in common but are not identical. Hippocampal lesions occurring acutely after status epilepticus show a high degree of selectivity for hilar interneurones, CA1 pyramidal neurones and CA3 pyramidal neurones. Hippocampal lesions in anterior temporal lobectomy specimens tend to involve the subfields less selectively with CA1 being only slightly more severely affected than dentate granule cells, CA3 and CA2 pyramidal neurones. The most severely damaged hippocampi may result from a combination of acute damage early in life (commonly from prolonged febrile convulsions) and cumulative damage associated with seizures. Less severe degrees of damage are probably a consequence of repeated seizures. The abnormal patterns of firing associated with epileptic activity are almost certainly responsible for cell death occurring acutely after status epilepticus; they may contribute to the progressive cell loss occurring in chronic epilepsy.
Meldrum
B
B
Department of Neurology, Institute of Psychiatry, London, U.K.
D000596:Amino Acids / Q000633:toxicity*; D000818:Animals; D001925:Brain Damage, Chronic / Q000503:physiopathology*; D004827:Epilepsy / Q000139:chemically induced* / Q000503:physiopathology; D006801:Humans
D000596:Amino Acids