Abstract

Complex partial seizures most often originate from the temporal lobe. The temporal lobe comprises rhinencephalic (limbic) structures, such as the hippocampus and amygdala located in the mesial surface of the lobe and neocortical structures located laterally. The syndrome of mesial temporal lobe epilepsy is the most common cause of complex partial seizures. This syndrome has specific historical features and characteristic pathology termed mesial temporal sclerosis. The characteristic pathological changes associated with intractable mesial temporal lobe epilepsy often occur within the hippocampus and are referred to as hippocampus sclerosis. Hippocampal sclerosis is found in 50 to 70% of the cases of intractable temporal lobe epilepsy who undergo temporal lobectomy. The hippocampal neuronal loss is often accompanied by reorganization of the mossy fiber system into the inner molecular layer of the dentate gyrus, leading to the formation of new synaptic contacts. The functional significance of this synaptic reorganization remains unclear; however, its existence may indicate that there is a lesion in the hippocampus and its interconnecting structures, which may not be apparent with conventional anatomical techniques. The immature brain also has a greater susceptibility to the development of prolonged provoked seizures in response to environmental stimuli, such as fever, infection, and head trauma. Consequently, it is quite likely that the initial precipitating injury may be associated with a seizure and, particularly a febrile seizure. Thus, it is assumed that these early seizures may lead to the development of mesial temporal sclerosis and subsequent temporal lobe epilepsy.

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