Mechanisms of development of temporal lobe epilepsy: clinical and experimental studies

Among the many forms of epilepsy, one of the most studied is epilepsy of the temporal lobe (temporal lobe epilepsy) associated with the pathology of the limbic system, and especially the hippocampus. Sections of the limbic system are the source of epileptic seizures in this form of the disease, which is confirmed by electroencephalographic data, including those obtained using embedded electrodes [81], and the clinical effectiveness of surgery. Removal of certain parts of the medial temporal cortex, including part of the hippocampus, can heal or reduce the frequency and severity of seizures [92]. On the basis of structural changes, two main types of epilepsy of the temporal lobe are distinguished: 1) with the presence of a volumetric process (tumor, congenital pathology, blood vessel aneurysm, hemorrhage) affecting the limbic system; 2) without the presence of clearly verified volumetric changes in the medial temporal lobe [23]. In the latter case, the only structural manifestation of temporal lobe epilepsy is hippocampal sclerosis. The name reflects the most striking morphological manifestations of the disease - the loss of neurons primarily in the CA1 and CA3 zones of the horn of the ammonia and the development of replacement gliosis. Intravital brain imaging using functional positron emission tomography, magnetic resonance imaging, and magneto-encephalography confirms changes in the hippocampus in temporal lobe epilepsy, usually in the form of a decrease in its volume [60]. There is also a positive correlation between intravital structural and biochemical (in particular, the number of AMPA-A receptors and the intensity of absorption of F-fluoro-2-deoxy-D-glucose) changes in the sclerosed hippocampus and data from the study of surgical material [75].