Abstracts

Rationale: Epilepsy is a group of disorders in the form of recurrent paroxysms of cerebral origin causing stereotypical symptoms. This disease has an autosomal dominant inheritance pattern with 60% penetrance, variable severity. Its development is multifactorial, the most common causes are disorders of development as a failure of neuronal migration, hippocampal malformations, hippocampal sclerosis and tumors. Temporal lobe epilepsy (TLE) refers to nosological processes associated with complex partial seizures such automatism, psychological symptoms and disconnections of the medium. The incidence is 25-50 new cases per 100 000 inhabitants per year. The prevalence in America is from 500 to 1000 patients per 100 000 inhabitants. Hippocampal sclerosis is the most studied epileptogenic focus, and represents 70% of patients with TLE. Epilepsy affects over 50 million people worldwide. Treatment is based on drugs according to type of epilepsy surgery in specific cases. Methods: We studied eight autopsy cases with diagnosis of temporal lobe epilepsy. We reviewed medical records and postmortem tissues, tissues were stained with hematoxylin-eosin, silver impregnation and immunohistochemistry for GFAP and examined photomicroscope. The cases studied were of both sexes with an age range of 20 to 76 years. The weight of the brains vary between 780 and 1250 grams. Results: All cases have developmental defects and failure of neuronal migration, neuronal depoblaci n, branched axons, neuronal dysplasia, heterotopias in cortex and white matter, cerebellar hypoplasia and dysplastic Purkinje neurons. There are also changes as neuronal death, hamartomatous vessels, demyelination, and degeneration depoblaci n Purkinje neurons. The cases have poor circulation changes related to hypoxia, and reactive astrocytes, gliosis, pyknosis, dendrites and bodies altered starch. Those with tuberous sclerosis show microcephaly, irregular gyri, neurofibrillary plaques, globose cells, and neuritic plaques. Tuberculosis cases observed neurons with karyorrhexis, globose cells, axons undulate, branched axons and parenchymal and meningeal tuberculosis. The case presents oligophrenia frontal lobe sclerosis, white matter atrophy with cyst formation, persistence of cavum septum, reduction of the cerebellar tonsils, signs dehipoxia, depoblacion neuronal and cortical spongiosis. Conclusions: Epilepsy is a disease of multifactorial origin that begins with a neurodevelopmental defect, so the importance of research in developmental biology for this disease, as well as advice to relatives and genetic counseling.