Mesial temporal lobe epilepsy (MTLE) is the most common form of focal epilepsy in adults. Mesial structures such as the hippocampus, amygdala and temporal cortex are the major affected structures in this syndrome. Studies with cerebral tissue from patients with MTLE have shown plastic changes related to seizures in the hippocampus, amygdala and temporal cortex. Although in MTLE the hippocampus act as a main seizure focus, changes in the amygdala and temporal cortex may occur because these structures are strongly interconnected. Psychiatric comorbidities are more frequently in patients with MTLE than in the general population. Although several studies have shown an association between epilepsy and psychiatric comorbidities, neuropathological mechanisms that may contribute to onset or maintenance of psychiatric symptoms in MTLE are poorly understood. The amygdala is responsible for processes related to emotions, and has a vital role in major depression and positive and negative symptoms seen in patients with psychosis. The temporal cortex is another structure that is altered in patients with MTLE and in psychiatric patients, as demonstrated by neuroimaging studies. Because of the importance of these structures in MTLE and psychiatric comorbidities, and taking into account the absence of published literature on the role of the amygdala and temporal cortex in MTLE associated with psychiatric comorbidities, our objective is to examine neuropathological changes as neuronal loss, gliosis, and axonal and dendritic alterations in these structures. In addition, we will analyze the expression of the FMRP protein (the fragile X mental retardation protein) and metabotropic glutamate receptor type 5 (mGluR5), proteins may be directly involved in mechanisms of neuronal plasticity. Amygdala and temporal cortices of MTLE patients with and without psychiatric comorbidities will be further compared to specimens from necropsy without a history of epilepsy.
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