Abstract
Temporal lobe epilepsy (also called mesial temporal lobe epilepsy), the most frequent form of partial epilepsy in adults, is clinically characterized by alterations in consciousness combined by various functional manifestations including sensory, motor, psychic, and autonomic.
On MR imaging, atrophy and T2-hyperintensity of hippocampus are the most relevant findings.
Significant neuronal loss is noted in the hippocampus; based on the most severly involved cornu ammonis (CA) region, three different types of hippocampal sclerosis are defined by the International League Against Epilepsy (ILAE).
The pathogenesis is not yet fully understood. An initial precipitating injury before the age of 4 years (e.g., complex febrile seizures, birth trauma) might be a contributing factor. Altered inhibitory mechanisms, interneurons, mossy cells, calretinin-immunoreactive neurons with Cajal–Retzius cell morphology, GABA transmission, and astrocytes might further contribute. Genes differently expressed play roles in structural integrity, axonal outgrowth, proliferation, gene-transcription control, calcium homeostasis, neuronal signaling, serotonin receptor (HTR2A), and neuropeptide Y receptor.
Treatment consists in the tailored neurosurgical resection of the sclerotic hippocampus, parts of the amygdala and the temporal cortex. Two-year postoperative seizure control is achieved in 60–80% and depends on the type of hippocampal sclerosis.
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Weis, S. et al. (2019). Epilepsies: Temporal Lobe Epilepsy. In: Imaging Brain Diseases. Springer, Vienna. https://doi.org/10.1007/978-3-7091-1544-2_45
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