What are the pathologies associated with cortical cell loss in temporal lobe epilepsy?
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Cortical cell loss in temporal lobe epilepsy (TLE) is associated with various pathologies. Neuronal dendritic reshaping and spine alterations are observed in type II focal cortical dysplasia, leading to severe cortical malformation and abnormal synaptic network organization . Additionally, TLE is characterized by the loss of layer 3 neurons in the medial entorhinal area, which contributes to seizure development . Generalized convulsive status epilepticus can cause focal cell loss in the hippocampus due to sustained glutamatergic excitatory neurotransmission and loss of GABAergic inhibitory neurotransmission, ultimately leading to hippocampal cell death . Furthermore, TLE is frequently associated with hippocampal sclerosis, possibly due to primary brain injury, leading to refractoriness to drug treatment and requiring surgical resection of mesial temporal regions .
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| Cortical cell loss in temporal lobe epilepsy is associated with focal neuronal injury due to sustained glutamatergic excitatory neurotransmission, leading to hippocampal cell death primarily mediated by NMDA glutamate receptors. | |
177 Citations | Cortical cell loss in temporal lobe epilepsy is linked to hippocampal sclerosis, neuronal loss, axonal sprouting, neurogenesis, and changes in receptor/channel functioning, exacerbated by vascular and astrocytic disruptions. |
| Pathologies associated with cortical cell loss in temporal lobe epilepsy include mesial temporal lobe epilepsy with hippocampal sclerosis (mTLE-HS) and malformation of cortical development (MCD), such as focal cortical dysplasia (FCD). | |
35 Citations | Cortical cell loss in temporal lobe epilepsy involves neuronal loss in the medial entorhinal area (MEA) and increased astrocyte and microglia activity, which can be mitigated by D-serine treatment. |
21 Citations | Dendritic reshaping, severe spine loss, and synaptic reorganization are associated with cortical cell loss in temporal lobe epilepsy, particularly in type II focal cortical dysplasia lesions. |
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