Neuronal loss In<unk> , there is loss of neurons in region CA1 and CA3 of the hippocampus. There is also damage to mossy cells and inhibitory interneurons in the hilar region of the hippocampus (region IV) and to the granule cells of the dentate gyrus. In animal models, neuronal loss occurs during seizures but in humans, neuronal loss predates the first seizure and does not necessarily continue with seizure activity. The loss of the GABA-mediated inhibitory interneurons may increase the hyperexcitability of neurons of the hippocampus leading to recurrent seizures. According to the "dormant basket cell" hypothesis, mossy cells normally excite basket cells which in turn, inhibit granule cells. Loss of mossy cells lowers the threshold of action potentials of the granule cells. GABA reversal In certain patients with<unk>  it has been found that the subiculum could generate epileptic activity. It has been found that GABA reversal potential is depolarising in the subpopulation of the pyramidal cells due to the lack of KCC2 co-transporter. It has been shown that it is theoretically possible to generate seizures in the neural networks due to down-regulation of KCC2, consistent with the chloride measurements during the transition to seizure and KCC2 blockade experiments. Granule cell dispersion in the dentate gyrus Granule cell dispersion is a type of developmental migration and a pathological change found in the<unk>  brain which was first described in 1990. The granule cells of the dentate gyrus are tightly packed forming a uniform, laminated layer with no monosynaptic connections. This structure provides a filter for the excitability of neurons. In<unk> , granule cells are lost, the structure is no longer closely packed and there are changes in the orientation of dendrites. These changes may or may not be epileptogenic. For instance, if the dendrites of granule cells reconnect, it may be in a way (through the laminar planes) that allows hyperexcitability. However, not all patients have granule cell dispersion. Aberrant mossy fiber sprouting Mossy fibers are the axons of granule cells. They project into the hilus of the dentate gyrus and stratum lucidum in the CA3 region giving inputs to both excitatory and inhibitory neurons. In the<unk>  brain, where granule cells are damaged or lost, axons, the mossy fibres, 'sprout' in order to reconnect to other granule cell dendrites. This is an example of synaptic reorganization. This was noted in human tissue in 1974 and in animal models in 1985. In<unk> , the sprouting mossy fibres are larger than in the normal brain and their connections may be aberrant. Mossy fibre sprouting continues from one week to two months after injury. Aberrant mossy fibre sprouting may create excitatory feedback circuits that lead to<unk> <unk>  seizures. This is evident in intracellular recordings. Stimulation of aberrant mossy fibre areas increases the excitatory postsynaptic potential response. However, aberrant mossy fiber sprouting may inhibit excitatory transmission by synapsing with basket cells which are inhibitory neurons and by releasing GABA and neuropeptide Y which are inhibitory neurotransmitters. Also, in animal models, granule cell hyper-excitability is recorded before aberrant mossy fibre sprouting has occurred.
Temporal lobe epilepsy
Frontal lobe epilepsy
Generalized epilepsy
Musicogenic epilepsy
Childhood absence epilepsy
Photosensitive epilepsy
Catamenial epilepsy
Northern epilepsy syndrome