Temporal lobe epilepsy etiology [Neurosurgery Wiki]

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====== Temporal lobe epilepsy etiology ======

Despite recent advances in our understanding of synaptic transmission associated with [[epileptogenesis]], the molecular mechanisms that control seizure frequency in patients with [[temporal lobe epilepsy]] (TLE) remain obscure. 

The most common cause of [[temporal lobe epilepsy]] is [[mesial temporal sclerosis]]. 

The expression of some proteins involved in the packaging of vesicular [[neurotransmitter]]s is altered in TLE. In addition, upregulated expression of [[annexin]] family proteins, which are also related to TLE, might play an important role in protection against TLE
((Zhang Y, Liu Y, Jia Y, et al. Proteomic profiling of sclerotic hippocampus revealed dysregulated packaging of vesicular neurotransmitters in temporal lobe epilepsy [published online ahead of print, 2020 Jul 1]. Epilepsy Res. 2020;166:106412. doi:10.1016/j.eplepsyres.2020.106412)).

Data demonstrate that [[mTOR]] signaling is significantly dysregulated in human TLE, offering new targets for pharmacologic interventions. Specifically, clinically available drugs that suppress mTORC1 without compromising mTOR2 signaling, such as rapamycin and its analogs, may represent a new group of antiepileptogenic agents in TLE patients
((Talos DM, Jacobs LM, Gourmaud S, Coto CA, Sun H, Lim KC, Lucas TH, Davis KA,
Martinez-Lage M, Jensen FE. Mechanistic target of rapamycin complex 1 and 2 in
human temporal lobe epilepsy. Ann Neurol. 2018 Jan 13. doi: 10.1002/ana.25149.
[Epub ahead of print] PubMed PMID: 29331082.
)).

Water [[homeostasis]] has been shown crucial for regulation of [[neuron]]al excitability. The control of water movement is achieved through a family of small integral membrane channel proteins called [[aquaporin]]s (AQPs). Despite the fact that changes in water homeostasis occur in sclerotic hippocampi of people with [[temporal lobe epilepsy]] (TLE) , the expression of AQPs in the epileptic brain is not fully characterised
((Salman MM, Sheilabi MA, Bhattacharyya D, Kitchen P, Conner AC, Bill RM,
Woodroofe MN, Conner MT, Princivalle AP. Transcriptome analysis suggests a role
for the differential expression of cerebral aquaporins and the MAPK signalling
pathway in human temporal lobe epilepsy. Eur J Neurosci. 2017 Jul 17. doi:
10.1111/ejn.13652. [Epub ahead of print] PubMed PMID: 28715131.
)).

Soluble human [[epoxide hydrolase 2]] is increased in both lateral and medial temporal tissues in temporal lobe epilepsy. Further studies should be conducted as inhibition of this enzyme has resulted in a significant decrease in or stopping of seizures and attenuated neuro-inflammation in experimental epilepsy models in the current literature
((Ahmedov ML, Kemerdere R, Baran O, Inal BB, Gumus A, Coskun C, Yeni SN, Eren B,
Uzan M, Tanriverdi T. Tissue Expressions of Soluble Human Epoxide Hydrolase-2
Enzyme in Patients with Temporal Lobe Epilepsy. World Neurosurg. 2017 Jun 29.
pii: S1878-8750(17)31032-X. doi: 10.1016/j.wneu.2017.06.137. [Epub ahead of
print] PubMed PMID: 28669871.
)).

===== Cavernous malformation related temporal lobe epilepsy =====

[[Cavernous malformation related temporal lobe epilepsy]] (CRTLE)