====== Hippocampal seizure ======

The association between [[epilepsy]] and the [[hippocampus]] is well known and important. [[Mesial temporal lobe epilepsy]] with [[hippocampal sclerosis]] is a syndromic diagnostic entity and indeed a quite common one. There are different theories on the pathophysiological pathways, as the [[hippocampus]] is often involved in seizures, even if they are not generated there. Whether hippocampal sclerosis is a cause or the effect of seizures is a subject of ongoing debate, but the predominant opinion is that [[seizure]]s probably do not cause relevant hippocampal volume loss in the mature brain. A diagnosis of epilepsy with [[hippocampal sclerosis]] is made based on typical semiological signs and symptoms, interictal and ictal EEG findings, cerebral imaging, and neuropsychological testing. Antiepileptic medication is indicated as a first-line treatment. Should the epilepsy prove to be medically intractable, which is commonly the case in these patients, an early evaluation regarding [[epilepsy surgery]] must be performed. Different epilepsy surgery techniques are available, from minimal ones like the selective amygdalohippocampectomy to more extensive ones like additional temporal lobe resection. Postoperative results concerning seizures and neuropsychological outcomes are very encouraging and depend on various predictive factors. Alternative procedures like stereotactic radiofrequency amygdalohippocampectomy and hippocampal stimulation are currently being assessed, partly with very promising results
((Chatzikonstantinou A. Epilepsy and the hippocampus. Front Neurol Neurosci. 2014;34:121-42. doi: 10.1159/000356435. Epub 2014 Apr 16. PMID: 24777136.)).
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Repeated [[seizure]] activity can lead to long-term changes in seizure dynamics and [[behavior]]. However, resulting changes in brain-wide dynamics remain poorly understood. This is due partly to technical challenges in precise seizure control and in vivo whole-brain [[mapping]] of circuit dynamics. 

Choy et al. developed an optogenetic kindling model through repeated [[stimulation]] of ventral hippocampal [[CaMKII]] [[neuron]]s in [[adult]] [[rat]]s. They then combined [[fMRI]] with [[electrophysiology]] to track brain-wide circuit dynamics resulting from non-afterdischarge (AD)-generating stimulations and individual convulsive [[seizure]]s. [[Kindling]] induced widespread increases in non-AD-generating stimulation response and ipsilateral [[functional connectivity]] and elevated [[anxiety]]. Individual seizures in kindled animals showed more significant increases in brain-wide activity and bilateral functional [[connectivity]]. Onset time quantification provided evidence for kindled [[seizure propagation]] from the ipsilateral to the contralateral [[hemisphere]]. Furthermore, a core of slow-migrating hippocampal activity was identified in both non-kindled and kindled seizures, revealing a novel mechanism of seizure sustainment and propagation
((Choy M, Dadgar-Kiani E, Cron GO, Duffy BA, Schmid F, Edelman BJ, Asaad M, Chan RW, Vahdat S, Lee JH. Repeated [[hippocampal seizure]]s lead to brain-wide reorganization of circuits and [[seizure]] propagation pathways. Neuron. 2021 Oct 23:S0896-6273(21)00778-9. doi: 10.1016/j.neuron.2021.10.010. Epub ahead of print. PMID: 34706219.)).