View source for Amygdala sclerosis in sudden and unexpected death in epilepsy

{{Reference

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Thom M, Griffin B, Sander JW, and Scaravilli F (1999) Amygdala sclerosis in sudden and unexpected death in epilepsy. Epilepsy Res 37:1 53–62.

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https://ac.els-cdn.com/S0920121199000315/1-s2.0-S0920121199000315-main.pdf?_tid=c65e118c-ced0-11e7-a592-00000aacb362&acdnat=1511278353_908ce71eabc6a76cd1cbff35eb52f3d0

|abstract=

Sclerosis of the amygdala is a not uncommon finding in patients with chronic epilepsy. The amygdala has efferent connections, via the central nuclei, to cardioregulatory centres in the medulla. Experimental studies have suggested that damage to the central nucleus may be of functional significance in patients with sudden and unexpected death in epilepsy (SUDEP) in particular with regard to their susceptibility to cardiac arrhythmias. We investigated this possibility by carrying out a quantitative immunohistochemical analysis of the patterns of neuronal loss and gliosis in three amygdala subnuclei (central, basal and lateral) in post mortem material from 15 SUDEP cases and seven normal controls. We identified significant neuronal loss in the medial division of the lateral amygdaloid nucleus in SUDEP cases but not in central or basal nuclei. These patterns of cell loss in the amygdala do not differ from previous studies in both humans and animal models of chronic epilepsy suggesting that there is not a specific pattern of amygdaloid sclerosis in SUDEP patients which could implicate a functional role for this nucleus in the mechanism of the sudden death.

|keywords=

Amygdala; Epilepsy; Sudden death

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*In light of the influence of the central nucleus of the amygdala on autonomic control ([[Cardiac and respiratory correlations with unit discharge in human amygdala and hippocampus|Frysinger and Harper, 1989]]), the possibility of damage to the amygdala as a precursor to SUDEP was investigated by study of postmortem tissue specimens. Neuronal loss was significant in the lateral nucleus but not the central or basal nuclei. This pattern was reported in previous studies of chronic epilepsy and is not specific to SUDEP.  More extensive discussion of potential involvement of the amygdala in SUDEP is in the Context section at [[Respiratory modulation of neuronal discharge in the central nucleus of the amygdala during sleep and waking states|Zhang et al., 1986]].

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