title: Amygdala sclerosis in sudden and unexpected death in epilepsy.
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.
authors.affiliation: Department of Neuropathology, National Hospital for Neurology and Neurosurgery, London, UK. mthom@ion.ucl.ac.uk
authors.forename: M
authors.initials: M
authors.lastname: Thom
authors.forename: B
authors.initials: B
authors.lastname: Griffin
authors.forename: J W
authors.initials: JW
authors.lastname: Sander
authors.forename: F
authors.initials: F
authors.lastname: Scaravilli
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000679:Amygdala / Q000473:pathology*; D003645:Death, Sudden / Q000473:pathology*; D004827:Epilepsy / Q000401:mortality / Q000473:pathology*; D005260:Female; D005911:Gliosis / Q000473:pathology; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D009474:Neurons / Q000473:pathology; D012598:Sclerosis; D013684:Telangiectasis / Q000473:pathology