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Abnormal activity in hypothalamus and amygdala during humour processing in human narcolepsy with cataplexy


Schwartz, S; Ponz, A; Poryazova, R; Werth, E; Boesiger, P; Khatami, R; Bassetti, C L (2008). Abnormal activity in hypothalamus and amygdala during humour processing in human narcolepsy with cataplexy. Brain: A Journal of Neurology, 131(2):514-522.

Abstract

Narcolepsy with cataplexy (NC) is a complex sleep-wake disorder, which was recently found to be associated with a reduction or loss of hypocretin (HCRT, also called orexin). HCRT is a hypothalamic peptide implicated in the regulation of sleep/wake, motor and feeding functions. Cataplexy refers to episodes of sudden and transient loss of muscle tone triggered by strong, mostly positive emotions, such as hearing or telling jokes. Cataplexy is thought to reflect the recruitment of ponto-medullary mechanisms that normally underlie muscle atonia during REM-sleep. In contrast, the suprapontine brain mechanisms associated with the cataplectic effects of emotions in human narcolepsy with cataplexy remain essentially unknown. Here, we used event-related functional MRI to assess brain activity in 12 NC patients and 12 controls while they watched sequences of humourous pictures. Patients and controls were similar in humour appreciation and activated regions known to contribute to humour processing, including limbic and striatal regions. A direct statistical comparison between patients and controls revealed that humourous pictures elicited reduced hypothalamic response together with enhanced amygdala response in the patients. These results suggest (i) that hypothalamic HCRT activity physiologically modulates the processing of emotional inputs within the amygdala, and (ii) that suprapontine mechanisms of cataplexy involve a dysfunction of hypothalamic-amygdala interactions triggered by positive emotions.

Narcolepsy with cataplexy (NC) is a complex sleep-wake disorder, which was recently found to be associated with a reduction or loss of hypocretin (HCRT, also called orexin). HCRT is a hypothalamic peptide implicated in the regulation of sleep/wake, motor and feeding functions. Cataplexy refers to episodes of sudden and transient loss of muscle tone triggered by strong, mostly positive emotions, such as hearing or telling jokes. Cataplexy is thought to reflect the recruitment of ponto-medullary mechanisms that normally underlie muscle atonia during REM-sleep. In contrast, the suprapontine brain mechanisms associated with the cataplectic effects of emotions in human narcolepsy with cataplexy remain essentially unknown. Here, we used event-related functional MRI to assess brain activity in 12 NC patients and 12 controls while they watched sequences of humourous pictures. Patients and controls were similar in humour appreciation and activated regions known to contribute to humour processing, including limbic and striatal regions. A direct statistical comparison between patients and controls revealed that humourous pictures elicited reduced hypothalamic response together with enhanced amygdala response in the patients. These results suggest (i) that hypothalamic HCRT activity physiologically modulates the processing of emotional inputs within the amygdala, and (ii) that suprapontine mechanisms of cataplexy involve a dysfunction of hypothalamic-amygdala interactions triggered by positive emotions.

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Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > Institute of Biomedical Engineering
04 Faculty of Medicine > University Hospital Zurich > Clinic for Neurology
Dewey Decimal Classification:170 Ethics
610 Medicine & health
Language:English
Date:February 2008
Deposited On:28 Nov 2008 15:42
Last Modified:05 Apr 2016 12:36
Publisher:Oxford University Press
ISSN:0006-8950
Additional Information:The definitive publisher-authenticated version is available online - official URLs : http://brain.oxfordjournals.org/cgi/content/full/131/2/514
Publisher DOI:10.1093/brain/awm292
Official URL:http://brain.oxfordjournals.org/cgi/content/full/131/2/514
PubMed ID:18094020
Permanent URL: http://doi.org/10.5167/uzh-6224

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