Two to three fMRI runs were repeated in each session for every patient. Each video was 8 min and 30 s and the relative fMRI scan time was 510 s. A, Each fMRI run was organized in 30 s of baseline during which the patient was instructed to watch a white cross on a black screen followed by one funny video. Representation of the polygraphic fMRI protocol.
The comparison of cataplexy versus laugh episodes revealed the involvement of a corticolimbic network that processes reward and emotion encompassing the anterior insular cortex, the nucleus accumbens, and the amygdala.Ĭataplexy emotion fMRI humor narcolepsy sleep disorders.Ĭopyright © 2015 the authors 0270-64584-12$15.00/0. During cataplexy, suprapontine BOLD signal increase was present in the amygdala, frontal operculum-anterior insular cortex, ventromedial prefrontal cortex, and the nucleus accumbens BOLD signal increases were also observed at locus ceruleus and in anteromedial pons.
During laughter (without cataplexy) an increased hemodynamic response occurred in a bilateral network involving the motor/premotor cortex and anterior cingulate gyrus. Cataplexy was marked by brief losses of mylohyoid muscle tone and by the observation of episodes of facial hypotonia, jaw drop, and ptosis. Emotion-induced laughter occurred in 16 patients, and of these 10 showed cataplexy for a total of 77 events (mean duration = 4.4 s). These findings confirm recent data obtained in the hypocretin knock-out mice and suggest that the absence of hypothalamic hypocretin control on mesolimbic reward centers is crucial in determining cataplexy induced by emotions. In narcolepsy caused by hypocretin/orexin deficiency, cataplexy is associated with a marked increase in neural activity in the amygdala, the nucleus accumbens, and the ventromedial prefrontal cortex, which represent suprapontine centers that physiologically process emotions and reward. To reach this goal drug-naive children and adolescents with recent onset narcolepsy type 1 were investigated. In this study we reported for the first time in humans the brain structures whose neural activity is specifically and consistently associated with emotion-induced cataplexy. Correlations analyses between these contrasts and disease-related variables and behavioral findings were performed. Whole-brain hemodynamic correlates of (1) a sign of fun and amusement (laughter) and of (2) cataplexy were analyzed and compared. fMRI data were acquired synchronously with EEG, mylohyoid muscle activity, and the video of the patient's face. Twenty-one drug-naive children/adolescent (13 males, mean age 11 years) with recent onset of narcolepsy type 1 (NT1) were studied with fMRI while viewing funny videos using a "naturalistic" paradigm. Animal data suggest that the amygdala and the ventromedial prefrontal cortex are key regions in promoting emotion-induced cataplectic attacks. 6 Department of Biomedical and Neuromotor Sciences, University of Bologna, 40123 Bologna, Italy, IRCCS Istituto delle Scienze Neurologiche, AUSL di Bologna, 40123 Bologna, Italy, and brain suprapontine mechanisms associated with human cataplexy have not been clarified.6 Department of Biomedical and Neuromotor Sciences, University of Bologna, 40123 Bologna, Italy, IRCCS Istituto delle Scienze Neurologiche, AUSL di Bologna, 40123 Bologna, Italy, and PMC article.5 Department of Clinical and Experimental Medicine, University of Parma, 43121 Parma, Italy.
4 Department of Biomedical, Metabolic, and Neural Sciences, University of Modena and Reggio Emilia, 41100 Modena, Italy.3 Department of Biomedical and Neuromotor Sciences, University of Bologna, 40123 Bologna, Italy, IRCCS Istituto delle Scienze Neurologiche, AUSL di Bologna, 40123 Bologna, Italy, and.Hospital, AUSL 41100 Modena, Italy, 2 Department of Biomedical, Metabolic, and Neural Sciences, University of Modena and Reggio Emilia, 41100 Modena, Italy, N.O.C.S.A.E. 1 Department of Biomedical, Metabolic, and Neural Sciences, University of Modena and Reggio Emilia, 41100 Modena, Italy, N.O.C.S.A.E.