Vaudano Anna Elisabetta, Pizza Fabio, Talami Francesca, Plazzi Giuseppe, Meletti Stefano
From the Department of Medicine and Surgery (A.E.V.), Sleep Medicine Center, University of Parma; Department of Biomedical, Metabolic, and Neural Science (A.E.V., S.M.) and Center for Neuroscience and Neurotechnology (A.E.V., S.M.), University of Modena and Reggio Emilia; Department of Biomedical and Neuromotor Sciences (F.P., G.P.), University of Bologna; IRCCS Istituto Delle Scienze Neurologiche di Bologna (F.P., G.P.); and Neurology Unit (F.T., S.M.), OCSAE Azienda Ospedaliero-Universitaria, Modena, Italy.
Neurology. 2019 Jan 28;92(5):e504-e515. doi: 10.1212/WNL.0000000000006853.
To investigate the neuronal correlates of spontaneous laughter in drug-naive pediatric patients with narcolepsy type I (NT1) compared to healthy controls by means of blood oxygen level-dependent (BOLD) MRI.
Twenty-one children/adolescents with recent onset of NT1 and 21 age- and sex-matched healthy controls were studied with fMRI while viewing funny videos using a naturalistic paradigm. Whole-brain hemodynamic correlates of spontaneous laughter were investigated in each group and compared by use of appropriate second-level general linear model analyses. If recorded, cataplexy events were treated as the effect of no interest at the single-participant level. Correlations analyses between these contrasts and behavioral findings were performed.
Emotion-induced laughter occurred in 16 patients (294 events) and 21 controls (357 events). In controls, laughter-related BOLD increases involved a widespread cortical and subcortical network including the bilateral motor and premotor areas, cingulated cortex, insula, and amygdala. In NT1, laughter induced BOLD signal increments in the motor cortex, right thalamus, and left subthalamic nucleus/zona incerta (STN/ZI). STN/ZI and thalamic changes were significantly higher during fMRI sessions with laughter without cataplexy compared to sessions in which laughter was associated with cataplexy.
Laughter expression in individuals with NT1 involves different brain circuits compared to controls by means of overactivation of cortical and subcortical regions belonging to the volitional control of laughter. The activation of the STN/ZI region observed predominantly in patients with NT1 during laugh episodes without cataplexy suggests that the ZI could act to prevent cataplexy.
通过血氧水平依赖（BOLD）磁共振成像，研究未经药物治疗的发作性睡病1型（NT1）儿童患者与健康对照者自发笑的神经关联。
对21名近期发病的NT1儿童/青少年以及21名年龄和性别匹配的健康对照者进行功能磁共振成像（fMRI）研究，他们使用自然主义范式观看有趣视频。在每组中研究自发笑的全脑血流动力学关联，并通过适当的二级一般线性模型分析进行比较。如果记录到猝倒事件，则在单参与者水平上将其视为无关效应。对这些对比与行为结果进行相关性分析。
16名患者（294次事件）和21名对照者（357次事件）出现了情绪诱发的笑。在对照者中，与笑相关的BOLD增加涉及广泛的皮质和皮质下网络，包括双侧运动和运动前区、扣带回皮质、岛叶和杏仁核。在NT1患者中，笑诱发了运动皮质、右侧丘脑和左侧底丘脑核/未定带（STN/ZI）的BOLD信号增加。与笑伴有猝倒的时段相比，在无猝倒的笑的fMRI时段中，STN/ZI和丘脑的变化显著更高。
与对照者相比，NT1患者的笑表达涉及不同的脑回路，这是通过属于笑的意志控制的皮质和皮质下区域的过度激活实现的。在无猝倒的笑发作期间，主要在NT1患者中观察到的STN/ZI区域的激活表明，未定带可能起到预防猝倒的作用。
