Department of Anatomy and Neurosciences, Amsterdam UMC (Location VUmc), Amsterdam, the Netherlands; Sleep-Wake Centre, Stichting Epilepsie Instellingen Nederland (SEIN), Heemstede, the Netherlands; Department of Neurology, Leiden University Medical Center, Leiden, the Netherlands.
Sleep-Wake Centre, Stichting Epilepsie Instellingen Nederland (SEIN), Heemstede, the Netherlands; Department of Neurology, Leiden University Medical Center, Leiden, the Netherlands.
Neuroimage Clin. 2019;24:101963. doi: 10.1016/j.nicl.2019.101963. Epub 2019 Jul 29.
Narcolepsy type 1 is caused by a selective loss of hypothalamic hypocretin-producing neurons, resulting in severely disturbed sleep-wake control and cataplexy. Hypocretin-producing neurons project widely throughout the brain, influencing different neural networks. We assessed the extent of microstructural white matter organization and brain-wide structural connectivity abnormalities in a homogeneous group of twelve drug-free patients with narcolepsy type 1 and eleven matched healthy controls using diffusion tensor imaging with multimodal analysis techniques. First, tract-based spatial statistics (TBSS) was carried out using fractional anisotropy (FA) and mean, axial and radial diffusivity (MD, AD, RD). Second, quantitative analyses of mean FA, MD, AD and RD were conducted in predefined regions-of-interest, including sleep-wake regulation-related, limbic and reward system areas. Third, we performed hypothalamus-seeded tractography towards the thalamus, amygdala and midbrain. TBSS analyses yielded brain-wide significantly lower FA and higher RD in patients. Localized significantly lower FA and higher RD in the left ventral diencephalon and lower AD in the midbrain, were seen in patients. Lower FA was also found in patients in left hypothalamic fibers connecting with the midbrain. No significant MD and AD differences nor a correlation with disease duration were found. The brain-wide, localized ventral diencephalon (comprising the hypothalamus and different sleep- and motor-related nuclei) and hypothalamic connectivity differences clearly show a heretofore underestimated direct and/or indirect effect of hypocretin deficiency on microstructural white matter composition, presumably resulting from a combination of lower axonal density, lower myelination and/or greater axon diameter.
发作性睡病 1 型是由于下丘脑产生食欲素的神经元选择性丧失引起的,导致严重的睡眠-觉醒控制障碍和猝倒。产生食欲素的神经元广泛投射到大脑中,影响不同的神经网络。我们使用弥散张量成像和多模态分析技术,评估了 12 名未经药物治疗的发作性睡病 1 型患者和 11 名匹配的健康对照者的脑白质微观结构组织和全脑结构连接异常的程度。首先,我们使用各向异性分数(FA)和平均、轴向和径向扩散系数(MD、AD、RD)进行基于束的空间统计学(TBSS)分析。其次,在包括睡眠-觉醒调节、边缘系统和奖励系统在内的睡眠-觉醒调节相关区域,进行平均 FA、MD、AD 和 RD 的定量分析。第三,我们进行了下丘脑到丘脑、杏仁核和中脑的种子追踪。TBSS 分析显示,患者大脑广泛存在 FA 值降低和 RD 值升高。患者左侧腹侧间脑的 FA 值和 RD 值降低,AD 值降低,且左侧下丘脑与中脑相连的纤维 FA 值降低。MD 和 AD 差异无统计学意义,且与疾病持续时间无关。脑白质广泛、局部的腹侧间脑(包括下丘脑和不同的睡眠和运动相关核)和下丘脑连接差异清楚地显示了食欲素缺乏对微观结构白质组成的直接和/或间接影响,这可能是由于轴突密度降低、髓鞘形成减少和/或轴突直径增加的综合作用。