Zhou Fuqing, Huang Suhua, Zhuang Ying, Gao Lei, Gong Honghan
Department of Radiology, The First Affiliated Hospital, Nanchang University, Nanchang 330006, China; Jiangxi Province Medical Imaging Research Institute, Nanchang, 330006, China.
Department of Radiology, Jiangxi Province Children's Hospital, Nanchang 330006, China.
Neuroimage Clin. 2016 May 26;15:458-465. doi: 10.1016/j.nicl.2016.05.011. eCollection 2017.
New neuroimaging techniques have led to significant advancements in our understanding of cerebral mechanisms of primary insomnia. However, the neuronal low-frequency oscillation remains largely uncharacterized in chronic primary insomnia (CPI). In this study, the amplitude of low-frequency fluctuation (ALFF), a data-driven method based on resting-state functional MRI, was used to examine local intrinsic activity in 27 patients with CPI and 27 age-, sex-, and education-matched healthy controls. We examined neural activity in two frequency bands, slow-4 (between 0.027 and 0.073 Hz) and slow-5 (0.010-0.027 Hz), because blood-oxygen level dependent (BOLD) fluctuations in different low-frequency bands may present different neurophysiological manifestations that pertain to a spatiotemporal organization. The ALFF associated with the primary disease effect was widely distributed in the cerebellum posterior lobe (CPL), dorsal and ventral prefrontal cortex, anterior cingulate cortex, precuneus, somatosensory cortex, and several default-mode sub-regions. Several brain regions (i.e., the right cerebellum, anterior lobe, and left putamen) exhibited an interaction between the frequency band and patient group. In the slow-5 band, increased ALFF of the right postcentral gyrus/inferior parietal lobule (PoCG/IPL) was enhanced in association with the sleep quality (ρ = 0.414, = 0.044) and anxiety index (ρ = 0.406, = 0.049) of the CPI patients. These findings suggest that during chronic insomnia, the intrinsic functional plasticity primarily responds to the hyperarousal state, which is the loss of inhibition in sensory-informational processing. Our findings regarding an abnormal sensory input and intrinsic processing mechanism might provide novel insight into the pathophysiology of CPI. Furthermore, the frequency factor should be taken into consideration when exploring ALFF-related clinical manifestations.
新的神经成像技术使我们对原发性失眠的大脑机制有了重大进展。然而，慢性原发性失眠（CPI）中的神经元低频振荡在很大程度上仍未得到充分描述。在本研究中，基于静息态功能磁共振成像的数据驱动方法低频振幅（ALFF），用于检测27例CPI患者和27例年龄、性别和教育程度匹配的健康对照者的局部内在活动。我们检测了两个频段的神经活动，慢4（0.027至0.073赫兹）和慢5（0.010 - 0.027赫兹），因为不同低频段的血氧水平依赖（BOLD）波动可能呈现与时空组织相关的不同神经生理表现。与原发性疾病效应相关的ALFF广泛分布于小脑后叶（CPL）、背侧和腹侧前额叶皮质、前扣带回皮质、楔前叶、体感皮质以及几个默认模式子区域。几个脑区（即右侧小脑、前叶和左侧壳核）表现出频段与患者组之间的相互作用。在慢5频段，右侧中央后回/顶下小叶（PoCG/IPL）的ALFF增加与CPI患者的睡眠质量（ρ = 0.414， = 0.044）和焦虑指数（ρ = 0.406， = 0.049）相关。这些发现表明，在慢性失眠期间，内在功能可塑性主要对过度唤醒状态作出反应，这是感觉信息处理中抑制作用的丧失。我们关于异常感觉输入和内在处理机制的发现可能为CPI的病理生理学提供新的见解。此外，在探索与ALFF相关的临床表现时应考虑频率因素。
