Altered resting-state hippocampal and caudate functional networks in patients with obstructive sleep apnea.
Altered resting-state hippocampal and caudate functional networks in patients with obstructive sleep apnea.
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DOI：
10.1002/brb3.994
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发表时间：
2018-06
影响因子：
3.1
通讯作者：
Kumar R
中科院分区：
文献类型：
--
作者：
Song X;Roy B;Kang DW;Aysola RS;Macey PM;Woo MA;Yan-Go FL;Harper RM;Kumar R
海马体和尾状核的脑结构损伤和代谢缺陷可能会导致阻塞性睡眠呼吸暂停 (OSA) 患者的认知和情绪缺陷。如果存在这种贡献，那么这些皮层下位点与介导情感症状和认知的皮层区域的静息态相互作用应该会受到干扰。我们的目的是检查相对于对照受试者的 OSA 中海马和尾状核与其他大脑区域的静息态功能连接 (FC)，并将这些变化与情绪和神经心理学评分联系起来。我们使用 3.0-Tesla 磁共振成像扫描仪从 70 名 OSA 和 89 名健康对照者那里获取了静息态功能磁共振成像 (fMRI) 数据，并评估了心理和行为功能以及睡眠问题。经过标准功能磁共振成像数据预处理后，生成双侧海马和尾状核的 FC 图，并进行组间比较（ANCOVA；协变量、年龄和性别）。与健康对照组相比，阻塞性睡眠呼吸暂停受试者表现出明显更高水平的焦虑和抑郁症状。在 OSA 受试者中，海马与丘脑、海马旁回、内侧和颞上回、岛叶和后扣带皮层的 FC 受到破坏。左右尾状核显示双侧额下回和右角回功能受损。此外，OSA 中边缘-纹状体-皮质 FC 的改变显示出与行为和神经心理学变量的关系。 OSA 中海马皮质 FC 受损可能是 OSA 抑郁和焦虑情绪水平的基础，而尾状皮质 FC 受损可能表明奖励处理和认知方面存在缺陷。这些发现为了解 OSA 情绪和认知缺陷共病的神经机制提供了见解。
Brain structural injury and metabolic deficits in the hippocampus and caudate nuclei may contribute to cognitive and emotional deficits found in obstructive sleep apnea (OSA) patients. If such contributions exist, resting‐state interactions of these subcortical sites with cortical areas mediating affective symptoms and cognition should be disturbed. Our aim was to examine resting‐state functional connectivity (FC) of the hippocampus and caudate to other brain areas in OSA relative to control subjects, and to relate these changes to mood and neuropsychological scores. We acquired resting‐state functional magnetic resonance imaging (fMRI) data from 70 OSA and 89 healthy controls using a 3.0‐Tesla magnetic resonance imaging scanner, and assessed psychological and behavioral functions, as well as sleep issues. After standard fMRI data preprocessing, FC maps were generated for bilateral hippocampi and caudate nuclei, and compared between groups (ANCOVA; covariates, age and gender). Obstructive sleep apnea subjects showed significantly higher levels of anxiety and depressive symptoms over healthy controls. In OSA subjects, the hippocampus showed disrupted FC with the thalamus, para‐hippocampal gyrus, medial and superior temporal gyrus, insula, and posterior cingulate cortex. Left and right caudate nuclei showed impaired FC with the bilateral inferior frontal gyrus and right angular gyrus. In addition, altered limbic‐striatal‐cortical FC in OSA showed relationships with behavioral and neuropsychological variables. The compromised hippocampal‐cortical FC in OSA may underlie depression and anxious mood levels in OSA, while impaired caudate‐cortical FC may indicate deficits in reward processing and cognition. These findings provide insights into the neural mechanisms underlying the comorbidity of mood and cognitive deficits in OSA.
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