Evidence in chronic fatigue syndrome for severity-dependent upregulation of prefrontal myelination that is independent of anxiety and depression
Evidence in chronic fatigue syndrome for severity-dependent upregulation of prefrontal myelination that is independent of anxiety and depression
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DOI：
10.1002/nbm.3261
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发表时间：
2015-03-01
影响因子：
2.9
通讯作者：
Del Fante, Peter
中科院分区：
文献类型：
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作者：
Barnden, Leighton R.;Crouch, Benjamin;Del Fante, Peter
对25例慢性疲劳综合征（CFS）患者和25例正常对照（NC）进行了基于体素的脑MRI回归分析，以CFS严重程度评分和CFS持续时间为依据，评估慢性疲劳综合征（CFS）中白色物质（WM）的受累情况。除了基于体素的形态测量，还对T-1和T-2加权自旋回波（T1 w和T2 w）MRI信号水平进行了一种新的基于体素的定量分析。严重程度评分包括Bell CFS残疾量表和基于10种最常见CFS症状的评分。医院焦虑和抑郁量表（HADS）抑郁和焦虑评分作为滋扰协变量。通过放宽集群形成的阈值，我们发现，T1 w信号升高，随着CFS的严重程度在腹外侧丘脑，内囊和前额叶WM。早期报道的中脑WM体积损失和神经炎症，以及这里提出的上调的前额叶髓鞘形成，与中脑的变化是一致的，与受损的神经传导，刺激在相同的电路中的丘脑中继皮质侧的塑性反应。T2 w信号与CFS持续时间以及CFS组与NC组T2 w信号的比较显示了右中颞叶WM的变化，其中受损的通信可以影响认知功能。调整抑郁症显着加强集群统计和增加集群大小在两个T1 w严重程度回归，但调整焦虑少。因此，抑郁和焦虑在这里是统计混杂因素，这意味着它们对前额叶WM的T1 w信号有方差贡献，但这与CFS严重程度的共定位方差无关。抑郁症本身的MRI回归仅检测到与WM体积的关联，也位于前额叶WM。我们认为，受损的相互脑-体和脑-脑通信通过中脑引起外周和中枢反应，有助于CFS症状。虽然焦虑、抑郁和CFS可能具有共同的生物学特征，但目前的证据表明CFS是一种独特的疾病。(c)2015作者NMR in Biomedicine，John Wiley & Sons，Ltd.
White matter (WM) involvement in chronic fatigue syndrome (CFS) was assessed using voxel-based regressions of brain MRI against CFS severity scores and CFS duration in 25 subjects with CFS and 25 normal controls (NCs). As well as voxel-based morphometry, a novel voxel-based quantitative analysis of T-1- and T-2-weighted spin-echo (T1w and T2w) MRI signal level was performed. Severity scores included the Bell CFS disability scale and scores based on the 10 most common CFS symptoms. Hospital Anxiety and Depression Scale (HADS) depression and anxiety scores were included as nuisance covariates. By relaxing the threshold for cluster formation, we showed that the T1w signal is elevated with increasing CFS severity in the ventrolateral thalamus, internal capsule and prefrontal WM. Earlier reports of WM volume losses and neuroinflammation in the midbrain, together with the upregulated prefrontal myelination suggested here, are consistent with the midbrain changes being associated with impaired nerve conduction which stimulates a plastic response on the cortical side of the thalamic relay in the same circuits. The T2w signal versus CFS duration and comparison of T2w signal in the CFS group with the NC group revealed changes in the right middle temporal lobe WM, where impaired communication can affect cognitive function. Adjustment for depression markedly strengthened cluster statistics and increased cluster size in both T1w severity regressions, but adjustment for anxiety less so. Thus, depression and anxiety are statistical confounders here, meaning that they contribute variance to the T1w signal in prefrontal WM but this does not correlate with the co-located variance from CFS severity. MRI regressions with depression itself only detected associations with WM volume, also located in prefrontal WM. We propose that impaired reciprocal brain-body and brain-brain communication through the midbrain provokes peripheral and central responses which contribute to CFS symptoms. Although anxiety, depression and CFS may share biological features, the present evidence indicates that CFS is a distinct disorder. (c) 2015 The Authors. NMR in Biomedicine published by John Wiley & Sons, Ltd.