Hyperintense sensorimotor T1 spin echo MRI is associated with brainstem abnormality in chronic fatigue syndrome.

Hyperintense sensorimotor T1 spin echo MRI is associated with brainstem abnormality in chronic fatigue syndrome.
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DOI:
10.1016/j.nicl.2018.07.011
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发表时间:
2018
期刊:
NeuroImage. Clinical
影响因子:
--
通讯作者:
Bhuta S
Bhuta S
中科院分区:
其他
文献类型:
--
作者:
Barnden LR;Shan ZY;Staines DR;Marshall-Gradisnik S;Finegan K;Ireland T;Bhuta S

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我们招募了 43 名符合福田标准的慢性疲劳综合症 (CFS) 受试者和 27 名健康对照者,并进行了 3T MRI T1 和 T2 加权自旋回波(T1wSE 和 T2wSE)扫描。 T1wSE 信号遵循 T1 弛豫率(1/T1 弛豫时间)并对髓磷脂和铁(铁蛋白)浓度做出反应。我们与 SPM12 进行了 MRI 信号水平组比较。使用 T2wSE 扫描进行分割后的空间归一化,并将其应用于配准的 T1wSE 扫描。对各个扫描进行全局信号水平标准化后,T1wSE 组比较检测到脑干区域 CFS 中的信号水平下降(基于簇的推理控制家庭错误率,PFWE = 0.002),而感觉运动皮层白质中大双侧簇的信号水平增加(簇 PFWE < 0.0001)。此外,脑干 T1wSE 值与 CFS(R2 = 0.31,P = 0.00007)和健康对照(R2 = 0.34,P = 0.0009)的感觉运动值呈负相关,并且回归是共线性的。鉴于已知的丘脑投射纤维可塑性,这种关系以前在健康对照或 CFS 中未曾报道,表明 CFS 中的脑干传导缺陷可能会刺激感觉运动皮层中髓磷脂的上调,以维持脑干 - 感觉运动连接。 VBM 没有发现区域灰质或白质体积的群体差异。我们认为,在 CFS 感觉运动 WM 中观察到的 T1wSE 增加表明髓鞘形成增加,这是对脑干缺陷的调节反应,尽管在本研究中无法测试因果关系。脑干髓磷脂的改变可能对大脑功能产生广泛的影响,应该成为未来研究的重点。
We recruited 43 Chronic Fatigue Syndrome (CFS) subjects who met Fukuda criteria and 27 healthy controls and performed 3T MRI T1 and T2 weighted spin-echo (T1wSE and T2wSE) scans. T1wSE signal follows T1 relaxation rate (1/T1 relaxation time) and responds to myelin and iron (ferritin) concentrations. We performed MRI signal level group comparisons with SPM12. Spatial normalization after segmentation was performed using T2wSE scans and applied to the coregistered T1wSE scans. After global signal-level normalization of individual scans, the T1wSE group comparison detected decreased signal-levels in CFS in a brainstem region (cluster-based inference controlled for family wise error rate, PFWE= 0.002), and increased signal-levels in large bilateral clusters in sensorimotor cortex white matter (cluster PFWE < 0.0001). Moreover, the brainstem T1wSE values were negatively correlated with the sensorimotor values for both CFS (R2 = 0.31, P = 0.00007) and healthy controls (R2 = 0.34, P = 0.0009), and the regressions were co-linear. This relationship, previously unreported in either healthy controls or CFS, in view of known thalamic projection-fibre plasticity, suggests brainstem conduction deficits in CFS may stimulate the upregulation of myelin in the sensorimotor cortex to maintain brainstem – sensorimotor connectivity. VBM did not find group differences in regional grey matter or white matter volumes. We argued that increased T1wSE observed in sensorimotor WM in CFS indicates increased myelination which is a regulatory response to deficits in the brainstem although the causality cannot be tested in this study. Altered brainstem myelin may have broad consequences for cerebral function and should be a focus of future research.
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