Hyperintense sensorimotor T1 spin echo MRI is associated with brainstem abnormality in CFS

Neuroimage Clin. 2018;20:102-109. doi: 10.1016/j.nicl.2018.07.011. Epub 2018 Jul 11.
Hyperintense sensorimotor T1 spin echo MRI is associated with brainstem abnormality in chronic fatigue syndrome.
Barnden LR1, Shan ZY2, Staines DR3, Marshall-Gradisnik S4, Finegan K5, Ireland T6, Bhuta S7.
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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.

Brainstem; Chronic Fatigue Syndrome; Motor; Myelin; Sensorimotor; T1wSE; Upregulation

This is from the Griffth cre. Here's the conclusions section of the paper:

In CFS T1wSE was elevated in sensorimotor WM and decreased in the brainstem. In both healthy controls and CFS, T1wSE (myelination in sensorimotor WM showed the same inverse correlation with T1wSE in the brainstem. This relationship, previously unreported in either healthy controls or CFS, suggested a possibility that in CFS a normal regulatory mechanism had responded to impaired brainstem signal conduction to stimulate elevated sensorimotor myelination. This com- plements evidence in CFS for severity dependent myelin upregulation in the internal capsule (Barnden et al., 2015). Deficits in brainstem function in CFS can have broad consequences for regulation of cerebral function in general and myelination in particular and should be a focus of future research in CFS.

Gotta be honest - my level of comprehension here is - something is up in the brainstem? Maybe to do with myelination? signals in another part of the brain are higher to compensate?
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It suggests the brain stem has reduced function, so other parts of the brain are trying to compensate by increasing myelin production. The brain stem has appeared in other papers (especially finding reduced blood flow) which night indicate that this is getting closer to the problem.

Brain stem problems would account for the range of symptoms we have.