Anti-Correlated Myelin-Sensitive MRI Levels in Humans Consistent with a Subcortical to Sensorimotor Regulatory Process... 2022 Barnden et al

Full title: Anti-Correlated Myelin-Sensitive MRI Levels in Humans Consistent with a Subcortical to Sensorimotor Regulatory Process—Multi-Cohort Multi-Modal Evidence

Abstract

Differential axonal myelination synchronises signalling over different axon lengths. The consequences of myelination processes described at the cellular level for the regulation of myelination at the macroscopic level are unknown. We analysed multiple cohorts of myelin-sensitive brain MRI. Our aim was to (i) confirm a previous report of anti-correlation between myelination in subcortical and sensorimotor areas in healthy subjects, (ii) and thereby test our hypothesis for a regulatory interaction between them. We analysed nine image-sets across three different human cohorts using six MRI modalities. Each image-set contained healthy controls (HC) and ME/CFS subjects. Subcortical and Sensorimotor regions of interest (ROI) were optimised for the detection of anti-correlations and the same ROIs were used to test the HC in all image-sets. For each cohort, median MRI values were computed in both regions for each subject and their correlation across the cohort was computed.

We confirmed negative correlations in healthy controls between subcortical and sensorimotor regions in six image-sets: three T1wSE (p = 5 × 10−8, 5 × 10−7, 0.002), T2wSE (p =2 × 10−6), MTC (p = 0.01), and WM volume (p = 0.02). T1/T2 was the exception with a positive correlation (p = 0.01). This myelin regulation study is novel in several aspects: human subjects, cross-sectional design, ROI optimization, spin-echo MRI and reproducible across multiple independent image-sets. In multiple independent image-sets we confirmed an anti-correlation between subcortical and sensorimotor myelination which supports a previously unreported regulatory interaction. The subcortical region contained the brain’s primary regulatory nuclei.

We suggest a mechanism has evolved whereby relatively low subcortical myelination in an individual is compensated by upregulated sensorimotor myelination to maintain adequate sensorimotor performance.

Open access, https://www.mdpi.com/2076-3425/12/12/1693

 

RAS = reticular activating system (also Wikipedia link)

The concluding paragraph is —

 

The original basic T1 spin-echo finding was reported in Hyperintense sensorimotor T1 spin echo MRI is associated with brainstem abnormality in CFS (2018, Fukuda). It was using an "old-fashioned" MRI sequence — although it was possibly ideal to discriminate this observation. This new paper supports that prior finding by replicating with five more modern sequences.

The conventional spin-echo sequence is slow and has been replaced by fast FSE/TSE (fast or turbo spin-echo, depending on manufacturer). Acquisition time is reduced, meaning less time required for the patient to stay very still in the scanner, but the signal-to-noise ratio is reduced.

 

Note they de-emphasise ME/CFS in this paper — they are simply looking at this inverse relationship, as present in HCs or patients. They report further on ME/CFS in the supplementary material, but this presumably repeats what was shown in the earlier paper. (The idea was that brainstem deficits were present in ME/CFS that were compensated for by upregulation in sensorimotor myelination.)

Datasets extended from 2006 - 2016 and used both 1.5T and 3T magnets.

The neurology and radiology is getting a bit complex, but that's probably most of what we need for now.

Spoiler: Sidebar

if such compensation tries to be more exaggerated in some pathological states, that opens up possibilities to explain symptoms that might vary both spatially and temporally — as the compensation might be more or less effective given any number of variable system inputs.

But hey — let's just do FND / conversion disorder / hysteria.