Hyperintense sensorimotor T1 spin echo MRI is associated with brainstem abnormality in chronic fatigue syndrome.
Barnden, Leighton R, Shan, Zack Y, Staines, Donald R et al. · NeuroImage. Clinical · 2018 · DOI
Quick Summary
Researchers used advanced MRI scans to compare the brains of 43 people with ME/CFS and 27 healthy people. They found that people with ME/CFS had different patterns in their brainstem (the base of the brain that controls basic functions) and in the sensorimotor areas (parts that control movement and sensation). The study suggests that the body may be compensating for problems in the brainstem by increasing protective coating around nerve fibers in motor control areas.
Why It Matters
This study identifies a potential structural brain abnormality in ME/CFS patients—altered myelin patterns in the brainstem and sensorimotor regions—which could explain some neurological symptoms like fatigue and movement difficulties. Understanding whether the brain is compensating for dysfunction may open new avenues for treatment development and help validate ME/CFS as a neurobiological condition.
Observed Findings
Decreased T1wSE signal in the brainstem region in CFS patients compared to healthy controls (PFWE=0.002)
Increased T1wSE signal in bilateral sensorimotor cortex white matter in CFS patients (PFWE<0.0001)
Negative correlation between brainstem and sensorimotor T1wSE values in both CFS (R²=0.31, p=0.00007) and healthy controls (R²=0.34, p=0.0009)
No significant differences in gray or white matter volumes between groups on voxel-based morphometry analysis
Inferred Conclusions
Altered myelin concentration in the brainstem may represent a primary abnormality in ME/CFS
Increased myelination in sensorimotor cortex white matter may be a regulatory/compensatory response to brainstem conduction deficits
The previously unreported brainstem-sensorimotor relationship suggests plasticity in thalamic projection fibers as a disease mechanism
Abnormal brainstem myelin may have broad consequences for cerebral function and should be a focus of future research
Remaining Questions
Is the decreased brainstem signal a cause or consequence of increased sensorimotor myelination, and can causality be established through longitudinal studies?
Do these MRI signal changes correlate with specific ME/CFS symptoms (fatigue severity, cognitive dysfunction, orthostatic intolerance) and do they predict clinical outcomes?
What This Study Does Not Prove
This study cannot establish causality; the authors cannot determine whether brainstem abnormality causes sensorimotor changes or vice versa. The cross-sectional design captures only a snapshot in time and cannot track disease progression or confirm that these changes are disease-specific rather than consequences of reduced activity. The relationship between MRI signal changes and actual clinical symptoms requires validation in larger longitudinal studies.
What is the biological mechanism driving increased myelination in sensorimotor cortex—is it truly compensatory plasticity or an independent pathological process?
Are these findings specific to ME/CFS or do they occur in other conditions with brainstem involvement or fatigue symptoms?