Findings from Functional MRI in ME/CFS and PCS

Prof. Dr. Carsten Finke gave an overview of neuroimaging methods in ME/CFS and Long COVID research. He covered structural magentic resonance imaging (MRI)/volumetry, diffusion tensor imaging (DTI), task-based and resting-state functional MRI (fMRI), arterial spin labelling (ASL), magnetic resonance spectroscopy (MRS), and positron emission tomography (PET), along with their respective contributions to characterising pathophysiology, neuroinflammation, perfusion, and metabolism. Structural MRI data from 47 post-COVID patients vs. 47 controls revealed modest but measurable volume reductions in the thalamus and pallidum. Complementary DTI findings provided findings correlating with physical fatigue and daytime sleepiness. MRS studies at 7 Tesla reported elevated lactate and glutamate levels alongside reduced choline, indicating disturbances in energy metabolism and neuroinflammatory changes; one study comparing ME/CFS and Long COVID patients identified differing metabolic patterns between groups. ASL data documented region-specific reductions in cerebral blood flow that correlated with clinical severity. In the functional MRI domain, he presented a 7 Tesla Stroop task study in which healthy participants showed increasing subcortical connectivity over time, whereas ME/CFS and Long COVID patients exhibited aberrant patterns in the default mode and salience networks alongside reduced hippocampal connectivity. A multimodal resting-state study (n=86 Long COVID patients with cognitive impairment) documented reduced connectivity between parahippocampal, orbitofrontal, and cerebellar regions, associated with memory deficits. A further thalamus seed-based analysis distinguished fatigued from non-fatigued Long COVID patients by connectivity profile. Prof. Dr. Finke also reported on a hyperbaric oxygen therapy (HBOT) study of 30 ME/CFS patients: elevated thalamic connectivity observed before treatment normalised after 40 HBOT sessions. He closed by underscoring that cohort heterogeneity remains a major challenge, and that identifying the driving pathomechanisms will require better-defined patient subgroups developed in close collaboration with immune phenotyping approaches.