NEUROLOGY
2018 was a particularly strong year for neuroimaging, with a multitude of studies deploying modern technologies and leveraging sophisticated analysis techniques to assess inflammatory, structural, and functional neurologic abnormalities.
In the absence of access to a patient brain biorepository, researchers have delved deep into the extent to which aberrant activity can be detected through noninvasive techniques and have produced notable results conclusively implicating neurologic dysfunction in ME/CFS disease pathophysiology.
Collectively, the work produced is a remarkable demonstration of altered neurological structure and function in ME/CFS patient brains, which consistently evidences a physiologic basis for patient-reported cognitive impairment and autonomic dysfunction using objective measures.
Zinn, et al. were able to discern differences in neurologic activity by electroencephalogram (EEG), a test that records electrical patterns in the brain.
Nakatomi, et al. observed widespread neuroinflammation associated with symptom severity by positron emission topography (PET) scan.
By functional MRI (fMRI),
Boissoneault, et al. and
Shan, et al. measured diminished functional connectivity (pattern of interactions between areas of the brain).
Barnden, et al. discovered deficits in neural conduction within the brainstems of CFS (Fukuda) patients, proposing that a compensatory increase in myelin (the “insulation” around neurons) may occur in this region and compromise cerebral function.
Staud, et al. evaluated differences in differences in cerebral blood flow patterns following a cognitive exertion task in ME/CFS subjects compared to healthy controls.
Boissoneault, et al. found cerebral blood flow and heart rate variability (differences in the amount of time between heartbeats) to be inversely correlated with fatigue levels.
Sevel, et al. tested the effectiveness of a machine learning platform in discerning neurologic structural abnormalities in ME/CFS.
Kimura, et al. measured microstructural abnormalities in patient brains by MRI, noting significant decreases in physical neurologic metrics in specific regions relative to healthy controls.
Rowe, et al. identified several ME/CFS patients whose cervical spinal stenosis (compression of the cervical spinal cord) contributed to their symptoms, as indicated by improvement following corrective surgery. The case series highlights the importance of careful neurologic examination of patients for this condition.
Addressing Naviaux’s
hypothesis that ME/CFS may involve processes at play in autism and the fact that the two diseases share symptoms of central sensitization (changes to the central nervous system that produce chronic pain) ,
Bileviciute-Ljungar, et al. measured features of autism in a CFS cohort, but did not observe an elevated rate of autistic traits.
Nilsson, et al. tested a dopamine and serotonin receptor agonist, (−)-OSU6162, in a clinical trial and found correlative but nonsignificant improvements in self-reported fatigue, especially in a subgroup receiving antidepressants.
