ME Australia blog post, by Sasha Nimmo, 12 July 2016: Six year study of abnormal brain changes in chronic fatigue syndrome patients
An Australian six year study evaluating progressive brain changes associated with chronic fatigue syndrome (Fukuda and Canadian Consensus Criteria definitions) shows patients’ brains deteriorate at an abnormal rate.
The study used optimized voxel based morphometry (VBM), a commonly-used automated tool for studying patterns of brain change in neurological diseases. It shows chronic fatigue syndrome (Fukuda & CCC) is a chronic illness with abnormal connections among brain regions and white matter deficits which continue to deteriorate.
The study, Progressive brain changes in patients with chronic fatigue syndrome: A longitudinal MRI study, was published in the Journal of Magnetic Imaging in April 2016.
The authors are from Griffith University’s National Centre for Neuroimmunology and Emerging Diseases and South Australia’s Lyell McEwin Hospital and Royal Adelaide Hospital. Many of this paper’s authors also published a paper about brain connectivity problems causing signalling problems in March 2016.
The six year study looked at the brains of 15 patients and 10 controls and found white matter decreased over time in the CFS patients. It also says hypoxia, which is a deficiency in the amount of oxygen reaching the tissues, could be causing neurodegeneration.
“The rate-of-change of regional white matter volumes in CFS patients was significantly different from that in controls in the left posterior part of the inferior fronto-occipital fasciculus (IFOF) and/or arcuate fasciculus. In this location, white matter volume relative to global white matter volume decreased with time in the CFS group while in controls it was unchanged.
This study detected continuing shrinkage of white matter in the left IFOF in patients with CFS, but not in controls. This result was consolidated by the pooled inter group comparisons revealing decreased regional white matter volumes in adjacent regions and decreased GM and blood volumes in contralateral regions and by regression analysis showing significant correlations of white matter and grey matter volumes and T2w intensities with CFS symptom scores in those regions.”
The IFOF connects networks of cognitive control, attention, language processing and working memory.
The study may explain symptoms such as impaired concentration, working memory loss, inability to focus vision and poor motor coordination.
This seems to agree with the findings of Boissoneault et al 2005 in the their paper Abnormal resting state functional connectivity in patients with chronic fatigue syndrome: an arterial spin-labeling fMRI study, which said “results demonstrate altered functional connectivity of several regions associated with cognitive, affective, memory, and higher cognitive function in ME/CFS (Fukuda criteria) patients. Connectivity to memory related brain areas (parahippocampal gyrus) was correlated with clinical fatigue ratings, providing supporting evidence that brain network abnormalities may contribute to ME/CFS pathogenesis”.
“Chronic functional hypoxia due to dysfunction of the neurovascular unit could also cause neurodegeneration. Of interest, a recent study found seventeen single nucleotide polymorphisms (SNPs) were significantly associated with CFS. Nine of these SNPs were associated with muscarinic acetylcholine receptors and eight with nicotinic ACh receptors (nAChRs). ACh, a neuromodulator in the brain, changes the state of neuronal networks throughout the brain and modifies their response to internal and external inputs. Control of synaptic Ca2+ concentration following nAChR stimulation is a major pathway for ACh to influence neuronal networks. Furthermore, nAChRs are also present in the cerebral vascular endothelium and smooth muscles. Thus, aberrant AChR function may impair cerebrovascular autoregulation and cause chronic functional hypoxia.
This study warrants further investigations to understand the pathomechanism of white matter deficits in the IFOF in CFS.”
The study was funded by the Judith Jane Mason Foundation.
Summary piece. The full paper came out in April.