A Comparison of Neuroimaging Abnormalities in Multiple Sclerosis, Major Depression and Chronic Fatigue Syndrome.., 2017, Morris et al

[Andy]

Full title: A Comparison of Neuroimaging Abnormalities in Multiple Sclerosis, Major Depression and Chronic Fatigue Syndrome (Myalgic Encephalomyelitis): is There a Common Cause?

There is copious evidence of abnormalities in resting-state functional network connectivity states, grey and white matter pathology and impaired cerebral perfusion in patients afforded a diagnosis of multiple sclerosis, major depression or chronic fatigue syndrome (CFS) (myalgic encephalomyelitis). Systemic inflammation may well be a major element explaining such findings. Inter-patient and inter-illness variations in neuroimaging findings may arise at least in part from regional genetic, epigenetic and environmental variations in the functions of microglia and astrocytes. Regional differences in neuronal resistance to oxidative and inflammatory insults and in the performance of antioxidant defences in the central nervous system may also play a role. Importantly, replicated experimental findings suggest that the use of high-resolution SPECT imaging may have the capacity to differentiate patients afforded a diagnosis of CFS from those with a diagnosis of depression. Further research involving this form of neuroimaging appears warranted in an attempt to overcome the problem of aetiologically heterogeneous cohorts which probably explain conflicting findings produced by investigative teams active in this field. However, the ionising radiation and relative lack of sensitivity involved probably preclude its use as a routine diagnostic tool.

Open access, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5842501/

White Matter Abnormalities in CFS
Early research investigating potential neuroanatomical abnormalities using MRI focused on WM using observer-dependent analysis [14, 179–181]. Natelson and others reported subcortical WM hyperintensities in 52 subjects fulfilling the original CDC selection criteria [182] compared with a control group who had undergone MRI investigation for head trauma [179]. On the other hand, Greco and others reported widespread demyelination in many of their CFS participants but at a group level, WM hyperintensities were not significantly different from healthy controls [180]. However, Lange and others also reported significantly increased WM hyperintensities in their CFS group who were free of comorbid anxiety or depression compared with healthy controls and CFS subjects with co-morbid psychopathology [183]. Interestingly, when the data obtained from the two CFS groups were combined, the levels of WM hyperintensities were not significantly different from the control group [183]. In another large study involving 48 CFS patients, Cook and others reported widespread WM abnormalities in their cohort whose extent correlated with symptom severity [14]. It should also be noted that a more recent MRI study using observer-dependent methods failed to detect any WM abnormalities in their CFS cohort although these patients were not recruited according to international consensus guidelines [184].

Recent studies based on T1- and T2-weighted MRI using VBM have universally reported significantly increased WM abnormalities in CFS subjects selected according to the “Fukuda” CDC criteria compared with healthy participants [185–188]. Puri and others reported reduced WM voxel volumes in the left occipital lobe while Barnden and others reported reduced WM voxel volumes in the frontal cortex, caudate and hypothalamus [185, 186]. Pertinently, Shan and others reported decreased WM volume in the left frontal occipital lobe and the fasciculus whose extent increased with self and clinically assessed symptom severity and also worsened over time [188]. Finally, Barnden and others reported reduced WM volume in the prefrontal cortex, the ventrolateral thalamus and internal capsule even following correction for the potential effects of anxiety and depression [187].