[Note: This is a preview abstract in advance of publication, posted Mar 1 by ME/CFS Australia (http://sacfs.asn.au). Ability to review the article, which appears to provide important evidence that ME/CFS is a neurological disorder, may flesh out our understanding. Dr. Kwiatek's call for study volunteers back in April 2010 is posted HERE.]
To explore brain involvement in chronic fatigue syndrome (CFS), we have extended statistical parametric mapping of brain magnetic resonance (MR) images to whole-brain voxel-based regressions against clinical scores. Using SPM5 we performed voxel-based morphometry (VBM) and analysed T1- and T2-weighted spin-echo MR signal levels in 25 CFS subjects and 25 normal controls (NC).
Clinical scores included CFS fatigue duration, a score based on the 10 most common CFS symptoms, the Bell score, HADS anxiety and depression, and hemodynamic [blood flow] parameters from 24 hour blood pressure monitoring.
We also performed group × hemodynamic score interaction regressions to detect locations where magnetic resonance regressions were opposite for CFS and normal controls, thereby indicating abnormality in the CFS group.
In the midbrain, white matter volume was observed to decrease with increasing fatigue duration.
For T1-weighted MR and white matter volume, group × hemodynamic score interactions were detected in the brainstem (strongest in midbrain grey matter), deep prefrontal white matter, the caudal basal pons and hypothalamus.
A strong correlation in CFS between brainstem grey matter volume and pulse pressure suggested impaired cerebrovascular autoregulation. [Regulation of blood flow in the brain.]
We argue that at least some of these changes could arise from astrocyte dysfunction. [Astrocytes are important star shaped ‘glial’ cells in the grey matter that play a number of roles including support of nerve-cell communications – and quality of memory formation, according to a study published Mar 4, 2011 by the journal Cell.]
These results are consistent with an insult to the midbrain at fatigue onset that affects multiple feedback control loops to suppress cerebral motor and cognitive activity and disrupt local central nervous system homeostasis, including resetting of some elements of the autonomic nervous system.
Source: NMR in Biomedicine [preview], Mar 1, 2011. Barnden LR, Crouch B, Kwiatek Rr, Burnet R, Mernone A, Chryssidis S, Scroop g, Del Fante P.