http://sacfs.asn.au/news/2011/03/03_01_publication_of_original_adelaide_cfs_mri_study.htm Publication of original Adelaide CFS MRI study Tuesday 1 March 2011 An MRI study which detected brainstem dysfunction and altered homeostasis in people with CFS is about to be published in the medical journal NMR in Biomedicine. Here's a preview: A brain MRI study of chronic fatigue syndrome: Evidence of brainstem dysfunction and altered homeostasis Authors: Leighton R. Barnden, Benjamin Crouch, Richard Kwiatek, Richard Burnet, Anacleto Mernone, Steve Chryssidis, Garry Scroop, Peter Del Fante Publication: NMR in Biomedicine Abstract [accepted, pre-proof] 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 parameters from 24 hour blood pressure monitoring. We also performed group =D7 hemodynamic score interaction regressions to detect locations where MR regressions were opposite for CFS and NC, 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 =D7 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. We argue that at least some of these changes could arise from astrocyte dysfunction. 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 CNS homeostasis, including resetting of some elements of the autonomic nervous system. Copyright =A9 2011 John Wiley& Sons, Ltd.