A brain MRI study of chronic fatigue syndrome: evidence of brainstem dysfunction and altered homeostasis, NMR in Biomedicine, 11 May 2011

May 12, 2011


Barnden, L. R., Crouch, B., Kwiatek, R., Burnet, R., Mernone, A., Chryssidis, S., Scroop, G. and Del Fante, P. (2011), A brain MRI study of chronic fatigue syndrome: evidence of brainstem dysfunction and altered homeostasis. NMR in Biomedicine, 24: n/a. doi: 10.1002/nbm.1692

Author Information
1 Department of Nuclear Medicine, The Queen Elizabeth Hospital, Adelaide, South Australia
2 School of Chemistry and Physics, University of Adelaide, Adelaide, South Australia
3 Division of Medicine, Lyell McEwin Hospital, Adelaide, South Australia
4 Endocrinology Department, Royal Adelaide Hospital, Adelaide, South Australia
5 Department of Radiology, The Queen Elizabeth Hospital, Adelaide, South Australia
6 Physiology Department, University of South Australia, Adelaide, South Australia
7 Adelaide Western General Practice Network, Adelaide, South Australia
Email: Leighton R. Barnden (Leighton.Barnden@health.sa.gov.au)

*Correspondence: Leighton R. Barnden, Department of Nuclear Medicine, The Queen Elizabeth Hospital, Adelaide, South Australia

*Correspondence:

Leighton Barnden, Department of Nuclear Medicine, The Queen Elizabeth Hospital, Woodville, SA 5011, Australia.

E-mail Leighton.Barnden@health.sa.gov.au

DOI: 10.1002/nbm.1692

Abstract

To explore brain involvement in chronic fatigue syndrome (CFS), the statistical parametric mapping of brain MR images has been extended to 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, the hospital anxiety and depression scale (HADS) anxiety and depression, and hemodynamic parameters from 24-h blood pressure monitoring. We also performed group × 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 × hemodynamic score interactions were detected in the brainstem [strongest in midbrain grey matter (GM)], deep prefrontal white matter (WM), the caudal basal pons and hypothalamus. A strong correlation in CFS between brainstem GM volume and pulse pressure suggested impaired cerebrovascular autoregulation. It can be argued 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 (ANS). Copyright © 2011 John Wiley & Sons, Ltd.


24 May 2011: “Please note that our primary findings survived statistical adjustment for anxiety and depression scores of the validated Hospital Anxiety and Depression Scale. We therefore suggest that our results represent the most convincing evidence now existing that the central nervous system is directly involved in CFS and that this occurs independent of psychological disorders.”

Read in full what they are now saying about this study at the ME/CFS (SA) Inc website.

7 thoughts on “A brain MRI study of chronic fatigue syndrome: evidence of brainstem dysfunction and altered homeostasis, NMR in Biomedicine, 11 May 2011”

  1. 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 (ANS).’

    Just like I always said, except these chaps have expressed it so much better than I ever could 🙂

    Significant study or what?

    1. I agree. I had myself decided that CFS was caused by an insult to the brainstem. It always seemed far more logical than other explanations. This needs to be replicated asap so that the bathwater can be discarded.

  2. Can someone explain to the layperson (me- an anxious mother whose daughter has had severe ME for nearly 7 years) what this actually means as it does seem a significant study but it needs simplifying for the non medical person. What are the implications for treatment of ME?

    1. Hi Rosemary,

      Implications for treatment are not something that can be gleaned from this study alone.

      That they seem to have found something identifiable is I think significant, BUT once again, it will need a better defined selection of patients, and independent verification.

      If someone picks this up – and if the authors run with it – then we might see something more concrete.

      Sorry x

  3. Thanks for the response. Is there anything we can do to lobby for ‘somone’ to pick this is- and who would that someone be?

    regards

    Rosemary

  4. If this finding is replacated and accepted it must also yield a legitimately scientific terminology to describe the desease as a welcome replacement for a multiplicity of terms which are either speculative or leveraged by the ‘all in the mind’ brigade for their own ends.

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