Our regular weekly summary of research paper abstracts received during the week that have not already been placed on the website.
Chronic fatigue syndrome: labels, meanings and consequences
J Psychosom Res. 2011 Jun;70(6):500-4. Epub 2011 Apr 9.
Wojcik W, Armstrong D, Kanaan R.
Department of Psychological Medicine, Institute of Psychiatry, King’s College London, London, UK.
In this month’s issue, we report a survey of members of the Association of British Neurologists, which asked if they viewed chronic fatigue syndrome (CFS) as a neurological condition – 84% of respondents did not. This is at odds with current classification in ICD-10. We discuss the difficulties of classifying CFS and myalgic encephalopmeylitis (ME), including historical and sociological factors, the pitfalls of the physical/psychological dichotomy and why classification matters to doctors and patients.
Chronic fatigue syndrome – a neuroimmunological model
Med Hypotheses. 2011 Jul;77(1):77-83. Epub 2011 Apr 6.
Arnett SV, Alleva LM, Korossy-Horwood R, Clark IA.
Research School of Biology, Australian National University, Australia.
The aetiological and pathophysiological basis of chronic fatigue syndrome (CFS) remains a controversial field of inquiry in the research community. While CFS and similar disease conditions such as fibromyalgia (FM) and post-infectious encephalopathy have been the focus of intense scrutiny for the past 20 years, results of research were often contradictory and a cohesive pathological model has remained elusive. However, recent developments in understanding the unique immunophysiology of the brain may provide important clues for the development of a truly comprehensive explanation of the pathology of CFS. We argue that CFS pathogenesis lies in the influence of peripheral inflammatory events on the brain and the unique immunophysiology of the central nervous system. There is also evidence that CFS patients have a relative immunodeficiency that predisposes to poor early control of infection that leads to chronic inflammatory responses to infectious insults. The neurological and endocrine changes have been described in CFS patients support the view that CFS has an inflammatory pathogenesis when considered as a whole. An inflammatory model of disease also provides an explanation for the marked female sex bias associated
with CFS. This review therefore posits the hypothesis that CFS as a disease of long-term inflammatory processes of the brain. We will also provide an investigative framework that could be used to justify the use of anti-TNF biological agents as a reliable and effective treatment approach to CFS, a syndrome that to date remains frustratingly difficult for both patients and health care professionals to manage.