Role Infectious Agents & Neurologic Dysfunction Reviewed

Harvard physician-researcher Anthony Komaroff and neurologist Tracey Cho review the literature on these two critical aspects of CFS. They report the evidence on central nervous system involvement as demonstrated in neuroendocrine studies, imaging tests using MRIs, functional MRIs, MRS and SPECT, EEG studies, tests of spinal fluid samples, and of pain and cognition. They report on autonomic system involvement and how studies have shown CFS to be distinct from depression. In reviewing the literature on infections, they examined the epidemiology and immunology of CFS as well as evidence of mitochondrial dysfunction, oxidative and nitrosative stress. The specific agents included in the review are Epstein-Barr virus, HHV-6, XMRV, polytropic MLVs, enteroviruses, parvovirus and bacterial infections. They conclude, “As with other diseases without a well-defined pathologic etiology, such as M.S., there may be multiple underlying triggers of an inflammatory process, which in certain susceptible individuals leads to the clinical manifestations of CFS.” (Seminars in Neurology, e-pub. Sept. 30, 2011)
Review of Neuroendocrine Abnormalities: In this summary of the literature, the authors find that the weight of current evidence supports the presence of the following factors related to hypothalamic–pituitary–adrenal (HPA) axis dysfunction in patients with CFS: mild hypocortisolism; attenuated diurnal variation of cortisol; enhanced negative feedback to the HPA axis; and blunted HPA axis responsiveness. Furthermore, HPA axis changes seem clinically relevant, as they are associated with worse symptoms and/or disability and with poorer outcomes to standard treatments for CFS. Given what is now a fairly consistent pattern of findings for the type of HPA axis changes found in CFS, we recommend that future work focuses on improving our understanding of the cause and relevance of these observed changes. (Nature Reviews Endocrinology, Sept. 27, 2011)

Tags: , September 27, 2011