This was recently brought to my attention through facebook and I thought it worthwhile posting it here to get your opinions
Jonathan Edwards. This research relates to a potentially promising hypothesis for the pathology of fibromyalgia however given the commonality between ME and FM it seems it could be of limited use in ME research - especially given that it ties together both the cardiovascular and nervous system, both of which appear to play roles within the pathology of ME.
Paper:
http://onlinelibrary.wiley.com/doi/10.1111/pme.12139/abstract
Article:
http://communities.washingtontimes....ct/17/fibromyalgia-solved-pathology-not-mind/
That aside I've recently been diagnosed with primary hyperparathyroidism as opposed to ME, so hopefully that can be sorted quite soon. I'm hoping to still play an active part both here on Phoenix Rising and hoping to return to university next year studying biomedical sciences, perhaps with a focus on immunity and autoimmunity - I guess I've been inspired. I'd like to personally thank Prof. Edwards for all the responses you've been making here.
First off congratulations on your alternative diagnosis Andrew of course I do hope you stick around - both here and around the subject area
Intrigued by some claims that AV shunt dysregulation may be 'diagnostic' for FMS I did a quick google around and found that its also common in type II diabetes and something called '
complex regional pain syndrome'.
Warning : the linked articles are a long read - but very worthwhile I believe for anyone interested.
The latter condition is particularly interesting. Not only are many of the clinical signs and symptoms (and physiological findings) similar to the wide range of multi-organ symptoms found in ME/CFS (and fibro) but many of the symptoms respond to ketamine (a nod to my ongoing fixation on glutamate as a symptom mediator) :
http://www.rsds.org/pdfsall/Systemic-Complications-of-CRPS.pdf
More importantly, while frequently considered a psychogenic illness, recent research now suggest a
neuroinflammatory model of complex regional pain syndrome that may be of
autoimmune origin and ticks many of the boxes as a potential model of ME/CFS (or fibro) onset and progression.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3661922/
Some key points of the model :
While a peripheral injury/trauma is often the initial trigger for CRPS, it needn't be. CRPS is also known with no apparent injury or even following psychological stress;
The model provides a mechanism whereby peripheral inflammation (potentially caused by autoantibodies - to either the beta(2)-adrenergic receptor (β2AR) or the muscarinic acetylcholine receptor (M2R) in CRPS) can propagate from the peripheral injury site to higher levelc of the nervous system and eventually impact on higher cognitive functions (avoiding the blood brain barrier issue by propagating via the parenchyma of the CNS e.g. glial cells);
This 'spreading neuroinflammation' can impact on many bodily systems/functions far from the original (if any) injury;
The condition becomes chronic;
Neuroinflammation leads to loss of sensory gating, excessive sensory gain and 'central sensitization' of the nervous system;
Symptoms may be subject to rapid deterioration and remission. etc.
Some excerpts :
The key concept here is that the development of autoimmunity to specific neuroautoantigens may be the initiating event for many cases of CRPS. Psychological stressors, physical trauma, infectious agents, and/or genetic susceptibility could all play a role in the breakdown of self-tolerance, and the onset of an autoimmune response. This set of etiological linkages fits well with documented clinical experience with CRPS (Mitchell 1872; Birklein et al. 2000). Psychological stressors and immunologic priming have been linked to the enhanced activation of microglia to nervous system injury (Frank et al. 2007; Hains et al. 2010).
Spreading neuroinflammation provides a non-psychogenic etiology to plausibly explain the progression and chronicity of certain disease states, as well as the migration of symptoms to different portions of the body. This mechanistic concept of spreading neuroinflammation within the CNS needs to be incorporated into differential diagnosis of neurological and neuropsychiatric disorders, as well as into the standard use of the Diagnostic and Statistical Manual for Mental Disorders (DSM). This would substantially advance the recognition and diagnosis of neuroinflammatory-mediated functional disorders within the biomedical community.
Cytokine production is a central part of the overlapping and interlocking mechanisms that produce neuroinflammatory disorders, including CRPS. Neuroendocrine alterations and disturbances in the metabolism of monoamines have been correlated with cytokine-induced mood and cognitive symptoms (Capuron et al. 2002; Dantzer et al. 2008; Doorduin et al. 2009; Engler et al. 2012). In addition, neuroimaging studies have revealed alterations in specific brain regions during cytokine treatment (Kullmann et al. 2012; Schneider et al. 2012). These changes could contribute to the development of fatigue, depression, and cognitive alterations in patients with neuroinflammation (Raedlera 2011; Schedlowski 2012). In CRPS patients, fatigue, paresis, depression, anxiety, and cognitive impairments are well documented (Mitchell 1872; Birklein et al. 2000; Apkarian et al. 2004).
