Is there a possibility that the small-fiber polyneuropathy explains palmer AV Shunt in FM?
Could the disruptions be due to immune disruption?
How would this affect sustenance of MTrP treatments?
Dear Dr. Albrecht, Dr. Behm, Dr. Ge Hy, and Dr. Oaklander,
Sincerely, Celeste Cooper, RN
Studies and articles:
CONCLUSIONS:“The excessive sensory innervation to the glabrous skin AVS is a likely source of severe pain and tenderness in the hands of FM patients. Importantly, glabrous AVS regulate blood flow to the skin in humans for thermoregulation and to other tissues such as skeletal muscle during periods of increased metabolic demand. Therefore, blood flow dysregulation as a result of excessive innervation to AVS would likely contribute to the widespread deep pain and fatigue of FM. SNRI compounds may provide partial therapeutic benefit by enhancing the impact of sympathetically mediated inhibitory modulation of the excess sensory innervation.”
ARTICLE, Women with Fibromyalgia Have A Real Pathology Among Nerve Endings to Blood Vessels, at Integrated Tissue Dynamics. This is a fantastic article that explains what happens in an easy to understand analogy. See entire article here.
“Scientists at Integrated Tissue Dynamics (Intidyn) and Albany Medical College have made a major discovery that should provide a more certain diagnosis of fibromyalgia, significant insight into the source and symptoms of the disease, and new strategies for its prevention and treatment. The Albany Med and Intidyn research team - headed by neurologists Charles Argoff, MD, and James Wymer, MD PhD and neuroscientists Phillip Albrecht, PhD, and Frank Rice, PhD - discovered that the skin in fibromyalgia patients has a major pathology involving nerve endings to a key type of blood vessel called arteriole-venule shunts… arteriole-venule shunts play a major role in the proper distribution of blood flow throughout the body, and the discovered pathology involving the nerve endings to the shunts provides a logical explanation for the widespread deep pain and fatigue symptomatic of fibromyalgia.
CONCLUSIONS:“The cytokine responses to mitogenic activators of PBMC isolated from patients with FM were significantly lower than those of healthy individuals, implying that cell-mediated immunity is impaired in FM patients. This novel cytokine assay reveals unique and valuable immunologic traits, which, when combined with clinical patterns, can offer a diagnostic methodology in FM.”
MY COMMENT:The role of cytokines in FM has been studied over more than a decade. I have never had a doubt regarding my own body that there is something askew in the immune system that accounts for the co-existence of particular disorders. Plasma levels have been consistently low, but not considered low enough to be significant. This research is looking at specific cytokines in specific cells, in specific ways, and the results will no doubt lead research in the right direction. I truly feel a bio-marker could be around the corner. Cc
CONCLUSIONS:“Descending pain modulation shifts from descending inhibition towards descending facilitation following muscle nociception in FM. Peripheral mechanical hyperalgesia and descending facilitation counterbalance the effect of descending inhibition in FM.”
MY COMMENT:This result should be no surprise in light of the stress contraction puts on a muscle when it has myofascial trigger points present. Cc
CONCLUSION:“These findings suggest that some patients with chronic pain labeled as "fibromyalgia" have unrecognized small-fiber polyneuropathy, a distinct disease that can be objectively tested for and sometimes definitively treated.”
ARTICLE: Small-Fiber Polyneuropathy Found in Fibromyalgia Patients. See entire article at Examiner.com, here.“Finally with the FM patients had a reduction in dermal unmyelinated nerve fibre bundles was found in skin samples of patients with fibromyalgia syndrome compared with patients with depression and with healthy control subjects, whereas myelinated nerve fibres were spared.”