MAGICAL MEDICINE: HOW TO MAKE AN ILLNESS ... - Invest in ME

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(http://www.entretiens‐du‐carla.com/publication.php?pub=fibro&pg=fatigue ).
This out‐dated perception has been shown to be invalid, for example:
• “Recent reports suggest that a subgroup of FMS subjects has an immune‐mediated disease. EDX
(electrodiagnostics) demonstrated a distal demyelinating polyneuropathy, suggestive of chronic inflammatory
demyelinating polyneuropathy (CIPD)” (Rheumatology 2008:47:208‐211)
• a report in Neuroscientist, February 12 th 2008 said: “Neurotransmitter studies show that fibromyalgia
patients have abnormalities in dopaminergic, opioidergic, and serotoninergic systems (and) studies of brain
anatomy show structural differences between the brains of fibromyalgia patients and healthy individuals.
The cerebral alterations offer a compelling explanation for the multiple symptoms of fibromyalgia”
• electron microscopy studies of skin biopsies from FM patients have shown unusual patterns of
unmyelinated nerve fibres as well as associated Schwann cells (Clin Rheumatol 2008:27(3):407‐411)
• high plasma levels of MCP‐1 and eotaxin provide evidence for an immunological basis of
fibromyalgia, ie. fibromyalgia is associated with inflammatory chemokines (Exp Biol Med 2008 5 th
June)
• altered intestinal permeability has been demonstrated in fibromyalgia patients (Rheumatology
2008:47(8):1223‐1227)
• changes in the levels of the neurotransmitter dopamine may explain brain gray matter reductions
experienced by people with fibromyalgia. A study by Wood et al from Louisiana State University
found significant reductions in gray matter in FM patients, confirming previous findings. The
study also found that FM patients showed a stronger correlation of dopamine metabolism levels and
gray matter density in areas of the brain where dopamine is known to control neurological
activity (American Pain Society news release, June 16, 2009)
• a blinded, controlled study of neurological signs and symptoms in FM by researchers from
the University of Washington, Seattle, demonstrated significant neurological findings on physical
examination, with FM patients having more neurological symptoms ‐‐ in multiple categories
– than controls. FM patients had greater dysfunction in cranial nerves IX and X (42% versus 8%),
and more sensory abnormalities (65% versus 25%); more motor abnormalities (33% versus 3%), and
more abnormal gait abnormalities (28% versus 7 %). The FM group also had significantly more
neurological symptoms, with the greatest differences being photophobia (70% versus 6%), poor
balance (58% versus 2%), and tingling in the arms or legs (54% versus 4%). Poor balance, tingling in
limbs, and numbness in any part of the body correlated with neurological examination findings in
the FM group (Watson NF, Buchwald D et al. Arthritis Rheum 2009:60(9):2839‐2844)
• Ablin, Buskila and Clauw from the University of Michigan reviewed several objective biomarkers
in fibromyalgia, commenting: “Although there was original scepticism that any objective abnormalities
would be identified in these individuals, at present there are many that have been reproducibly identified, and
most point to dysregulation of central nervous system function as a key underlying pathogenic mechanism in
this and related illnesses” (Curr Pain Headache Rep 2009:13(5):343‐349).
It is troubling that the Wessely School so persistently dismiss or ignore the evidence that fibromyalgia is not
a somatisation disorder and that they disregard the evidence that FM and ME/CFS have distinct biological
profiles, for example:
• levels of somatomedin C are lower in FM patients but are higher in ME/CFS patients (J psychiat Res
1997:31:1:91‐96)