Monday, June 19, 2017

Fibromyalgia at the 2017 EULAR Annual Meeting in Madrid - a disease of the peripheral or central nervous system

Fibromyalgia: a disease of the peripheral or central nervous system – that is indeed a provocative question. Or not at all!

C. Sommer talked on [1]: “PERIPHERAL PATHOLOGY IN FIBROMYALGIA”. “In recent years, an involvement of the thinly myelinated nerve fibers of the A-delta type and the unmyelinated C-fibers has been reported in fibromyalgia patients.” And: “While the reasons for this small fiber pathology and its contribution to FMS pain are still unclear, a new research field has emerged that will focus on uncovering the underlying pathophysiology.” So what?! The findings are undisputed, though we still lack data on larger cohorts. I see in focusing on a peripheral pathology a clinging to a straw for drug interventions that have been not so successful.

E. Kosek’s talk has been on [2]: “CENTRAL PATHOLOGIES IN FIBROMYALGIA”. She stated: “Although mechanisms such as muscle ischemia and peripheral nerve fibre pathology have been implicated in fibromyalgia, currently no known peripheral pathology can fully account for the pain. Therefore, the pain in fibromyalgia is most likely explained by a complex interaction between peripheral and central mechanisms.” There are known functional and structural abnormalities in the brains of fibromyalgia patients (MRI). Fibromyalgia patients showed an inability to activate the descending pain inhibitory system. E. Kosek talked on elevated IL-8 in the cerebrospinal fluid and translocator protein (TSPO) in glia cells indicating neuro-inflammation, possibly due to glia cell activation. A positive response to a 12 weeks treatment with a serotonin-noradrenalin re-uptake inhibitor (SNRI) has been seen only in patients with a short duration of fibromyalgia. She referred to the Jensen et al. Study [3]: “In contrast, cognitive behaviour therapy did not affect clinical pain or pain sensitivity but increased activations of cerebral regions implicated in executive cognitive control during painful stimulation and thus likely reappraisal of painful stimuli.” Kosek also looked at physical exercise and ended: “The results demonstrated that different treatment modalities affected specific brain mechanisms, indicating that at least some of the cerebral abnormalities in FM are reversible.”

To sum it up: Fibromyalgia has a complex pathology, which is only understood in parts. Peripheral and central mechanisms interact in the development of fibromyalgia. Before acute pain mutates into chronic pain analgesics should be used; the importance of analgesics dwindles quickly. Serotonin-noradrenalin re-uptake inhibitors play a role in early fibromyalgia; I don’t think that fibromyalgia patients are generally referred to rheumatologists in this stage of the disease. Cognitive behavior therapy in combination with physical exercise are most likely to alleviate fibromyalgia symptoms.

Links and references:
[1] DOI: 10.1136/annrheumdis-2017-eular.7088
[2] DOI: 10.1136/annrheumdis-2017-eular.7142
[3] Jensen et al. Pain 2012:153(7):1495–503


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