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From Winter 2016/7 Forum

Fibromyalgia (FM) is often found to be comorbid with other diseases including CFIDS/ME. In a recent issue of the medical journal entitled PAIN, researchers from the University of Colorado in Boulder discovered a brain signature that identifies fibromyalgia sufferers with 93 percent accuracy. This work, when replicated, could be a potential breakthrough for both diagnostic purposes and treatment! The medical magzine is published by the International Association for the Study of Pain. The researchers are going further in the studies to find subtypes of FM

Medscape has had quite a few articles on FM recently. One segment said, “Fibromyalgia is a disorder of unknown etiology characterized by widespread pain and tenderness, abnormal pain processing, and other symptoms, without apparent inflammation or damage to joints, muscles, or other tissues. Can you differentiate this common disorder from other conditions that cause chronic pain, and do you know how best to treat it?” We found the treatments a bit lacking.

Tonix Pharaceuticals announced they are discontinuing their TNX 102 SL which was sublingual tablets of cyclobenzaprine for treating the pain of FM since a 12 week trial on patients did not reduce their pain by much — if any. Tonix will continue their work for PTSD and has partnered with the Department of Defense.

Dr. Kosek and others from Sweden authored a paper (Brain Behav Immun.) earlier this year that was entitled “The translocator protein gene is associated with symptom severity and cerebral pain processing in fibromyalgia.” The abstract explained “The translocator protein (TSPO) is upregulated during glia activation in chronic pain patients. TSPO constitutes the rate-limiting step in neurosteroid synthesis, thus modulating synaptic transmission. Related serotonergic mechanisms influence if pro- or anti-nociceptive neurosteroids are produced.” Knowing this, the authors found “This study investigated the effects of a functional genetic polymorphism regulating the binding affinty to the TSPO, thus affecting symptom severity and cerebral pain processing in fibromyalgia patients. Gene-to-gene interactions with a functional polymorphism of the serotonin transporter gene were assessed. Fibromyalgia patients (n=126) were genotyped regarding the polymorphisms of the TSPO (rs6971) and the serotonin transporter (5-HTTLPR/rs25531). Functional magnetic resonance imaging (n=24) was used to study brain activation during individually calibrated pressure pain.

“Compared to mixed/low TSPO affinity binders, the high TSPO affinity binders rated more severe pain (p=0.016) and fibromyalgia symptoms (p=0.02). A significant interaction was found between the TSPO and the serotonin transporter polymorphisms regarding pain severity (p<0.0001).”

Most of these authors were from the Karolinska Institute and they wrote, “Functional connectivity analyses revealed that the TSPO high affinity binding group had more pronounced pain-evoked functional connectivity in the right frontoparietal network, between the dorsolateral prefrontal area and the parietal cortex.” Those are specific areas of the brain.

They concluded with information that has never been found before in fibromyalgia and wrote, “Fibromyalgia patients with the TSPO high affinity binding genotype reported a higher pain intensity and more severe fibromyalgia symptoms compared to mixed/low affinity binders, and this was modulated by interaction with the serotonin transporter gene.”


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