Effect of Steroids on Patients With Fibromyalgia/Chromic Widespread Pain: An Observational Study
Objective: Fibromyalgia causes widespread chronic pain. Pain management and treating underlying conditions are of utmost importance. Recent studies found an association of thyroid autoimmunity with fibromyalgia. Pain management of patients with anti-thyroid ...
We found that 51.6% of the patients responded well to the steroid therapy
Repeated cold stress, an animal model for fibromyalgia, elicits proprioceptor-induced chronic pain with microglial activation in mice - Journal of Neuroinflammation
Background Fibromyalgia is characterized by chronic pain, fatigue, and other somatic symptoms. We have recently revealed that proprioceptor hyperactivation induces chronic pain in a rat model of myalgic encephalomyelitis. The present study explores whether similar proprioceptor-induced pain is elicited in a mouse model of fibromyalgia. Methods Repeated cold stress (RCS) was used as a fibromyalgia model. Pain behavior was examined using the von Frey test, and neuronal activation was examined immunohistochemically as activating transcription factor (ATF)3 expression. The Atf3:BAC transgenic mouse, in which mitochondria in hyperactivated neurons are specifically labeled by green fluorescent protein, was used to trace the activated neuronal circuit. PLX3397 (pexidartinib) was used for microglial suppression. Results RCS elicited long-lasting pain in mice. ATF3, a marker of cellular hyperactivity and injury, was expressed in the lumbar dorsal root ganglion (DRG) 2 days after RCS initiation; the majority of ATF3-expressing DRG neurons were tropomyosin receptor kinase C- and/or vesicular glutamate transporter 1-positive proprioceptors. Microglial activation and increased numbers of microglia were observed in the medial part of the nucleus proprius 5 days after RCS initiation, and in the dorsal region of the ventral horn 7 days after RCS. In the ventral horn, only a subset of motor neurons was positive for ATF3; these neurons were surrounded by activated microglia. A retrograde tracer study revealed that ATF3-positive motor neurons projected to the intrinsic muscles of the foot (IMF). Using Atf3:BAC transgenic mice, we traced hyperactivated neuronal circuits along the reflex arc. Green fluorescent protein labeling was observed in proprioceptive DRG neurons and their processes originating from the IMF, as well as in motor neurons projecting to the IMF. Microglial activation was observed along this reflex arc, and PLX3397-induced microglial ablation significantly suppressed pain behavior. Conclusion Proprioceptor hyperactivation leads to local microglial activation along the reflex arc; this prolonged microglial activation may be responsible for chronic pain in the present model. Proprioceptor-induced microglial activation might be the common cause of chronic pain in both the fibromyalgia and myalgic encephalomyelitis models, although the experimental models are different.
Neutrophils infiltrate sensory ganglia and mediate chronic widespread pain in fibromyalgia | PNAS
Conclusion: “We used a model of hyperalgesic priming to induce chronic widespread pain in mice that resulted in robust and persistent ipsilateral and contralateral behavioral hypersensitivity and sensitization of spinal cord neurons. Adoptive transfer of neutrophils from primed mice and from patients with fibromyalgia syndrome confers mechanical pain to recipient naïve mice, sensitizes evoked action potential firing of spinal cord neurons, and causes neutrophil infiltration into the dorsal root ganglia. These data demonstrate that neutrophils are fundamental for the development of chronic widespread pain through infiltration of peripheral sensory ganglia. Further studies characterizing the neutrophil phenotype in fibromyalgia syndrome may shed light on mediators of the cross talk between these polymorphonuclear granulocytes and sensory neurons. Our findings suggest that targeting neutrophils may be useful therapeutic targets for pain control in fibromyalgia.”
Unbiased immune profiling reveals a natural killer cell-peripheral nerve axis in fibromyalgia
Conclusion: “This study identified a neuro-immune interface between peripheral nerves and NK cells in FMS patients that suggests a novel mechanism for FMS pathogenesis and a new direction in the development of therapeutic options to treat this poorly managed syndrome.”
Neuropeptides CRH, SP, HK-1, and Inflammatory Cytokines IL-6 and TNF Are Increased in Serum of Patients with Fibromyalgia Syndrome, Implicating Mast Cells
Passive transfer of fibromyalgia symptoms from patients to mice - PubMed
We can “give” fibromyalgia to mice by transferring fibromyalgia patients’ antibodies to them. Symptoms resolve when antibodies are taken away. Strongly suggests fibromyalgia has an autoimmune component.
I take Nuvigil (armodafinil) which is an isomer of Provigil (modafinil), which was shown to reduce neuroinflammation. Nuvigil takes away a lot of my pain.
%3Amax_bytes(150000)%3Astrip_icc()%2FGettyImages-1150384558-58231110548b4034b13f4582244c384b.jpg?width=92&height=&ar=&mode=&format=avif&dpr=2)