Fibromyalgia Syndrome

Overview of Fibromyalgia Syndrome (fibromyalgia syndrome. FS) is a non-sexual articular rheumatism, clinical manifestations of musculoskeletal pain and multiple Fajiang. and the location of special tenderness point. Fibromyalgia Syndrome can be secondary to trauma, various rheumatism, bone arthritis (osteoarthritis, the OA), Rheumatoid arthritis (rheumatoid arthritis, RA) and various non-rheumatic diseases (such as hypothyroidism, cancer). This type of fibromyalgia syndrome is called secondary Fibromyalgia Syndrome (secondary fibromy syndromen algia), if not accompanied by other disorders, they were called primary fibromyalgia syndrome (primary fibromyagia syndrome ). Cause pathogenesis of the disease mechanism is not yet clear. Reported in the literature and sleep disorders, abnormal secretion of neurotransmitters and immune disorders. 1. Sleep disorders of sleep disorders involving 60-90% of patients. Sleep easy for the performance of them, dreams, early morning lack of energy, fatigue, body pain and morning stiffness flu. Night EEG records found Europium wave of intervention ??elta; wave sleep. Interference with volunteers ringing non-rapid eye movement sleep (non rapid eye movement) can induce These graphics EEG and clinical symptoms. Other factors affect sleep as mental stress, environmental noise may increase symptoms of fibromyalgia syndrome. It is speculated that this ??normal sleep in fibromyalgia syndrome came straight hair plays an important role. 2. Abnormal secretion of neurotransmitters serotonin reported in the literature (serotonin, 5-HT) and substance P (SP) and other neurotransmitters in the incidence of the disease plays an important role. Serotonin is the precursor tryptophan, a food protein tryptophan absorption in the intestine, the majority of plasma protein binding. small part of the state was free. Free tryptophan could be carried through the vector of blood-brain barrier into the brain tissue. Then, in the 5-HT neurons by hydroxylation and decarboxylation role Generation 5-HT. Released into the synaptic gap of 5-HT, in part by the presynaptic nerve endings uptake, some of mitochondrial monoamine oxidase activity generated role of 5-hydroxytryptamine indole acetic acid (5-hydroxyindo le acetic acid). 5-HT also exists in the gastrointestinal mucosa, platelets and breast cells, as it is difficult through blood-brain barrier, Therefore, the central nervous system and peripheral blood of the 5-HT belong to the two systems. After study found : ?٠fibromyalgia syndrome patients plasma free tryptophan and transshipment rate (trannsport ratio) reduce. And reduce the extent of musculoskeletal pain was related to that of plasma concentration and rotation rate, the lower the more obvious pain. ?ڠplatelet membrane of the high affinity 5-HT receptor, Imipramine with 5-HT competitive combination of platelet receptor, Tritium-labeled imipramine in the platelet membrane of 5-HT receptor density, found fibromyalgia syndrome than normal by the role. ?۠muscle fibers before the syndrome is the human brain tissue 5-HT than normal noticeably reduced. Experiments show ,5-HT can regulate non-rapid eye movement sleep, reduce sensitivity to pain, improve depression, can also enhance the analgesic effect of anesthesia. Amitriptyline (arrhythmia) and amine benzene ring heptene (cyclobenzaprin e) 5-HT to 5-hydroxy-indoleacetic acid B enzyme conversion, and increased 5-HT concentrations, it is of fibromyalgia syndrome is effective. Instead, give tryptophan hydroxylase inhibitor-of PCPA (parachlorophenylalami ne) appear like fibromyalgia syndrome pain, out of this drug, the pain disappeared. Another with the fibromyalgia syndrome is a neurotransmitter substance P. Littlejohn found, physical or chemical stimulation induced fibromyalgia syndrome patients with congestive obvious reaction of the skin, Such an overreaction may persist, with the stimulation of peripheral damage. As these exciting and skin-injury receptor (polymodal cutaneous nociceptor) Anti - radioactive release from the nerve endings pathology of Substance P, which can cause local vasodilator, Vascular permeability increase and a neurogenic inflammation (neurofibromas inflammmation ). Nerve endings release of substance P, the dorsal root ganglion sensory neurons of the primary will be no more synthetic substance P, in order to maintain a constant level. Synthesis of substance P also to the peripheral and central two-way transmission, the central nervous system of substance P levels increased. Because of its slow but strong and lasting excitement, the central nervous system will have been affected to some extent. It was also discovered that in normal or high levels of 5-HT exist, Substance P sensory nerve impulses to the dissemination of a damping effect. Lack of 5-HT, it will lose this control, resulting in hyperalgesia. 3. Immune disorder some authors reported in fibromyalgia syndrome patients dermal-epidermal junction and an immune reaction deposition, used electron microscopy found fibromyalgia patients comprehensive muscle capillary endothelial cell swelling, suggest acute vascular injury; tissue hypoxia and permeability-increasing. Patients often to the unexplained weight gain, swelling of hands and diffuse nocturia and may increase the permeability increase. In addition, a preliminary study found that IL-2 (interleukin-2. IL-2) levels in fibromyalgia syndrome increased. Receiving IL-2 treatment of cancer patients born fibromyalgia syndrome - like symptoms, including extensive pain, sleep disorders, morning stiffness and tenderness there, and so on. Europium also found that interferon can cause fatigue. These phenomena suggest immune disorder. Vivo cytokine levels and abnormal fibromyalgia syndrome came straight to the hair.