The cause of Fibromyalgia is not known but it’s likely that a number of factors contribute to its development. Researchers have a number of theories about the causes or triggers of the syndrome. Some of the theories include:

Injury or trauma to either the musculoskeletal or nervous system (Peripheral Sensitization)

This can lead to a phenomenon of peripheral sensitization of the sensory nervous system through nociceptive activation. This can be seen in such conditions as arthritic disorders, peripheral nerve damage as in diabetic neuropathy or postherpetic neuralgia and in sympathetic modulation as in reflex sympathetic dystrophy (aka complex regional pain syndrome)

Neurological alterations (Central Sensitization)

Many researchers agree that Fibromyalgia is a disorder of central processing with neuroendocrine /neurotransmitter dysregulation. In other words Fibromyalgia is a pain amplification syndrome. This central sensitization theory states that people with Fibromyalgia have a lower threshold for pain due to increased brain sensitivity to pain signals. Researchers believe repeated nerve stimulation causes the brains of Fibromyalgia patients to change. This change involves an abnormal increase in levels of certain neurotransmitters, chemicals in the brain that cause nerves to communicate, and is believed to result from overwhelming the “gated” protective mechanism of afferent sensory inputs into the dorsal root ganglion of the spinal column. A “wind­up” phenomenon, repetitive stimulation of C-fibers leading to a progressive increase in electrical charges from second order neurons in the spinal cord resulting in amplification of sensory impulses in the CNS, develops creating greater painful discomfort than is seen in normal people. Large my­elinated A-fibers, smaller C-un­myelinated fibers, and autonomic B-fibers carry sensory information that is perceived as amplified pain, hypervigilance, and allodynia. Unfortunately, it is not known what initiates the process of central sensitization but it is interesting to note that cen­tral sensitization is seen in other syndromes in­cluding irritable bowel syndrome (IBS), irritable bladder syndrome, chronic pelvic pain, chronic fatigue syndrome, tension headache, and temporomandibular joint dysfunc­tion syndrome.

Sleep disturbances

Some researchers theorize that disturbed sleep patterns may be a cause rather than just a symptom of Fibromyalgia.

Changes in muscle metabolism

It has been suggested that deconditioning and decreased blood flow to muscles may contribute to fatigue and decreased endurance. Endurance is a function of how efficient the body is at getting oxygen and nutrients to the muscle and then carting away the waste products. Therefore, anything that affects one of these variables can play a role. Metabolic alterations and abnormalities in the hormonal substance that influence nerve activity may also play a role.

Infectious agents

Some researchers theorize that a viral or bacterial infection may trigger Fibromyalgia. While it is not an exhaustive list, some of the agents implicated have included hepatitis C, Epstein-Barr virus, Lyme disease.

Endocrine disturbances

Thyroid disease is commonly associated with Fibromyalgia and may play a contributing role in its cause.

Post-traumatic stress

A smoothly functioning hormonal stress response system controlled by the hypothalamus-pituitary-adrenal (HPA) axis helps the body remain stable under physiological and psychological stress through the actions of three hormones. Fibromyalgia patients have been shown to have reduced function of the HPA hormone system. Some researchers also believe that in individuals with post-traumatic stress disorder (PTSD), the HPA axis response is dysregulated. Individuals with PTSD have low circulating levels of cortisol. In one study of motor vehicle accident victims, low cortisol levels immediately after the accident were associated with the development of PTSD and high cortisol levels were associated with the development of depression. Additionally, psychological trauma, resulting from childhood physical abuse or maltreatment, exerts enduring negative effects on the developing brain and induces a cascade of physiological effects, including changes in hormones and neurotransmitters in vulnerable brain regions.

Abnormalities of the autonomic (sympathetic) nervous system

People with Fibromyalgia appear to have a problem with a vast network of nerve pathways throughout the brain, spinal cord, and body known as the autonomic nervous system. The autonomic nervous system may be thought of as the “automatic” nervous system that runs the life support functions typically not under conscious control. These functions include heart rate, blood vessel contraction, sweating, salivary flow and intestinal movements.

Hormonal influence

Researchers have found little correlation with the sex hormone estrogen despite the fact that Fibromyalgia is more common in women than men. However, many women find that their symptoms greatly improve during pregnancy.  Additionally, Fibromyalgia patients produce less cortisol in response to stress than do healthy people, possibly having to do with a defect in the HPA axis. When the body is deficient in cortisol, the symptoms of Fibromyalgia are mirrored. However, it is not clear how important cortisol deficiency is in the onset or course of Fibromyalgia but it is known that giving patients corticosteroid medications does not improve the condition.

Genetic influence

One theory suggests a genetic predisposition to developing an autonomic or central nervous system disorder (i.e., a disorder of the brain and spinal cord) that affects the response to severe pain. Another theory evolved from the parent-child relationships seen in Fibromyalgia that suggest a genetic cause. One study has shown that an autosomal dominant basis exists for Fibromyalgia.

Fibromyalgia and reduced pressure pain thresholds have been shown to aggregate strongly within families. An individual is 8.5 times more likely to develop Fibromyalgia if they have a family member with Fibromyalgia versus a family member with rheumatoid arthritis.

 

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