Here’s a blog entry I wrote for my physiology course, naturally it’s not a complete understanding of fibromyalgia, but contains some interesting info from some scholarly articles that I read. Ignore the portion on drug therapies if that’s beyond your interest! -K
Fibromyalgia is a controversial chronic pain syndrome that is not entirely understood, nor always easily treated. It is estimated that 2% of the American population has it with a proportion of 9:1 women to men affected. People commonly have associated symptoms including chronic fatigue, insomnia, mood disorders, depression, headaches, and other problems. Risk factors include self-reported depression, psychiatric disorders, psychosocial stresses, physical injury/trauma in the workplace, and a link has been explored between the development of fibromyalgia and infections including Lyme disease, HIV, other viral infections, and Hepatitis A and B. Researchers are exploring genetic risk factors and have found that first-degree relatives of people with fibromyalgia are eight times more likely to develop fibromyalgia, a genetic link that is stronger than that of family members developing rheumatoid arthritis.
The main characteristic of the condition is that patients have process pain signals abnormally. The increased sensitization to pain either occurs in the peripheral nerves or the central nervous system. An injury is often associated with peripheral nerve sensitization, whereas an actual change within the CNS can cause spinal cord excitability, increased size of pain reception fields, and the lowering of pain thresholds. Other research has shown that pain signals are increased, such that the nerve cells release more Substance P (a neuropeptide associated with pain sensation) and excitatory amino acids than normal. This has a domino effect in that the next nerve cells become hyperexcited and in turn release more Substance P and excitatory amino acids. Glial cells also join the pain party in increasing the excitement and pain signaling. The concept of Temporal summation in Guyton/Hall is amplified in patients with fibromyalgia, who experience more pain and for longer periods of time than normal patients. Some researchers view this as evidence that the problem is in the CNS.
Treatment at this point seems to entail a multi-therapy approach. Drugs include tricyclic antidepressants such as amitriptyline and nortriptyline, cyclobenzaprine, tizanidine, SSRIs, pregabalin and gabapentin and SNRIs are all involved in treatment. Research indicates that combinations often work better. There is not enough data to indicate the effectiveness of opioids, and NSAIDs were not found to be effective. Therapies outside of drugs are encouraged and being explored, such as exercise, and mental health therapies. Because it is such a complex syndrome, research will continue into treatments, pharmacologic and nonpharmacologic alike.
Saxena, Amit, M.D., and Bruce M. Solitar, M.D. “Fibromyalgia Knowns, Unknowns and Current Treatment.” Bulletin of the NYU Hospital for Joint Disease. 2010. http://www.ncbi.nlm.nih.gov/pubmed/20969544
Staud, Roland. “Biology and Therapy of fibromyalgia: pain in fibromyalgia syndrome.” Division of Rheumatology and clinical immunology, McKnight Brain Institute, University of Florida. 2006. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1526632/?tool=pubmed