Although Fibromyalgia Syndrome (FMS), is one of the most common chronic pain syndromes, we still don't know much about it.The debilitating condition, which is marked by fatigue and widespread pain, has been understudied for decades. While it's generally believed to be caused by the brain, there is no way to know how it starts or how to treat it. Many patients feel utterly gaslighted by doctors, who claim it doesn't exist.Recent research using mice has provided further evidence that fibromyalgia may not be a real condition, but could also have an autoimmune response.Researchers injected mice with antibodies from 44 people with the syndrome. They noticed some classic symptoms, such as muscle weakness, tenderness and increased heat/cold sensitivity. Their pain-sensing nerves were more sensitive all around them.However, mice injected with antibodies from 39 healthy individuals showed no symptoms.These pain-causing antibodies weren't found in patients' central nervous systems, so the authors believe fibromyalgia may be a condition of the immune system and not an illness that arises in the brain.This is not surprising as 80% of people suffering from fibromyalgia (fibromyalgia) are women. However, brain imaging studies have led many scientists to believe that fibromyalgia may be neurological in origin.Recent genetic studies have shown that fibromyalgia may be an autoimmune condition.Andreas Goebel, a pain medicine student at the University of Liverpool, says, "When I started this study in the UK I expected that some cases of fibromyalgia may be auto immune."It turned out that the same antibodies which caused pain in mice were also found in all 44 people with fibromyalgia in the United Kingdom as well as in Sweden.This study only examines how human antibodies function in mice. Further research is needed to discover how these antibodies cause pain and fatigue.However, these findings suggest that fibromyalgia could have an autoimmune cause and not be neurological. These pain-causing antibodies were found to be able to bind to both human and mouse neurons in the study. This could indicate that these markers may be responsible for some of the neurological changes seen in brain scans.This could explain why antidepressants and gentle exercise don't work well for many people.The drugs that target the control of antibody levels could prove to be more effective.After a few weeks, the mice were freed from all pain-causing antibodies and the animals returned to normal.If the pain-causing antibody are managed, fibromyalgia symptoms may be quickly reversed.We already have drugs that can do this, thankfully. We just have to test them.David Andersson, a neuroscientist from King's College London, says that "our work has uncovered an entire new area of therapeutic options" and should offer real hope for fibromyalgia sufferers.Andersson plans to expand his research by using antibodies from patients with chronic COVID (myalgic encephalomyelitis/chronic tired syndrome) in similar mouse studies. These two chronic conditions have many symptoms in common with fibromyalgia. They have also been linked to autoimmune problems.Although the question of whether fibromyalgia can be considered neurological or immunological remains open to debate, this evidence certainly casts doubt on previous assumptions."If these results are replicated and extended upon, then there would be an extraordinary prospect for a new treatment of people with Fibromyalgia," Des Quinn (chair of Fibromyalgia Action UK) told The Guardian."However, these results require further investigation and confirmation before they can be universally applied."The Journal of Clinical Investigation published the study.
