Table of ContentsView AllTable of ContentsWhat Is Autoimmunity?Is Fibromyalgia an Autoimmune Disease?What Research Says
Table of ContentsView All
View All
Table of Contents
What Is Autoimmunity?
Is Fibromyalgia an Autoimmune Disease?
What Research Says
Some research suggests FM may be an autoimmune disease involving neuroinflammation, an inflammatory response within the brain and spinal cord, and small-fiberneuropathy, which is weakness and pain from nerve damage.That hypothesis isn’t getting widespread acceptance in the medical community, though.
This article looks at what this research says about the evidence for autoimmunity, neuroinflammation, and small-fiber neuropathy in fibromyalgia. It also discusses why not all inflammation is created equal and why these research findings—if accurate—are important.
Autoimmunity describes an immune reaction directed against normal organs/tissues of the body that causes damage, inflammation, or disease. The body’s immune system, which ordinarily attacks intruders like viruses, bacteria, and even cancer cells, mistakes healthy cells or tissue for dangerous pathogens and then attacks and tries to destroy them.
Autoimmune diseases can affect single or multiple organs. Examples of organ-specific autoimmune diseases include:
Systemic autoimmune diseases can cause different issues, as their effects are felt throughout the body. Examples include:
Symptoms of autoimmune diseases vary widely depending on the organ(s) affected. However, some symptoms are common among many disorders. General symptoms may include:
Symptoms may worsen, improve, and then worsen again in an unpredictable manner.
For decades, fibromyalgia’s very existence was controversial. But not anymore. Early on, some doctors who believed in FM classified it as “arthritis-like.”
Many medical experts suspected autoimmunity because of the condition’s similarities to known autoimmune diseases such as lupus, Sjögren’s disease, rheumatoid arthritis, and multiple sclerosis.
However, early research failed to turn up the hallmarks of autoimmune disease, including:
Later, FM was considered a pain condition that was believed to be neurological or neuroimmune. The termcentral sensitivity syndromedeveloped as an umbrella term for FM and related illnesses, includingmyalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS),irritable bowel syndrome (IBS), andmigraine.
Now, FM is seen as a complex, multi-symptom illness. What’s more, some evidence suggests it isn’t actually missing those hallmarks of autoimmunity:
What You Need to Know About the Nervous System
Fibromyalgia has always borne a striking resemblance to autoimmune diseases.
Research published in 2019 laid out the many factors they have in common:
Autoantibodies
Researchers believe they may have found the smoking gun of autoimmunity in FM as well. They discovered that several autoantibodies were unusually high in people with FM, including those for:
None of these were found in every person with FM. Rates ranged from about 19%to 73%.
Gangliosides may be an important aspect of FM autoimmunity. They’re believed to be involved in small-fiber neuropathy.
Giving Fibromyalgia to Mice
In a groundbreaking 2021 study, researchers took antibodies (immunoglobulin G, IgG) from people with FM and injected them into mice. The mice then:
Researchers say the FM IgG appeared to target white-matter brain cells (glia), gray-matter brain cells (neurons), and certain nerve fibers. This shows how immune system activity can cause neurological symptoms.
The ability to transfer FM like this is nothing short of revolutionary. On top of providing evidence about what’s causing symptoms, it could point to new diagnostic tests and treatments.
How Your Immune System Reacts to the Common Cold
Diagnosis and Treatment
If more research validates findings of autoimmunity in fibromyalgia, it could lead todiagnostic tests. Because fibromyalgia is currently adiagnosis of exclusion, that would be an important change.
A 2022 study focused on identifying biomarkers for diagnosing and managing fibromyalgia, found that study participants with FM had elevated levels of 19 inflammatory serum proteins, indicating widespread inflammation.
Manyimmunosuppressive drugsfor autoimmune diseases are already on the market. That greatly expands treatment options, especially since the drugs could be used off-label right away.
Whether current immunosuppressants are safe and effective for FM remains to be seen.
Why Autoimmune Diseases Affect More Women Than Men
Neuroinflammation
Several studies have now confirmed neuroinflammation in fibromyalgia. Some also have looked at where it is in the brain and what may be driving it.
Inflammation is a complex immune response to injury and infection. It’s a necessary function. But when it becomes chronic, inflammation causes tissue damage. It’s especially harmful to the nervous system.
Verywell / Shideh Ghandeharizadeh
The nervous system and immune system work together to create neuroinflammation. FM research links several cells and one molecule to the process.
Neurological components include:
Immune system components include:
A 2021 study looked at where brain inflammation is in FM.Researchers found several areas with abnormal inflammation compared with healthy people in the control group.
Some of these areas play roles in functions that are often dysregulated in people with FM. They include:
They also found abnormally low inflammation-related activity in the:
Neuroinflammation in the amygdala, left medial frontal, and left superior parietal gyri was associated with higher pain scores. Neuroinflammation in the left amygdala, left medial frontal, and left superior frontal gyri was associated with higher stress responses, which included measures of fatigue, tension, frustration, depression, somatization, and aggression.
How Your Brain Works
A Different Type of Inflammation
Neuroinflammation has different effects than “typical” inflammation in the joints and soft tissues. Typical inflammation causes pain in many conditions, such as arthritis and multiple sclerosis.
Neuroinflammation doesn’t cause the same issues. Instead, it causes neurological problems that lead to neurological symptoms.
FM pain is believed to come from central sensitization, which is a heightened response to pain in the central nervous system. Research suggests neuroinflammation is behind central sensitization.
Inflammatory markers for fibromyalgia tend to be slightly elevated. However, the cells and molecules involved in the neuroinflammation of FM may provide new diagnostic markers to look for.
Drugs that suppress microglia and astrocytes may be useful for treating neuroinflammation. They include:
Other existing treatments for neuroinflammation include:
Several other drugs are under development for neuroinflammation, most of them developed as potentialParkinson’s disease treatments.Anti-inflammatory drugsare often prescribed for neuroinflammatory diseases as well. However, they’ve historically been considered ineffective for FM pain.
Small-Fiber Neuropathy
Small-fiber neuropathy (SFN) is nerve damage that’s only in the small sensory nerves of the skin.It’s probably best known in association withtype 2 diabetes.
As in FM, the pain comes and goes and is described as:
Also like FM, SFN involves the abnormal pain typeshyperalgesiaandallodynia. Hyperalgesia makes your pain signals more intense, basically “turning up the volume” of pain. Allodynia makes things hurt that shouldn’t, like a loose waistband or a hand rubbing lightly against your skin.
The 8 Types of Fibromyalgia Pain
SFN and fibromyalgia also have these symptoms in common:
FM research suggests some damaged nerves are part of anti-inflammatory processes. That provides another explanation for neuroinflammation.
Typical SFN vs. Fibromyalgia SFN
The typical diagnostic test for SFN is askin punch biopsy. A small amount of skin is removed with a circular tool and examined under a microscope. The focus is on nerve fiber density in the skin.
SFN is treatable, and small nerves continue to grow throughout life. That means they can repair the damage.
Standard SFN treatments are already heavily used for fibromyalgia. They include:
In a pilot study, treatment withintravenous immunoglobulin(IVIg) has been shown to improve SFN in FM. This treatment is known to be effective against autoimmune-related neuropathy. Biopsies confirmed that nerves showed less damage after treatment.
Ganglioside autoimmunity may suggest treatment options as well. Gangliosides are suspected of being involved with diabetes-related small-fiber neuropathy. Some early animal research has suggested that ganglioside-targeted treatments may improve neuropathic pain.
Currently, researchers are working on drugs called ganglioside GM3 synthase inhibitors.Evidence suggests that these may work as both oral medication and topical treatments.
Summary
Research has uncovered evidence that FM is an autoimmune disease. Neuroinflammation and small-fiber neuropathy appear to be important elements of it. Autoantibodies could provide diagnostic markers for FM. Immunosuppressants may be treatment options. Neuroinflammation and SFN also offer potential diagnostic markers. Existing treatments are on the market. Some experimental drugs are in the works as well.
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