Fibromyalgia(FM) may be anautoimmune disease, where your immune system attacks healthy cells by mistake.

For years, the evidence seemed to point away from that.

This issue is still far from decided, but opinion may be swaying back toward autoimmunity.

Areas Impacted by Neuroinflammation in Fibromyalgia

Verywell / Shideh Ghandeharizadeh

It also discusses why not all inflammation is created equal and why these research findingsif accurateare important.

What Is Autoimmunity?

Autoimmune diseases can affect single or multiple organs.

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.

Is Fibromyalgia an Autoimmune Disease?

For decades, fibromyalgias very existence was controversial.

Early on, some doctors who believed in FM classified it as arthritis-like.

Now, FM is seen as a complex, multi-symptom illness.

Rates ranged from about 19%to 73%.

Gangliosides may be an important aspect of FM autoimmunity.

Theyre believed to be involved in small-fiber neuropathy.

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 whats causing symptoms, it could point to new diagnostic tests and treatments.

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.

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.

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.

Its a necessary function.

But when it becomes chronic, inflammation causes tissue damage.

Its 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.

Some of these areas play roles in functions that are often dysregulated in people with FM.

A Different punch in 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.

When tissues expand beyond their normal size, they cause pain by putting pressure on surrounding structures.

Arthritic fingers hurt because theyre inflamed.

Neuroinflammation doesnt cause the same issues.

Instead, it causes neurological problems that lead to neurological symptoms.

Research suggests neuroinflammation is behind central sensitization.

Inflammatory markers for fibromyalgia tend to be slightly elevated.

Drugs that suppress microglia and astrocytes may be useful for treating neuroinflammation.

However, theyve historically been considered ineffective for FM pain.

Hyperalgesia makes your pain signals more intense, basically turning up the volume of pain.

Allodynia makes things hurt that shouldnt, like a loose waistband or a hand rubbing lightly against your skin.

That provides another explanation for neuroinflammation.

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.

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.

Summary

Research has uncovered some evidence that FM may be 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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