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What was fibromyalgia before?

Fibromyalgia is a complex chronic pain disorder characterized by widespread musculoskeletal pain, fatigue, sleep problems, and emotional distress. The exact causes are still unknown, but research suggests it involves abnormalities in how the brain processes pain signals. While fibromyalgia is now a recognized medical condition, this was not always the case.

When was fibromyalgia first identified?

The term “fibromyalgia” first emerged in the medical literature in the 1970s. However, the symptoms we now associate with fibromyalgia have been described for centuries:

  • In the early 1800s, symptoms resembling fibromyalgia were referred to as “muscular rheumatism.”
  • In the mid-1800s, terms like “fibrositis” and “muscular rheumatism” were used to describe widespread pain and tenderness.
  • In 1904, a condition called “fibrositis” with symptoms of diffuse aches and tender points was described.

But fibromyalgia was not defined as a distinct clinical entity until the 1970s when researchers began studying the condition more systematically.

1976 – First official definition

The first official definition of fibromyalgia came in 1976 when researcher Dr. Hugh Smythe presented criteria for the condition at the American Rheumatism Association meeting. He proposed the term “fibrositis” to describe patients with chronic widespread pain, fatigue, and tender points throughout the body.

1981-1990 – New name and criteria

In 1981, the term “fibromyalgia” was proposed by Dr. Muhammad Yunus as an alternative to fibrositis. The term blended “fibro” meaning fibrous tissues, “my” meaning muscles, and “algia” meaning pain.

In the 1980s, the American College of Rheumatology began studying fibromyalgia more systematically. In 1990, the ACR published the “1990 Criteria for the Classification of Fibromyalgia” which laid out the first official diagnostic guidelines.

When did fibromyalgia become an accepted diagnosis?

While research on fibromyalgia ramped up in the 1980s, it was still poorly understood and controversial in the medical community. Many doctors remained skeptical about recognizing it as a true clinical condition. But over time, research and clinical experience led to greater validation and acceptance:

  • In 1987, the FDA approved the first medication for fibromyalgia – cyclobenzaprine.
  • In 2007, the FDA approved pregabalin (Lyrica), the first medication specifically approved for fibromyalgia.
  • In 2010, the ACR published revised diagnostic criteria that are still used today.
  • The 2010 criteria reduced the number of tender points required for diagnosis from 11 of 18 to just a general regional distribution.

These developments reflected the medical community’s growing understanding of fibromyalgia as a legitimate syndrome driven by central nervous system dysfunction rather than solely a musculoskeletal issue.

How common is fibromyalgia?

Early studies estimated fibromyalgia affected around 3-6 million Americans, though true prevalence was difficult to ascertain since the condition lacked defined diagnostic criteria. Current estimates suggest fibromyalgia affects around 2-6% of the global population with between 2-4% prevalence in the US. This equates to around 10 million Americans and over 100 million people worldwide.

Some key facts about fibromyalgia prevalence:

  • Between 75-90% of fibromyalgia patients are women.
  • Onset is most common between ages 30-50.
  • Prevalence rises with age, peaking around age 70.
  • Fibromyalgia often runs in families.

The following table summarizes some statistics on fibromyalgia prevalence globally:

Country/Region Estimated Prevalence
United States 2-6%
Canada 3.3-5.8%
Europe 2.5-6%
Mexico 2.4%
South Korea 1.2-6.2%
Japan 1.7%

What were early explanations for fibromyalgia pain?

With no clear external cause, early theories tried to pin fibromyalgia pain on psychological factors or inflammation in muscles and joints. These included:

Psychogenic theories

Some believed fibromyalgia was purely a psychological condition or “psychogenic rheumatism” caused by mental factors like hysteria or depression. This contributed to perceptions that it was “all in people’s heads.”

Inflammatory theories

Terms like fibrositis suggested inflammation of muscle, ligament, and tendon tissues caused the widespread pain. Early criteria focused heavily on identifying tender points at certain muscle-tendon junctions.

Trauma theories

Physical trauma like automobile accidents were hypothesized as potential triggers since many patients reported onset after an injury. However, no clear evidence linked trauma alone to developing fibromyalgia.

Viral or immune theories

Some research suggested viral infections or autoimmune dysfunction could be potential triggers. However, no clear infection or autoantibodies have been consistently identified.

Deconditioning theories

Lack of physical conditioning and muscle strength was proposed as enabling chronic pain. But strengthening exercises alone showed limited ability to resolve fibromyalgia pain.

How does our understanding of fibromyalgia differ today?

While the exact causes are still unclear, today fibromyalgia is thought to be rooted in central nervous system dysfunction – specifically in how the brain processes pain signals – rather than a problem with muscles, joints, viruses, or emotions. Key aspects of the modern understanding include:

Central sensitization

Research shows people with fibromyalgia have increased sensitivity to pain signals due to abnormal sensory processing in the nervous system. This “central sensitization” leads to heightened pain from even minor stimuli.

Pain circuits

Brain imaging shows people with fibromyalgia have altered activation of neural pain circuits, including increased activity in areas related to pain processing and emotional aspects of pain.

Neurochemical imbalances

Imbalances in neurotransmitters that modulate pain response, such as serotonin, norepinephrine, and substance P, are believed to dysregulate pain signaling.

Neuroendocrine disruption

Dysfunction in the hypothalamic-pituitary-adrenal axis influences stress responses and may relate to pain sensitivity, fatigue, and cognitive problems in fibromyalgia.

Genetic factors

Certain genetic variants affecting neurotransmitter systems have been associated with increased fibromyalgia risk, pointing to a biological basis.


In summary, fibromyalgia has moved from a controversial, misunderstood condition to an accepted clinical disorder recognized as being rooted in dysfunctional central pain processing. While gaps remain in our understanding, continued research centered around the neurobiology of fibromyalgia will hopefully lead to improved treatments.