Mechanisms involved
This condition is explained through the mechanisms below. Each one is taught as ordinary physiology first.
Primary
Secondary / contributing
Pain-processing visual
The volume changes. The signal can stay small.
Pain is real
Amplification changes the output; it does not make the experience imagined.
Sleep changes gain
Unrefreshing sleep weakens descending inhibition and raises sensitivity.
Several inputs add
Pain, sensory load and autonomic strain can feed the same processing system.
Conceptual, not a diagnostic test. Fibromyalgia is a positive clinical diagnosis; this diagram shows the pain-processing model behind lowered thresholds and impaired inhibition.
Immune cells involvedWho is actually in the tissue
Not an inflammatory arthritis — but not immunologically silent either.
Selected cell
Mast cell
Tissue sentinel packed with histamine, tryptase and prostaglandin granules. When it degranulates it recruits and sensitizes nearby nerve endings.
Skin mast cell numbers are raised in several studies, sitting alongside small fiber changes.
Schematic drawings, not micrographs. Immune findings here describe mechanism and association; none of them are diagnostic tests.
What it is
Diagnosed by widespread pain and symptom severity over at least three months, using the ACR criteria. It is a positive diagnosis based on pattern, not a label applied when tests are negative, and it can coexist with any structural disease rather than replacing it.
How the mechanisms produce this
- Quantitative sensory testing shows lowered thresholds and impaired descending inhibition — this is the pain-processing mechanism made measurable.
- Non-restorative sleep both results from and worsens the amplification, forming the central loop.
- Autonomic involvement is common and explains the orthostatic and gut symptoms that often accompany it.
- Small-fiber abnormalities are found in a meaningful subset, blurring the peripheral-central line.
What tends to help
- Exercise has the strongest evidence of anything available — but must be graded and paused for post-exertional malaise.
- Sleep treated as a primary target, not an afterthought.
- Duloxetine, amitriptyline or pregabalin trialled with defined endpoints; opioids perform poorly.
- Coexisting structural disease investigated on its own merits, not dismissed under the label.
Where the evidence is thin
Whether fibromyalgia is one condition or several with a shared endpoint is unresolved.