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Fibromyalgia

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Fibromyalgia

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fibromyalgia tender points diagram

Anatomical diagram and infographic illustrating the 18 specific tender points used in the diagnosis of fibromyalgia, as defined by the 1990 American College of Rheumatology (ACR) criteria. The image features two stylized human silhouettes—one anterior and one posterior—with bilateral orange/red dots marking the location of the tender points. The points are distributed across the body including: suboccipital muscle insertions (occiput), low cervical intertransverse spaces (C5-C7), midpoint of the upper trapezius border, supraspinatus origins above the scapular spine, second costochondral junctions, 2 cm distal to the lateral epicondyles, upper outer quadrants of the gluteal muscles, posterior to the greater trochanteric prominence, and the medial fat pad of the knee proximal to the joint line. A text panel on the right provides a structured list of these nine bilateral pairs, totaling 18 points, with brief anatomical descriptions for each site. This educational material is designed for clinical training in rheumatology and physical examination techniques.

Anatomical diagram and infographic illustrating the 18 specific tender points used in the diagnosis of fibromyalgia, as defined by the 1990 American College of Rheumatology (ACR) criteria. The image features two stylized human silhouettes—one anterior and one posterior—with bilateral orange/red dots marking the location of the tender points. The points are distributed across the body including: suboccipital muscle insertions (occiput), low cervical intertransverse spaces (C5-C7), midpoint of the upper trapezius border, supraspinatus origins above the scapular spine, second costochondral junctions, 2 cm distal to the lateral epicondyles, upper outer quadrants of the gluteal muscles, posterior to the greater trochanteric prominence, and the medial fat pad of the knee proximal to the joint line. A text panel on the right provides a structured list of these nine bilateral pairs, totaling 18 points, with brief anatomical descriptions for each site. This educational material is designed for clinical training in rheumatology and physical examination techniques.

A medical illustration depicting the pathophysiology of central sensitization and pain processing pathways, specifically in the context of fibromyalgia. The graphic features a neuroanatomical diagram of the ascending and descending pain pathways alongside human figures marking tender point locations. The ascending pathway (orange line) begins at peripheral nociceptors, travels through the peripheral nerve to the dorsal ganglia of the spinal roots, enters the dorsal horn of the spinal cord, and terminates in the brain (CNS), where 'PAIN' perception occurs. A descending inhibitory pathway (green line) is shown originating in the brain but is intersected by a black prohibition symbol, indicating 'Descending fibers inhibition' failure or dysfunction. An inset image displays anterior and posterior human silhouettes with yellow circles marking 18 classic fibromyalgia tender points, including the neck, chest, elbows, hips, and knees. Text annotations explain that sensitization of nociceptive fibers causes pain perception from non-painful sensory stimuli, illustrating the concepts of hyperalgesia and allodynia.

A medical illustration depicting the pathophysiology of central sensitization and pain processing pathways, specifically in the context of fibromyalgia. The graphic features a neuroanatomical diagram of the ascending and descending pain pathways alongside human figures marking tender point locations. The ascending pathway (orange line) begins at peripheral nociceptors, travels through the peripheral nerve to the dorsal ganglia of the spinal roots, enters the dorsal horn of the spinal cord, and terminates in the brain (CNS), where 'PAIN' perception occurs. A descending inhibitory pathway (green line) is shown originating in the brain but is intersected by a black prohibition symbol, indicating 'Descending fibers inhibition' failure or dysfunction. An inset image displays anterior and posterior human silhouettes with yellow circles marking 18 classic fibromyalgia tender points, including the neck, chest, elbows, hips, and knees. Text annotations explain that sensitization of nociceptive fibers causes pain perception from non-painful sensory stimuli, illustrating the concepts of hyperalgesia and allodynia.

A comparative anatomical diagram of the human brain illustrating functional connectivity (FC) changes in patients with fibromyalgia across three conditions: Baseline, Sham transcranial Direct Current Stimulation (tDCS), and Real tDCS. The diagrams utilize sagittal brain outlines to map regions of interest including the primary motor/somatosensory cortex (M1/S1), thalamic nuclei (VL/VPL), anterior/posterior insula (ant/post ins), periaqueductal gray (PAG), amygdala (amyg), and cerebellum (cer). At baseline, red solid lines indicate that stronger FC between M1/S1, VL/VPL, ant ins, and PAG predicts a better analgesic response. Under the Sham tDCS condition, dashed blue lines represent a main effect of connectivity changes, while solid blue lines show decreased FC correlating with analgesia between the thalamus and posterior insula/M1. In the Real tDCS condition, distinct pathways of decreased FC are shown between the VL/VPL thalamus and the medial prefrontal cortex (mPFC), supplementary motor area (SMA), and cerebellum, highlighting the neural mechanisms of neuromodulation-induced pain relief.

A comparative anatomical diagram of the human brain illustrating functional connectivity (FC) changes in patients with fibromyalgia across three conditions: Baseline, Sham transcranial Direct Current Stimulation (tDCS), and Real tDCS. The diagrams utilize sagittal brain outlines to map regions of interest including the primary motor/somatosensory cortex (M1/S1), thalamic nuclei (VL/VPL), anterior/posterior insula (ant/post ins), periaqueductal gray (PAG), amygdala (amyg), and cerebellum (cer). At baseline, red solid lines indicate that stronger FC between M1/S1, VL/VPL, ant ins, and PAG predicts a better analgesic response. Under the Sham tDCS condition, dashed blue lines represent a main effect of connectivity changes, while solid blue lines show decreased FC correlating with analgesia between the thalamus and posterior insula/M1. In the Real tDCS condition, distinct pathways of decreased FC are shown between the VL/VPL thalamus and the medial prefrontal cortex (mPFC), supplementary motor area (SMA), and cerebellum, highlighting the neural mechanisms of neuromodulation-induced pain relief.

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Fibromyalgia

Definition

Fibromyalgia is the term used to describe chronic widespread musculoskeletal pain for which no alternative structural or inflammatory cause can be identified. It belongs to a broader class now called nociplastic pain (previously "centralized pain" or "central sensitization syndrome") - conditions where pain arises from altered nociception without clear evidence of tissue damage or nerve injury, driven predominantly by CNS dysfunction. - Goldman-Cecil Medicine, p. 2885
The same patients may be labeled differently depending on which specialist they see: chronic fatigue syndrome (fatigue-dominant), irritable bowel syndrome (GI-dominant), interstitial cystitis, temporomandibular disorder, tension headache, or vulvodynia. These are increasingly grouped as chronic overlapping pain conditions. - Goldman-Cecil Medicine, p. 2885

Epidemiology

  • Chronic widespread pain affects 4-12% of the general population at any given time
  • Fibromyalgia prevalence estimates range from 2-20% across various studied populations
  • Occurs ~1.5x more often in women than men (though not exclusively a female condition)
  • Prevalence is consistent across countries, ethnicities, and cultures
  • Particularly prevalent in those with comorbid inflammatory rheumatic diseases (RA, OA)
  • Goldman-Cecil Medicine, p. 2887; Firestein & Kelley's Textbook of Rheumatology, p. 598

Pathophysiology

Fibromyalgia is best understood as a disorder of pain processing, not a peripheral musculoskeletal disease.

Central Mechanisms (Primary)

The core abnormality is central sensitization - an amplification of pain signals within the CNS. This involves:
  • Failure of descending inhibitory pain pathways (dysfunctional diffuse noxious inhibitory control)
  • Heightened activity in ascending nociceptive pathways
  • Altered functional connectivity in key brain regions (thalamus, insula, prefrontal cortex, periaqueductal gray)
  • Results in hyperalgesia (exaggerated pain to painful stimuli) and allodynia (pain from normally non-painful stimuli)

Peripheral Mechanisms (Contributing)

Recent evidence suggests peripheral contributions in subgroups:
  • Autoantibodies binding to Fc receptors on peripheral sensory neurons
  • Autoantibodies directed against satellite cells in dorsal root ganglia, increasing nociceptor sensitivity
  • Widespread small fiber neuropathy in some subpopulations
These peripheral findings have not yet led to targeted treatments, but they challenge the purely CNS model. - Firestein & Kelley's Textbook of Rheumatology, p. 598

Pain Mechanism Classification

FeatureFibromyalgia (Nociplastic)NociceptiveNeuropathic
CauseCNS/systemic problemInflammation/damageNerve damage/entrapment
DistributionWidespread, diffuseWell-localizedDermatomal/stocking-glove
Key featuresAllodynia, fatigue, "fibro fog"Activity-relatedLancinating, numbness
  • Goldman-Cecil Medicine, p. 2888

Clinical Features

Core Symptoms

  1. Widespread musculoskeletal pain - both sides of body, above and below waist, axial involvement
  2. Sleep disturbance - non-restorative sleep, alpha-wave intrusion into deep sleep
  3. Diurnal fatigue - often profound, worsened by overexertion
  4. Cognitive dysfunction ("fibro fog") - impaired memory, concentration, word-finding
  5. Mood disturbance - depression and anxiety are common comorbidities

Associated Symptoms & Comorbidities

  • Irritable bowel syndrome
  • Tension/migraine headaches
  • Paresthesias and stiffness (without true neurological deficit)
  • Hyperacusis, photosensitivity, chemical sensitivity
  • Pelvic pain, urinary urgency (interstitial cystitis overlap)
  • Temporomandibular disorder
  • Raynaud phenomenon
  • Firestein & Kelley's Textbook of Rheumatology, p. 598

Diagnosis

ACR 2010/2016 Criteria (Current)

The older 1990 ACR criteria required a clinician to identify ≥11 of 18 specific tender points on physical exam. These have been largely replaced because tender points were unreliable and excluded men.
The 2010/2016 criteria use a patient-reported symptom approach:
  • Widespread Pain Index (WPI): number of body areas painful in the past week (out of 19 areas)
  • Symptom Severity Scale (SSS): rates fatigue, waking unrefreshed, cognitive symptoms, and somatic symptoms (0-12)
  • Diagnosis requires: WPI ≥7 + SSS ≥5 or WPI 4-6 + SSS ≥9
  • Symptoms must be present at similar level for ≥3 months
  • No other disorder sufficiently explains the pain
The 18 tender points (9 bilateral pairs) from the historic 1990 criteria are shown below for reference:
18 Fibromyalgia Tender Points - ACR 1990 Criteria

Central Sensitization - Pain Pathway Diagram

Central Sensitization and Descending Inhibition Failure in Fibromyalgia

Treatment

Fibromyalgia responds best to a multimodal, CNS-targeted approach. Opioids and NSAIDs are largely ineffective.

Non-Pharmacological (First Line)

  • Aerobic exercise - the single most evidence-based intervention; even modest exercise significantly reduces pain and fatigue
  • Cognitive-behavioral therapy (CBT) - addresses catastrophizing and sleep hygiene
  • Patient education - explaining the central sensitization mechanism reduces distress and improves outcomes
  • Sleep hygiene - treating non-restorative sleep is key
  • Multidisciplinary pain programs

Pharmacological

Three drugs are FDA-approved specifically for fibromyalgia:
DrugClassMechanismNotes
Duloxetine (Cymbalta)SNRI↑ serotonin + norepinephrineAlso treats comorbid depression
Milnacipran (Savella)SNRI↑ norepinephrine > serotoninHigher norepinephrine selectivity
Pregabalin (Lyrica)α2δ ligand↓ calcium channel activity, ↓ excitatory neurotransmissionAlso improves sleep
Other commonly used agents:
  • Tricyclic antidepressants (amitriptyline, cyclobenzaprine) - low-dose, improve sleep
  • Gabapentin - similar mechanism to pregabalin, off-label
  • Tramadol - weak opioid + SNRI; modest evidence (avoid strong opioids)
  • Low-dose naltrexone - emerging evidence for anti-inflammatory/glial modulation effect

What to Avoid

  • Strong opioids - worsen central sensitization over time (opioid-induced hyperalgesia)
  • NSAIDs/corticosteroids - no meaningful benefit for nociplastic pain
  • Excessive investigation and surgery based on pain complaints alone

Prognosis

Fibromyalgia symptoms exist on a continuum - they may progress or regress rather than defining a fixed disease state. With proper multimodal management, most patients achieve meaningful symptom reduction. Comorbid inflammatory conditions (RA, OA) can worsen fibromyalgia pain, and fibromyalgia predicts worse outcomes from biologic therapies or arthroplasty - though those treatments can still provide benefit. - Firestein & Kelley's Textbook of Rheumatology, p. 598

Recent Evidence (2024-2026)

  • A 2025 systematic review (PMID 40576703) found the Mediterranean diet may reduce fibromyalgia symptoms through anti-inflammatory and low-antigenic properties - a promising lifestyle adjunct.
  • A 2025 meta-analysis (PMID 40053352) confirmed very high prevalence of depression and anxiety among adults with chronic pain conditions including fibromyalgia, reinforcing the need for integrated psychological care.
Sources: Goldman-Cecil Medicine (International Ed.); Firestein & Kelley's Textbook of Rheumatology; Adams & Victor's Principles of Neurology; Morgan & Mikhail's Clinical Anesthesiology; Stahl's Essential Psychopharmacology
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