Fibromyalgia

Populations and Risk Factors

• Women affected approximately 6–9:1 over men (85–90% of diagnosed cases); onset most common between ages 30 and 50
• Strong association with prior physical trauma (motor vehicle accident, surgery) or severe emotional trauma/abuse — these are hypothesized triggers for central sensitization onset
• First-degree relatives have an 8-fold increased risk, suggesting genetic predisposition affecting pain processing pathways
• Comorbidities are the rule rather than the exception: irritable bowel syndrome (IBS) in 30–70%, temporomandibular joint disorder (TMJ) in 25%, chronic migraine or tension headache in 50%, anxiety and depression in 30–50%, chronic fatigue syndrome (significant overlap)
• Sleep disorders (particularly disrupted Stage IV non-REM sleep) are present in virtually all FMS patients and may be both a cause and consequence of the condition
• Viral infections (EBV, hepatitis C, HIV) associated with onset in some cases
• Obesity increases risk — mechanical load and systemic inflammation may contribute to central sensitization maintenance

Causes and Pathophysiology

Central Sensitization — The Core Mechanism

• Definition: Central sensitization is a state in which the central nervous system (spinal cord dorsal horn neurons and cortical/subcortical pain-processing areas) amplifies incoming sensory signals, causing normal-intensity stimuli to be perceived as painful (allodynia) and mildly painful stimuli to be perceived as severely painful (hyperalgesia). This is the fundamental mechanism underlying fibromyalgia — the problem is not in the peripheral tissues but in how the CNS processes sensory input.
• Neurochemical basis: FMS patients demonstrate measurably elevated levels of excitatory neurotransmitters and reduced levels of inhibitory neurotransmitters:
• Substance P: elevated 2–3 times normal in cerebrospinal fluid — a pain-facilitating neuropeptide that amplifies nociceptive transmission at the spinal cord level
• Glutamate: elevated in the insula (a key pain-processing cortical area) — the primary excitatory neurotransmitter in the CNS
• Serotonin and norepinephrine: reduced in descending inhibitory pain pathways — these neurotransmitters normally dampen ascending pain signals; their deficiency removes the "braking system" on pain transmission. This explains why SNRIs (duloxetine/Cymbalta, milnacipran/Savella) are effective — they increase serotonin and norepinephrine at the synapse.
• Dopamine: reduced in the basal ganglia — contributes to fatigue, motivational deficits, and anhedonia
• Why this matters for palpation: The elevated Substance P and glutamate mean that palpation pressure applied at normal therapeutic intensity may be perceived as intensely painful. Tender points are not sites of local tissue pathology — they are sites where the amplified CNS signal is most readily provoked. This is why tender points are hypotonic (no local muscle spasm) and do not refer pain (no trigger point mechanism).

Wind-Up Phenomenon

• Temporal summation (wind-up): When repetitive low-frequency stimuli are applied to the same area, FMS patients experience progressively increasing pain — each successive stimulus feels more painful than the last, rather than habituating as in healthy controls. This is a direct marker of dorsal horn hyperexcitability.
• Clinical significance for MT: Sustained pressure over a single area, repetitive strokes at the same depth, or prolonged deep work can invoke wind-up. Techniques must vary in location, pressure, and rhythm to avoid temporal summation. The therapist cannot rely on "working through" the tenderness — continued pressure will make it worse, not better.

Sleep Disruption Cycle

• Stage IV sleep intrusion: Alpha wave intrusion into delta (Stage IV) non-REM sleep is documented in FMS patients. Stage IV sleep is when growth hormone (GH) is released — GH is essential for tissue repair, immune modulation, and pain threshold maintenance. Disrupted Stage IV sleep reduces GH release, which lowers pain thresholds, which increases pain, which further disrupts sleep — a self-perpetuating cycle.
• Why this matters clinically: FMS fatigue is distinct from normal tiredness — it is neurologically driven and not proportional to activity. Patients describe "waking up more tired than when they went to bed." Sleep quality is a more important treatment target than pain intensity in many FMS patients.

HPA Axis Dysfunction

• Neuroendocrine disruption: The hypothalamic-pituitary-adrenal (HPA) axis shows blunted cortisol response to stress in FMS patients. Cortisol is anti-inflammatory and modulates pain processing. The blunted stress response leaves patients more vulnerable to pain amplification and contributes to the fatigue, cognitive dysfunction, and immune dysregulation seen in FMS.

Exercise Paradox

• The paradox: Regular aerobic exercise is the single most effective non-pharmacological intervention for FMS — it raises pain thresholds, improves sleep, increases endogenous endorphins, and reduces fatigue over time. However, excessive or sudden-onset exercise triggers post-exertional malaise (PEM) — a flare of pain, fatigue, and cognitive dysfunction lasting 24–72 hours. The therapeutic window is narrow: intensity must start far below normal recommendations and increase very gradually.

Signs and Symptoms

Pain Characteristics

• Widespread musculoskeletal pain present for at least 3 months — described as aching, burning, throbbing, or stabbing; location shifts and migrates rather than remaining fixed
• Pain does not follow dermatomal, myotomal, or peripheral nerve distributions — it is diffuse and often described as "everywhere" or "all over"
• Allodynia: light touch, clothing pressure, or normal social contact (handshake) may provoke pain
• Hyperalgesia: mildly painful stimuli (bumping into a table, moderate pressure) produce disproportionate pain responses

Fatigue and Sleep

• Fatigue is often rated as more disabling than pain — described as "bone-deep exhaustion" unrelieved by rest
• Non-restorative sleep: "I sleep 8 hours but wake up feeling like I didn't sleep at all"
• Cognitive dysfunction ("fibrofog"): impaired concentration, word-finding difficulty, short-term memory lapses, difficulty with multitasking

Diagnostic Criteria Comparison

Common Comorbidities

• Irritable bowel syndrome (IBS): 30–70% — shared central sensitization mechanism
• Chronic migraine or tension headache: ~50%
• Temporomandibular joint disorder (TMJ): ~25%
• Anxiety and/or depression: 30–50% — both cause and consequence of chronic pain
• Chronic fatigue syndrome: significant symptom overlap; may be the same spectrum
• Restless leg syndrome, interstitial cystitis, vulvodynia — all hypothesized to share central sensitization pathways

Assessment Profile

Subjective Presentation

• Chief complaint: "I hurt all over." "I'm exhausted all the time and nothing helps." Patients often describe years of symptoms with multiple prior diagnoses that did not explain the full picture. Pain location shifts — "some days it's my back, some days it's my legs, some days it's everything."
• Pain quality: Widespread aching with superimposed burning, stabbing, or throbbing; pain migrates and shifts location; intensity fluctuates day-to-day and hour-to-hour; disproportionate to any identifiable tissue pathology; may include allodynia (pain from light touch) and hyperalgesia (amplified pain from mild stimuli)
• Onset: Often insidious, though many patients identify a triggering event (MVA, surgery, viral infection, severe emotional trauma); symptoms build gradually over weeks to months; diagnosis is typically delayed 2–5 years from symptom onset
• Aggravating factors: Sustained activity or overexertion (triggers PEM), cold and damp weather, poor sleep, emotional stress, repetitive stimulation of the same area (wind-up), prolonged static postures
• Easing factors: Gentle low-intensity movement (walking, aquatic exercise), warmth (warm baths, heat packs — improves pain tolerance in most patients), pacing activity with rest intervals, improved sleep quality, stress reduction
• Red flags: Focal neurological deficits (numbness in a specific dermatomal pattern, true weakness in a myotomal distribution) → suggest peripheral nerve pathology, not FMS; progressive unilateral joint swelling with warmth → inflammatory arthritis, not FMS; unexplained weight loss with fatigue → screen for malignancy or endocrine disorder

Observation

• Local inspection: Usually normal appearance — no swelling, redness, atrophy, or deformity; pain is "invisible," which contributes to patient frustration, invalidation, and secondary psychological distress; may show fatigue in facial expression, guarded or slow movement patterns
• Posture: May show generalized protective posturing — slightly flexed trunk, elevated shoulders, shallow breathing pattern; postural deviations present are typically pre-existing and not caused by FMS; some patients adopt a bracing/rigid posture from chronic pain anticipation
• Gait: Usually normal; may show guarded, slow, or cautious gait pattern from pain avoidance rather than structural cause; no antalgic pattern attributable to a specific joint

Palpation

• Tone: Characteristically normal to hypotonic at tender point sites — this is the critical distinction from myofascial pain syndrome (MPS), where trigger points are hypertonic bands. FMS tender points are not areas of muscle spasm; they are sites where the amplified CNS pain signal is most readily provoked. Some patients may have concurrent MPS trigger points (comorbid conditions), which should be identified and treated differently from tender points.
• Tenderness: Diffuse, widespread tenderness not confined to specific anatomical structures; positive at multiple bilateral sites; historical 18 tender point sites include: occiput, low cervical (C5–C7 anterior), trapezius (midpoint), supraspinatus (near medial scapular border), second rib (costochondral junction), lateral epicondyle, gluteal (upper outer quadrant), greater trochanter, medial knee (fat pad). Pressure threshold is reduced — pain provoked at lower force than expected (~4 kg on dolorimetry vs. 6–8 kg in healthy controls). Tenderness does NOT follow dermatomal or myotomal distributions and does NOT refer pain to distant sites.
• Temperature: Normal — no localized warmth or coolness; no inflammatory process producing temperature changes; if warmth is detected over a joint, consider comorbid inflammatory arthritis rather than FMS
• Tissue quality: Generally normal muscle tissue quality — no fibrotic bands, nodules, or ropy texture attributable to FMS itself; tissue may feel "puffy" or mildly edematous in some patients (possibly from deconditioning or medication side effects); any fascial restriction, trigger point bands, or fibrotic changes found are comorbid findings (MPS, deconditioning) and should be treated on their own merit

Motion Assessment

• AROM: Typically full but painful — range is not structurally limited; patients may voluntarily limit movement from pain anticipation or fear-avoidance behavior; morning stiffness is common but less severe and shorter-duration than RA; stiffness improves with gentle movement
• PROM / end-feel: Normal tissue-stretch end-feel — there is no capsular restriction, bony block, or structural limitation; PROM equals or slightly exceeds AROM; the presence of a capsular end-feel or hard end-feel suggests a comorbid condition (OA, adhesive capsulitis) rather than FMS; pain at end-range is from central sensitization, not tissue pathology
• Resisted testing: Normal strength; pain may be reported with contraction but there is no true weakness or myotomal pattern; if focal weakness is found, investigate peripheral nerve pathology as a separate finding; grip strength may be subjectively reduced from pain avoidance but dynamometry typically shows normal force production

Special Test Cluster

Critical distinction — tender points vs. trigger points: If a palpable hypertonic band with a referred pain pattern is found, that is a trigger point (MPS), not a tender point (FMS). The two conditions commonly coexist. Treat trigger points with standard TrP techniques; approach tender point areas with the central sensitization precautions described in MT Considerations.

Differential Assessment