Polymyalgia Rheumatica (PMR)

Populations and Risk Factors

• Almost exclusively adults over 50 years; peak incidence between ages 70 and 80; virtually never occurs before age 50
• Women affected approximately 2–3:1 over men
• Strongest prevalence in people of Northern European (Scandinavian) descent; rare in Black and Asian populations
• Genetic predisposition: HLA-DR4 association; familial clustering observed
• Possible environmental or infectious triggers (temporal clusters suggest seasonal or infectious component, but no specific agent identified)
• 15–20% of PMR patients develop giant cell arteritis (GCA); conversely, 40–60% of GCA patients have PMR symptoms — the two conditions likely represent different manifestations of the same disease spectrum
• Onset may follow stressful life events, viral illness, or vaccination in genetically susceptible individuals

Causes and Pathophysiology

Periarticular Inflammation

• Primary target: The inflammatory process in PMR targets the periarticular structures of proximal joints — subacromial bursae, subdeltoid bursae, trochanteric bursae, glenohumeral and hip joint synovium, bicipital tenosynovitis, and interspinous bursae of the cervical spine. Imaging studies consistently show bursitis and synovitis rather than myositis — the muscles themselves are not directly inflamed.
• Why the name is misleading: "Polymyalgia" (many muscle pains) was coined based on clinical presentation (patients report muscle pain), but the actual pathology is periarticular inflammation that produces pain perceived in the proximal muscles. The distinction is clinically important: muscle enzymes (CK) are normal in PMR (elevated CK suggests polymyositis instead), and biopsy of the muscles shows no inflammatory infiltrate.
• IL-6 as the key driver: Interleukin-6 is markedly elevated in PMR and is the primary mediator of the systemic inflammatory response — it drives the acute-phase reaction (elevated ESR, CRP, fibrinogen), produces constitutional symptoms (fatigue, malaise, fever, weight loss), and contributes to the morning stiffness pattern. IL-6 levels correlate with disease activity and predict relapse during steroid tapering.

Morning Stiffness Mechanism

• Why >45 minutes: During sleep, reduced movement allows inflammatory exudate to accumulate in the periarticular bursae and synovial spaces of the shoulders and hips. The subacromial and trochanteric bursae become distended with inflammatory fluid. Upon waking, the swollen, inflamed bursae resist movement until the mechanical activity of using the joints gradually redistributes the fluid and reduces pressure. In PMR, this takes 45 minutes to several hours — distinguishing it from the briefer stiffness of OA (<30 minutes) and paralleling the stiffness duration of RA.
• Bilateral symmetry: The characteristic bilateral, symmetrical distribution (both shoulders and both hips simultaneously) results from the systemic nature of the inflammatory process — IL-6-driven immune activation targets periarticular tissues throughout the proximal skeleton rather than focusing on a single joint.

Proximal Weakness Pattern

• Functional weakness without primary muscle pathology: Patients have difficulty raising arms above the shoulders, combing hair, dressing, rising from chairs, and climbing stairs. This functional impairment results from pain inhibition and periarticular restriction — not from muscle atrophy or myositis. The muscles are capable of generating force, but pain from inflamed bursae and tendons limits willingness to contract through range. This distinction is critical: if true proximal muscle weakness with elevated CK is found, the diagnosis shifts to polymyositis.
• Disuse atrophy (secondary): Prolonged activity avoidance from pain and stiffness produces genuine proximal muscle atrophy over weeks to months — deltoid, supraspinatus, gluteus maximus, and quadriceps bulk diminishes. This secondary atrophy creates a self-reinforcing cycle: less muscle support increases load on inflamed periarticular structures, increasing pain, increasing avoidance.

Giant Cell Arteritis Connection

• Shared disease spectrum: PMR and GCA share the same HLA-DR4 genetic predisposition, the same IL-6-driven inflammatory pathway, and frequently coexist. Current understanding treats them as different clinical expressions of a single vasculitic/inflammatory disease: GCA represents the vascular manifestation (large-vessel granulomatous vasculitis), while PMR represents the periarticular manifestation.
• GCA mechanism: Granulomatous inflammation of the intima and media of medium and large arteries — most commonly the temporal artery, ophthalmic artery, and aorta. Inflammation narrows the arterial lumen, producing ischemia to the tissues supplied. When the ophthalmic artery or its branches are involved, ischemia to the optic nerve causes sudden, irreversible vision loss — this is why GCA is a medical emergency.
• Transition risk: PMR can develop into GCA at any time during the disease course — even during treatment. This means massage therapists must screen for GCA symptoms at every session, not just at initial assessment.

Signs and Symptoms

Proximal Musculoskeletal Presentation

• Bilateral shoulder pain and stiffness — the most common presenting feature (70–95%); pain is deep, aching, and located in the deltoid region, upper arms, and neck
• Bilateral hip and pelvic girdle pain and stiffness — present in approximately 50–70%; pain in the buttocks, lateral hips, and proximal thighs
• Morning stiffness lasting >45 minutes (often 1–2 hours) — hallmark feature; stiffness is worst on waking and gradually improves with activity
• Difficulty with overhead activities: combing hair, reaching shelves, dressing upper body
• Difficulty rising from chairs, getting out of a car, climbing stairs — from hip girdle involvement
• Pain is bilateral and symmetrical — asymmetric or unilateral presentation should raise suspicion for other conditions
• Night pain that awakens the patient — particularly when rolling onto the affected shoulder

Constitutional Symptoms

• Fatigue and malaise — often profound and debilitating
• Low-grade fever and weight loss
• Depression and loss of appetite
• General sense of illness disproportionate to localized joint complaints

Red Flags — Giant Cell Arteritis

• New-onset temporal headache — unilateral or bilateral, often severe, located over the temporal arteries
• Jaw claudication — pain or fatigue in the jaw muscles during chewing that resolves with rest; caused by ischemia of the masseter from temporal artery inflammation
• Visual disturbances — blurred vision, diplopia, amaurosis fugax (transient monocular blindness), or sudden permanent vision loss
• Temporal artery abnormalities — tenderness, nodularity, decreased or absent pulse on palpation
• Scalp tenderness — pain when brushing hair or resting head on a pillow
• Any combination of these symptoms in a PMR patient = EMERGENCY REFERRAL; do not treat; send to emergency department immediately

Assessment Profile

Subjective Presentation

• Chief complaint: "Both my shoulders are so stiff in the morning I can barely get dressed. It takes over an hour to loosen up." Patients often describe a sudden or subacute onset (over 1–2 weeks) of bilateral shoulder and hip pain that is worst in the morning and gradually improves with movement throughout the day. They frequently report that they "feel 20 years older overnight."
• Pain quality: Deep, aching pain in the shoulders, upper arms, hips, and thighs; pain is constant but worst in the morning and after periods of inactivity; not sharp or lancinating (sharp pain in the temporal region suggests GCA); patients often have difficulty localizing the pain — they gesture broadly at the shoulder and hip girdle rather than pointing to a specific spot
• Onset: Subacute (1–4 weeks) in most cases; some patients describe a sudden onset over a few days; occasionally preceded by a viral illness or stressful event; age at onset invariably >50 years
• Aggravating factors: Prolonged inactivity (worst in the morning and after sitting), overhead reaching, rising from seated position, climbing stairs, rolling in bed at night, damp cold weather (anecdotal but commonly reported)
• Easing factors: Movement and activity (stiffness improves with use — opposite of mechanical joint pathology that worsens with use); warmth; NSAIDs provide partial relief; low-dose prednisone produces dramatic relief within 24–72 hours (this rapid corticosteroid response is itself a diagnostic criterion)
• Red flags: New temporal headache, jaw claudication (pain with chewing), visual changes (blurring, double vision, transient or permanent vision loss), scalp tenderness → giant cell arteritis; EMERGENCY REFERRAL; do not treat; risk of permanent blindness

Observation

• Local inspection: No visible joint swelling or deformity (periarticular inflammation is deep and not usually visible externally); mild swelling may be observed over the bicipital groove (bicipital tenosynovitis) or trochanteric region; generalized appearance of stiffness and discomfort; patient may appear older and more fatigued than expected
• Posture: Shoulders elevated and protracted from protective guarding; arms held close to the body to minimize shoulder movement; bilateral upper trapezius elevation; forward head posture from chronic cervicothoracic guarding; hip flexion bias when standing from gluteal and iliopsoas guarding; overall "guarded" posture reflecting bilateral proximal pain
• Gait: Stiff, shuffling gait — particularly in the morning or after prolonged sitting; shortened stride from hip girdle restriction; difficulty initiating movement from sitting to standing (pushes up with arms from chair rather than using legs); gait improves as the session progresses (movement reduces stiffness)

Palpation

• Tone: Bilateral hypertonicity in the shoulder girdle musculature — upper trapezius, levator scapulae, deltoid, supraspinatus, infraspinatus; bilateral hip girdle hypertonicity — gluteus medius, TFL, iliopsoas, piriformis, quadratus lumborum; hypertonicity is protective guarding (reactive to periarticular inflammation) rather than primary muscle pathology; cervical extensors and paraspinals are hypertonic from compensatory posturing; the bilateral symmetry of the tone pattern is characteristic
• Tenderness: Subacromial and subdeltoid bursal tenderness on palpation (may require specific palpation technique — tenderness anterior and lateral to the acromion); bicipital groove tenderness (bicipital tenosynovitis); greater trochanteric tenderness (trochanteric bursitis); proximal deltoid, upper arm, and lateral hip tenderness — patients often describe the tenderness as "in the muscle" but it originates from underlying periarticular structures; bilateral symmetry of tenderness distribution is characteristic; normal CK distinguishes from polymyositis
• Temperature: No significant local warmth — periarticular inflammation is deep enough that surface temperature is usually normal; generalized warmth may be present with low-grade fever during active disease; compare shoulders and hips bilaterally for symmetry
• Tissue quality: No fibrotic or structural tissue changes specific to PMR; with prolonged disease, secondary deconditioning produces reduced muscle bulk in the proximal musculature (deltoid, supraspinatus, gluteals, quadriceps); tissue feels generally tense and guarded rather than ropy or nodular

Motion Assessment

• AROM: Bilateral reduction in shoulder AROM — particularly abduction and external rotation (pain-limited, not capsular-limited); bilateral reduction in hip ROM — particularly flexion and internal rotation when rising from sitting; morning AROM is dramatically worse than afternoon AROM (>45 minutes of stiffness improvement with activity); a patient who cannot raise arms above shoulders in the morning but can do so by afternoon demonstrates the characteristic pattern; cervical AROM may be reduced from interspinous bursal inflammation
• PROM / end-feel: PROM exceeds AROM — the joint itself is not restricted; end-feel is guarded/protective (muscle guarding from pain before anatomical end-range is reached) rather than capsular/leathery (which would suggest adhesive capsulitis) or hard/bony (which would suggest OA); when the patient relaxes and the examiner gently takes the joint through range, significantly more movement is available than the patient can produce actively — this gap between AROM and PROM is characteristic
• Resisted testing: Pain on resisted testing of shoulder abduction and external rotation (due to underlying subacromial bursitis and supraspinatus tendon inflammation, not primary muscle weakness); resisted hip flexion painful from iliopsoas bursal inflammation; importantly, if the patient can generate force despite pain, this confirms pain inhibition rather than true muscle weakness — true proximal weakness with elevated CK suggests polymyositis

Special Test Cluster

Note: At every session, screen for GCA symptoms before treatment: ask about new headaches, jaw pain with chewing, visual changes, and scalp tenderness. Palpate temporal arteries bilaterally. If any GCA symptom is present, do not treat — refer to emergency department immediately.

Differential Assessment