Polymyalgia Rheumatica (PMR)
Inflammatory syndrome of shoulder and hip girdle stiffness in adults over 50; dramatic response to low-dose steroids.
Also known as: PMR, polymyalgia
Overview
Inflammatory syndrome of older adults characterized by bilateral aching and morning stiffness of the shoulder and pelvic girdle, markedly elevated inflammatory markers, and rapid response to low-dose corticosteroids. Closely related to giant cell arteritis.
Epidemiology
Almost exclusively in adults over 50; peak incidence 70-80. Female predominance 2-3:1. More common in people of Northern European ancestry. About 15-20% of PMR patients develop GCA, and about 40-50% of GCA patients have PMR features.
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Risk factors
- Age >50 (essentially required)
- Female sex
- Northern European ancestry
- HLA-DR4 association
- Coexisting or prior giant cell arteritis
Pathophysiology
Subclinical large-vessel and bursal inflammation driven by IL-6 and innate immune activation. Subdeltoid bursitis, biceps tenosynovitis, and hip trochanteric bursitis underlie the proximal stiffness rather than primary muscle disease.
Clinical presentation
Symptoms
- Subacute onset of bilateral shoulder and hip girdle aching and stiffness
- Morning stiffness >45 minutes (often hours)
- Difficulty rising from a chair or lifting arms above the head
- Constitutional symptoms in 30-50%: fatigue, low-grade fever, anorexia, weight loss
- No true muscle weakness once pain is controlled
Signs / physical exam
- Restricted active shoulder and hip motion limited by pain, not weakness
- Tenderness over deltoids, trapezii, trochanters
- Normal muscle strength on confrontation testing
- Screen carefully for GCA features: temporal artery tenderness, jaw claudication, scalp tenderness, visual symptoms
Differential diagnosis
- Giant cell arteritis — Headache, scalp tenderness, jaw claudication, vision changes; coexists with PMR — always screen for cranial symptoms
- Rheumatoid arthritis (elderly-onset) — Symmetric small-joint synovitis, RF/CCP positive, erosions on imaging; may overlap clinically
- Inflammatory myopathy (polymyositis, dermatomyositis) — True muscle weakness, elevated CK, EMG/biopsy changes
- Hypothyroidism — Proximal stiffness, elevated CK, low TSH/T4
- Statin myopathy — Recent statin use, elevated CK, weakness more than stiffness
- Fibromyalgia — Diffuse pain, normal ESR/CRP, age usually <60
- Paraneoplastic / lymphoma — Atypical features, poor or delayed steroid response, weight loss; pursue malignancy workup if response inadequate
- Osteoarthritis of shoulders/hips — Mechanical pain, normal inflammatory markers, no constitutional symptoms
Diagnostic workup
Diagnostic criteria
2012 EULAR/ACR provisional criteria: age ≥50, bilateral shoulder pain, abnormal CRP or ESR, plus weighted morning stiffness, hip involvement, absence of other joint pain, and absence of RF/anti-CCP.
Labs
- ESR — characteristically >40 mm/h (often >50-100); CRP elevated and may be more sensitive
- CBC — normochromic normocytic anemia, thrombocytosis
- CK — normal (excludes inflammatory myopathy)
- TSH (exclude hypothyroidism)
- RF, anti-CCP, ANA — usually negative; help exclude RA and SLE
- Comprehensive metabolic panel (baseline before steroids)
Imaging
- Shoulder ultrasound or MRI — subacromial-subdeltoid bursitis, biceps tenosynovitis, glenohumeral synovitis (supportive but not required)
- Temporal artery ultrasound or biopsy if GCA features develop
- PET-CT in atypical cases — can show large-vessel uptake
Diagnostic algorithm
| Feature | PMR | Giant Cell Arteritis |
|---|---|---|
| Age | >50 | >50 |
| Key symptoms | Shoulder/hip stiffness, morning stiffness >45 min | New headache, jaw claudication, scalp tenderness, visual loss |
| ESR/CRP | Markedly elevated | Markedly elevated |
| Imaging | Bursitis on US/MRI | Temporal artery US (halo) or biopsy |
| Initial steroid dose | Prednisone 12.5-25 mg/day | Prednisone 40-60 mg/day (or 1 g IV pulse if vision threat) |
| Overlap | 15-20% develop GCA | 40-50% have PMR features |
Treatment
First-line
- Prednisone 12.5-25 mg/day — dramatic improvement within 48-72 hours is both therapeutic and diagnostic
- Slow taper over 1-2 years guided by symptoms and inflammatory markers (typical schedule: reduce by 2.5 mg every 2-4 weeks until 10 mg, then 1 mg every 1-2 months)
- Bone-protective therapy: calcium 1000-1200 mg/day, vitamin D 800-2000 IU/day, plus bisphosphonate if at risk (almost all elderly patients on chronic steroids qualify)
- PPI for GI protection if NSAIDs or anticoagulants coadministered
Complications
- Relapse during taper (very common — usually managed with small dose increases)
- Steroid-related: osteoporosis, hyperglycemia/diabetes, hypertension, weight gain, cataracts, infection, adrenal insufficiency
- Progression to or unmasking of giant cell arteritis
- Misdiagnosis: occult RA, malignancy, or polymyositis
PANCE pearls
- A truly dramatic response to 15-20 mg of prednisone within 72 hours is one of the most useful clinical signs in rheumatology.
- Always screen for GCA at every PMR visit — sudden vision loss is a preventable catastrophe.
- Normal CK separates PMR from inflammatory myopathies.
- Failure to taper below 10 mg or atypical features should prompt reconsideration of the diagnosis.
References
- EULAR/ACR 2012 — 2012 Provisional Classification Criteria for PMR (Dasgupta et al., Ann Rheum Dis 2012)
- EULAR/ACR 2015 — 2015 Recommendations for the Management of PMR (Dejaco et al., Ann Rheum Dis 2015)
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