Polymyalgia Rheumatica
An inflammatory condition seen in older adults causing severe aching and morning stiffness in the shoulders, neck, and hips, responding remarkably well to low-dose steroids.
Emergency Management: Concurrent Giant Cell Arteritis presenting with vision changes requires immediate escalation of Prednisone to 40-60 mg daily (or IV Methylprednisolone for visual loss) to prevent permanent blindness.
Polymyalgia rheumatica (PMR) is a chronic inflammatory disorder of unknown etiology predominantly affecting individuals over the age of 50. It is characterized by symmetric aching and prolonged morning stiffness in the proximal musculature of the shoulder and pelvic girdles and the neck.
Detailed Overview
PMR is one of the most common inflammatory rheumatic diseases in the elderly. It is closely associated with Giant Cell Arteritis (GCA); roughly 15-20% of patients with PMR develop GCA, and 40-50% of GCA patients have PMR symptoms. The disease does not cause true muscle weakness, but rather pain so severe that it limits movement. PMR responds dramatically and rapidly to low-dose systemic corticosteroids, which is considered both therapeutic and diagnostically supportive. Without treatment, it significantly impairs quality of life.
Epidemiology & Demographics
Incidence is 50 per 100,000 individuals over age 50. Almost never occurs before age 50. Incidence peaks in the 70s. Females are affected 2-3 times more often than males. More common in populations of Northern European descent.
Etiological Mechanism
Unknown, but suspected to be an interplay of genetic predisposition (HLA-DRB1 alleles) and environmental triggers (possibly viral infections like adenovirus or parvovirus B19) leading to immune system dysregulation.
Primary Causes
An autoimmune inflammatory response targeting the synovium and bursae of large proximal joints.
PMR is characterized by synovitis, bursitis, and tenosynovitis of the proximal joints (especially subacromial/subdeltoid bursitis and trochanteric bursitis). It is a systemic macrophage and T-cell mediated immune response. An increase in pro-inflammatory cytokines, particularly Interleukin-6 (IL-6), drives the systemic acute-phase response, causing elevated ESR and CRP. Unlike rheumatoid arthritis, PMR does not result in erosive joint destruction or autoantibody production (RF/anti-CCP are negative). The pain is due to inflammation of the periarticular structures rather than the muscle fibers themselves, explaining the lack of elevated muscle enzymes (normal CK).
Diagnostic Criteria & Guidelines
Clinical diagnosis based on age >50, bilateral shoulder/pelvic aching, morning stiffness >45 mins, elevated ESR/CRP, and a rapid, dramatic response to low-dose glucocorticoids within 48-72 hours.
Low-dose systemic glucocorticoids: Prednisone 15-20 mg PO daily. Patients should experience a 70-100% improvement within 3 days. Once symptoms and inflammatory markers normalize (usually 2-4 weeks), taper Prednisone gradually (e.g., by 2.5 mg every 2-4 weeks down to 10 mg, then by 1 mg every 4 weeks). Calcium 1200 mg and Vitamin D 800 IU daily for bone protection.
Second-Line & Adjunctive Therapy
Methotrexate 10-15 mg PO weekly with Folic acid 1 mg daily. Used as a steroid-sparing agent in patients who experience relapses during tapering or have high risk for glucocorticoid toxicity (e.g., severe diabetes, severe osteoporosis).
Surgical & Procedural Management
None indicated for PMR.
Patient Counseling & Advice
Warn the patient NEVER to stop Prednisone abruptly due to the risk of adrenal crisis. Educate them on the symptoms of Giant Cell Arteritis (new severe headaches, jaw pain when chewing, vision changes) and to seek emergency care immediately if they occur.
Follow-Up & Monitoring Schedule
Clinical review and ESR/CRP testing every 4-8 weeks during the tapering phase. Dual-energy X-ray absorptiometry (DEXA) scan at baseline to assess fracture risk, and consider starting a bisphosphonate (e.g., Alendronate) prophylactically.
Preventive Strategies
No known prevention for the disease itself. Prevention focuses on avoiding steroid-induced osteoporosis via calcium, vitamin D, and bisphosphonates.
Excellent prognosis for symptom resolution. The course of the disease typically lasts 1 to 2 years, after which steroids can be successfully stopped in most patients. Relapses occur in about 50% of patients during the taper.