Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.
Recognise polymyalgia rheumatica as an inflammatory pain-and-stiffness syndrome in older adults, exclude mimics and coexisting giant-cell arteritis, use a diagnostic glucocorticoid regimen with structured taper, and investigate atypical response.
PMR is an inflammatory syndrome of older adults characterised by bilateral shoulder and often hip-girdle pain and stiffness. Symptoms are worst after rest and interfere with dressing, turning in bed and rising. Examination shows restricted active movement from pain while passive movement and true strength may be relatively preserved. There is no single confirmatory test; diagnosis combines age, inflammatory pattern, raised markers, exclusion of mimics and a carefully observed treatment response.
Baseline assessment prevents steroid from obscuring infection, cancer and inflammatory alternatives. Ask about weight loss, fever, focal bone pain, synovitis, weakness and neurological symptoms. Examine temporal arteries, vision, pulses, joints, shoulder mechanics, hip movement, formal power and nodes. Ultrasound can show bilateral subdeltoid bursitis, biceps tenosynovitis and hip synovitis, but these findings are supportive rather than unique.
A standard starting dose of prednisolone 15 mg/day should produce clear global improvement within days. Complete immediate resolution is not required, and response alone is nonspecific. Persistently severe symptoms, normal markers in an atypical presentation, inability to taper, objective weakness or focal findings prompt reassessment. Higher starting doses increase toxicity and can conceal a wrong diagnosis; lower doses risk undertreatment.
PMR occurs almost exclusively after age fifty, with immune ageing and HLA susceptibility producing inflammation around shoulder and hip girdle synovial structures.
Seasonal variation and occasional clustering suggest environmental triggers, but no specific infection is established and antibiotics have no routine role.
PMR and GCA share immune pathways and frequently coexist; PMR symptoms do not protect against cranial or large-vessel arterial disease.
Subdeltoid bursae, biceps tendon sheaths, glenohumeral and hip synovial structures become inflamed, producing pain and prolonged stiffness without primary muscle-fibre destruction.
IL-6 and other inflammatory mediators cause morning stiffness, fatigue, fever, anaemia and raised CRP or ESR in typical active disease.
Patients struggle to raise arms or rise because movement hurts and stiffens, but formal power is preserved when pain is overcome.
Inflammation can recur during taper, while glucocorticoid withdrawal, adrenal suppression and structural shoulder disease can mimic a true relapse.
New symmetrical shoulder pain with prolonged morning stiffness and difficulty dressing or turning in bed is the core PMR phenotype.
Hip aching, fatigue, low fever, weight loss and raised inflammatory markers commonly accompany shoulder symptoms but are not individually specific.
Formal strength is usually intact once pain is accommodated; objective weakness, atrophy or CK elevation suggests myopathy or neurological disease.
Headache, scalp pain, jaw claudication or any visual symptom changes treatment immediately to the GCA pathway.
Young age, focal symptoms, normal markers, severe night pain, peripheral synovitis or poor steroid response requires diagnostic review.
Persistent peripheral synovitis, small-joint swelling, RF or anti-CCP and erosive change favour rheumatoid arthritis, although onset can initially mimic PMR.
Objective weakness, CK elevation, rash, dysphagia, thyroid or adrenal findings indicates muscle or endocrine disease rather than pain-limited movement.
Endocarditis, osteomyelitis, tuberculosis, myeloma, lymphoma and solid cancer can produce shoulder pain, systemic symptoms, anaemia and raised inflammatory markers.
Rotator-cuff disease, osteoarthritis, cervical disease and fibromyalgia cause pain but differ in stiffness duration, inflammatory markers and systemic trajectory.
Unrecognised cranial or large-vessel vasculitis can cause irreversible blindness, stroke, limb ischaemia and delayed aortic aneurysm or dissection.
Diabetes, hypertension, infection, osteoporosis, cataract, glaucoma, skin fragility, mood disturbance, myopathy and adrenal suppression accumulate during treatment.
Repeated inflammatory flares or overly rapid taper can prolong exposure, while misclassified mechanical pain may prompt unnecessary dose escalation.
Pain, sleep loss, deconditioning and steroid myopathy can impair dressing, transfers and independence even when inflammatory markers improve.
Pain arises mainly from bursae and synovial structures; true weakness or CK elevation should redirect assessment.
Steroid can temporarily improve cancer, infection and many painful conditions, so baseline evaluation and longitudinal fit remain essential.
Arteritis can emerge after an apparently uncomplicated PMR diagnosis and requires a much higher emergency dose.
Rotator-cuff and osteoarthritis symptoms may persist after inflammatory stiffness resolves and should not automatically prolong steroid.
Symptoms below physiological doses may reflect inflammatory relapse, withdrawal or adrenal insufficiency and require different responses.
Starting prednisolone before asking about visual symptoms and therefore giving an inadequate PMR dose to GCA.
Calling inability to lift painful arms weakness without formal power testing and CK.
Using steroid response as the only diagnostic criterion.
Increasing dose for every shoulder ache without checking CRP, mechanics, infection and adrenal symptoms.
Tapering rapidly after initial response and creating relapse and repeated high-dose exposure.
Omitting fracture, glucose, blood-pressure, infection and eye prevention during a long course.
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A 72-year-old has typical bilateral shoulder and hip stiffness, raised CRP, preserved true power and no cranial or visual symptoms. Mimics have been assessed. What is the usual initial treatment?
National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.
Editorial contact: Doctor’s Passport editorial team. Source-check date is separate from clinical approval. Report a content problem ·
Treatment often lasts one to two years or longer. Taper only when symptoms and markers are controlled, and distinguish relapse from steroid withdrawal, adrenal insufficiency, osteoarthritis and rotator-cuff pain. Begin bone, glucose, pressure, vaccination, gastric and infection prevention at treatment start. Methotrexate may reduce steroid burden in relapse-prone or toxicity-prone patients; biologic treatment is specialist and commissioning dependent.
Exclude infection and screen GCA first. Monitor glucose, pressure, mood, eyes, bone, infection and adrenal suppression; steroid response is supportive, not diagnostic, and prolonged treatment must not stop abruptly.
Weekly administration is essential because daily methotrexate can be fatal. Check FBC, liver and renal function, withhold during serious infection, avoid trimethoprim or co-trimoxazole, and stop at least one month before maternal conception; specialist selection is required.
Avoid oesophageal emptying disorders, inability to sit upright, hypocalcaemia and severe renal impairment; review dental risk and treatment duration. Check the selected SmPC because the weekly regimen is off-label for some male or glucocorticoid-induced-osteoporosis indications.