Polymyalgia rheumatica

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

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.

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.

Key points

PMR causes new bilateral shoulder aching with morning stiffness longer than forty-five minutes in adults over fifty, commonly with hip-girdle pain and raised CRP or ESR.
Confirm pain-limited movement rather than true weakness; abnormal power, CK, reflexes, sensation, rash or dysphagia requires an alternative neuromuscular assessment.
Ask about headache, scalp tenderness, jaw claudication, visual symptoms, limb claudication and aortic pain at diagnosis and every follow-up.
Obtain FBC, CRP, ESR, renal, liver, calcium, ALP, glucose, thyroid and CK, with RF or anti-CCP, protein electrophoresis, imaging and infection tests guided by phenotype.
Start prednisolone 15 mg orally once daily for a typical uncomplicated presentation after baseline assessment; a substantial clinical response within about one week supports but does not prove diagnosis.
Maintain 15 mg for three weeks, reduce to 12.5 mg for three weeks, then 10 mg for four to six weeks, followed by reductions of 1 mg every four to eight weeks if remission persists.
Do not use PMR-dose steroid for possible GCA; suspected cranial disease needs 40–60 mg prednisolone and visual symptoms require an emergency high-dose pathway.
Relapse means recurrent PMR symptoms with a supportive marker rise after alternatives are assessed; return to the previous effective dose and taper again rather than restarting the entire schedule automatically.
Consider methotrexate early in repeated relapse, prolonged treatment or high steroid-toxicity risk with rheumatology monitoring.
Poor or incomplete response should trigger diagnostic review for GCA, RA, myositis, infection, malignancy and structural shoulder disease rather than repeated empirical steroid increases.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Age-related immune disease

PMR occurs almost exclusively after age fifty, with immune ageing and HLA susceptibility producing inflammation around shoulder and hip girdle synovial structures.

Environmental influence

Seasonal variation and occasional clustering suggest environmental triggers, but no specific infection is established and antibiotics have no routine role.

GCA spectrum association

PMR and GCA share immune pathways and frequently coexist; PMR symptoms do not protect against cranial or large-vessel arterial disease.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Periarticular inflammation
Subdeltoid bursae, biceps tendon sheaths, glenohumeral and hip synovial structures become inflamed, producing pain and prolonged stiffness without primary muscle-fibre destruction.
2
Cytokine systemic response
IL-6 and other inflammatory mediators cause morning stiffness, fatigue, fever, anaemia and raised CRP or ESR in typical active disease.
3
Pain-limited movement
Patients struggle to raise arms or rise because movement hurts and stiffens, but formal power is preserved when pain is overcome.
4
Relapsing treatment course
Inflammation can recur during taper, while glucocorticoid withdrawal, adrenal suppression and structural shoulder disease can mimic a true relapse.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Bilateral girdle stiffness

New symmetrical shoulder pain with prolonged morning stiffness and difficulty dressing or turning in bed is the core PMR phenotype.

Hip and systemic features

Hip aching, fatigue, low fever, weight loss and raised inflammatory markers commonly accompany shoulder symptoms but are not individually specific.

Preserved true power

Formal strength is usually intact once pain is accommodated; objective weakness, atrophy or CK elevation suggests myopathy or neurological disease.

Concurrent GCARed flag

Headache, scalp pain, jaw claudication or any visual symptom changes treatment immediately to the GCA pathway.

Atypical or refractory course

Young age, focal symptoms, normal markers, severe night pain, peripheral synovitis or poor steroid response requires diagnostic review.

Red flags requiring action

Any visual symptom, jaw claudication or new cranial pain requires immediate GCA assessment before routine PMR review.
Objective muscle weakness, dysphagia, rash or markedly raised CK suggests inflammatory myopathy rather than uncomplicated PMR.
Fever, night sweats, focal pain, lymphadenopathy, weight loss or poor steroid response requires infection and malignancy assessment.
Peripheral synovitis, erosions or persistent small-joint swelling may indicate elderly-onset rheumatoid arthritis.
Relapse symptoms with low blood pressure, vomiting or severe weakness during rapid taper may represent adrenal insufficiency.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
CRP, ESR and FBCFirst step
Why
Support inflammatory activity, identify anaemia or thrombocytosis and create a taper baseline.
Interpretation and limitations
Most cases raise at least one marker, but results are nonspecific; a normal result makes typical PMR less likely and demands careful review.
02
Renal, liver, calcium, ALP, glucose, TSH and CK
Why
Find metabolic, endocrine, muscle and treatment-safety alternatives before glucocorticoid.
Interpretation and limitations
CK should be normal in PMR; abnormal calcium, ALP, thyroid or liver tests can redirect toward malignancy, bone, endocrine or muscle disease.
03
RF, anti-CCP and protein electrophoresis
Why
Assess elderly-onset rheumatoid arthritis or paraprotein disease when clinical features support them.
Interpretation and limitations
Anti-CCP or persistent peripheral synovitis favours RA; paraprotein requires haematological context and does not automatically explain symptoms.
04
Shoulder and hip ultrasound
Why
Support periarticular inflammation and identify structural alternatives in an uncertain presentation.
Interpretation and limitations
Bilateral bursitis and biceps tenosynovitis support PMR but also occur in other disease and must match the clinical syndrome.
05
GCA imaging pathway
Why
Investigate cranial or large-vessel arteritis when symptoms, markers or steroid-resistant PMR raise concern.
Interpretation and limitations
Temporal or axillary ultrasound and PET-CT, CTA or MRA are selected by phenotype; testing must not delay emergency GCA glucocorticoid.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Elderly-onset rheumatoid arthritis

Persistent peripheral synovitis, small-joint swelling, RF or anti-CCP and erosive change favour rheumatoid arthritis, although onset can initially mimic PMR.

Inflammatory or endocrine myopathy

Objective weakness, CK elevation, rash, dysphagia, thyroid or adrenal findings indicates muscle or endocrine disease rather than pain-limited movement.

Infection or malignancy

Endocarditis, osteomyelitis, tuberculosis, myeloma, lymphoma and solid cancer can produce shoulder pain, systemic symptoms, anaemia and raised inflammatory markers.

Mechanical shoulder and widespread pain

Rotator-cuff disease, osteoarthritis, cervical disease and fibromyalgia cause pain but differ in stiffness duration, inflammatory markers and systemic trajectory.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01First-line diagnosisExclude mimics and screen for GCAFirst stepFirst lineAn adult over fifty has new bilateral girdle pain and prolonged morning stiffness.

1Document stiffness, function, systemic, cranial and visual symptoms and examine temporal arteries, pulses, joints, shoulder mechanics and true muscle power.
2Obtain inflammatory, blood, metabolic, thyroid and muscle tests and add RA, paraprotein, infection or imaging assessment from atypical features.
3If the phenotype is typical and GCA is absent, start prednisolone 15 mg/day and arrange clinical and marker review within one to two weeks.

02Preferred taperReduce only in remissionPreferredSymptoms improve substantially and inflammatory markers normalise or return toward baseline.

1Continue 15 mg for three weeks, then 12.5 mg for three weeks and 10 mg for four to six weeks.
2Below 10 mg reduce by 1 mg every four to eight weeks while symptoms and markers remain controlled, individualising for relapse and toxicity.
3At each step screen GCA and record bone, glucose, pressure, infection, eye, mood and adrenal risks.

03RelapseConfirm inflammation before increasingGirdle pain or stiffness returns during taper or after treatment stops.

1Reassess CRP or ESR, GCA, infection, RA, mechanical shoulder or hip disease, fibromyalgia, steroid withdrawal and adrenal insufficiency.
2For confirmed PMR relapse return to the previous dose that controlled symptoms, then repeat a slower taper after remission.
3AlternativeRefer repeated relapse, inability to reduce or toxicity for methotrexate or specialist alternative and diagnostic reconsideration.

04GCA diversionChange dose and destination immediatelyNew cranial, visual, neurological, limb-vascular or aortic features appear.

1Give prednisolone 40–60 mg immediately for suspected GCA, or emergency visual-ischaemia rescue when sight symptoms occur.
2Arrange same-day ophthalmology for visual change and fast-track rheumatology ultrasound or biopsy without waiting for markers.
3Continue PMR and large-vessel follow-up only after the arterial emergency is secured.

Key medicines and prescribing safety3 treatments · regimens, roles and cautions

First-line anti-inflammatory treatment and a structured therapeutic trial in a typical presentation.

Prednisolone

Start 15 mg orally once daily for uncomplicated PMR; after three weeks reduce to 12.5 mg for three weeks, then 10 mg for four to six weeks, then by 1 mg every four to eight weeks if remission persists.

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.

Off-label steroid-sparing option added early or after relapse in selected PMR patients.

Methotrexate with folic acid

For repeated relapse or high steroid-toxicity risk, specialists commonly start 7.5–15 mg orally once weekly with folic acid at least 5 mg on another day and titrate by response.

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.

Reduces fragility fracture during prolonged glucocorticoid exposure in patients whose fracture risk warrants medicine treatment.

Alendronic acid

When fracture prevention is indicated, use 70 mg orally once weekly with adequate calcium and vitamin D, taken fasting with plain water while remaining upright for at least thirty minutes.

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.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Giant-cell arteritis

Unrecognised cranial or large-vessel vasculitis can cause irreversible blindness, stroke, limb ischaemia and delayed aortic aneurysm or dissection.

Glucocorticoid toxicity

Diabetes, hypertension, infection, osteoporosis, cataract, glaucoma, skin fragility, mood disturbance, myopathy and adrenal suppression accumulate during treatment.

Relapse and prolonged dependency

Repeated inflammatory flares or overly rapid taper can prolong exposure, while misclassified mechanical pain may prompt unnecessary dose escalation.

Functional decline

Pain, sleep loss, deconditioning and steroid myopathy can impair dressing, transfers and independence even when inflammatory markers improve.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Review response within one to two weeks of starting treatment; lack of substantial improvement triggers diagnostic reconsideration.
At every visit ask explicitly about headache, scalp tenderness, jaw claudication, visual symptoms, limb claudication and aortic pain.
Track CRP or ESR alongside symptoms at taper steps, recognising markers can be normal during mechanical pain and raised during infection.
Monitor pressure, weight, glucose or HbA1c, bone density and fracture risk, eyes, mood, infection and steroid myopathy.
Record cumulative steroid dose, relapses and the lowest effective dose and consider rheumatology referral when taper repeatedly fails.
Provide steroid sick-day and emergency advice and assess HPA-axis suppression before final withdrawal when exposure has been prolonged.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

PMR is not muscle inflammation

Pain arises mainly from bursae and synovial structures; true weakness or CK elevation should redirect assessment.

Response is not proof

Steroid can temporarily improve cancer, infection and many painful conditions, so baseline evaluation and longitudinal fit remain essential.

Every relapse screens GCA

Arteritis can emerge after an apparently uncomplicated PMR diagnosis and requires a much higher emergency dose.

Mechanical pain survives remission

Rotator-cuff and osteoarthritis symptoms may persist after inflammatory stiffness resolves and should not automatically prolong steroid.

Taper tests both disease and adrenal axis

Symptoms below physiological doses may reflect inflammatory relapse, withdrawal or adrenal insufficiency and require different responses.

11Common pitfallsFrequent interpretation and management errors.

01
Starting prednisolone before asking about visual symptoms and therefore giving an inadequate PMR dose to GCA.
02
Calling inability to lift painful arms weakness without formal power testing and CK.
03
Using steroid response as the only diagnostic criterion.
04
Increasing dose for every shoulder ache without checking CRP, mechanics, infection and adrenal symptoms.
05
Tapering rapidly after initial response and creating relapse and repeated high-dose exposure.
06
Omitting fracture, glucose, blood-pressure, infection and eye prevention during a long course.