Epicondylitis — Tennis and Golfer's Elbow

• Lateral epicondylitis ("tennis elbow") — the common extensor origin, principally extensor carpi radialis brevis. Pain over the lateral epicondyle, reproduced by resisted wrist extension and by gripping. Far more common than the medial form, and most patients have never played tennis; it follows any repetitive gripping or wrist-extension work.
• Medial epicondylitis ("golfer's elbow") — the common flexor–pronator origin. Pain over the medial epicondyle, reproduced by resisted wrist flexion and pronation. The ulnar nerve runs just posterior in the cubital tunnel, so check for coexisting ulnar symptoms.
• Diagnosis is clinical; imaging is reserved for atypical presentations or failure to improve.
• Differential: radial tunnel syndrome, cervical radiculopathy (C6), elbow osteoarthritis, and ulnar collateral ligament injury on the medial side.
• Management is conservative and the natural history is favourable over months to a year: activity modification, eccentric strengthening physiotherapy, counterforce bracing, and topical or oral NSAIDs. Corticosteroid injection gives short-term relief but worse outcomes at one year, which is a commonly tested nuance. Surgery is a last resort.

Mechanism-based causes

• Repetitive eccentric overload of the common extensor origin: the dominant cause of lateral disease. Gripping, wrist extension, forearm supination/pronation and vibration transmitted through hand tools produce submaximal, repeated tensile strain on the extensor carpi radialis brevis (ECRB) enthesis.
• Repetitive wrist flexion and forced pronation: the medial equivalent — golf (especially a "fat" shot striking the ground), throwing, racquet serves with topspin, bowling, carpentry, and manual pulling.
• Acute overload superimposed on chronic degeneration: a single heavy lift or an unaccustomed backhand can convert a silent tendinosis into symptomatic disease; this is the stem where symptoms "started after one weekend of painting."

Modifiable risk factors

• Occupational exposure: forceful repetitive gripping, high-force/high-repetition combined tasks, and vibrating tool use — the exposure pattern emphasised in the ACOEM elbow disorders guideline. Meat cutters, plumbers, carpenters, cooks, keyboard/mouse users.
• Sport technique and equipment: faulty single-handed backhand, grip circumference too small, high string tension, heavy racquet.
• Smoking and obesity: both are associated with tendinopathy and with poorer recovery, plausibly via microvascular compromise of an already hypovascular enthesis.
• Diabetes mellitus: classically over-represented in medial epicondylitis; glycation-related collagen cross-linking impairs tendon remodelling.
• Systemic corticosteroids and fluoroquinolones: recognised tendinopathy risks (best characterised for the Achilles, but a fair distractor in an elbow stem).

Non-modifiable risk factors

• Age: peak incidence in the fourth to fifth decades, when tendon healing capacity has declined but activity remains high — not the young elite athlete.
• Sex: roughly equal, though occupational cases skew with the workforce.
• Dominant limb: the great majority of cases occur on the dominant side.
• Prior contralateral or other tendinopathy, suggesting a constitutional predisposition to failed tendon healing.

• The vulnerable structure: the ECRB origin lies deep to the extensor digitorum communis on the anterior aspect of the lateral epicondyle and rubs against the lateral edge of the capitellum during flexion–extension. Its undersurface is relatively hypovascular, so mechanical abrasion plus poor perfusion converge on one small area of enthesis — which is why point tenderness is slightly distal and anterior to the bony prominence rather than on it.
• Repetitive submaximal strain → microtearing: eccentric loading (the wrist extensors decelerating wrist flexion during grip and impact) generates tensile forces exceeding the tendon's remodelling capacity. Collagen microtears accumulate faster than they are repaired.
• Failed healing response, not inflammation: the repair that follows is disordered. Histology shows angiofibroblastic hyperplasia (Nirschl) — immature type III collagen replacing organised type I fibres, increased mucoid ground substance, fibroblast proliferation, and neovascularisation without inflammatory cells. Acute-phase inflammatory infiltrate is characteristically absent, which is why the "-itis" is a misnomer and why systemic anti-inflammatories modify symptoms rather than disease.
• Why it hurts: the ingrowing neovessels are accompanied by unmyelinated sensory nerve fibres expressing substance P and CGRP. Nociceptor ingrowth into a normally aneural tendon substance explains load-dependent, well-localised pain in the absence of swelling, erythema, or warmth.
• Why grip is weak and painful: forceful grip requires synergistic wrist-extensor co-contraction to stabilise the wrist. Loading the degenerated ECRB origin during grip both provokes pain and triggers reflex inhibition, producing measurable grip-strength loss — hence pain shaking hands or lifting a full cup.
• Why it is provoked by passive stretch: elbow extension with forearm pronation and wrist flexion maximally lengthens the common extensor origin, reproducing pain (Mill's manoeuvre).
• Medial side, same biology: the flexor–pronator origin (pronator teres, flexor carpi radialis) degenerates identically, but the ulnar nerve in the cubital tunnel lies immediately posterior, so perineural scarring or coexisting traction neuritis adds numbness in the ring and little fingers in a substantial minority.

Symptoms

• Lateral elbow pain radiating into the extensor forearm, aching at rest and sharp with use — nociceptor ingrowth into degenerated tendon loaded during wrist extension.
• Pain and weakness with gripping: dropping a coffee cup, difficulty turning a doorknob or shaking hands. Grip demands extensor co-contraction, so the lesion is loaded even when the task looks like "flexion."
• Morning stiffness that eases, and pain that worsens through a work shift rather than a brief inflammatory flare pattern.
• No systemic features: no fever, no swelling, no other joint involvement — this separates it from inflammatory arthritis or septic olecranon bursitis.

Signs — lateral

• Point tenderness just distal and anterior to the lateral epicondyle over the ECRB origin, not over the joint line.
• Cozen test: resisted wrist extension with the fist clenched, forearm pronated and the wrist radially deviated, performed with the examiner stabilising the elbow and palpating the lateral epicondyle; reproduction of lateral pain is positive. Described with the elbow flexed to about 90° in some sources and extended in others — the loading principle, not the elbow angle, is what is being tested.
• Mill's test: passive wrist flexion with pronation and full elbow extension stretches the origin and provokes pain.
• Maudsley test: resisted extension of the middle finger, which selectively loads ECRB.
• Chair-lift test: pain lifting a chair with the forearm pronated.
• Reduced grip strength, worse with the elbow extended than flexed.

Signs — medial

• Tenderness over the medial epicondyle/flexor–pronator origin, pain on resisted wrist flexion and resisted pronation, and on passive wrist extension with the elbow extended.
• Ulnar nerve screen is mandatory: Tinel sign at the cubital tunnel, ring/little-finger paraesthesia, intrinsic weakness.
• Valgus stress testing should be normal; pain or laxity suggests ulnar collateral ligament injury in a thrower.

• Diagnosis is clinical. Localised tenderness at the common extensor or flexor–pronator origin plus reproduction of pain on resisted wrist extension (lateral) or resisted wrist flexion/pronation (medial), in a patient with a compatible repetitive-load history and an otherwise normal elbow exam, is sufficient. No laboratory test is indicated; ESR/CRP are normal and ordering them is a distractor.

When to image (ACR Appropriateness Criteria, chronic elbow pain)

• Plain radiographs first if there is trauma, mechanical locking, restricted or painful range of motion, joint effusion, or failure to improve after an adequate conservative trial. Films are usually normal; a minority show calcification or spurring at the epicondyle (enthesophyte), and radiographs exclude osteoarthritis, loose bodies, osteochondritis dissecans, and occult fracture.
• Ultrasound is the practical next test — inexpensive, dynamic, and operator-dependent. Findings: hypoechoic thickening of the common extensor origin, loss of the normal fibrillar pattern, intrasubstance clefts/partial tearing, cortical irregularity of the epicondyle, and neovascularity on power Doppler — the sonographic signature of tendinosis rather than tenosynovitis.
• MRI is the best anatomic test and the one obtained before surgery or when the diagnosis is genuinely in doubt: increased T2/STIR signal and thickening within the ECRB origin, with grading of partial versus full-thickness tear, plus assessment of the lateral ulnar collateral ligament (lateral) or ulnar collateral ligament (medial). Note that MRI signal change correlates poorly with symptoms, so imaging should not override the exam.
• Electrodiagnostic studies (EMG/NCS) are most useful medially, to confirm ulnar neuropathy at the cubital tunnel when there is ring/little-finger numbness, intrinsic weakness, or a positive Tinel sign. In suspected radial tunnel syndrome electrodiagnostics are characteristically normal or non-diagnostic, so a negative study neither confirms nor excludes it — the diagnosis rests on pain and tenderness several centimetres distal to the epicondyle over the supinator. Frank denervation of finger and thumb extensors instead indicates posterior interosseous nerve syndrome.

Named instrument

• The Patient-Rated Tennis Elbow Evaluation (PRTEE) is the validated pain-and-function questionnaire used to track outcomes in trials and clinics. There is no diagnostic scoring system — do not expect a criteria set analogous to Jones or Centor.

First-line (all patients)

• Activity/ergonomic modification: reduce forceful repetitive gripping, enlarge tool and racquet grips, correct backhand technique. This removes the causative load.
• Eccentric-loading physiotherapy: the intervention with the best evidence for reversing tendinosis, because controlled eccentric strain stimulates collagen realignment and tenocyte remodelling (e.g. isometric progressing to eccentric wrist-extensor loading, Tyler twist with a flexible bar).
• Counterforce (tennis-elbow) strap worn a few centimetres distal to the epicondyle, dispersing force away from the degenerated origin.
• Wrist extension (cock-up) orthosis, holding roughly 15–30° of wrist extension to unload the ECRB origin, may be added for lateral disease — but the supporting evidence is limited/low-strength and it should not displace counterforce bracing plus eccentric loading.
• NSAIDs — topical first: topical diclofenac gives short-term analgesia with minimal systemic exposure; a short course of an oral NSAID (e.g. naproxen) is acceptable. Analgesia only — it does not alter the tendinosis. Acetaminophen is a reasonable adjunct.

Escalation / second line

• Corticosteroid injection (e.g. methylprednisolone with lidocaine): meaningful relief at weeks, but worse pain, function, and higher recurrence at one year than physiotherapy or wait-and-see — the classic tested nuance. Use sparingly, never repeatedly.
• Other options with limited or mixed evidence: autologous blood or platelet-rich plasma injection, extracorporeal shockwave therapy, topical nitroglycerin, dry needling/percutaneous tenotomy. The AAOS guidance on lateral elbow tendinopathy grades most of these as low-strength or inconclusive.

Definitive

• Surgery only after roughly 6–12 months of genuine, supervised conservative care: open Nirschl-type debridement/excision of degenerative ECRB tissue, or arthroscopic/percutaneous release; medially, flexor–pronator debridement with ulnar nerve decompression or transposition if neuropathy coexists.

Avoid

• Repeated or high-volume intratendinous steroid (fat atrophy, depigmentation, tendon rupture), prolonged immobilisation (stiffness and deconditioning), and opioids, which have no role in tendinopathy.

Of the disease

• Chronic refractory pain and grip weakness: a minority remain symptomatic beyond a year. Mechanism is persistent failed healing with ongoing neovascular/nerve ingrowth; the signal is unchanged pain despite documented adherence to eccentric loading.
• Partial or complete rupture of the common extensor origin: sudden increase in pain with a palpable defect and marked loss of resisted wrist extension; suggested by full-thickness tear on MRI.
• Secondary ulnar neuropathy (medial disease): perineural scarring in the cubital tunnel — ring/little-finger numbness, positive elbow flexion/Tinel test, later first dorsal interosseous wasting. Progressive intrinsic weakness warrants urgent surgical referral to prevent permanent denervation.
• Deconditioning and work disability from guarding and prolonged rest.

Of treatment

• Corticosteroid injection: subcutaneous fat atrophy and skin depigmentation over the injection site (cosmetically obvious in darker skin), post-injection pain flare, transient hyperglycaemia in diabetics, and tendon rupture with repeated intratendinous injection. Paradoxically inferior one-year outcomes — the recurrence itself is the complication examiners want.
• Post-injection infection: because epicondylar injections are peritendinous and extra-articular, the expected infectious complication is cellulitis, an injection-site abscess, or septic olecranon bursitis, not septic arthritis — true septic arthritis follows intra-articular injection or haematogenous seeding. Fever, spreading erythema, fluctuance, or pain on passive range of motion after an injection requires aspiration/drainage with cultures and empiric antibiotics covering staphylococci and streptococci, including MRSA coverage when purulent, as framed by the IDSA skin and soft tissue infection guideline. Never re-inject an infected site.
• NSAID toxicity: GI ulceration/bleeding, renal impairment, hypertension — the reason topical formulations are preferred in older or comorbid patients.
• Surgical complications: iatrogenic lateral ulnar collateral ligament injury from over-aggressive posterior release causing posterolateral rotatory instability (apprehension and clunk on the pivot-shift test); posterior interosseous nerve injury with finger-drop; ulnar nerve injury or subluxation after medial release; wound infection, haematoma, elbow stiffness, and persistent pain in a subset.

• Tendinosis, not tendinitis: biopsy shows angiofibroblastic hyperplasia with disorganised type III collagen and neovascularisation and no inflammatory infiltrate. If a stem offers "neutrophilic inflammation of the tendon," it is wrong.
• **Lateral = ECRB = resisted wrist extension (Cozen, Mill's, Maudsley); medial = flexor–pronator = resisted wrist flexion and pronation. Tenderness is just distal and anterior** to the lateral epicondyle, not on the joint line.
• Best next step in a classic presentation is not imaging — it is activity modification plus an eccentric-strengthening physiotherapy programme, with a counterforce strap and topical NSAID. Radiographs/MRI only for atypical features, mechanical symptoms, trauma, or failure to improve.
• The single most tested nuance: corticosteroid injection helps at weeks but yields worse pain and function at one year than physiotherapy or watchful waiting. Choose it only for short-term, work-critical relief — and never repeatedly.
• The association to know: medial epicondylitis and ulnar neuropathy at the cubital tunnel. Ring/little-finger numbness in a golfer with medial elbow pain means examine the ulnar nerve and consider EMG.
• Common distractor — radial tunnel syndrome: proximal radial/posterior interosseous nerve compression at the arcade of Frohse/supinator, causing aching lateral forearm pain with tenderness several centimetres distal to the epicondyle and night pain, characteristically without motor weakness and with normal or non-diagnostic electrodiagnostics. If the stem gives finger drop / weak thumb and finger extension with no sensory loss, that is posterior interosseous nerve syndrome, a different entity. C6 radiculopathy is the other trap: look for neck pain, a positive Spurling, and reflex change.
• Most patients with "tennis elbow" have never played tennis — the dominant-arm manual worker is the typical stem, peaking in the fourth to fifth decades.
• Natural history is favourable: the majority resolve within 6–12 months; surgery (Nirschl debridement of ECRB) is reserved for failure of prolonged supervised conservative care.