Epicondylitis is a chronic degenerative disease of the tendon origins arising from the elbow epicondyles. Lateral epicondylitis ('tennis elbow') affects the common extensor tendon origin (extensor carpi radialis brevis — ECRB most commonly), medial epicondylitis ('golfer's elbow') affects the common flexor-pronator tendon origin. Lateral form is 5-10 times more common than medial with 1-3% prevalence in general population. Most frequent in adults aged 35-50, dominant on the dominant hand side. Histopathologically, chronic angiofibroblastic degeneration ('tendinosis') dominates rather than acute inflammation — collagen disorganization, fibroblast proliferation, mucoid degeneration, and neovascularization are seen. MRI shows T2 signal increase, thickening, and partial tear findings at the affected tendon origin. US offers equivalent sensitivity with advantages of dynamic assessment and treatment guidance.
Age Range
30-60
Peak Age
45
Gender
Equal
Prevalence
Very Common
Epicondylitis is a chronic overuse injury caused by repetitive wrist and forearm movements, with pathophysiology explained by the 'failed healing' model. In lateral epicondylitis, ECRB is most commonly affected because it is anatomically prone to impingement between the lateral epicondyle and radial head (capitellum) — during elbow extension and pronation, the undersurface of ECRB is subjected to friction with the radial head. Repetitive eccentric loading (such as wrist extension during gripping) creates microtrauma at the tendon origin → normal healing response initiates but ongoing mechanical stress disrupts healing → failed healing cycle → angiofibroblastic degeneration develops. Histopathologically: (1) disorganization and fragmentation of collagen type I fibers, (2) immature fibroblast proliferation (predominantly type III collagen production — mechanically weak), (3) mucoid degeneration (proteoglycan and glycosaminoglycan accumulation), (4) neovascularization (disorganized vascular proliferation — with pain receptors), (5) notable absence of inflammatory cells — thus 'tendinosis' is more accurate than 'tendinitis.' The physics basis of T2 signal increase in tendinosis on MRI: in normal tendon, tightly packed collagen fibers produce very low signal with ultra-short T2 (~1-5 ms); in degeneration, collagen disorganization and mucoid material accumulation (proteoglycan + bound water) partially lengthen T2 → intermediate-high signal. In partial tear areas, collagen fiber disruption and free fluid infiltration → focal hyperintense defect. In medial epicondylitis, ulnar neuropathy (50%) may accompany due to proximity to ulnar nerve — cubital tunnel syndrome should be investigated.
T2 fat-sat MRI showing signal increase, thickening, and morphologic disruption at tendon origin from lateral or medial epicondyle — confirms epicondylitis diagnosis with clinical symptoms. If partial tear is superimposed, focal undersurface defect is seen.
On coronal and axial T2 fat-sat images, focal or diffuse T2 signal increase is seen at the common extensor tendon origin (especially ECRB) from the lateral epicondyle. Normal tendon origin shows homogeneous low signal — from tight packing of collagen fibers. Signal increase reflects degeneration (tendinosis), edema, and/or partial tear. In partial tear, focal high-signal defect at the undersurface (articular side) of the tendon — best seen on axial images. In complete tear, defect extends through entire tendon thickness with retraction of tendon ends. Capitellar cartilage beneath ECRB should be evaluated — cartilage damage may develop from chronic ECRB degeneration.
Report Sentence
T2 signal increase and thickening are noted at the common extensor tendon origin (ECRB) at the lateral epicondyle, consistent with lateral epicondylitis.
On T2 fat-sat, edema is seen around the tendon origin and epicondylar periosteum — hyperintense signal increase. Peritendinous edema indicates active process and should be evaluated independently from tendinosis. In lateral epicondylitis, the lateral collateral ligament complex (LCL — especially lateral ulnar collateral ligament LUCL) may also be involved — T2 signal increase and thickening. LCL involvement increases risk of posterolateral rotatory instability and is important for surgical planning. Joint effusion may accompany — especially in chronic cases and those with LCL involvement. In medial epicondylitis, medial collateral ligament (MCL — especially anterior band) should be evaluated — may be associated with medial instability.
Report Sentence
Peritendinous and periosteal edema are noted around the lateral epicondyle, consistent with active lateral epicondylitis.
On B-mode US, thickening, hypoechoic signal change, and loss of fibrillar pattern at the common extensor or flexor tendon origin are seen. Normal tendon origin is thin, hyperechoic with smooth fibrillar pattern. In tendinosis: thickening (>4 mm, normal 3-4 mm), hypoechoic areas (mucoid degeneration), fibrillar pattern disruption. In partial tear, focal anechoic or hypoechoic defect — more common at articular surface (deep portion). In complete tear, defect through entire thickness with retraction. US is ideal for bilateral comparative assessment — both elbows compared with symmetric probe positioning. Dynamic assessment can evaluate tendon mobility and crepitation during elbow flexion-extension.
Report Sentence
Thickening, hypoechoic signal change, and fibrillar pattern disruption are noted at the common extensor tendon origin on US, consistent with lateral epicondylitis.
Increased vascularity (neovascularization) at the affected tendon origin is seen on power Doppler — indicating active degenerative process. Normal tendon origin has no or minimal Doppler signal. Neovascularization represents new capillary vessels developing in response to degeneration and generally accompanies pain sources — therefore Doppler-positive areas help identify pain-generating regions. US-guided sclerosing agent injection (polidocanol) targets these neovascular areas with demonstrated pain-relieving effect. Doppler signal decrease in treatment response monitoring correlates with clinical improvement.
Report Sentence
Neovascularization at the common extensor tendon origin is noted on power Doppler, consistent with active lateral epicondylitis.
On PD fat-sat or T2 fat-sat axial images, a focal hyperintense defect at the undersurface (articular/deep portion) of the common extensor tendon origin — partial tear. ECRB undersurface tears are the most common form because this surface is subjected to mechanical friction with the radial head. Defect size is reported as percentage of tendon thickness: <50% low-grade partial tear, >50% high-grade partial tear. Surrounding edema and signal increase around the tear. Coronal images assess tear line and extent. In complete tear, defect through entire tendon thickness with retraction of tendon ends — rare but an important condition requiring surgery.
Report Sentence
Focal hyperintense defect at the undersurface of the common extensor tendon origin is noted, consistent with partial tear.
On coronal and axial T2 fat-sat images, T2 signal increase, thickening, and morphologic disruption at the common flexor-pronator tendon origin from the medial epicondyle are seen. Pronator teres and flexor carpi radialis (FCR) are the most commonly affected components. In medial epicondylitis, ulnar nerve pathology may accompany due to proximity — ulnar nerve thickening, T2 signal increase, or subluxation at cubital tunnel level should be investigated (50% coexistence). MCL anterior band should also be evaluated — may be associated with medial instability, especially in throwing athletes (baseball pitchers).
Report Sentence
T2 signal increase at the common flexor-pronator tendon origin at the medial epicondyle is noted, consistent with medial epicondylitis.
Criteria
Degeneration at common extensor tendon origin (ECRB most common). Lateral epicondyle tenderness, grip weakness, positive Cozen/Mill test.
Distinct Features
5-10 times more common than medial. ECRB undersurface tears most common. LCL involvement may accompany (posterolateral rotatory instability). Conservative treatment 80-90% successful — arthroscopic debridement or open surgery for refractory cases.
Criteria
Degeneration at common flexor-pronator tendon origin (pronator teres, FCR most common). Medial epicondyle tenderness, pain with wrist flexion/pronation.
Distinct Features
Ulnar nerve pathology accompanies in 50% (cubital tunnel syndrome). MCL anterior band involvement possible (medial instability — throwing athletes). Lower surgical need than lateral form.
Criteria
Focal tear defect superimposed on tendinosis. Focal hyperintense defect at undersurface (articular side) or bursal surface.
Distinct Features
Surgical indication strengthened for high-grade partial tear (>50%) or complete tear. PRP injection being tried for moderate tears. Axial MRI best shows defect size and location.
Distinguishing Feature
Distal biceps tendon pathology (insertional tendinopathy or tear) can clinically mimic lateral/medial epicondylitis — both cause elbow pain. On MRI, distal biceps shows signal abnormality at radial tuberosity insertion, epicondylitis at epicondylar origin. Axial images differentiate by anatomic localization.
Distinguishing Feature
Lateral collateral ligament (LCL) injury may coexist with lateral epicondylitis but is a separate pathology. LCL injury causes posterolateral rotatory instability — positive pivot-shift test. LCL signal change on MRI is evaluated independently from tendon origin.
Distinguishing Feature
Osteochondral lesion (capitellum or trochlea) is important differential of elbow pain — MRI shows articular cartilage defect and subchondral bone signal change. Epicondylitis is extra-articular tendon origin pathology — cartilage and subchondral bone are normal (except periosteal edema).
Urgency
routineManagement
conservativeBiopsy
Not NeededFollow-up
3-monthEpicondylitis treatment is predominantly conservative with 80-90% of patients recovering in 6-12 months. First step: NSAIDs (2-4 weeks), ice, activity modification, counterforce brace (reduces load on tendon origin), eccentric strengthening exercises (physiotherapy — most effective conservative method). Second step: US-guided corticosteroid injection (effective short-term but high recurrence rate 50-70%), PRP injection (studies showing superiority over corticosteroid medium-term), sclerosing agent injection (polidocanol — neovascular targeting). Third step (non-responsive to 6-12 months conservative — 5-10% of patients): arthroscopic or open surgical debridement (excision of degenerative tendon tissue + ECRB origin repair). In medial epicondylitis with accompanying ulnar nerve pathology, cubital tunnel decompression may be added. Postoperative rehabilitation takes 3-6 months.
Epicondylitis resolves with conservative treatment in 80-90% of patients. First-line treatment is rest, ice, NSAIDs, and eccentric exercises. Corticosteroid injection provides short-term relief. PRP injection and surgical debridement are options in resistant cases. MRI should assess tear extent in cases not responding to conservative treatment.