Physical Medicine and Rehabilitation for Epicondylitis

Updated: Aug 30, 2018
  • Author: Sharon J Gibbs, MD; Chief Editor: Stephen Kishner, MD, MHA  more...
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Medial epicondylitis (ME) is an overuse injury affecting the flexor-pronator muscle origin at the anterior medial epicondyle of the humerus. ME is often discussed in conjunction with lateral epicondylitis (LE), which occurs much more frequently. ME is the most common cause of medial elbow pain, although the clinician is likely to see at least 5 cases of LE for every case of ME. Patients who develop medial elbow pain appreciate their physician's knowledge of the subtle differences in the diagnosis and treatment of the two disorders. [1, 2] (See images below.)

Medial epicondyle. Medial epicondyle.
Strengthening exercises are performed once pain ha Strengthening exercises are performed once pain has subsided with active range of motion. The starting position (slight pronation) of an eccentric exercise for medial epicondylitis is shown. In order to prevent further injury, a trained therapist should instruct patients in exercises to confirm proper weight and technique.
The eccentric exercise proceeds until full supinat The eccentric exercise proceeds until full supination has been reached.


ME involves primarily the flexor-pronator muscles (ie, pronator teres, flexor carpi radialis, palmaris longus) at their origin on the anterior medial epicondyle. Less often, ME also affects the flexor carpi ulnaris and flexor digitorum superficialis. Repetitive stress at the musculotendinous junction and its origin at the epicondyle leads to tendinitis in its most acute form and to tendinosis in its more chronic form. [3] In addition, an ulnar neuropraxia caused by compression of the ulnar nerve in or around the medial epicondylar groove has been estimated to occur in up to 50% of ME cases.

The tendinosis that occurs is primarily the result of failure of the damaged tendon to heal. Microscopic examination of the involved tissue shows granulation tissue, fibrovascular and fibrocartilaginous tissue, tendon microfragmentation, calcification, and necrosis. Histologically, damage to the involved tendons has been described as angiofibroblastic hyperplasia tendinosis and fibrillary degeneration of collagen. [4] A simple, acute inflammatory reaction is noted to be a much less common finding than are the previously described tendinosis changes.




No studies indicate a race predilection.


A male-to-female ratio of 2:1 has been reported.


Peak incidence is in patients aged 20-49 years, but ME is also seen in teens and older adults, especially if they engage in hobbies, jobs, or sports activities that make them prone to overuse injuries.