Causes / typical injury mechanism: In general, anterior interosseous nerve (AIN) compression syndrome is caused by transient neuritis (Parsonage-Turner syndrome), compression, or rarely, from compartment syndrome. Compression can occur at the deep head of the pronator teres (most commonly), fibrous arch of the flexor digitorum superficialis (FDS), thrombosed radial ulnar or anterior interosseous artery, accessory head of the flexor pollicis longus (FPL), accessory muscle from the FDS to the flexor digitorum profundus (FDP), or aberrant muscles (palmaris profundus, flexor carpi radialis brevis [FCRB]).

Parsonage-Turner syndrome involves bilateral AIN symptoms caused by brachial neuritis.

Classic history and presentation: AIN compression syndrome classically presents in a patient in the fourth decade of life with vague, poorly localized pain in the forearm and cubital fossa with motor deficits. Usually, these patients primarily complain of pain and do not have sensory changes. Most commonly, the motor deficits manifest as difficulty bringing the index finger and thumb together, difficulty with buttoning clothing, and difficultly forming a fist.

Prevalence: Less than 1% of all upper limb nerve syndromes

• Age – fourth decade
• Sex / gender – equal in males and females

Risk factors: Viral brachial neuritis, upper extremity trauma such as supracondylar fractures, penetrating injuries, cast fixation, and venipuncture.

Pathophysiology: AIN compression syndrome can be caused by transient neuritis (Parsonage-Turner syndrome), direct AIN compression, or compartment syndrome. Parsonage-Turner syndrome involves bilateral AIN symptoms caused by brachial neuritis.