Anatomy, Shoulder and Upper Limb, Forearm Anterior Interosseous Nerve

Structure and Function

The AIN provides motor innervation to deep forearm muscles, including flexor digitorum profundus (radial half/index and middle finger), flexor pollicis longus, and pronator quadratus. It also provides some sensation to the distal radioulnar and carpal joints and joint capsule. The AIN does not provide cutaneous innervation.[1]

Physiologic Variants

Martin-Gruber anastomosis occurs in 10% to 15% of all forearms (motor nerve connection between the median and ulnar nerves). In 50% of these cases, the nerve communication from the median nerve arises from the AIN branch. Therefore, palsy of the AIN could lead to palsy of the intrinsic muscles of the hand normally supplied by the ulnar nerve.[2]

Surgical Considerations

AIN Compressive Neuropathy

The surgical decompression of the AIN is indicated only if a prolonged period of nonoperative treatment fails. The technique may include the release of the superficial arch of flexor digitorum superficialis and lacertus fibrosus, detachment of superficial head of pronator teres, ligation of any crossing vessels, and removal of any space-occupying lesion.[3]

Pediatric Supracondylar Fracture

Closed reduction and percutaneous pinning are indicated in type II and III supracondylar fractures, flexion type, or medial column collapse. The urgency of this surgery depends on the clinical presentation. Of note, an isolated AIN injury is not an urgent surgical consideration and can be done electively.[4]

Clinical Significance

Clinical Examination

The anterior interosseous nerve examination is performed by testing the motor function of the flexor digitorum profundus, flexor pollicis longus, and pronator quadratus. The flexor digitorum profundus tendon is tested by asking the patient to bend the tips of the second and third digits while stabilizing the proximal interphalangeal joints. Uninjured patients can flex the distal interphalangeal joints. The flexor pollicis longus can be tested by instructing the patient to bend the interphalangeal joint of the first digit. The pronator quadratus is tested by positioning the patient's arm at the side with the elbow flexed to 90 degrees and the forearm in supination. The examiner then asks the patient to pronate the forearm while providing resistance. As with all orthopedic examinations, the affected extremity should be compared with the unaffected extremity.[5]

AIN Syndrome

Anterior interosseous nerve syndrome typically presents with forearm pain and partial or complete dysfunction of muscles innervated by the anterior interosseous nerve, including the flexor pollicis longus, flexor digitorum profundus to the second digit and third digit, and pronator quadratus. The anterior interosseous nerve may become entrapped at any of the following locations: the tendinous edge of the deep head of pronator teres (most common cause), flexor digitorum superficialis arcade, edge of the lacertus fibrosus, accessory head of the flexor pollicis longus (Gantzer muscle), accessory muscle from the flexor digitorum superficialis to the flexor digitorum profundus, and aberrant muscles (flexor carpi radialis brevis, palmaris profundus). However, transient neuritis is the most common cause. Complete anterior interosseous nerve palsy typically causes partial or complete loss of motor function in the flexor digitorum profundus to the second digit, flexor digitorum profundus to the third digit, flexor pollicis longus, and pronator quadratus. The function of the flexor digitorum profundus to the third digit may be preserved because of cross-innervation by the ulnar nerve. The patient may demonstrate grip and pinch weakness, specifically with flexion of the first, second, and third digits. The patient may be unable to make an okay sign (Kiloh-Nevin sign) because of an inability to flex the first digit interphalangeal joint and the distal interphalangeal joint of the second digit, indicating complete loss of function of the flexor pollicis longus and flexor digitorum profundus to the second digit. This weakness can be further evaluated by asking the patient to pinch a sheet of paper between the first and second digits using only the fingertips while the examiner slowly pulls the paper away. Patients with anterior interosseous nerve syndrome may compensate for flexor pollicis longus and flexor digitorum profundus to the second digit weakness by using intrinsic hand muscles innervated by the ulnar nerve. The patient may also demonstrate weakness with resisted pronation with the elbow maximally flexed, which tests the pronator quadratus. Patients with Martin-Gruber anastomosis can present with weakness of the intrinsic hand muscles typically supplied by the ulnar nerve. The anterior interosseous nerve does not provide sensory innervation to the skin, so isolated anterior interosseous nerve palsy does not cause sensory deficits.

The differential diagnosis for patients presenting with suspected anterior interosseous nerve syndrome includes trauma, flexor pollicis longus tendon rupture, proximal sites of nerve compression (ie, cervical nerves, brachial plexus), thoracic outlet syndrome, pronator syndrome, carpal tunnel syndrome, and Parsonage-Turner syndrome. Parsonage-Turner syndrome can present as bilateral anterior interosseous nerve neuropathy caused by viral brachial neuritis. Parsonage-Turner syndrome is more likely if the motor loss is preceded by intense shoulder pain and a viral prodrome. Flexor pollicis longus rupture is typically seen in patients with rheumatoid arthritis or a history of trauma and is distinguished from anterior interosseous nerve compressive neuropathy with passive flexion and extension of the wrist. An intact flexor pollicis longus tendon causes the first digit interphalangeal joint and second digit distal interphalangeal joint to flex during this motion. Electromyography and nerve conduction studies can help rule out other, more proximal lesions and assess the severity of anterior interosseous nerve compressive neuropathy. Imaging is typically not helpful for the diagnosis and treatment of anterior interosseous nerve syndrome. The majority of patients improve with nonoperative treatment, including rest and splinting in 90 degrees flexion for 8 to 12 weeks. Surgical decompression of the anterior interosseous nerve is indicated if nonoperative treatment fails.[3][6][7]

Pronator Teres Syndrome

AIN syndrome should be distinguished from pronator teres syndrome, a distinct but similar proximal median neuropathy. Pronator teres syndrome is characterized by vague forearm pain associated with paresthesia of the median nerve. This is distinguished from AIN neuropathy, which is a pure motor palsy.[5]

Pediatric Supracondylar Fractures

Anterior interosseous nerve neuropraxia is the most common nerve palsy associated with pediatric supracondylar fractures. Anterior interosseous nerve palsy is found in 7.6% to 8.6% of supracondylar fractures and alone accounts for 47% of all nerve-related complications and 70% of median nerve injuries. The mechanism of injury is typically a fall onto an outstretched hand. Patients most often present with pain and refusal to move the elbow. Physical examination findings consistent with a supracondylar fracture include gross deformity, swelling, ecchymosis in the antecubital fossa, and limited active elbow motion. Patients with anterior interosseous nerve neuropraxia are unable to flex the interphalangeal joint of the first digit and the distal interphalangeal joint of the second digit (inability to make an okay sign). The mechanism of injury for the anterior interosseous nerve in supracondylar fractures is tenting of the nerve on the fracture or entrapment in the fracture site. Radiography findings indicative of a pediatric supracondylar fracture include the posterior fat pad sign, a lucency on a lateral view along the posterior distal humerus and olecranon fossa that is highly suggestive of occult fracture around the elbow. Other findings include displacement of the anterior humeral line and alteration of the Baumann angle. Nearly all cases of neuropraxia following supracondylar humerus fractures resolve spontaneously. Operative treatment is indicated based on the severity of the fracture.[4][8]