Anterior Interosseous Syndrome

Etiology

Several causes of anterior interosseous nerve syndrome have been well documented. Injuries to the anterior interosseous nerve resulting from direct external trauma do not meet the diagnostic criteria for anterior interosseous nerve syndrome.[6] Documented external traumatic causes include forearm and elbow fractures, penetrating injuries such as stab wounds, cast fixation, venipuncture, and complications arising from open reduction and internal fixation of fractures. Only spontaneous cases presenting with weakness of the muscles innervated by the anterior interosseous nerve qualify as true anterior interosseous nerve syndrome.

Many physicians, particularly surgeons, consider anterior interosseous nerve syndrome a form of compressive neuropathy. However, several clinical features set this condition apart from other compressive neuropathies. In contrast to the more gradual onset seen in typical compression syndromes, paralysis in anterior interosseous nerve syndrome often develops suddenly and resolves spontaneously. Recurrence remains uncommon, unlike the higher recurrence rates observed in other compressive neuropathies.

Electrodiagnostic studies in many patients with anterior interosseous nerve syndrome reveal a more widespread median motor involvement extending beyond the muscles specifically innervated by the anterior interosseous nerve.[7] The most frequently identified cause involves an idiopathic immune-mediated neuritis. An intrinsic compressive lesion in the forearm, including conditions such as compartment syndrome and localized compression neuropathy, represents the second most common etiology.[8][7]

The most common site of intrinsic anterior interosseous nerve entrapment or compression is the tendinous edge of the deep head of the pronator teres muscle. Other potential sites include:

• The proximal edge of the flexor digitorum superficialis (FDS) arch (the FDS arcade)
• Gantzer's muscle (accessory head of the FPL muscle)
• FDS or FDP accessory muscles
• Arterial thrombosis (radial or ulnar artery has been implicated)
• Lacertus fibrous

A careful analysis of the anterior interosseous nerve anatomy in the forearm will indicate that compression of the anterior interosseous nerve cannot explain most of the anterior interosseous nerve syndromes. The anterior interosseous nerve branches from the median nerve 5 to 8 cm distal to the lateral epicondyle beneath the pronator teres. The nerve passes between the FDP and FPL muscles. There should be sensory involvement if the compression occurs proximal to the anterior interosseous nerve. Compression distal to the anterior interosseous nerve branch point should have only selective FDP or FPL denervation. Observing all 3 muscle involvements is difficult secondary to compressive etiology.

Anterior interosseous nerve syndrome should be clinically differentiated from stenosing tenosynovitis or pathologies limited to local pathology affecting the flexor tendons alone (ie, flexor tendon adhesions or partial versus complete flexor tendon rupture). The nerve is typically compressed by the fibrous bands that often originate from the deep head of the brachialis fascia and the pronator teres, and this pressure can increase with minor variations.[9]

An FPL tendon rupture is also a possibility among patients with rheumatoid arthritis. To exclude the differential diagnosis, the wrist must be flexed passively and extended to confirm that the individual has an intact tenodesis effect.[10] Rheumatoid disease and gouty arthritis may be predisposing factors in anterior interosseous nerve entrapment.

Epidemiology

Anterior interosseous nerve syndrome is rare when compared with other entrapment neuropathies, comprising <1% of all upper extremity palsies. No difference between the incidence of the anterior interosseous nerve in men and women or between dominant and nondominant upper extremities has been demonstrated.

Pathophysiology

The exact pathophysiology can occur secondary to primary entrapment, direct trauma, or in more ambiguous or vague clinical presentations. The condition also manifests following viral neuritis. Very similar syndromes can be caused by more proximal lesions, such as brachial plexus neuritis. In the latter, clinicians should have a heightened diagnostic suspicion in patients presenting with motor loss following prodromal symptoms consisting of intense shoulder pain or recent viral illness or exposure.[11][12]

History and Physical

Clinical Features

True anterior interosseous nerve syndrome generally presents with motor deficits alone, without accompanying sensory changes. Most patients report a sudden or acute onset of poorly localized pain in the forearm and cubital fossa, often as the primary complaint. Symptoms, eg, numbness, tingling, or other sensory deficits, remain absent. Patients frequently describe difficulty bringing the distal phalanges of the thumb and index finger together.

On physical examination, the pinch grip test or "OK" sign typically yields a positive result; instead of forming a proper circle with the thumb and index finger, the patient presses the sheet between an extended thumb and index finger (see Image. Pinch Grip Test). Additional complaints may include difficulty forming a fist or fastening buttons. Sensation remains intact on examination.[13][14]

Evaluation

Alongside a thorough history and detailed neurological examination, electrodiagnostic studies play a critical role in evaluating anterior interosseous nerve syndrome of spontaneous origin. Sensory nerve conduction studies of the median nerve should yield normal results, given the absence of sensory innervation to the anterior interosseous nerve. Electromyography typically reveals abnormalities in the flexor pollicis longus, the radial portion of the flexor digitorum profundus, and the pronator quadratus, aiding in the distinction between neurologic amyotrophy and compression neuropathy.[15] Magnetic resonance imaging (MRI) also offers significant value in assessing patients with suspected anterior interosseous nerve syndrome.[16]

Treatment / Management

Nonsurgical Management

The consensus on the preferred management of anterior interosseous nerve syndrome includes conservative interventions, eg, a period of rest, observation, and splinting of the elbow at 90 degrees of flexion (or the position of most comfort for the patient). Most patients experience improvement and even recovery within 6 to 12 weeks of activity modification.[17] Other conservative modalities to consider include NSAIDs and physical therapy, including reduced pain and massage techniques if tolerated. 

Surgical Modalities

Surgical treatment consists of exploration, neurolysis, and decompression after several months of failed nonoperative modalities. The literature reports 75% or more significant positive outcomes following surgery, with higher rates reported in patients with an identifiable, apparent space-occupying mass. Unless a clear cause is identified, surgical intervention is typically offered only in select cases, and the option is discussed following at least 3 months of failed conservative treatment.[18][19](B3)

During median nerve surgical decompression, meticulous dissection is necessary to establish the exact sites of compression and is critical in identifying and releasing compressing edges or fibrous bands. Because many anterior interosseous nerve syndrome cases are caused by inflammatory neuritis rather than compressive neuropathy, other surgical options may be considered to improve hand function, including tendon transfers and reconstructive surgeries.

Differential Diagnosis

Anterior interosseous nerve entrapment or compression injury presents a challenging clinical diagnosis due to its predominantly motor function and frequent misidentification as a ligamentous finger injury. The differential diagnosis includes stenosing tenosynovitis, flexor tendon adherence or adhesion, flexor tendon rupture, and brachial neuritis. Brachial plexus neuritis may present with a similar clinical picture.[9][10]

Selective fascicular involvement of the median nerve trunk above the elbow has emerged as a recently recognized cause of anterior interosseous nerve syndrome, displaying the characteristic clinical and electromyographic features. Diagnosis of this variant relies on advanced MRI techniques and an increasing number of supporting case reports.[16]

Pertinent Studies and Ongoing Trials

Anterior interosseous nerve studies are usually retrospective. No randomized controlled trials have been performed since the condition is relatively rare. Patients who have undergone surgery typically have good postoperative records; many will resolve with conservative treatment. Therefore, the natural history of the disease seems to be benign. Those retrospective studies have shown the surgical and nonsurgical methods to be equivocal.[10]

Prognosis

The prognosis is usually good, and most cases don't require surgical treatment. If conservative therapy fails beyond 3 months, surgery might be offered in select cases.[20]

Complications

Complications of anterior interosseous syndrome primarily involve persistent motor deficits that affect fine motor function, particularly impairing the ability to perform tasks requiring thumb and index finger coordination, eg, writing, buttoning clothing, or gripping objects. Delayed or incorrect diagnosis may lead to prolonged dysfunction, as the condition is often mistaken for tendon injuries or other neuropathies. In cases where spontaneous recovery does not occur, chronic weakness and muscle atrophy may develop, especially if the underlying cause is unrecognized or untreated. Surgical complications, although uncommon, may include nerve damage, scarring, or failure to relieve symptoms if the entrapment site is not accurately identified. Misdiagnosis of traumatic injuries as true anterior interosseous syndrome can also result in ineffective treatment plans. Additionally, patients with autoimmune conditions, eg, rheumatoid arthritis or gout, may face higher risks for tendon rupture or inflammatory recurrence, further complicating the clinical picture. Incomplete recovery, especially in cases with diffuse median nerve involvement or immune-mediated neuritis, may lead to long-term functional limitations, making early identification and appropriate management essential to minimizing adverse outcomes.