Review on the Anterior Interosseous Nerve Syndrome
The anterior interosseous nerve (AIN) is a branch of the median nerve (1). The AIN is typically found approximately 5cm from the lateral epicondyle and will typically dive below or through the pronator teres before it travels through the interosseous membrane of the wrist (3). The AIN provides motor innervation to the flexor pollicis longus (FPL), the flexor digitorum profundus (FDP) of the second and third digit, and the pronator quadratus (1).
The pathophysiology of AIN syndrome is controversial. The AIN can be injured from trauma or iatrogenically from surgical injury (1). However, symptoms can also be secondary to entrapment from an accessory flexor digitorum profundus (1). Entrapment of the AIN occurs infrequently and only amounting for less than 1% of the upper limb entrapment syndromes (2). AIN entrapment is found most commonly in patients in their 40s. There are alternative theories as to the pathophysiology of AIN syndrome, which includes the theory that the motor weakness seen in AIN syndrome is due to neuritis and not entrapment (4).
Patients with AIN will have no sensory deficit on examination (1). Hand paresthesias and forearm pain can be representative of a proximal median nerve entrapment and not AIN syndrome (1). Providers will find motor weakness with AIN syndrome. This can be tested with resistance of the FPL and FDP of the index finger (4). During the clinical examination, patients with AIN syndrome have weakness in making an O with their thumb and index finger (5). This can also be tested by having the patient try to hold a piece of paper with their finger tips when somebody tries to pull the paper away (3). Due to the weakness, providers need to rule out a tendon tear rupture of the FPL (7). This can be accomplished by passively bringing the wrist into extension and visualizing flexion of the interphalangeal joint of the thumb due to contraction of the FPL (7). Patients also will complain of a deep pain in their forearm (5). It is also important to assess for previous shoulder pain, as the motor palsy can be manifestation of previous Parsonage Turner Syndrome (7).
Identifying compression of the AIN on MRI can be difficult (4). Although the entrapment may not be visualized, there can be enhancement within the muscles affected by the nerve root entrapment (5). When diagnosis is not clear, electrodiagnostic testing can be performed to help differentiate neuralgic amyotrophy verse a compression neuropathy (5).
The majority of acute cases of AIN syndrome will resolve spontaneously (5). However, there may be some residual weakness in select patients (6). Other conservative measures like bracing, NSAIDs, oral steroids, and physical therapy can aid in symptom improvement (5). Timing for surgical intervention can vary. Surgical evaluation can be done if the symptoms persist past 6-8 weeks, but some surgeons will advocate waiting 12 weeks (3).
AIN syndrome typically presents with forearm pain and weakness in the FPL and FDP of the index finger. Diagnosis can be made clinically or aided with EMG and/or MRI. Symptoms are typically self limiting, but surgical exploration can be done in patients who to have spontaneous recovery.
By Gregory Rubin, DO
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