Anterior interosseous nerve syndrome: an unusual case of peripheral nerve compression in a high-level baseball pitcher

Article information

Arch Hand Microsurg. 2025;30(2):136-140

Publication date (electronic) : 2025 May 30

doi : https://doi.org/10.12790/ahm.25.0003

Harin Bhavin Parikh, Adam Gabriel Wright-Chisem, Steven Soohwan Shin

Department of Orthopaedics, Cedars-Sinai Medical Center, Los Angeles, CA, USA

Corresponding author: Harin Bhavin Parikh Department of Orthopaedics, Cedars-Sinai Medical Center, 444 S. San Vicente Blvd, Suite 603, Los Angeles, CA 90048, USA Tel: +1-916-690-0456 Fax: E-mail: harin.parikh@cshs.org

Received 2025 February 7; Revised 2025 April 5; Accepted 2025 April 14.

Abstract

Introduction

Anterior interosseous nerve (AIN) syndrome is characterized by difficulty in making an “OK” sign due to weakness of the flexor pollicis longus (FPL) and flexor digitorum profundus to the index and middle fingers [1]. In addition, weakness of the pronator quadratus is also detected with electromyography/nerve conduction studies in patients with suspected AIN syndrome [1]. Patients may have deep forearm pain due to involvement of proprioceptive fibers. Etiologies reported in the literature include external compression versus neuralgic amyotrophy (Parsonage-Turner Syndrome) [2]. Thus, treatment options are varied, ranging from observation to surgical decompression. In this case report, we describe the treatment of a high-level baseball pitcher presenting with AIN syndrome who successfully returned to the sport following surgical decompression. AIN syndrome in high-level athlete is rare, and to our knowledge not been commonly reported in the literature. Treating providers should aim to alleviate nerve compression and facilitate a safe return to play when possible. The patient has provided written consent for publication of this case.

Case report

A 31-year-old left-handed man presented to our clinic in-season for evaluation of deep left forearm pain and hand weakness. He was a high-level pitcher for a professional club. His symptoms began three months prior to presentation without any history of traumatic injury. Of note, he had changed his throwing mechanics to involve more pronation and a greater throwing velocity earlier in the season. Following the progressive onset of his symptoms, he was unable to pitch effectively in practice or during games and thereafter refrained from all baseball activity without improvement in symptoms.

He had a history of left elbow pain and numbness and tingling in his left hand seven years prior, at which time he was diagnosed with an ulnar collateral ligament tear at the elbow and associated cubital tunnel syndrome. He underwent ulnar collateral ligament reconstruction with cubital tunnel release and subcutaneous ulnar nerve transposition at that time. He had an uneventful postoperative recovery and was able to return to full activity until the onset of his current symptoms.

On physical exam, he had focal tenderness to palpation over his left pronator teres and proximal forearm without atrophy. He had 4/5 strength of his left FPL and index finger flexor digitorum profundus. He otherwise had full strength with examination of the posterior interosseous and ulnar nerves. Sensation was intact in the median, radial, and ulnar distributions. He had pain with resisted pronation; however, he did not have pain or instability with any other provocative maneuvers including the milking maneuver and moving valgus stress test. He had a negative Tinel sign over the proximal forearm overlying the pronator musculature, ulnar nerve, and at the volar wrist overlying the carpal tunnel.

Plain radiographs of his elbow did not reveal any bony abnormality explaining the patient’s symptoms. An magnetic resonance imaging (MRI) was obtained, which was unremarkable for any muscle edema seen in AIN or non-AIN-innervated muscles. In addition, no hourglass or torsional lesions of the AIN were identified on MRI imaging of the elbow or forearm. Electrodiagnostic studies were performed, notable for increased motor latency of AIN-innervated muscles.

Based on the patient’s weakness in the AIN distribution and deep proximal forearm pain, the possibility of AIN syndrome was discussed. Options ranging from continued observation to surgical exploration and decompression were discussed. Given the patient’s career as a high-level baseball pitcher, it was important to him to return to throwing as soon as possible. Thus, he elected to proceed with surgical intervention, performed approximately 4 months after the onset of symptoms.

The patient was positioned supine with the left upper extremity placed on a hand table. A “lazy S” incision was used to approach the proximal forearm volarly with the incision directed from medial to lateral (Fig. 1). As subcutaneous tissues were spread, cutaneous terminal branches of the medial antebrachial cutaneous nerve were protected. The lacertus fibrosus was identified and sharply incised, revealing the underlying median nerve (Fig. 2). The superficial head of the pronator teres was identified and reflected medially, further exposing the median nerve. The pronator teres muscle belly was found to be quite robust (Fig. 3). This was preserved given the importance of the patient to pronate during the throwing motion; however, the overlying fascia was incised to address any possible pronator syndrome. The flexor digitorum superficialis (FDS) arch was then identified and incised. Of note, this fibrous arch was found to significantly compress the median nerve (Fig. 3). The median nerve was traced proximally as it ran along the leash of Henry and compressive bands along the flexor-pronator mass were released. The deep head of the pronator teres was identified and reflected off of the median nerve. This allowed for visualization of the AIN as it branched off the median nerve; the AIN was traced and decompressed distally (Fig. 4).

Fig. 1.

A “lazy S” incision made from the medial aspect of the elbow proximally to the lateral aspect of the forearm distally.

Fig. 2.

Lacertus fibrosus isolated prior to division, elevated with a Freer elevator.

Fig. 3.

Pronator teres and flexor digitorum superficialis arch. Note the robust nature of the pronator teres muscle belly. Also pictured is the median nerve (white arrow) passing underneath the flexor digitorum superficialis arch (blue arrow) prior to the release of the arch.

Fig. 4.

Anterior interosseous nerve (blue vessel loop) following surgical decompression. Note the take-off of the anterior interosseous nerve from the median nerve (white arrow). Also pictured is the leash of Henry (green arrow).

Postoperatively, the patient was placed into a bulky soft dressing without a plaster splint. Immediate passive and active range of motion was initiated. The patient was allowed to weight-bear on the extremity as tolerated. By 6 weeks postoperative, he noted significant improvement in his deep forearm pain and improvement in FPL and index finger FDS function. He was ultimately cleared to return to full activity and throwing without restrictions and returned to sport the following competitive season.

Discussion

In throwing athletes including high-level baseball pitchers, elbow injuries are a common cause of disability [3-5]. Interestingly, elbow injuries represent the highest number of days missed of all musculoskeletal injuries [6]. Common elbow injuries sustained in these athletes include those to the ulnar collateral ligament, flexor-pronator mass, posteromedial impingement, and cubital tunnel syndrome [6].

Although many pitchers face cubital tunnel syndrome and undergo eventual cubital tunnel release, the incidence of other upper extremity compressive neuropathies in this population is rare. To our knowledge, this is the first report of AIN syndrome in a high-level baseball pitcher. The patient initially complained of deep forearm pain and was found to have weakness in the AIN nerve distribution. Interestingly, a prior retrospective analysis of 14 patients found that 9 (64%) complained of deep forearm pain [7]. This could be explained by intraoperative findings including a robust pronator teres muscle belly and fibrous FDS arch. With attention given to the release of the pronator fascia and FDS arch during the surgery, this appeared to have led to significant improvement in the patient’s symptoms.

Our patient presented with weakness with resisted thumb interphalangeal joint flexion and index finger distal interphalangeal flexion. Other patients with more extensive weakness may present with the characteristic "Kiloh-Nevin" sign of AIN syndrome, on an inability to make an "OK" sign with the thumb and index finger. [1]. Pronator syndrome was considered as a potential diagnosis given the patient’s vague forearm pain. However, patients with pronator syndrome generally present with numbness in the median nerve distribution [1]. Our patient did not have paresthesias; instead, he was found to have motor weakness with flexion of the thumb and index finger, characteristic of pure motor palsy [1]. In addition, AIN syndrome was further supported with electromyography and nerve conduction studies. Of note, the points of compression in both syndromes are similar [1].

The above patient’s career as a high-level baseball pitcher played a significant role in the decision to proceed with surgical decompression to treat his symptoms. Prior studies recommend an initial period of nonoperative management with forearm flexor-pronator muscle stretching, activity modification, and anti-inflammatory medications [1]. Prior reports have found favorable results with nonoperative treatment at 1 year; however, more recent studies suggest that patients may benefit from nerve exploration and decompression if no nerve recovery is seen three months after the onset of symptoms [2,7]. Our patient did not want the unpredictability of continued observation and therefore made the decision to proceed with operative intervention after failed nonoperative management for three months. The timing of surgical intervention was critical in allowing him to return to regular pitching the following season.

Important structures to identify and release during an AIN decompression include the lacertus fibrosus, the FDS arch, Gantzer’s muscle (if present), and the superficial head of the pronator teres [1]. An important consideration was that as a baseball pitcher, the patient was heavily reliant on active pronation during the pitching motion [8]. Understanding the contribution of the pronator teres muscle to active pronation, the decision was made to defer the release of the superficial head of the pronator teres and lengthening of the deep head [9]. Though not characteristic of the classically described AIN decompression technique, we believed that this would give the patient the best chance at symptomatic improvement while maximizing his chances to return to high-level activity without risking a decrease in pronation strength during the throwing motion. This was evidenced by his favorable recovery postoperatively. If the patient did not have improvement in his symptoms, MRI imaging would have been performed to investigate more proximal sites of compression in the arm. Future studies may look to investigate the size of the pronator teres muscle belly in relation to the incidence of symptoms of AIN syndrome to shed further light regarding this potential phenomenon in high-level athletes.

In this report, we present the case of a high-level baseball pitcher who presented with AIN syndrome refractory to an initial period of nonoperative management. His career as a baseball pitcher influenced our decision to deviate from the traditional treatment algorithm, including a quicker progression to surgical management and preservation of the pronator teres during decompression to maximize pitching ability. We believe that these measures were necessary to allow the patient to quickly regain motor strength and return to full activity. Thus, providers should be cognizant of AIN syndrome as a potential cause of deep forearm pain and motor weakness in high-level baseball pitchers and customize management according to the demands of their profession. Though recently considered as an amyotrophic neuralgia, structural causes in the forearm of these high-level athletes should be investigated using MRI and electrodiagnostic studies allowing for more informed treatment decision-making.

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