Successful recovery of anterior interosseous nerve palsy caused by blunt trauma at the forearm level: a case report
Article information
Abstract
Anterior interosseous nerve syndrome (AINS) is typically characterized by dysfunction of the pure motor branch of the median nerve, primarily affecting the flexor pollicis longus and the flexor digitorum profundus (FDP) of the index finger, and occasionally involving the FDP of the middle finger and the pronator quadratus. Although various etiologies such as compressive neuropathy and isolated neuritis have been proposed, the most recent review describes AINS as a form of neuralgic amyotrophy. Its treatment remains a matter of debate; the most frequently discussed approach is conservative treatment followed by surgical intervention above the medial epicondyle level if recovery is not achieved. In the case described herein, a hematoma resulting from blunt trauma at the forearm level compressed the anterior interosseous nerve (AIN), with clinical features and diagnostic findings very similar to those of typical AINS. Early surgical removal of the hematoma led to complete recovery without complications. Despite the current understanding of AINS pathophysiology and treatment, this case emphasizes the need to consider the possibility of AIN palsy due to forearm lesions. We report on the clinical course and successful treatment of this case to highlight this important consideration.
Introduction
The anterior interosseous nerve (AIN) is the largest motor branch of the median nerve, arising in the upper forearm to innervate the flexor digitorum profundus (FDP) muscles of the index and middle fingers, as well as the flexor pollicis longus (FPL) muscle. In the distal forearm, the AIN also supplies the pronator quadratus (PQ) muscle [1-3].
AIN palsy was first described by Tinel [4] in 1918 as “dissociated paralysis of the median nerve.” Parsonage and Turner [5] reported cases associated with neuralgic amyotrophy, which was later characterized by Kiloh and Nevin [6] as isolated neuritis, and Fearn and Goodfellow [2] proposed entrapment neuropathy as a potential etiology. Since then, various pathophysiologies have been proposed, and the most recent studies describe typical AIN syndrome (AINS) as a form of neuralgic amyotrophy [1,7,8].
While AINS can manifest following an upper-extremity traumatic event, direct traumatic injury to the AIN itself is not typically classified as “AIN syndrome” due to its distinct underlying pathophysiology and rarity [1]. Similarly, weakness of the AIN-innervated muscles due to an extrinsic mass, such as a tumor or hematoma, is infrequent and also represents a different pathophysiological process [1,8].
We report a case of AIN palsy that presented with clinical features and diagnostic findings similar to typical AINS but was caused by a lesion resulting from blunt trauma at the mid-forearm level. We aim to describe the clinical course leading to successful recovery following early surgical intervention.
Case report
A 42-year-old left-handed man presented with flexion failure of the interphalangeal (IP) joint of the left thumb and the distal interphalangeal (DIP) joint of the index finger. Three weeks before he visited our hospital, the patient had sustained trauma when his left forearm was trapped in a machine door for 15 minutes.
Records from the initial hospital visit indicated a 2-cm laceration on the dorsoulnar side of the mid-forearm, accompanied by pain and swelling at the injury site on volar aspect of the left forearm. Palpation revealed no significant abnormalities. The patient reported no symptoms in the neck or shoulder areas, and there was no relevant medical or surgical history. At the time of injury, no sensory changes or motion limitations were observed from the left forearm to the hand. Plain radiography showed no fractures or periosteal reactions. Only a primary closure for the skin breakage was performed, with no immobilization. The pain persisted after injury, and the main symptoms began to manifest 4 to 5 days later.
Prior to visiting our hospital, the patient continued with daily activities for 2 weeks after injury. However, due to the lack of symptom improvement, including flexion failure of the IP joint of the left thumb and the DIP joint of the index finger, he presented to our outpatient clinic for further evaluation. Examination revealed a flexion strength of grade 2/5 for both the IP joint of the left thumb and the DIP joint of the DIP joint of the left index finger, making it impossible for the patient to perform the ‘O’ sign (Fig. 1).
Preoperative photographs. (A) Flexion failure of the interphalangeal joint of the left thumb. (B) Flexion failure of the distal interphalangeal joint of the left index finger. (C) The patient was unable to form the ‘O’ sign.
Passive range of motion (ROM) was remarkable, indicating no joint abnormalities. The movements of all other distal and proximal muscles were normal. However, the sensory testing revealed a tingling sensation on the volar aspect of the thumb, index finger, and middle finger, which corresponded to the median nerve territory, with no tenderness or Tinel sign. On palpation, a mass-like lesion, approximately 5 cm in size, was identified at the distal one-third of the volar aspect of the forearm, with a defined boundary and immobility.
Plain radiography showed an oval-shaped diffuse haziness at the distal one-third level of the forearm. Magnetic resonance imaging (MRI) T2-weighted images revealed a 6-cm mass-like lesion with low signal intensity around the musculotendinous junction of the FDP at the distal one-third level (Fig. 2).
Preoperative magnetic resonance imaging T2-weighted images (A, axial view; B, coronal view) revealed a well-defined mass-like lesion. The size of the lesion is approximately 6.1×2.5×2.0 cm, with heterogeneous low signal intensity observed around the musculotendinous junction of the flexor digitorum profundus tendon (arrows), indicative of potential intramuscular hematoma.
Three weeks after injury, electromyography (EMG) was performed, detecting fibrillation (2+) and positive sharp waves (3+) in the PQ, FPL, FDP, and pronator teres muscles. Nerve conduction studies showed a reduction in both motor and sensory nerve conduction amplitudes of the left median nerve to less than half of the contralateral side, suggesting denervation due to physical interference. Based on these findings, we planned surgical exploration with the suspicion that a hematoma within the FDP muscle group was compressing the AIN as it branched from the median nerve. Additionally, it was essential to assess for any potential damage to the FPL, the FDP tendon of the index finger, and the median nerve trunk.
A 5-cm linear incision was made at the site of the palpable mass on the volar aspect of the distal forearm. The subcutaneous layer was intact, with no issues in the flexor digitorum superficialis and flexor carpi radialis muscles. An oval-shaped intramuscular hematoma was observed within the FDP muscle, accompanied by necrotic changes and significant soft tissue swelling in the FDP muscle of the index finger. Additionally, approximately 40% rupture of the tendon at the musculotendinous junction. This area of injury aligned with the course of the AIN branching from the median nerve, suggesting that the damage was caused by blunt trauma, with the mass effect from the hematoma and soft tissue swelling contributing to compression. The median nerve and the FPL tendon were intact, with no adhesion or fibrous arch formation in the surrounding tissues. The necrotic muscle and the ruptured ends of tendon were excised. Furthermore, the distal tendon was transferred to the middle finger FDP tendon using the Pulvertaft weaving technique (Fig. 3).
Intraoperative photographs. (A) An oval-shaped mass-like lesion, suspected to be an intramuscular hematoma, was found at the musculotendinous junction of the flexor digitorum profundus (FDP) tendon, with the muscle showing diffuse swelling. (B) Necrotic changes were observed in the FDP muscle of the index finger, along with a 40% tendon rupture at the musculotendinous junction. (C) It was confirmed that there were no visible injuries to the FPL tendon and the median nerve. The FDP2 tendon, which was dissected from the musculotendinous junction for tendon transfer, is also shown. *, FPL tendon; ▲, median nerve; •, FDP2 tendon. (D) A tendon transfer from FDP3 was performed to reconstruct FDP2.
After surgery, the patient began to show improvement in thumb IP joint motion starting from the 4th week. ROM tests demonstrated a progressive improvement in the thumb IP joint, with 20° of flexion observed in the 4th week, increasing to 40° in the 7th week, 75° in the 10th week, and reaching 85° by the 12th week (Fig. 4). Additionally, the tip pinch grip test measured 2.3 kg on the affected side, compared to 2.3 kg on the contralateral side. The DIP joint of the index finger showed 40° of flexion in the 4th week, improving to 80° in the 12th week. Ultimately, the patient was able to perform the ‘O’ sign (Fig. 5).
Serial improvement in the range of motion of the thumb interphalangeal joint over time (4, 7, 10, 12 weeks).
(A) Improvement in the range of motion of the distal interphalangeal joint (arrow) of the index finger at 12 weeks after surgery. (B) The patient was able to achieve the "O" sign.
The two-point discrimination test in the 4th week showed static and moving tests at 44 mm (contralateral 33 mm) for the thumb, 15 mm (contralateral 33 mm) for the index finger, and 55 mm (contralateral 33 mm) for the middle finger. By the 12th week, all affected fingers showed static and moving tests of 33 mm, similar to the contralateral side.
This study was approved by the Institutional Review Board of Gwangmyeong Sungae General Hospital (No. 2024-N-008). Written informed consent was obtained from the patient for the publication of this report including all clinical images.
Discussion
AIN palsy is a rare disorder, and its pathophysiology and clinical course are not yet fully understood. It was first described by Tinel [4] in 1918 as “dissociated paralysis of the median nerve.” Since then, various etiologies such as neuralgic amyotrophy, supracondylar fractures of the humerus, forearm fractures, anomalies of the median artery, trauma from elbow orthoses, thrombophlebitis, and complications from catheterization or phlebotomy have been proposed as etiologies for AIN palsy [9,10].
Recent studies have described AINS, the most recognized clinical presentation of AIN palsy, as a form of neuralgic amyotrophy [1,7,8]. It is believed to result from fascicular constrictions or hourglass lesions of the median nerve, typically occurring at or above the medial epicondyle [1]. These constrictions are generally identified within the anterior interosseous fascicular group and are not related to lesions in the forearm [1].
The patient we report experienced AIN palsy following trauma to the forearm, which can be distinguished from typical AINS by several key features: the primary lesion was located at the mid-forearm level, the onset of symptoms was delayed by 4 to 5 days after injury, and sensory disturbances in the hand were present. These findings suggest that the hematoma within the FDP muscle, resulting from the trauma, exerted a mass effect on the forearm structures, leading to compression of the median nerve trunk and AIN. This pathophysiological mechanism is supported by the imaging and clinical findings.
The management of AINS remains a topic of controversy. Authors who consider the cause of AINS to be entrapment neuropathy advocate for surgical exploration and nerve decompression, whereas those who attribute it to neuritis of the AIN favor conservative treatment. Spinner [9], while acknowledging the effectiveness of conservative management, recommended surgical intervention if paralysis shows no improvement 6 to 8 weeks after symptom onset. Hill et al. [11] further suggested that surgical exploration and nerve decompression should be considered if paralysis persists beyond 12 weeks. Since the 1990s, however, operative management of AINS has been discouraged due to the belief that surgery does not alter the natural course of the condition [12,13]. This principle is grounded in observations that approximately two-thirds of patients with AINS spontaneously recover function within 6 months of onset and is further supported by inconsistent outcomes from surgical exploration of the forearm [1,7]. Consequently, the duration of conservative treatment has been extended before considering surgical intervention. Seror [14] recommended surgical treatment only after at least 1 year of conservative management without improvement in paralysis, while Futami [15] went further to suggest that surgical indications are minimal and that conservative treatment should be pursued for up to 2 years after symptom onset.
Nonetheless, given that recovery is often incomplete and that a subset of patients does not recover, alternative treatment options have been explored. Considering the imaging and surgical findings that demonstrate AIN fascicular swelling and constrictions proximal to the elbow in AINS, it is reasonable to focus surgical intervention on this region, such as through external decompression or internal microneurolysis [1,7,8]. On the other hand, operative procedures within the forearm have not been shown to improve outcomes compared to nonoperative treatment [12].
In contrast, the treatment approach for our reported case did not follow the typical AINS protocol. The patient’s history and diagnostic findings clearly indicated that the pathology was localized to the forearm. The presence of a 6-cm lesion on MRI, suspected to be an intramuscular hematoma in the distal forearm, along with EMG findings indicating denervation due to physical interference, led to the diagnosis of compressive neuropathy. Given the pathophysiology described earlier, early surgical intervention was deemed essential not only to remove the hematoma but also to assess for any physical damage to the nerves, tendons, and muscles at the injury site. In surgery, compression of the AIN and median nerve was observed at the mid-forearm level, caused by intramuscular hematoma and edematous changes in the FDP muscle, along with approximately 40% rupture of the tendon at the musculotendinous junction. Subsequent dissection of both proximal and distal areas confirmed the integrity of the median nerve and the FPL tendon.
Considering the various etiologies and treatment approaches that have been proposed for typical AINS, the case we are reporting of direct trauma at the forearm level presents a distinct and uncommon pathophysiology. We highlight that, in instances of trauma-induced AIN palsy, careful attention to forearm pathology is crucial for accurate diagnosis and effective management. This finding reinforces the understanding that not all AIN palsy cases share the same etiology as typical AINS, and therefore, treatment strategies should be tailored accordingly.
Notes
Conflicts of interest
The authors have nothing to disclose.
Funding
None.