Supracondylar Apophysis of the Humerus: Rare Cause of High Compression of the Median Nerve^[*]

Abstract

Supracondylar apophysis (SA) is a bony prominence that originates from the anteromedial aspect of the distal humerus with a lower projection and which, although usually asymptomatic, due to the relationship with adjacent structures can cause symptoms. We describe the case of a 42-year-old woman with pain complaints radiating from her elbow to her hand, with 6 months of evolution. On objective examination, the patient had a sensory deficit in the median nerve territory and decreased grip strength. Radiographs of the distal humerus were performed, in which a bone spike was visible, and magnetic resonance imaging showed thickening of the median nerve epineurium. Electromyography showed severe axonal demyelination of the median nerve proximal to the elbow. A median nerve compression caused by a SA was diagnosed. The patient underwent surgery and, 1 year after the operation, she had a complete clinical recovery. Supracondylar apophysis is a rare, but possible and treatable cause of high median nerve compression.

Keywords

supracondylar apophysis - median nerve - compressive neuropathy - median nerve compression

Introduction

Supracondylar apophysis (SA) is an anatomical structure described by Knox in 1841. This bone prominence of variable size originates from the anteromedial face of the distal humerus, protrudes inferiorly and represents a vestigial remnant typical of climbing animals. The fibrous band known as the Struthers ligament, usually appears as a continuation of the SA and forms a foramen in which the median nerve and the brachial artery can be compressed in their path.[1] The prevalence of this anatomical structure varies widely in studies (0.7–2.5%); however, it is unanimous that it is rare and more marked in the Caucasian ethnicity and in females.[2]

Case Report

A 42-year-old Caucasian woman with no major medical history was observed in an Orthopedics consultation due to progressive pain complaints radiating from the elbow to the left hand, with 6 months of evolution. On objective examination, the patient had a sensory deficit in the median nerve territory and decreased grip strength. No palpable swelling in the left upper limb, no positive Tinel throughout the median nerve path, and no vascular changes. Then, she underwent imaging exams to study the symptoms presented, which revealed: on the radiographs of the distal humerus, a bone spike of inferior orientation ([Fig. 1]), and magnetic resonance imaging showed a thickening of the epineurium of the median nerve suggestive of nerve compression. On electromyography, the patient had severe axonal demyelination of the median nerve proximal to the elbow. Therefore, a compression of the median nerve was diagnosed by a SA.

Fig. 1 Radiographs (face and profile views) of the left elbow showing the supracondylar apophysis of the distal humerus.

The patient underwent surgery to excise this structure through an anterior route of the distal humerus. Intraoperatively, compression of the median nerve was confirmed ([Figs. 2] and [3]) and excision of the SA and Struthers ligament was performed without complications. In the postoperative evaluation at 2 months, the patient had a significant improvement in neurological symptoms with gain in grip strength and decreased paresthesia. An electromyography was performed that showed an appreciable recovery of the left median nerve with normalization of the motor neurography. One year after the surgery, there was a complete regression of symptoms and strength recovery, comparable to the contralateral side.

Fig. 2 Intraoperative images of the anterior plane dissection. Observation of several structures involved: median nerve, brachial artery, Struthers ligament, and supracondylar apophysis.

Fig. 3 Image of the supracondylar apophysis after excision.

Discussion

Supracondylar apophysis is an anatomical structure usually without clinical manifestations; however, in some cases, it can become symptomatic and manifest by swelling and/or symptoms of compression of the median nerve and brachial artery.[3] Soliere[4] reported, in 1929, the first case of clinical changes caused by the presence of a SA. This entity represents a diagnostic challenge, given the clinical presentation similar to the most common neuropathy of the upper limb—Carpal tunnel syndrome and also by the multiple possible sites of compression of the median nerve at the level of the elbow, which include: between the heads of the pronator teres, in the aponeurotic arch formed by the proximal insertion of the forearm flexor muscles, and in the lacertus fibrosus.[5] The possibility of treating heterotopic ossification or osteochondroma must also be part of the differential diagnoses, since this presents differentiating characteristics that pass through the orientation of the bone spike—not pointing towards the joint and continuing with the cortical humerus.[6]

Some clinical cases of neurovascular compression associated with this structure are described in the literature: Aydinlioglu et al.[7] described a case of bilateral compression of the median nerve by the SA; May-Miller et al.[8] reported a very rare case of compression of the cubital nerve, and there are also reports of fracture of this structure.[9]

In the clinical suspicion of neuropathy caused by the SA, imaging exams combined with electromyography are diagnostic, as in the clinical case we describe. The treatment recommended in symptomatic patients is surgical and consists of excision of the SA and of the Struthers ligament, when the latter is present, thus allowing confirmation of the decompression of the involved structures. As described in the literature and verified in the clinical case presently described, this treatment option is associated with good functional results in the short and long term.[10]

In conclusion, SA is a rare, but possible and treatable, cause of high median nerve compression.

Conflito de Interesses

Os autores declaram não haver conflito de interesses.

^* Work developed at the Department of Orthopedics and Traumatology, Centro Hospitalar Universitário de São João, Porto, Portugal.

Financial Support

The authors declare that they have received no financial support for the research, authorship and/or publication of the present article.

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Publication History

Received: 29 April 2020

Accepted: 06 July 2020

Article published online:
29 October 2020