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.
