Intermittent ulnar nerve compression due to accessory abductor digiti minimi muscle: crucial diagnostic role of nerve ultrasound

Nerve entrapment is a common pathologic condition with a diagnosis that relies on clinical and neurophysiologic evaluations. Nerve entrapment can be caused by anatomic variations, such as accessory muscles. In the past, the diagnosis could only be made during surgical exploration, 1–4 but recently ultrasonography (US) has allowed us to find atypical structures surrounding and compressing nerves. 5 Among muscle variations, the accessory abductor digiti minimi (AADM) is the most common aberrant muscle in the Guyon canal, with an incidence of 22.4%. 6,7 The AADM has been reported to entrap the ulnar nerve at the wrist. 8–14 We present a case of US diagnosis of ulnar nerve compressed by an AADM. A 24-year-old, right-handed man came to our attention for a 6-year history of right handgrip weakness after repetitive manual activity (especially wrist extension). In the last year right wrist pain also occurred. Clinical examination revealed no weakness or atrophy in the hand muscles. No sensory deficits were detected, although the patient complained of paresthesia of the medial 3 fingers. Sensory and motor conduction velocity and amplitude of the radial, median, and ulnar nerves bilaterally were normal, revealing no axonal/demyelinating damage. Needle electrmyography was not performed. US evaluation of the right ulnar nerve from the wrist to the axilla showed no alterations in nerve dimension or echogenicity. In the ventral portion of the distal third of the forearm, we found an atypical muscular structure that ran over the ulnar nerve and the Guyon canal, reaching the abductor digiti minimi muscle. The muscle seemed to pass over the Guyon canal ligament and near the ulnar artery (Fig. 1A and B). This accessory muscle was innervated by accessory branches from the right ulnar nerve (Fig. 1C). Evaluation of the left hand revealed a similar structure. The position and electrophysiologic features of the accessory muscle suggested it was an AADM. Dynamic US showed an increased anteroposterior diameter of the muscle during handgrip, which produced compression on the underlying ulnar nerve. Magnetic resonance imaging of the hands confirmed the presence of the AADM. The patient underwent surgical intervention. The surgeon followed the drawing we had made on the skin based on the US examination and confirmed the presence of a 7-cm-long muscular structure (Fig. 1D), which was removed. Two weeks after surgery the patient reported symptom improvement. US in this case provided crucial anatomic evidence of an accessory muscle that otherwise would not have been diagnosed. We hypothesize that the intermittent symptoms were related to transient neuroapraxic block after hand stress. Moreover, handedness and anatomic features probably caused more nerve stress on the right side than on the left. It is likely that the normal neurophysiologic and clinical picture and transient symptoms would have led the patient to not have surgical treatment. By identifying the actual cause of symptoms, US allowed us to proceed with a tailored therapeutic approach. Surgical exploration confirmed the US findings and decompressed the nerve. Knowledge of anatomic variation is essential for the surgeon to perform the best intervention for the patient.