Ulnar Neuropathy in Hansen Disease

OBJECTIVE: To assess the relationship between the cross-sectional area (CSA) of the ulnar nerve by ultrasound (US) with clinical and electrophysiologic findings in Hansen ulnar neuropathy. METHODS: Twenty-one patients (42 arms) with Hansen disease (mean age 30.0 ± 12.97, range 13-61 years, borderline tuberculoid 29%, borderline lepromatous, 19% lepromatous leprosy 42%, and pure neuritic type 10%) were examined clinically for ulnar sensory and motor weakness. The ulnar nerve was ultrasonographically examined from the wrist to the axilla, and CSA was measured at the level of maximum enlargement. Ulnar sensory nerve conduction was recorded orthodromically with ring electrodes placed at the fifth digit and amplitude of sensory nerve action potential (SNAP) recorded 3 cm proximal to the distal wrist crease. Motor conduction velocity (MCV) was recorded at the wrist-below the elbow, below the elbow-above the elbow, and above the elbow-axilla segments. RESULTS: Out of the 42 arms with Hansen disease, 76% had clinically motor weakness, and 43% had sensory loss in the upper limbs innervated by the ulnar nerve. As compared with healthy subjects, the patients with Hansen ulnar neuropathy had a statistically significant reduction in SNAP (P ≤ 0.0001) and MCV (P ≤ 0.0001). It was observed that the maximum enlargement of the ulnar nerve in all the patients was a few centimeters above the elbow segment. The mean CSA of ulnar nerve above the medial epicondyle was 18 ± 15 mm as compared with controls 4.83 ± 1.12 mm (P < 0.0001). In addition to nerve thickening, US depicted abnormality in morphology. In 55%, the nerve was hypoechoic, and in 7.1%, the nerve pattern was oligofascicular. Color Doppler (CD) flow signals were observed in all the nerves with loss of fascicular pattern and in 40% of the nerves that were hypoechoic. A statistically significant correlation was found between CSA of ulnar nerve above the medial epicondyle vs. MCV at BE-AE and compound muscle action potentials (CMAP) above the elbow in the patients with clinical motor weakness (r = -0.55, P < 0.001) and (r = -0.57, P < 0.001), respectively. There was no statistical significant correlation between CSA and SNAP in the patients with (r = -0.52, P = 0.23) and without (r = -0.07, P = 0.83) sensory loss. CONCLUSIONS: In leprosy patients, a positive correlation exits between the presence of motor weaknesses of the ulnar nerve innervated muscles, sonographically thickening of the ulnar nerve, and motor conduction slowing of the ulnar nerve at the BE-AE segment. In addition, US provided information on nerve morphologic alterations regarding the echo texture and location of nerve enlargement.