Abstract

Lateral epicondylitis (LE) is a condition that is caused by repetitive wrist extension activities and involves inflammation of the extensor tendon attachments at the lateral epicondyle. Symptoms associated with LE have been demonstrated to diminish with manual cervical manipulation, and electromyographic (EMG) signal abnormalities have been identified in individuals with LE suggestive of a cervical radiculopathy component. PURPOSE: This study was designed to determine: (i) if the quantitative EMG parameters related to motor unit potential (MUP) morphology, motor unit (MU) firing patterns or motor unit number estimates (MUNEs) detected from the affected extensor carpi radialis brevis (ECRB) muscle of patients with LE are different from those detected in healthy control subjects and whether these measures are suggestive of nerve pathology in patients. METHODS: Ten patients (47.9 ± 10.2 years) with clinically determined LE and eight healthy subjects (30.9 ± 7.9 years) participated in the study. Maximum M-waves, and needle- and surface- detected EMG data were recorded from the ECRB muscle during 30-second contractions performed at 10% of maximum voluntary contraction force. DQEMG™ was used to extract needle-detected and surface- detected (S) MUP morphology and MU firing rates. Maximum M-wave amplitudes were divided by the amplitude of the mean SMUP in each subject to obtain MUNEs. Kruskall-Wallace tests were used to determine between-group differences. RESULTS: Patients with LE had significantly larger MUP area-to-amplitude ratio (1.70 ± 0.58 vs. 1.23 ± 0.41), MUP duration (10.08 ± 3.10 ms vs. 6.90 ± 2.36 ms), SMUP amplitude (118.87 ± 111.10 μV vs. 60.15 ± 27.00 μV), and SMUP area (536.8 ± 528.1 μVms vs. 297.4 ± 189.5 μVms) compared to healthy control subjects (p<0.05). MU firing rates were significantly higher in the healthy control subjects (14.29 ± 2.47 Hz) than patients with LE (13.72 ± 2.69 Hz; p<0.05). The MUNEs were not significantly different between the groups (p>0.05). CONCLUSIONS: The MUP morphology differences between patients with LE and healthy control subjects are suggestive of neurogenic changes in the MUs of the ECRB muscle in the patients with LE; however the MUNEs did not suggest that there was any axonal loss.

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