- 著者
- Gen Horiguchi Takafumi Aoki Hiromoto Ito
- 出版者
- 日本医科大学医学会
- 雑誌
- Journal of Nippon Medical School (ISSN:13454676)
- 巻号頁・発行日
- vol.78, no.4, pp.208-213, 2011 (Released:2011-08-26)
- 参考文献数
- 16
- 被引用文献数
- 1
The main cause of carpal tunnel syndrome (CTS) remains unknown. Stiffness of the subcutaneous area of the volar aspect of the carpal tunnel is present in many patients and suggests that the stiffness of muscles attached to the transverse carpal ligament is increased. We performed an electrophysiological study to investigate muscle activities and to clarify whether the stiffness of muscles attached to the transverse carpal ligament is involved in the pathogenesis of CTS. The subjects of this study included 16 patients with early CTS showing no motor dysfunction. Both thenar muscles (opponens pollicis, abductor pollicis brevis, and flexor pollicis brevis) and hypothenar muscles (opponens digiti minimi, abductor digiti minimi, flexor digiti minimi brevis) were investigated. Surface electrodes were placed on each muscle, and maximum voluntary contractions with the thumb and little finger in opposition were maintained for 3 seconds in all patients and in 7 control subjects. Electromyographs were subjected to fast Fourier transform analysis, and the root mean square (RMS) and the mean power frequency (MPF) were determined for each muscle. The RMS of the opponens pollicis was significantly less in hands affected by CTS (292.8 μV) than in healthy hands (405.9 μV). The RMS did not differ between affected hands and healthy hands for the other 2 thenar muscles but did differ significantly for the hypothenar muscles. The MPF did not differ between affected hands and healthy hands for any muscle. The results show that electrophysiological differences are present among muscles innervated by the median nerve and that hypothenar muscles originally unrelated to median nerve dysfunction are also affected in early CTS. These results suggest that modulation of muscles attached to the transverse carpal ligament is involved in the pathogenesis of CTS.