Читать книгу Musculoskeletal Disorders - Sean Gallagher - Страница 44

The median nerve is one of the numerous structures passing through the carpal tunnel in the wrist. These include nine tendons (four flexor digitorum superficialis, four flexor digitorum profundus, and the flexor pollicis longus), various blood vessels, and the median nerve. The carpal tunnel is bounded superficially by the flexor retinaculum, has a deep border formed by palmar aspects of several carpal bones, is bounded laterally by the medial surface of the trapezium, and is bounded medially by the lateral surface of the hamate bone.

Various studies have provided findings which suggest that damage development to neural and tendinous tissues may be associated with symptom development (Barbe et al., 2020; Bove et al., 2019; Chikenji, Gingery, Zhao, Passe et al., 2014; Clark, Al‐Shatti, Barr, Amin, & Barbe, 2004; Clark et al., 2003; Elliott et al., 2009; Elliott, Barr, Clark, Wade, & Barbe, 2010; Ettema, Zhao, An, & Amadio, 2006; Jain et al., 2014). Studies that have biopsied tissues in CTS cases have suggested that the development of median nerve compression may be the consequence of connective tissues experiencing degeneration due to repeated mechanical stress (Festen‐Schrier & Amadio, 2018; Schrier, Vrieze, & Amadio, 2020; Schuind, Ventura, & Pasteels, 1990). Structures affected by repeated stress can include flexor tendons and their synovial sheath (Kerr, Sybert, & Albarracin, 1992). Degenerative noninflammatory fibrosis and thickening of the synovium have been implicated as a factor in median nerve pathology (Chikenji, Gingery, Zhao, Passe et al., 2014; Ettema et al., 2006; Sternbach, 1999). Tendon fibrosis changes may impact the gliding mechanism of the subsynovial connective tissue (SSCT), which moves en bloc with the tendons and median nerve (Ghasemi‐Rad et al., 2014). Increases in vascularity, fibroblast density, and collagen fiber size have been reported in resected synovial specimens and are also indicative of synovial degeneration (Jinrok et al., 2004). If a decrease in SSCT motion were to result from fibrosis, the movement of the tendons would likely increase shear strain in the SSCT (Ghasemi‐Rad et al., 2014). The degree of shear strain would be expected to vary with wrist posture, with the maximum shear predicted at 60 degrees of wrist flexion (Yoshii et al., 2008). High velocity tendon motion has been suggested to place the SSCT at a particularly high risk of shear injury (Yoshii et al., 2011). Hand and finger motions may also result in friction between the flexor digitorum muscles and the median nerve, also potentially leading to cumulative trauma development (Yoshii et al., 2008).

Noninflammatory tendon damage (tendinosis) has also been noted in CTS cases (Kerr et al., 1992). Tendinosis is characterized by microtears in the substance of the tendon and connective tissue, collagen degeneration, and fiber disorientation (Sharma & Maffulli, 2005). These characteristics are also observed during in vitro fatigue failure studies of tendons and studies of fatigue failure in animal studies (Barbe et al., 2013b; Schechtman & Bader, 1997; Shepherd & Screen, 2013; Sun et al., 2010). Patients with this syndrome also demonstrate decreased areal bone mineral density (BMD) in distal forearm bones (i.e., radius and ulna) and reduced bone in hand phalanges, as observed using quantitative ultrasound measurements (Erselcan, Topalkara, Nacitarhan, Akyuz, & Dogan, 2001; Kisala, Pluskiewicz, & Adamczyk, 2019).