prevalence than that reported in males (Breivik et al., 2005; Picavet & Schouten, 2003; Treaster & Burr, 2004). Age is another significant factor, with an increased general prevalence in older individuals and a notable increase of shoulder pain prevalence in the 45–64 age‐group (Pribicevik, 2012). In addition, adolescents aged 12–18 years appear to have a greater than average shoulder pain prevalence. In 2014, 88,980 nonfatal shoulder injuries and illnesses occurred that involved days away from work (Bureau of Labor Statistics, 2015).
A systematic review examining physical occupational risk factors for shoulder pain disclosed that jobs involving high force demands, highly repetitive work activities, adoption of non‐neutral shoulder postures, and exposure to vibration and duration of employment were observed to be common physical occupational risk factors (Van der Windt, Thomas, & Pope, 2000). This review also examined psychosocial factors (e.g., job dissatisfaction, lack of control at work, poor social support, and/or psychological demands); however, while certain psychophysical factors were found to be significant, these factors were assessed to be inconsistent across the studies examined. Moderate to high levels of physical demand have commonly been associated with the development of shoulder pain (Ariens et al., 2000; Bergenudd, 1987; Devereux, Vlachonikolis, & Buckle, 2002; Malchaire, Cock, & Vergracht, 2001; Miranda, Punnett, Viikari‐Juntura, Heliövaara, & Knekt, 2008). Exposure to vibration has also been implicated in the development of shoulder pain (Ariens et al., 2000; Miranda et al., 2008; Stenlund, Goldie, & Hagberg, 1993; van der Windt et al., 2000). Continuous low‐intensity muscle contractions also increase the prevalence of neck‐shoulder complaints and syndromes, including acromioclavicular syndrome (Balogh et al., 2019; Huysmans, Blatter, & Beek, 2012; Visser & van Dieen, 2006). Finally, the adoption of non‐neutral shoulder postures has been associated with shoulder outcomes in a number of studies (Larsson, Sogaard, & Rosendal, 2007; Miranda et al., 2008; Pope et al., 1997; van der Windt et al., 2000). Many studies have failed to examine potential interactions between these physical risk factors; however, Frost and Andersen (1999) provide data suggestive of an interaction between force and repetition and shoulder tendinitis.
Anatomy/pathology
Rotator cuff (RC) injuries are generally considered to be the result of a degenerative disorder of the RC tendons, which begins with acute tendinitis (inflammation) that leads to tendinosis (degeneration), ultimately leading to tendon tears (partial or full), as shown in Figure 2.6 (Neer, 1983). There is mounting evidence of some level of inflammation in all tendon injuries (Abraham, Shah, & Thomopoulos, 2017). Animal models of RC pathology in which the tissue are collected long before a surgical repair endpoint show clear evidence of inflammation in rotator cuff tendon proper, epitendon, or surrounding capsule (Abraham et al., 2017; Kietrys, Barr, & Barbe, 2011; Thomas et al., 2014). Yet, histological studies of the affected RC tendons tend to show a minimal amount of inflammatory cells at the time of surgery (Fukuda, Hamada, & Yamanaka, 1990), and serum biomarker studies of patients with long‐term RC injuries show increased levels of circulating markers of enzymes that contribute to tissue degradation (matrix metalloproteinases), angiogenesis (increased production of vascular endothelial growth factor, VEGF), and axonal sprouting that may be related to the enhanced pain associated with RC injuries (summarized in Gold et al., 2016). These inflammation and degeneration changes are typically intrinsic factors that can enhance RC injuries (Seitz, McClure, Finucane, Boardman, & Michener, 2011). Extrinsic factors can also enhance RC injuries and impingement of the RC tendons. Some injuries are also thought to be the result of a combination of extrinsic and intrinsic factors.
Risk factors/activities associated with shoulder tendinopathy
The development of RC disorders is associated with a number of factors, including personal characteristics (such as age and gender), occupational exposures, and certain sports‐related activities. Among personal characteristics, factors such as gender and age tend to be most highly implicated in RC injuries (details). In terms of physical exposures, a history of occupations involving heavy lifting and/or highly repetitive tasks has been linked to the increased risk of RC disorders, which often result in greater than average lost time from work compared to other MSDs. In terms of physical exposures, a history of occupations involving heavy lifting and/or highly repetitive tasks have been linked to increased risk of RC disorders, which often result in greater than average lost time from work compared to other MSDs. In 2014, 88,980 nonfatal shoulder injuries and illnesses occurred that involved days away from work (Bureau of Labor Statistics, 2015).
Figure 2.6 Partial and full tears in supraspinatus tendons, a rotator cuff tendon. (a) The location of the supraspinatus tendon. (b–d) X‐ray images of a partial‐thickness tear in the supraspinatus tendon. In a neutral position (b), a partial tear was not evident; hence, changes were interpreted as tendinosis. Crass position (c) and modified Crass position (d) show a hypoechoic region (arrows) interpreted as a partial tear in a fat‐suppressed T2‐weighted magnetic resonance image. (e and f) Full‐thickness tear (arrows) of a supraspinatus tendon (arrows). Neutral position (e), Crass position (f), and modified Crass position (g).
Modified from Shah, N. P., Miller, T. T., Stock, H., & Adler, R. S. (2012). Sonography of supraspinatus tendon abnormalities in the neutral versus Crass and modified Crass positions: A prospective study. Journal of Ultrasound in Medicine, 31(8), 1203–1208. doi: 10.7863/jum.2012.31.8.1203. Wiley.
High shoulder pain prevalence is often seen in athletic pursuits, particularly those requiring forceful and repetitive motions that involve throwing or other activities where the hands and/or elbows are active above the level of the shoulder. High stresses are placed on the shoulder in activities such as baseball pitching, football throwing, tennis, volleyball, and swimming. These repetitive high‐stress activities are likely to result in microdamage and damage propagation that may exceed the repair capacity of shoulder musculoskeletal tissues (Bani Hani et al., 2021).
Subacromial impingement may also occur at the subacromial joint. It is thought to be the result of fatigue in the stabilizing structures of the shoulder (the tendons and ligaments), resulting in humeral subluxation and subsequent impingement of the supraspinatus tendon between the head of the humerus and the inferior surface of the acromion. It has been reported that the most frequent shoulder diagnoses in athletes involve RC dysfunction with signs of supraspinatus tendon impingement (Baring, Emery, & Reilly, 2007; McHardy, Pollard, & Luo, 2007; Pink & Tibone, 2000). That said, there can also be degenerative changes in the joint structure itself. In one study, the frequency of radiologically detected lesions in shoulders of 152 miners using vibration tools was 40.7% and included degenerative changes (34.5%) that were mainly in the acromioclavicular joint (17.8%) (Kakosy et al., 2006).
Upper Extremity Muscle Disorders: Fatigue, Myalgia, and Fibrosis
Characteristics/description
Muscle fatigue denotes a transient decrease in the force and power capacity of skeletal muscle activity (Enoka & Duchateau, 2008). Repetitive or sustained contraction of skeletal muscle can lead to a progressive and reversible loss in the ability to produce the desired force (Allen, Lamb, & Westerblad, 2008; Ortenblad, Lunde, Levin, Andersen, & Pedersen, 2000). Myalgia is also known as muscle pain and is a symptom of many diseases and disorders, including prolonged repetitive work (Bongers, Ijmker, Heuvel, & Blatter, 2006; Hadrevi et al., 2019; Sjøgaard, Lundberg, & Kadefors, 2000). Muscle fibrosis is characterized by fibroblast and myofibroblast cell proliferation and excessive accumulation of extracellular matrix proteins in fascial tissues, such as collagen and fibronectin (Contreras, Rebolledo, Oyarzun, Olguin, & Brandan,
