Musculoskeletal Disorders. Sean Gallagher
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Facet joints (Figure 2.3), or more properly zygopophyseal joints, are a small set of joints formed by the superior and inferior articular processes of adjacent vertebrae. These joints are believed, when loaded, to develop wear and tear of the gliding surfaces of the joint, which may lead to arthritis over time (Eisenstein & Parry, 1987; Farfan, 1973). Bending forward and/or side‐to‐side bending is believed to place damaging stress concentrations on the cartilage surface of the joints, leading to degeneration (Farfan, 1973). As the facet joint begins to degenerate, small defects in the joint surfaces appear. As with the disc, the cartilage surfaces of the facet joints have limited blood supply, which impedes the body’s ability to repair the damage. This limited repair capacity makes the facet joint susceptible to degeneration. In fact, degeneration of the facet joints is believed by some to be a result of disc degeneration (Vernon‐Roberts & Pirie, 1977). This is because when a disc degenerates, it loses height. When this occurs, it causes the bone and cartilage of the facet joint (normally separated) to come into contact and grind against each other, causing degeneration of the surfaces. Studies have suggested that up to 45% of patients with back pain demonstrate facet pain and that approximately 15% of chronic LBP cases may be due to facet joint pain (Schwarzer, Aprill, & Bogduk, 1995).
The sacroiliac joint is formed where the sacrum of the spine joins the iliac bone in the pelvis, is innervated by the first four sacral nerves, and is a demonstrated source of LBP (Schwarzer et al., 1995). Data from studies involving nerve‐blocking agents suggest the prevalence of sacroiliac pain to be 2–30% in chronic LBP sufferers (Chawla, 2018).
Pathological mechanisms associated with spinal nerve root pain (or radicular pain) are not well understood. It has been hypothesized that spinal nerve roots may be vulnerable to compression, potentially leading to pain. Some early studies found that nerve roots might exhibit an inflammatory response when exposed to viable nucleus pulposus material from an intervertebral disc (McCarron, Wimpee, Hudkins, & Laros, 1987). However, degenerated nucleus pulposus material appears not to provoke such an inflammatory response (Chawla, 2018). Exposure of spinal nerve roots to the proinflammatory cytokine TNF‐α is another suggested cause, as it would be expected to provoke neuropathic pain in spinal nerves (Klyne, Barbe, & Hodges, 2017; Klyne & Hodges, 2020).
Physical risk factors/activities associated with LBP
Most experts agree that heavy physical work, lifting, prolonged static work postures, frequent bending and twisting, and exposure to vibration may contribute to back injuries. A systematic review of physical work factors performed by the NIOSH found strong evidence of a causal relationship between both lifting/forceful movements and exposure to whole‐body vibration and LBP. Evidence suggesting a causal relationship to LBP was also found for adoption of awkward postures and heavy physical work (NIOSH, 1997). A further systematic review performed by the (National Research Council–Institute of Medicine, 2001) demonstrated that activities such as manual materials handling, frequent twisting and bending, heavy physical load, and exposure to whole‐body vibration demonstrated positive association to risk of low back disorders in the preponderance of studies investigating such factors. These findings have been supported by more recent data on the relationship between LBP and occupational activities, in which tasks such as carrying, lifting heavy weight while in trunk flexion, and adoption of awkward postures (including bending, squatting, twisting, and kneeling) demonstrated higher LBP risk (Amorim et al., 2019).
UE Tendon and Muscle Disorders
MSDs of the distal UE are prevalent in the working world and have substantial economic costs (Dale et al., 2013; Descatha, Leclerc, Chastang, & Roquelaure, 2003; Gerr et al., 2002; Silverstein et al., 2010; Tanaka, Petersen, & Cameron, 2001). These MSDs can affect each segment of the upper extremity, from the shoulder to the hand. Risk factors for wrist and hand MSDs include repetitive pushing, hand force, combined exposure to both force and repetition, sustained gripping (e.g., computer or hand tool use), repetitive redundant movement of the thumb and digits (e.g., typing or texting), sustained or repeated static loading of the weight of an instrument or tool, and use of vibrating tools (Barr, Barbe, & Clark, 2004; Fry, 1986; Gold, Mohamed, Ali, & Barbe, 2014; Gupta & Mahalanabis, 2006; Kakosy, Nemeth, Kiss, Laszloffy, & Kardos, 2006).
Hand‐intensive jobs that feature forceful and repetitive activities are associated with both the onset and severity of hand and wrist MSDs (Barr et al., 2004; Viikari‐Juntura & Silverstein, 1999). Other physical risk factors shown to exacerbate risk include adoption of non‐neutral wrist and forearm postures, sustained gripping, sustained or repeated static loading of the weight of an instrument or tool, high impact jolting, exposure to hand‐arm vibration (HAV), and exposure to cold temperatures (NIOSH, 1997; NRC‐IOM, 2001). Continuous movement of a joint into end of range, for example, with repeated hyperextension of metacarpophalangeal joints, may be another causative factor due to enhanced inflammation in joint and tendon tissues (Gold et al., 2014; Walsh, Delahunt, & McCarthy, 2011). Individuals with prolonged heavy or one‐sided hand workloads or increased high impact “jolting” of the hand show increased incidence of hand osteoarthritis, with higher incidence in females (Bernard, Wilder, Aluoch, & Leaverton, 2010; Blumenfeld et al., 2014; Rossignol et al., 2005). The following sections discuss some of the more common UE disorders, their characteristics, prevalence and incidence, anatomy and pathology, and risk factors.
Hand‐wrist tendinopathy
Description/characteristic features
Wrist tendinopathy is a broad term used to characterize disorders involving damage or irritation to tendons and/or their synovial sheaths located in and around the wrist joint. Such disorders comprise the most common complaints evaluated by hand care professionals (McCauliffe, 2010). These disorders were formerly characterized as wrist tendinitis; however, recent research has demonstrated that these disorders demonstrate relatively few inflammatory cells (McCauliffe, 2010). Instead, these tendon disorders often appear to be the result of a disruption in the structural integrity of the tendon. This has led some to prefer use of the term tendinosis (implying a breakdown in the collagen structure of a tendon) or the broader and more clinically used term tendinopathy (a term implying a general disease process of the tendon).
Wrist tendinopathy usually affects a single tendon, but in some cases, it involves two or more tendons. Symptoms may start with a mild pain that progressively worsens with continued activity. The pain often presents as diffuse, as opposed to a localized, and may extend up to the forearm or into the fingers. Pain may be variously described as a dull ache, a burning sensation, or a sharp stabbing pain. Symptoms may be so painful that they may result in significant adverse effects on the activities of daily living. Even common tasks such as turning doorknobs or lifting a coffee cup may prove painful. Symptoms more rarely observed include numbness, loss of motion, or pain at rest. Often, wrist tendinopathy occurs at points where the tendons cross each other or pass over a bony prominence. These are possible sites of irritation and can lead to discomfort when moving the wrist joint. De Quervain’s disease is often characterized by the development of pain