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Non-specific Arm Pain
SUMMARY
Non-specific arm pain (NSAP) is a common chronic upper limb pain disorder that has previously been referred to as repetitive strain injury. NSAP is frequently associated with tasks that involve repetitive upper limb activities, such as intense computer use and light production work. What differentiates NSAP from other specific work-related upper limb conditions is the lack of obvious tissue injury on clinical testing. It is only recently that the complex mechanisms underlying NSAP are beginning to be revealed. Although psychosocial stressors contribute to the symptoms, the underlying pathophysiology appears to be a subtle neuromusculoskeletal injury that involves inflammation and tissue ischemia. Such features are likely to be a consequence of frequent low-force, highly repetitive muscle activity that is carried out in constrained and sustained working postures. Patients consistently show features of a minor neuropathy, with clear signs of nerve trunk mechanical sensitivity and changes in peripheral nerve function. The consequences of such a minor nerve injury have been underestimated. It is now apparent that peripheral nerve inflammation in the absence of axonal degeneration is sufficient to drive abnormal nociceptive activity (e.g., axonal mechanical sensitivity). These changes would contribute to symptoms and also lead to chronicity. Simple analgesics and non-steroidal anti-inflammatory medications are usually ineffective in treating NSAP. However, in persons with signs of peripheral nervous system involvement, neuropathic pain medications should be considered. Preventing the onset of NSAP involves attention to the work environment and how the individual interacts within that environment, for example, by reducing psychological and ergonomic stressors.
Introduction
Upper limb pain is a major health issue in the Western world. At any point in time it is estimated that 9%–26% of the adult population experiences such pain ( ). In a working population, most of these cases (70%–90%) will be related to working practices ( ). Upper limb pain is reported to be second only to low back pain as a cause of work-related illness ( ). For this reason, upper limb disorders have a significant social and economic impact ( ). The direct and indirect costs of upper limb disorders to businesses in Britain are estimated to be ≤5251 per injured worker ( ). In the United States, the total compensable cost for repetitive motion disorders in 2009 was estimated to be $1.97 billion ( ).
Painful upper limb symptoms that are the result of obvious injury or inflammation following acute trauma or systemic disease are, in the main, easily classified. Examples of specific conditions include carpal tunnel syndrome (CTS), wrist tenosynovitis, tendonitis, and tendinopathy. Treatments are clearly defined and a reliable prognosis can be made. However, a proportion of patients with reports of upper limb pain do not fit any common clinical diagnosis. These patients can be grouped under the classification of non-specific arm pain (NSAP). In the total picture of work-related upper limb pain, NSAP accounts for about the same number of cases as all the specific conditions combined ( ).
Most readers are familiar with the term “repetitive strain injury” (RSI), which has become ubiquitous in both the press and the general population as a label for patients with NSAP. The term RSI came into widespread use during an apparent epidemic of the condition in Australia during the early 1980s, which coincided with the replacement of typewriters with computer keyboards ( ). It is, however, not a new condition, and historically a very clear description of the symptoms of NSAP was presented by the surgeon Samuel Solly during a clinical lecture on scriveners’ palsy in 1864 (reprinted in ). The term RSI is contentious because it clearly implies etiology (repetitive strain) and pathology. RSI has also been used synonymously for other specific upper limb disorders such as CTS and tenosynovitis. Although we prefer the classification NSAP, a number of different terms are also used in other countries to refer to this patient group ( Table 50-1 ).
Table 50-1
List of Terms That Are Synonymous with Non-specific Arm Pain
| ACRONYM | DESCRIPTIVE LABEL | GEOGRAPHIC REGION |
|---|---|---|
| CTD | Cumulative trauma disorder ∗ | USA |
| NSAP | Non-specific arm pain | UK |
| NSFP | Non-specific forearm pain | UK |
| OCB | Occupational cervicobrachial disorder | Japan |
| OOS | Occupational overuse syndrome | Australia, New Zealand |
| RMD | Repetitive motion disorder ∗ | USA |
| RSI | Repetitive strain injury ∗ | Australia, Canada, Greece, Netherlands, UK |
| WRMD | Work-related musculoskeletal disorder ∗ | Canada |
| WRULD | Work-related upper limb disorder ∗ | Ireland, Sweden, Netherlands, UK |
Key Signs and Symptoms
With only slight variations, the diagnostic criteria for NSAP are generally agreed ( ). Unlike the specific upper limb conditions, patients with NSAP do not have any apparent signs of tissue injury, and the results of nerve conduction studies, when performed, are normal (i.e., there is no frank nerve injury). Although NSAP is considered a diagnosis of exclusion, patients have a similar pattern of symptoms ( ), with symptoms of diffuse hand, wrist, and arm pain frequently accompanied by non-dermatomal or single dermatomal paresthesia. Symptoms frequently affect the dominant arm but may be bilateral, though more severe on the dominant side. The spread of symptoms often includes the shoulder girdle. Patients also report pain with limb movement, deep muscle tenderness, muscle weakness (with no sign of muscle wasting), hyperalgesia, allodynia, and difficulty coordinating fine finger movements ( Fig. 50-1 ). Postural deviations are common, particularly forward displacement of the head and shoulder girdle in combination with scapular protraction ( ). Increased muscle stiffness, especially of the scalene, pectoral, and forearm muscle groups, is also reported. Consistent with these postural changes, more than 70% of patients with NSAP have been described as having neurogenic thoracic outlet syndrome ( ). In addition, psychological distress such as depression and anxiety may form part of the clinical picture of NSAP, although measures of psychological morbidity show no difference from patients with specific work-related upper limb disorders (e.g., CTS) ( ).
Clinical Evidence of Neuropathy
Patients with NSAP show signs of peripheral nervous system involvement. There are notable changes in the function of sensory as well as autonomic nerve fibers. Of particular interest are reports of elevated vibration thresholds in areas of the hand innervated by the median and ulnar nerves ( ), which indicate altered myelinated (Aβ) nerve fiber function. Such changes are considered to be an early sign of neuropathy ( ), in particular, a minor neuropathy ( ). In the upper limb there are also decreases in histamine-induced flare and cutaneous vasoconstriction in response to cold stimuli, which signify altered function of unmyelinated (C-fiber) sensory and sympathetic nerve fibers, respectively ( ).
An almost defining clinical feature of NSAP is the presence of nerve trunk mechanosensitivity, a further indication of pathology of the peripheral nervous system ( ). Positive and painful responses are frequently reported when the physical examination is expanded to include tests of nerve trunk mechanosensitivity. For example, arm pain symptoms can be reproduced by digital pressure over the median nerve at the carpal tunnel (e.g., Tinel’s test) and over the supracondylar ridge and ulnar nerve at the wrist and cubital tunnel ( ). Upper limb movements that apply strain to the brachial plexus and median and ulnar nerves (referred to as nerve movement tests) ( ) also cause painfully reduced joint rotation. It is reported that more than 70% of patients with NSAP have painful responses to either median or ulnar nerve movement tests ( ). In fact, the majority of these patients have painful responses to both nerve movement tests, as well as tenderness to digital pressure at multiple sites over both nerves, corresponding to the diffuse nature of NSAP ( Fig. 50-2 ).
Risk Factors
NSAP is commonly reported by individuals who perform rapid and/or intensive repetitive work ( ), such as office workers who spend long hours using display screen (computer) equipment, musicians, and production line workers. Despite the frequency of reported symptoms, there is still some controversy over the “work-relatedness” of NSAP ( ). In a prospective study, repetitive movements of the arm and wrist were found to be predictive of NSAP ( ). Several studies have also provided evidence of a positive association between painful symptoms and the duration of computer mouse use ( ), as well as regular keyboard use (>4 hr/day) ( ). In a meta-analysis of epidemiological studies that examined specific neck and arm symptoms, the found evidence that exposure to highly repetitive work, combined with forceful exertion and/or sustained posture, increased the risk for neck and shoulder pain, as well as CTS. If the description of NSAP is limited to the forearm (i.e., non-specific forearm pain; ), some authors believe that it is associated with psychological stress and not with mechanical exposure ( ). In line with this, somatizing tendencies ( ), as well as pain catastrophizing ( ), are also considered risk factors for NSAP.
A lack of perceived support from colleagues and supervisors, as well as a high workload and time pressure, has been shown to increase risk for the development of upper limb pain ( ). Interestingly, those generally inclined to a “perfectionist” attitude may also have increased risk for the development of NSAP in the workplace ( ). However, it appears that it is increased exposure to physical risk factors such as prolonged computer use combined with high job demand and psychosocial stressors that is important in the development of work-related upper limb pain ( ). When considering risk factors, activities outside the workplace (e.g., hobbies, sport) must also be included.
External risk factors are only part of what determines whether NSAP will develop. Muscle strength, as well as anatomic variation (i.e., carpal tunnel dimension), may also predispose certain individuals ( ). Obesity is a risk factor for CTS and may therefore have implications for NSAP. There are also significant correlations between obesity and systemic inflammation ( ), which may increase the risk for development of a diffuse chronic pain condition. In considering these biological differences, it is important to remember that many painful conditions show significant dependence on genetic factors. For example, twin studies indicate greater concordance of CTS in monozygous than in dizygous twins, thus indicating that about 50% of the incidence can be assigned to genetic factors ( ). Furthermore, results from the 1958 British Birth Cohort Study suggest that genetic variants of the β 2 -adrenergic receptor gene may be associated with chronic widespread musculoskeletal pain ( ).
Pathophysiology
Despite a 150-year history of NSAP ( ), it is only recently that significant progress has been made in understanding the pathophysiology of this potentially disabling condition. The lack of obvious signs of tissue injury, which has led some researchers to suggest a psychological mechanism, as well as the legal controversy surrounding NSAP, has hindered research on organic causes of this painful condition. However, two important re-occurring factors appear to be important in the etiology of NSAP: first, the fact that patients usually associate their symptoms with sustained low-force, high-repetition activities such as keyboard or mouse use and, second, that these repetitive tasks are often carried out in working postures involving maintenance of the joints in non-neutral positions ( ) ( Fig. 50-3 ). Our current understanding of the mechanisms suggests that the development of symptoms is a consequence of inflammation and ischemia. For example, in patients with work-related upper limb disorders, elevated levels of systemic inflammatory mediators (interleukin-1β [IL-1β], tumor necrosis factor-α [TNF-α], and IL-6), as well as C-reactive protein, correlate with pain severity ( ). In addition, there is emerging evidence, using magnetic resonance imaging, of median and ulnar nerve inflammation at the wrist and distal end of the forearm, as well as the brachial plexus, in patients with NSAP ( Fig. 50-4 ; ). Because of the lack of obvious tissue injury on clinical testing, inflammation and ischemia are probably responses to subtle injury, microtrauma, or even the normal physiological processes that are a result of repetitive movements combined with sustained postures. Research is now beginning to focus on the consequences of these processes. The following section discusses in detail some of the underlying mechanisms that lead to inflammation and ischemia and how such processes may cause symptoms (summarized in Fig. 50-5 ).
Effects of Repetitive Movements on Musculoskeletal Tissue
Muscle
Much of our understanding of the effects of low-force, high-repetition activity on muscle integrity has been gained from an animal model of repetitive motion injury ( ). In this model, animals are trained to repeatedly reach and grasp food pellets. This low-force, high-repetition task is sufficient to cause a decline in motor performance by week 5 such that either rats cannot (or will not) perform the tasks or movement patterns become particularly clumsy ( ). The most notable pathological feature of this model is the development of inflammation within muscle, tendon, and bone, which correlates with the decline in motor performance. Inflammation is indicated by the presences of macrophages in these tissues, as well as by increased local and systemic levels of inflammatory cytokines such as IL-1 and TNF-α ( ). Another interesting feature of this model is the pathological remodeling of bone that occurs within a few weeks ( ). Immature woven bone is deposited at sites of tendon and ligament attachment, a change that may have future biomechanical consequences. Both inflammatory and motor responses are dependent on the rate of the task, with low repetition causing a dampened response. With tasks of higher intensity or following chronic exposure to repeated muscle strain, the effects are exacerbated, and signs of muscle and tendon sheath fibrosis become apparent ( ).
The main finding from these studies is that inflammation can occur without significant muscle damage. It is speculated that intensive low-force, highly repetitive activity initially leads to repeated episodes of low-grade tissue inflammation ( ). In some individuals, this low-grade inflammation may not fully resolve, and over time, tissue viability may be compromised. A vicious cycle may be set up whereby repeated tissue loading leads to chronic inflammation. It should be noted that inflammation is also a major component of delayed-onset muscle soreness ( ), which occurs after repeated eccentric muscle loading. In this instance, the inflammatory response acts as a trigger for muscle hypertrophy. The associated muscle soreness is seen to decrease with repeated muscle training.
Muscle biopsy samples from patients with NSAP, as well as from individuals who perform intensive repetitive activities, have also revealed signs of subtle muscle pathology. In patients with NSAP, clinical severity correlated with changes in the first dorsal interosseous muscle ( ). These changes included an increase in type I (low-threshold, fast-twitch) muscle fibers, fiber hypertrophy, and signs of mitochondrial dysfunction. Muscle fiber hypertrophy is probably a training effect from the repetitive activity. Interestingly, consistent with the work of , evidence of muscle inflammation was also present. Other studies have observed changes in the trapezius muscle of patients with work-related neck–shoulder pain, although these studies did not examine inflammation ( ; ; ). A common feature in all these studies is signs of mitochondrial disturbances in type I muscle fibers, a change that is thought to indicate muscle ischemia ( ). Such mitochondrial dysfunction, along with evidence of inadequate capillary supply to type I and IIA fibers ( ), provides a mechanism of hypoxia and ischemic muscle pain as a possible factor contributing to the production of symptoms. Both muscle ischemia and inflammation would lead to activation and sensitization of muscle afferent terminals ( ), which in turn would result in central sensitization and muscle pain. However, the relationship between muscle biopsy findings and pain perception is unclear, and similar findings are frequently noted in work-exposed pain-free subjects (reviewed in ). Electromyography has also revealed changes in the forearm muscles of patients with NSAP that indicate a muscle pathology ( ), although once again, the relationship between these findings and pain is unclear.
A further hypothesis suggests that the continuous activation of type I muscle fibers during sustained low-force, high-repetition activities could result in selective overuse of these fibers ( ). Although studies have demonstrated continuous activation of individual motor units during wrist movements ( ), there is only limited evidence that such overuse can damage muscle fibers ( ) sufficiently to cause pain.
Blood Flow
Reduced blood flow to the forearm muscles has been reported at rest and during exercise in patients with NSAP ( ). These findings are consistent with histopathological signs of ischemia in muscle biopsy specimens, which together would suggest a vascular component of NSAP. Although the cause of these disturbances in blood flow is unclear, some evidence suggests that certain patients with NSAP have raised forearm extensor compartment pressure ( ). An increase in compartment pressure could lead to a compromised blood supply to the contracting forearm muscles during sustained repetitive activity, which may contribute not only to muscle ischemia but also to microtrauma and inflammation. Interestingly, many patients with NSAP who had undergone decompression surgery on the extensor muscle compartment continued to experience neuropathic pain symptoms ( ). In addition to mechanical restriction of blood flow, an autonomic change leading to vasomotor function ( ) may compromise blood flow in these patients.
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