The abundant evidence of an association between work-related biomechanical factors and CTS has been accumulated, for the most part, using cross-sectional study designs. Many such studies appear confounded by the presence of numerous conditions that are associated with and contribute to CTS and that may be unrelated to occupational hand use. Anatomically, factors that decrease the size of the carpal tunnel or increase the volume of the contents of the carpal tunnel will increase the intratunnel pressure. Persistent increased carpal tunnel pressure, in turn, may increase the likelihood of developing CTS. Physiologically, various neuropathic and inflammatory conditions and conditions that alter fluid balance also increase the risk of developing CTS. In addition, some evidence links work-related musculoskeletal symptoms to psychosocial factors such as monotonous work, perception of high workload, perception of time pressure, low control, and low social support. Lastly, the possibility of a genetic predisposition to CTS cannot be disregarded. For example, a familial history of CTS was found to be present in 27% of 421 patients with electrodiagnostically confirmed CTS (9).
The resilience of the arguments linking CTS to the biomechanics of occupational hand use emerges from the knowledge base related to the physiology of peripheral nerve compression injury, the parallel between CTS symptoms and peripheral nerve compression injury, and the epidemiological evidence. Anatomically, the carpal tunnel is unfortunately well designed to induce median nerve compression injury. The floor of the carpal tunnel, formed by the carpal bones, and the roof of the tunnel, formed by the transverse carpal ligament, create a stiff passageway for its tightly packed contents. Because the compliance of the carpal tunnel is low, increased volume of the carpal tunnel contents, or a decrease in the dimension of the carpal tunnel, increases the pressure within the carpal tunnel. Increased carpal tunnel pressure, considered an important causal factor of CTS, exerts deleterious effects on the microvascular systems of the nerve epineurium, perineurium, and endoneurium. Sustained and increased carpal tunnel pressure causes predictable physiologic responses in the median nerve that give rise to acute and chronic CTS symptoms. The physiologic responses include numbness and paresthesia, epineurial and intrafascicular edema, epineurial scarring, impairment in intraneural circulation, structural changes such as distended internodes and myelin derangement, marked sensory changes, and weakness of the thenar muscles.
Structural and functional changes to the median nerve are crucial for discriminating CTS from nonCTS pathologic conditions. In particular, median nerve motor and sensory changes secondary to CTS, assessed electrophysiologically to quantify conduction velocity, are considered by some as the gold standard for diagnosing CTS. However, impaired median nerve conduction velocity across the carpal tunnel does not necessarily imply CTS. This is highlighted by a prospective study on the natural history of CTS. An 11-yr longitudinal study of median nerve sensory conduction velocity, clinical symptoms, and confirmed CTS was performed on 289 industrial workers (8). Diagnosis of CTS was based on the simultaneous presence of a specific symptom complex and abnormal median nerve conduction. The original study group consisted of 942 hands in 471 workers in 1984. Two follow-up studies, in 1989 and 1994–1995, consisted of 630 hands in 316 workers and 578 hands in 289 workers, respectively. In 1984, 41 hands in the primary study group were classified as having CTS. The longitudinal results from these 41 subjects revealed that the number of hands demonstrating electrodiagnostically confirmed median nerve conduction velocity slowing did not parallel the number of hands having confirmed CTS (Fig. 2). This illustrates the potential for dissociation between confirmed CTS and electrodiagnostic evidence of slowing of the median nerve conduction velocity. In addition, interpretation of electrodiagnostic results can be problematic.
Electrodiagnostic protocols that do not account for between-subject factors such as age, gender, body mass index, wrist geometry, electrode placement, body anthropometrics, and hand temperature may induce a bias. Furthermore, median nerve conduction velocity may be impaired by nerve compression at sites other than the carpal tunnel. Electrodiagnostic testing of the median nerve at the carpal tunnel does not necessarily rule this out. For example, the median nerve can be compressed by the flexor aponeurosis at the elbow and it can also become compressed between the two heads of the pronator teres. These situations, which are not uncommon, can decrease median nerve conduction velocity across the carpal tunnel.
Nevertheless, even if the electrodiagnostic results are unambiguous, the presence of physical and medical conditions that may cause, or may be associated with, CTS and that are independent of occupational-related hand-use must be addressed. For example, pregnancy, hypothyroidism, rheumatoid arthritis, gout, diabetes mellitus, long-term hemodialysis, familial occurrence of CTS, previous hand or wrist injury, hypertrophy of the lumbrical muscles, alcohol or tobacco use, obesity, and physical inactivity or low physical fitness increase the risk for developing CTS. It seems reasonable that the presence and potential contribution of these, as other conditions, should be ruled out before carpal tunnel syndrome can be unambiguously attributed work-related factors. If the presence of these risk factors cannot be ruled out, then the extent to which occupational hand use may be causally associated with the CTS is diminished.
The epidemiological evidence of the work-relatedness of CTS has been the most debated. Center stage in the debate is the population of workers thought of as being at greatest risk for developing carpal tunnel syndrome, those whose jobs require extensive use of their hands. The NIOSH position is that the “evidence is clear that exposure to a combination of the job factors studied increases the risk for CTS.” The evidence was reported as “strong,” and strong was defined as reflecting a very likely causal relationship between intense or long duration exposure, or both, to a combination of risk factors. Generalized, quantitative, and validated definitions of “intense” and “long duration” are at best difficult to acquire, but these terms have been somewhat characterized within certain industries. Nevertheless, the extent to which these characterizations are transferable to other industries is simply unknown.
The particular combination of risk factors for which the evidence was considered strong appears to have been primarily the forcefulness of hand use and the extent to which the hand was subjected to repetitive forceful hand use. The strength of the evidence was based on the presence of a positive relationship in at least several studies and study designs in which chance, bias, and confounds were reasonably rejected. Other criteria conventionally used to establish causality were not explicitly considered. In addition to the strength of association, these criteria include the consistency of the effect, biological plausibility, dose response, temporal sequence, specificity, the absence of other plausible explanations, and establishing sufficiency vs necessity-based causation.
More than 30 epidemiological studies examining workplace factors and their relationship to CTS were reviewed. Ultimately, nine of these studies were selected and used to support the conclusion of providing “strong evidence.” One of the studies was not published in a refereed journal (5).
Most of the studies used statistical designs that have a limited ability to address causality. For example, cross-sectional designs cannot provide evidence of the temporal relationship between exposure and effect. In one cross-sectional study, the dominant significant contributor was gender (4). In another study, the odds ratio for forcefulness (but not repetition) of hand use was significant (2). The discussion section of another cross-sectional study identified numerous statistical confounds and inadequate statistical power (12). One study was a retrospective survey, the data of which were extracted from the 1988 National Health Interview Survey (13). Although important, this type of experimental design has inherent weaknesses that reduce the confidence with which attributions of causality may be asserted.
In two cases, the findings of the studies were re-interpreted in a manner that seems in direct opposition to the interpretation of the authors. One author wrote of “very little evidence for the concept of cumulative trauma as a prominent cause of CTS in American industry” (10). Another author concluded that there was “no consistent association” between occupational hand use and prevalence or severity of slowing of median nerve conduction velocity (6). This author latter concluded that slowing of the median nerve conduction velocity was not correlated with occupational hand use (7). Indeed, after the 5-yr period of this prospective study, slowing was found to be more associated with age and hand dominance than with occupational hand use.
The study by Silverstein et al. (11), who studied the influence of high force and high repetition jobs on the prevalence of CTS, did demonstrate a significant and independent contribution to CTS risk of both force and repetition. The odds ratios for CTS and high repetition and high force were 2.9 and 5.5, respectively. However, in the study by Chiang et al. (2), based on the logistic regression and which addresses the issue of dose response, the effect of high force, but not repetition, was significant. Last, Chiang et al. (1) studied more than 200 workers in a frozen food plant and determined the relationship between CTS, exposure to cold, and job-related repetitive movements. These authors reported that high repetitiveness (especially in combination with cold temperatures) was associated with CTS. Based on the a priori boundaries established by NIOSH for inclusion, it seems that the extent to which the included studies collectively establish a strong causal relationship between exposure to a combination of factors and risk of developing CTS is not unambiguous.
Are there job-specific biomechanical factors to which the development of CTS may be unambiguously and causally associated? There is a substantial and impressive body of literature presenting evidence of association between exposure to biomechanical risk factors and CTS. Despite our criticisms and objections, we do not contest a general relationship between exposure to some biomechanical risk factors and increased risk for developing CTS. However, the evidence of an unambiguous relationship is not compelling. Certainly, some occupations have a very high prevalence of CTS compared with the general population. Further, the job-specific hand use is strongly, but not necessarily uniquely, associated with the development of the pathologic features. It is possible that a synergy between risk factors amplifies the physiological response to the biomechanical risk factors. Presently, it seems prudent to avoid general rules of thumb that, in some arenas, are conventionally applied to all occupations and all workers to link occupational hand use to CTS. The lines of evidence are not consistent or continuous from the cellular and tissue levels, where the knowledge base is strong, to organism levels of investigation, where the knowledge base is not as strong.
1The news item, which was originally carried by Reuters, was recently confirmed in a personal communication between MDG and an attorney from the Broward County Bar Association, Workman’s Compensation Section.
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Keywords:©2003 The American College of Sports Medicine
biomechanics; cumulative trauma disorder; hand; industrial injury; repetitive motion injury; wrist