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National Research Council (US) Steering Committee for the Workshop on Work-Related Musculoskeletal Injuries: The Research Base. Work-Related Musculoskeletal Disorders: Report, Workshop Summary, and Workshop Papers. Washington (DC): National Academies Press (US); 1999.
Work-Related Musculoskeletal Disorders: Report, Workshop Summary, and Workshop Papers.
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Soft Tissue Responses to Physical Stressors: Muscles, Tendons, and Ligaments
James Ashton-Miller
Reported soft tissue injuries can be the result of stresses (e.g., of posture, motion, or vibration) from a single, mechanical event or from repetitive events. The risk of such injury increases with acute or chronic changes in intrinsic factors (age, gender, inherited tissue anatomy, pain responses) related to an individual's physical capacity and extrinsic factors (work and life-style factors) related to the physical demands of the environment. Responses to soft tissue injuries include a complex cascade of events involving inflammatory responses, which mark the first phase of the healing process, followed by a remodeling phase in which tissues are restored. A smooth transition through these healing phases requires that physical loading of tissues be temporarily reduced, in part because of pain and discomfort. This should be followed by a careful increase of physical loading during remodeling to avoid exacerbating symptoms.
Muscles
Muscles can suffer from a variety of injuries, including contraction induced injuries, single-event muscle strain injuries, and fatigue. There is considerable scientific exploration of these types of muscle injury. Three models of muscle injury promise the most return in understanding work-related muscle disorders. The first is an ''eccentric contraction model" in which muscles are subjected to a single, rapid stretch or a series of repetitive contractions. Research using this model has been conducted over the past 15 years in human and animal studies. The animal studies, in particular, have demonstrated that if a period of healing is allowed, the same forces can be later applied without reinjury. Age can affect the ability of the muscles to heal, and exercise, at any age, improves muscle strength and endurance, though it does not compensate for all the advantages of youth.
A second promising model has been developed to investigate muscle fatigue. This model is driven by theories that a muscle's ability to sustain power output is a function of its fiber composition and oxidative capacity. Recent in vivo laboratory studies of human muscle have used noninvasive spectroscopy to measure changes in tissue oxygenation in response to varying levels and duration of force. Decreased oxygen levels with increasing force were demonstrated (in nearly linear proportions) and also were associated with higher reports of discomfort by the study subjects.
The third model suggests that muscle stiffness, tenderness, and pain are associated with the release of substances, such as potassium chloride and lactic acid, during muscle contraction. Laboratory experiments testing this model involve either induced muscle fatigue or the injection of irritants into human muscle tissue. Both subjectively reported pain and myoelectric activity are monitored. The results of these studies also suggest that different muscle groups have different pain levels (jaw muscles, for example, are more sensitive than neck muscles).
Tendons and Ligaments
Tendons, ligaments, retinaculae, intervertebral discs, and the fasciae of muscles are all connective tissues between bone and muscles. The primary structural component of these tissues is collagen, which is demonstrably susceptible to external stresses. In the case of ligaments, theory suggests that strains can reduce the crimp or waviness of collagen fibrils in the ligaments and increase susceptibility to injury. Most studies of ligament injuries have focused on the knee; these studies show that ligaments are generally slow to heal and repair themselves (up to 2 years in animal studies). Aging also appears to affect the tensile strength and elasticity of the ligaments. Biomechanical, in vitro laboratory studies have shown that human hand tendons can be weakened under the friction generated by awkward hand or wrist postures when the hand is gripping an object. Animal studies show that repetitive strains on tendons can cause degenerative changes—increased inflammation, more capillaries, edema and fibrosis. These study findings could be augmented by in vivo evidence of the link between cumulative strain and tendon and ligament injury.
The ability to study cause and effect in overuse-related injuries is hampered by difficulties in accurately estimating the relationships between force and human muscles and tendons throughout different parts and activities of the day—commuting, work, and home and leisure activities. A laudable goal would be to reduce work-related stress on tissues sufficiently so that whether injured "on" or "off" the job, tissues can heal and repair in a reasonable time without risk of becoming chronic conditions.
Soft Tissue Responses to Physical Stressors: Nerves
David Rempel, Lars Dahlin, and Göran Lundborg
We focus on the effects of compression on peripheral nerve functioning as demonstrated in human and animal studies. Peripheral nerve dysfunction associated with nerve compression typically occurs where nerves pass through a tight tunnel formed by stiff tissue boundaries. The resulting "confined space" limits tissue movement and can lead to sustained tissue pressure. Well-known examples are compression of the median nerve at the wrist, of the ulnar nerve at the wrist or elbow, and the spinal root nerves at the vertebral foramen. Clinical reports suggest that lesions that take up some of this confined space (tumors, cysts, and so forth) can cause nerve injury. So too can edema and extracellular matrix in the soft tissues (such as those associated with pregnancy and congestive heart failure). Other conditions, such as diabetes mellitus or an inflammatory reaction, can also increase the susceptibility of nerves to compression injuries.
The studies we examined to illustrate the effects of nerve compression on peripheral nerves included human and animal laboratory studies of the physiologic, pathophysiologic, biochemical, and histologic effects of "loading." Four of these studies demonstrate the state of the evidence on peripheral nerves as well as its limitations.
The first of these studies is an histological study on laboratory rats. In this study, varying levels of nerve compression were applied to the sciatic nerves. Endoneurial fluid pressure was measured at several time intervals up to 24 hours after the removal of compression. Greater levels of compression were associated with greater and longer lasting levels of endoneurial fluid pressure. Histologic examination of nerve tissue showed edema and degenerating nerve fibers after 8 hours even at the lowest levels of induced compression used in the study.
A second, similar study examined nerve compression over longer time periods—up to 4 weeks, under relatively high levels of nerve compression. The histologic results were edema, inflammatory reactions, and fibrosis within hours of compression. After 2 to 3 weeks, marked fibrosis, demyelination, and axonal degeneration were evident.
Related studies of animals exposed to vibration of the hind limbs for 4 hours over a period of 5 days suggest similar edema and structural nerve changes.
These two studies deal with sciatic nerves. Two other illustrative studies deal with nerves in the fingers and wrists. One study examined carpal tunnel nerve pressure in 20 people by asking them to press a load cell with their index fingers and then pinch the same cell between thumb and index finger. Both the pressing and pinching tasks led to increasing extraneural pressure in the carpal tunnel, but the pinching task was associated with pressures twice as high as the pressing task. The other study involved 10 men (ages 17-30) exposed to hand vibration in their work who were matched with 12 male cadavers of similar ages without such work exposures. Biopsies of the nerve just proximal to the wrist in both the living subjects and the control group (cadavers) showed pathological changes to the nerve in all 10 subjects and in one of the controls. Nerve changes included the breakdown of myelin and fibrosis.
These studies demonstrate a clear biological effect: that nerves are particularly sensitive to loading at relatively low levels of compression and exhibit changes that can persist. Humans exposed to hand vibrations or performing certain maneuvers can experience elevated extraneural pressures that in laboratory animals would result in nerve injury. All of these studies are limited in some ways: limited exposures to compression, lack of statistical comparisons, investigation of only one area of nerve dysfunction when multiple nerves are involved, and measurement difficulties that limit understanding of precise dose-response relationships. Further research could overcome some of the limits and usefully add to our understanding of these biological effects.
Discussion
The papers provide evidence for several conclusions about soft tissue response to physical stress. Although certain loads can be tolerated or adapted to, all soft tissues, including muscle, tendon, ligament, fascia, synovia, cartilage, intervertebral disc, and nerve, fail if subjected to sufficient force. Data from cadaver studies provide ranges within which such failures occur, as do animal models of some soft tissues tested in laboratory studies. Even at levels clearly below these failure ranges, however, there is scientific evidence from laboratory studies that soft tissue responses include inflammation, muscle fatigue, and ultrastructural degeneration that does not heal without cessation or restriction of the provoking force. As Figure 1 illustrates, intrinsic factors, such as age and conditioning, can influence soft tissue response and recovery, as can extrinsic factors, including the work environment and life-style characteristics.
The discussants of the Ashton-Miller and Rempel et al. papers did not generally dispute the conclusions presented, though many believe that greater attention to some aspects of the scientific evidence on soft tissue responses to stress could provide additional, important insights on tissues responsible for work-related musculoskeletal disorders. Suggested research areas included:
- studies of the synovium (the tissue lining the tendons and joints);
- recent biological work on cytokines and growth factors considered important in tissue inflammation, healing, and repair;
- more scrutiny of studies using electromyography (EMG) to monitor muscle fatigue and pain (EMG measurement is noninvasive, objective, and can be used to establish biomarkers for muscle injury); and
- studies of the effects of peripheral tissue inflammation on the central nervous system, especially in cases where muscle pain lasts much longer than expected.
Several other themes emerged from the discussions of these papers. The need for more research and more integrative research was a major theme. The long-term or chronic effects of soft tissue responses to stressors was one area in which discussants believed further research was critical. Steven Lehman, University of California at Berkeley, raised this issue in discussing the need to better understand the physiology of low-force, long-duration work and its effects on motor control, muscle fatigue, pain, and the recovery process. Carlo de Luca, Boston University, suggested the use of electromyography as a method for studying muscle fatigue.
The clinicians among the discussants stressed that, although most of the laboratory evidence presented in the papers corroborated their own case observations, that laboratory evidence deals primarily with acute stressors while they find the most difficult cases to be those involving chronic stressors. Susan Mackinnon, Washington University School of Medicine, noted that her experience indicates that an understanding of patient symptoms requires an understanding of chronic nerve compression. She described a model of chronic nerve compression in rats and primates that closely mimics the pathological changes seen in humans. These pathological changes (ranging from edema to degeneration) are paralleled by the symptoms of patients in clinical testing. Patient complaints typically begin with intermittent numbness brought on by specific postures, but not apparent when the patient is resting. As compression continues or increases, numbness becomes more persistent and, eventually, permanent. There are also neural and physiological symptoms which begin with complaints of aching and progress to weakness and finally, to muscle atrophy.
We need a good model of chronic nerve compression.
(Robert Szabo, University of California, Davis)
Robert Szabo, University of California, Davis, reinforced Mackinnon's comments, noting that the Rempel et al. paper's discussion of laboratory studies on nerve compression over time did not highlight the clinical relevance of the findings. The findings show a progressive degeneration of nerve health under sustained compression, which suggests that nerve compression effects can be viewed on a spectrum divided into early, intermediate, and late categories. In clinical terms, early stages respond most favorably to conservative treatment (such as steroid injections and splinting for carpal tunnel syndrome). For intermediate stages of nerve compression, involving numbness and parasthesia, patients respond well to nerve decompression via the surgical release of the carpal tunnel. In late stages, patients often have permanent sensory loss with long-standing edema and fibrosis: these patients may benefit from carpal tunnel release, but this will not eliminate all their symptoms.
Putting these clinical views on chronic nerve compression in an even broader context, Thomas Mayer, PRIDE, Dallas, Texas, reported that even when all forms of acute nerve compression and musculotendinous sprains and strains are considered, they account for a small portion of medical care and medical costs (see box).
It has been known for 2 to 3 decades that 90 percent of the musculoskeletal claims comprise only 20 percent of the medical and indemnity expenditures . The 10 percent of cases extending beyond the acute phase of soft tissue healing account for 80 percent of the system costs for low back pain.
(Thomas Mayer, PRIDE, Dallas, Texas)
Another common "need for research" theme among the paper discussants was the need to generate links between specific anatomically distinct disorders (as they are clinically observed) and specific underlying patterns of pathology. J. Steven Moore, Texas A&M, summarized this view by noting that models that relate (1) specific patterns of musculoskeletal loading to (2) distinct internal stress in specific anatomical structures that (3) elicit tissue responses that (4) lead to observed tissue changes—are critical to diagnosis, treatment, and epidemiological tracking of musculoskeletal disorders and the circumstances under which people are exposed to such disorders. Echoing these remarks, Kai-Nan An, Mayo Clinic, noted that inconsistencies in the definitions and diagnosis of work-related repetitive stress injuries makes the true incidence of such injuries and the factors that provoke them difficult to identify.
Overall, the paper authors and discussants agreed that sound research shows that muscles, tendons, ligaments, and nerves can fail when subjected to sufficient force and that they can heal and repair themselves over time under the appropriate conditions (restriction or cessation of force and gradual reconditioning). However, there was also agreement that work remains to be done in establishing the links between impetus to injury to soft tissue response, on one side, and optimal conditions (either physical or environmental) for healing and repair of injury, on the other.
We now have the biomechanical and mechanobiological concepts and techniques to begin rigorous study that could lead to progress in prevention and treatment of these [musculoskeletal] disorders. The challenge is to bring first-rate mechanics, biology, and clinical perspectives together in order to approach the [research] problems in a unified, consistent manner.
(Dennis Carter, Stanford)
- Biological Responses of Tissues to Stressors - Work-Related Musculoskeletal Diso...Biological Responses of Tissues to Stressors - Work-Related Musculoskeletal Disorders
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