[Table of Contents] -- Appendix 1 - Appendix 2
A. LOW-BACK DISORDERS
Low-back pain has long been associated with the performance of heavy physical work (Hales and Bernard, 1996; Klein, Jensen, and Sanderson, 1984; Rowe, 1969, 1971). Recently, a NIOSH review (Bernard and Fine, 1997) concluded that several materials-handling characteristics and whole body vibration are associated with low-back disorders. The National Academy of Sciences (1998) also concluded that there is an association between certain work factors and low-back disorders. To understand the mechanisms by which work causes or contributes to the genesis or expression of low-back pain, it is first necessary to comprehend basic low-back anatomy and potential sources of pain. The majority of low-back disorders involve soft tissues (muscle and ligament) or the three-disc complex (the intervertebral disc and two facets). The latter may involve degenerative disc disease, disc herniation or osteoarthritic conditions. To understand how the performance of work causes lumbar disc disease, a review of lumbar anatomy, disc biochemistry, and disc biomechanics is critical. With this foundation, pathogenic models are better appreciated. Several references are available for further review (Bogduk and Twomey, 1991; Chaffin and Andersson, 1991; Williams., McCulloch, and Young, 1990; Wiesel et al., 1996).
A.1.a Epidemiology and Sources of Low-Back Pain
Several authorities have estimated that up to 70% to 80% of adults will experience an episode of low-back pain during their lifetime requiring temporary activity modification (Andersson, 1981; Bigos et al., 1994; Frymoyer and Cats-Baril, 1991; Bernard and Fine, 1997). On an annual basis, low-back pain will cause perhaps 2% to 5% of the population to seek medical advice or miss work (Waddell, 1987). While the 1-year prevalence of low-back pain in the general U.S. population may be as high as 15% (Andersson, 1991), estimates in the working age population are as high as 50% (Sternbach, 1986; Vallfors, 1985). In Quebec, a review of 347,131 claims for work-related injuries made to the Workers' Compensation Board during 1981 (Quebec, 1987) revealed that 1.7% of the population was compensated at least once during the year for a work-related spinal disorder. Seventy percent (70%) of these claims involved the lumbar region. Kelsey and White (1980) estimated a similar (2%) annual incidence of compensable low-back problems in American workers. There is some suggestion that back pain associated with work activities may be underreported. Behrens et al. (1994) reviewed self-reported back pain, lasting 1 week or more, in the U.S. working population from the 1988 Occupational Health Supplement to the National Health Interview Survey. The overall 12-month prevalence of back pain due to injury was 2.5%, and due to repetitive activity was 4.5%. Rates varied with occupation, with the highest reported incidence for injury-related back pain observed in truck drivers (6.7%), and the greatest incidence of repetitive activity-related back pain noted for mechanics (10.5%). In another analysis, Guo et al. (1995) estimated 12-month self-reported rates of back pain attributed to work as high as 22.6% in male construction workers and 18.8% in female nurse aides. As noted, this was a self-reported survey with no validation of the episodes, but it does suggest that many episodes of back pain associated with work activities may not be reported.
With regard to duration of low-back pain, it appears that up to 90% of low-back pain episodes will resolve within about 4 to 7 weeks (Bergquist-Ullman, 1977; Bigos et al., 1994; Deyo, 1987; Von Korff et al., 1993). However, 5% to 10% of patients will develop pain persisting for 6 months or more (Klenerman et al., 1995; Nachemson and Bigos, 1984; Spengler et al., 1986). Once experienced, recurrent episodes of low-back pain appear common. Rowe (1963 and 1965) estimated a 75% to 83% rate of recurrence for low-back pain or sciatica, with 50% to 60% of the recurrences in the year following the initial episode (Rowe, 1969). Similarly, trends for recurrence in the first 2 years were noted by Troup, Martin, and Lloyd (1981) and Lloyd, and Troup (1983). Bergquist-Ullman and Larsson (1977) looked at auto workers with acute low-back pain, and found a 62% recurrence by the first year with an additional 18% by year 2. Regrettably, perhaps 1% of Americans may be temporarily disabled and another 1% chronically disabled by low-back pain at any given time (Andersson, 1991).
There is some debate as to the exact etiology of low-back pain, and some authorities suggest that it is possible to make a precise diagnosis in perhaps only 20% of patients presenting with acute low-back pain (Frymoyer, 1988; Nachemson, 1976; White and Gordon, 1982). Theories for anatomic sources include the muscles, ligaments, vertebrae, intervertebral discs, facet joints, and spinal nerve roots (Riihimaki, 1991). However, Section A.4 on the three-joint complex (disc and two facet joints) and the nerve root will explore what appears to be the most significant anatomic locations for discogenic low-back pain. Proposed etiologies for low-back pain that have been advanced include the roles of nerve compression, tissue ischemia, sensitization of nerve endings, inflammatory mediators, spinal instability, and other postulates (Frymoyer, 1988; Nachemson, 1992). The majority of cases of work-related low-back pain are attributed to mechanical causes, such as muscle and ligament strains and sprains and disc herniations. Degenerative disc or facet disease, spinal stenosis, spondylolisthesis and compression fractures have also been attributed, at least in part, to work.
One additional difficulty in evaluating the etiology of low-back pain is that 56% of patients reporting an episode of work-related low-back pain note an insidious onset of pain rather than a single, point-in-time event with immediate low-back pain (Bergquist-Ullman and Larsson, 1977). This study found that cases with an insidious onset experienced prolonged recovery. Part of the explanation for this may lie in the absence of nociceptors in the disc itself and the facet joints (except for the synovial lining) (Pope et al., 1991). These load-bearing structures may therefore become injured without immediate recognition (e.g., sudden pain), and the eventual manifestation of low-back pain may only occur after a series of point-in-time events have sufficiently injured these spinal structures to the point where nociceptors become irritated (e.g., in the outer one-third annulus or facet synovium).
The lumbar spine is required to redistribute forces related to both intrinsic weight bearing and extrinsic load carrying. It is composed of five vertebral bodies separated by intervertebral discs acting as shock absorbers and stabilizers, as well as the posterior vertebral ring composed of pedicles, laminae, spinous and transverse processes, and facet joints that enclose and protect the spinal cord and spinal nerve roots. The lumbar vertebrae are numbered from the upper (cephalad) or first lumbar vertebra (L1) to the lower (caudad) or fifth lumbar vertebra (L5). Lumbar vertebrae are larger and wider than those in the dorsal and cervical spine, with the fifth vertebra generally the largest. This affords a larger surface area for the intervertebral disc and for load distribution. Disc anatomy and function will be discussed further in Section A.4. At the lower end of the lumbar spine is the sacrum, a large, triangular bone representing the fusion of five sacral vertebrae, and the small coccyx.
Consistent with the greater vertebral size, the lumbar pedicles are shorter and wider than in the dorsal spine. Lumbar facets are posterior articular processes where the adjacent vertebrae interface. These joints help permit motion and bear some of the compressive load in addition to helping maintain stability of the spine against torsion and shear. Facet joints are synovial, and they contain nerve innervation in the synovial lining. Anterior and posterior longitudinal ligaments attach to the superior and inferior margins of the lumbar vertebrae, and are innervated by pain fibers. The ligamentum flavum is a non-innervated structure that runs down the vertebral ring, and may hypertrophy after injury. This may become significant when a hypertrophied ligament infolds during spinal extension in an individual with disc bulging and facet arthropathy, thereby creating relative spinal stenosis. The interspinous ligament, also non-innervated, runs down the posterior margins of the spinous processes, posterior projections from the vertebral ring.
In adults, the spinal cord terminates as the conus medullaris at about the level of the first lumbar vertebra in the upper lumbar spine. Branching off from the conus is a bundle of lumbosacral nerve roots that resemble a horse's tail, called the cauda equina. These nerve roots pass through the lumbar and sacral portions of the spinal canal surrounded by the vertebrae, intervertebral discs, pedicles, laminae, facet joints, and spinal ligaments and eventually emerge as individual nerve roots through the intervertebral foramina. The neural foramen is bordered by the transverse processes of adjacent vertebrae, and the spinal nerve root takes its name from the adjacent (cephalad) vertebrae. The spinal cord is covered by the thecal sac, composed of meningeal tissue and cerebrospinal fluid.
Nerve roots in the lumbosacral spine include ventral (motor) and dorsal (sensory) components. Ventral roots contain motor axons sending signals to distal areas and control various skeletal muscle motor functions. Dorsal roots comprise primarily sensory axons receiving signals from distal areas or dermatomes. Thus, symptoms and signs of nerve root compression will vary with the location of the compressive lesion. As the intrathecal nerve roots reach the intervertebral foramen, the root sleeve gradually encloses the nerve more tightly, and eventually become extrathecal. Cell bodies for sensory axons are located in an extrathecal area of swelling called the dorsal root ganglion. These ganglia are encountered in or close to the intervertebral foramina. Axons of the nerve roots consist of collagen tissue called the endoneurium. This is covered by a thin root sheath that separates the endoneurium from a small amount of cerebrospinal fluid, and the epineurium and perineurium covering. Blood flow derives from segmental arteries that divide into three branches when approaching the intervertebral foramen. Nociceptors are present in facet synovium and outer layers of annulus (or extension of the posterior longitudinal ligament).
There are several important muscles of the low back. The psoas muscles are major spinal flexors that originate at the anterior vertebral borders and combine with the iliacus from the crest of the pelvic ilium and insert on the pelvis and lesser trochanter of the hip. Posteriorly, the erector spinae muscles attach to the spinous processes and laminae down to the sacrum to act as major spinal extensors. The interspinales muscles run between the five spinous processes of the lumbar spine and contribute to extension. Several other coactivating muscles assist in spinal stabilization and rotation. The rectus abdominis extends from the lower border of the rib cage to the pelvis and assist in flexion and maintenance of lordosis. The obliques and transversus are coactivators, and contribute to the generation of increased intraabdominal pressure, which some feel helps decrease compressive loading on the spine. External moments imposed on the lumbar spine during lifting are proportional to the weight and distance of the load from the spine and the weight and location of the individual's body segments. This results in a state of equilibrium where the external moments are counteracted by internal moments, primarily created by muscle contractions of flexors balancing extensors with additional stabilization from co-activators. Ligaments provide passive resistance or restorative moment to muscles. It is not clear, however, under what lifting conditions the ligaments play a significant biomechanical role.
A.3 Soft Tissue/Mechanical Low-Back Disorders
As noted earlier, the exact etiology of low-back pain is unknown in many cases, and therefore, there is a lack of universal agreement on the contribution of muscle and ligament sprains and strains to work-related low-back disorders. In part, the difficulty in diagnosis relates to the inability to easily palpate deep low-back muscles, the lack of imaging information on low-back muscle disorders, and the absence of surgical pathologic specimens to evaluate. However, an understanding of muscle anatomy, function (static and dynamic loading), repair mechanisms, and muscular contributions to low-back function requires consideration of the role of muscle and ligament sprains and strains in work-related low-back disorders.
A.3.a Static Loading
In evaluating the pathogenesis of soft-tissue low-back disorders, there are considerations related to static and dynamic work activities. Simple maintenance of posture requires balancing of counteracting mechanical forces about the spine. As discussed in the section on tissue pathology, static loading affects muscle and connective tissue. During static trunk flexion, low-back extensor muscles must progressively increase their activity to maintain trunk flexion (Andersson et al., 1977; Schultz et al., 1982). During continuous static loading from prolonged sitting at work, muscles may undergo energy depletion with the development of fatigue. Normally, individuals may respond by standing up, walking about, or otherwise shifting positions. However, in monitored data entry positions or similar work settings, this may not be permitted. Muscle fatigue may then result in additional load bearing by the intervertebral disc. Studies have demonstrated that lumbar muscle activity decreases with the use of back rests (Andersson et al., 1974,1979; Hosea et al., 1986). Using myoelectric measurements, Andersson et al. (1974) ascertained that activity of the erector spinae progressively decreased as the angle of the back rest advanced from 10 degrees of forward inclination to backward inclination. This results from a partial reduction of the lumbar spine load imposed by the upper body as the load is transmitted to the back rest (Andersson and Marras, 1996; Chaffin and Andersson, 1991). In addition, during unsupported sitting, the lumbar spine flattens, and the use of lumbar supports and back rests can reduce the loss of normal lordosis (Andersson et al., 1979). Using a back rest inclination of 110 degrees and a 4 cm lumbar support, the authors were able to demonstrate that lumbar posture could be similar to normal standing posture. Maintenance of adequate seated posture has further implications for the intervertebral disc, with lower intervertebral disc pressures noted during supported sitting as opposed to unsupported sitting (Andersson et al., 1974). Inadequate seating can contribute to the development of low-back pain. Individuals who sit in chairs that are too high and have their feet unsupported experience elevated pressure on the back of their thighs (Akerblom, 1969; Bush, 1969; Schoberth, 1962, as cited in Chaffin and Andersson, 1991). Burandt and Grandlean (1963) observed the tendency of subjects in high seat pans to slide forward in their seats to support their feet, negating the benefit of a back rest.
A.3.b Dynamic Loading
Dynamic loading of the lumbar spine has other implications for muscle and ligament. Stresses induced in the low back during manual materials handling relate to the load weight and the characteristics of the lift, as discussed in Appendix II. As a result of their anatomic positions, large spinal movements are created from relatively small degrees of muscle shortening. Unfortunately, this results in the generation of relatively large muscle and joint forces, with potential for tissue overloading and injury. This could be particularly important during excessive or rapid movement (Andersson and Marras, 1996), or at the point of muscle fatigue. A study by Hukins et al. (1990) revealed that greater forces are exerted on ligaments as the speed of motion increases. In addition, elastic limits of the ligaments and disc may be exceeded (Adams and Dolan, 1981). Bush-Joseph et al. (1988) evaluated the effect of the speed of lifting on the external load moment. Subjects were asked to lift at slow, medium, and high speeds. There was a direct linear correlation between increasing speed of lifting and increased peak moment. Furthermore, a study by Marras and Mirka (1992) revealed that muscles must generate a higher percentage of electromyographic (EMG) maximal activity to maintain a constant muscle force as the speed of trunk velocity increases with bending.
Both lifting frequency and load weight affect back muscle work capacity, in part related to fatigue. Using EMG assessments, Kim and Chung (1995) observed that lifting at 10% of maximum voluntary isometric strength (MVIS) at a rate of 6 times a minute was more fatiguing than lifting at 20% MVIS at a rate of 3 times per minute. Frequent loading of the lumbar spine with moderate to heavy weights can also cause general physical fatigue with elevation in heart rate and energy expenditure. Uncoordinated muscle activation that could result from local and systemic fatigue could then place other tissues at increased risk with continued lifting (Garg, 1986).
A.3.c Postural Issues
Additional postural factors during lifting significantly affects muscle function and risk of injury. Skeletal muscle is more likely to rupture during eccentric contraction (Friden and Lieber, 1994), a factor involved in many manual materials-handling tasks. In addition, muscle length affects the amount of force that muscle can generate, with maximal force produced when muscles are at their resting lengths (Andersson and Marras, 1996; Chaffin and Andersson, 1991). Therefore, lifting in positions where skeletal muscles are elongated or shortened can increase the risk of injury to these tissues.
Using EMG evaluation of muscle function during lateral flexion of the lumbar spine, Andersson, Ortengren, and Herberts (1977) demonstrated increased activity on the side contralateral to bending. Other researchers have determined that asymmetric loading in lateral flexion and axial rotation causes high levels of antagonistic activity in abdominals and back extensors. This is associated with increased myoelectric activity on the side of spine contralateral to the load, although there is still significant activity on the ipsilateral side (Astrand, 1987; Kelsey, 1975; Magora, 1970; Merriam et al., 1983). Andersson (1977) noted that increased intervertebral disc pressure and intraabdominal pressure occurs when the trunk is loaded in lateral flexion and axial rotation, with rotation being the greater factor.
A.3.d Muscle Velocity and Acceleration
Marras has indicated that several trunk muscle characteristics and demands associated with dynamic lifting may better assess the risk of developing a low-back disorder from manual materials handling. The authors analyzed 400 lifting jobs in 48 industries using a triaxial goniometer (Lumbar Motion Monitor or LMM) that was worn by working subjects. A combination of five trunk motion and workplace factors was able to reasonably predict jobs posing high risk for low-back disorders (Marras et al., 1995). These factors include the lift frequency, load moment, trunk sagittal range of motion, trunk lateral velocity and trunk twist acceleration (Marras et al., 1995). A recent NIOSH Health Hazard Evaluation provided additional verification that the LMM has predictive capacity equal to the NIOSH Lifting Equation in job analysis (NIOSH, 1993), with perhaps greater ease of administration.
Recently, Marras et al. (1990, 1993, 1995) studied the trunk angular motion characteristics of normal and chronic low-back pain subjects. Used in a clinical setting, the LMM appears to have good ability to accurately distinguish between normal individuals and those with chronic low-back pain or structural disease. The authors used anatomic and pain categories previously selected by the Quebec Task Force Study on Spinal Disorders (1987). Normative trunk motion values for age and gender were derived in a study of 339 males and females from ages 20 to 70 years who had never experienced significant low-back pain. While wearing the LMM, subjects performed trunk flexion and extension in five symmetric and asymmetric motion planes (0 degrees, 15 degrees and 30 degrees right and left) while trunk angular position, velocity, and acceleration were recorded with the LMM. In a repeatability study, 20 healthy normal subjects who had never experienced a low-back disorder were tested with the LMM once a week for 5 weeks. No statistically significant differences were observed among the trunk motion characteristics between the five weekly test sessions using multivariate analysis of variance. Correlation coefficients were computed to select reliable trunk motion variables to be used in the next phase of the study. Correlations varied as a function of the angle of asymmetry and measured variables, with motion characteristics in the zero plane demonstrating correlation coefficients of 0.88 to 0.96 (number of conditions performed, twisting range of motion, sagittal range of motion at 0 degrees, sagittal extension velocity at 0 degrees, sagittal extension acceleration at 0 degrees, continuous velocity, continuous acceleration, lateral right range of motion at 0 degrees).
In the next phase, the eight highly reliable trunk motion characteristics evaluated in the healthy subjects were compared with measurements in subjects with chronic low-back pain (96 males and 75 females) who were recruited for study from secondary and tertiary referral practices. These individuals had been symptomatic for a least 7 weeks and had been sufficiently studied, including with appropriate imaging studies, to permit accurate Quebec classification. Dynamic trunk motion characteristics were normalized for age and sex, and using quantitative discriminant analysis, the 510 subjects were correctly classified in 94% of cases as being either healthy or having chronic low-back pain(stage-one analysis).
In a stage-two analysis, nine variables (the eight previously mentioned and continuous position) correctly classified 80% of subjects into one of eleven groups (normal, low-back pain alone, low-back pain with proximal or distal radiation, disc herniation with high or low pain scores, spondylolisthesis, spinal stenosis, postoperative, nonorganic components, other) via modified classification using splines. It was also noted that trunk range-of-motion parameters commonly used to quantify impairment had poor ability to discriminate normal vs. chronic low-back pain, nor was it useful in classification. Furthermore, a characteristic pattern of recovery from low-back pain was noted, with normalization occurring first in range of motion followed by velocity and later acceleration of dynamic trunk motion. It was opined that the LMM's ability to quantify unloaded free-dynamic motion and account for the co-activation of additional structures (e.g., internal and external obliques, lattissimus dorsi) affecting erector spinae function was in part responsible for its enhanced discriminating ability compared to alternate imaging techniques.
Whole-body vibration may also affect skeletal muscle and predispose an individual to work-related low-back pain. Etiologies for this may include bursts of cyclic muscle contraction, muscle fatigue, decreased ability of fatigued muscles to protect spinal structures from loads, continuous compression and stretch of structures, decreased blood flow, and altered neuropeptides (Brinckmann et al., 1996; Friden and Lieber, 1994; Hansson and Holm, 1991; Seidel, 1988). The following section discusses this further.
A.4 Three-Joint Complex (Disc and Two Facets) and the Nerve Root
Epidemiologic evidence suggests that work exposures involving heavy lifting or manual materials handling and vibration are associated with low-back disorders, including disc disorders (Bernard and Fine, 1997). Excessive or repeated spinal loading and inadequate rest periods to permit repair mechanisms to function may be associated with biomechanical stresses that damage intervertebral disc cartilage endplates. This may then disturb metabolic transport, hastening the development of degenerative disc disease and disc herniation with secondary nerve root compression or inflammation.
A.4.a Brief Epidemiology and Theories on Etiologies of Pain
The three-joint complex refers to the intervertebral disc and two facet joints. This complex permits the spine to absorb compression and resist torsion and shear, while permitting translation and rotation of the spine. Rowe (1971) opined that up to 70% to 80% of recurring, chronic low-back pain will eventually be diagnosed as discogenic. Discogenic pain can include clear and consistent symptoms and signs expected with lumbar disc herniation and specific nerve root pathology, as well as chronic low-back pain associated with increased pressure in the intervertebral disc or degenerative disc disease. In patients with lumbar disc herniations, approximately 90% to 95% occur at the lower three intervertebral disc spaces (lumbar 3/4 disc or lumbar 4th nerve root, lumbar 4/5 disc or lumbar 5th nerve root, lumbosacral L5/Sl or sacral 1st nerve root) (Deyo, Rainville, and Kent, 1992). Increased compressive and torsional forces transmitted to the lower levels of the lumbar spine probably account for this observation. Peak incidence of lumbar disc herniation occurs in adults during the working years from ages 30 to 55 (Spangfort, 1972). The onset of symptoms may be acute, subacute, or chronic, and the relationship to a single lifting incident may not always be obvious (Berquist-Ullman and Larsson, 1977). Symptoms and physical findings depend on the location of the disc herniation and the degree of nerve compression.
Interesting observations regarding the tissue origin of low-back pain in surgical patients were made by Kuslich et al. (1991). The authors reported the results of 193 surgeries performed for lumbar disc herniation or spinal stenosis. The surgeons used a technique called "progressive local anesthesia" wherein tissue was infiltrated as the operation proceeded and was based on the individual's requirement for pain control. Patients were either fully awake or lightly sedated. This afforded the opportunity to stimulate successive tissue using mechanical force of blunt surgical instruments or by application of low voltage electrical current. Pain was rated on a 0 to 5 analog scale and patients were asked if the intensity and location of their pain were similar to the preoperative discomfort. Local xylocaine was used to control any residual pain that persisted after cessation of tissue stimulation.
The authors' observations were that stimulation of compressed, swollen, or stretched nerve root commonly produced sciatic pain that was similar to the characteristics noted before surgery. Similar results were noted at the caudal dura, nerve root sleeve, ganglion, and the nerve distal to the ganglion. In patients who had undergone prior laminectomies and who developed perineural fibrosis, the scar tissue was not sensitive, but the adjacent nerve root was. In contrast, the author reported that normal, uncompressed, or unstretched nerve roots were generally not tender, and forceful retraction more commonly produced only mild paresthesias. Stimulation of the annulus fibrosus produced no pain in one third, and moderate to severe pain in the others. Most often, central low-back pain was again similar to preoperative pain. Similar findings were noted with stimulation of the posterior longitudinal ligament. The author questioned whether variations in innervation of the annulus could account for these findings. In cases where there was tight lateral stenosis, the joint capsule of the superior articulating facet was frequently observed to contact the posterior surface of the disc, and stimulation at this point produced low-back pain. Pressure or currettage of the vertebral endplate resulted in deep, severe low-back pain, though usually different than preoperative pain. Of significance, the authors suggested that other tissues such as muscle, lumbar fascia, ligamentum flaum, lamina, and spinous processes were not significant causes of sciatic-type low-back pain.
In another experimental study by Smyth and Wright (1958), patients undergoing lumbar discectomy had silk threads placed around the lumbar nerve roots and out through the skin. Postoperatively, the threads were manipulated to place tension on the nerve roots. Radicular pain was perceived by individuals who had manipulation of previously compressed nerve roots. However, only paresthesias were experienced when this was performed on non-compressed nerve roots. The findings are in agreement with Kuslich et al. (1991).
Several mechanisms have been proposed for the development of nerve root pain, including mechanical deformation, compression, ischemia, and inflammatory mediators. There are few experimental studies regarding the effects of spinal nerve root compression; however, it appears that the spinal nerve root may be more susceptible to compression than peripheral nerves (Olmarker and Rydevik, 1991). In an in vivo experiment on the porcine cauda equina, a plastic balloon was fixed over the spinal canal and compression was induced by inflating the balloon (Olmarker et al., 1989a, 1989b, 1990a, 1990c). While arterial flow to nerves did not cease until pressures approached the mean arterial pressure, venous flow stopped at relatively low pressures of between 5 and 10 mm Hg. The resultant compression-induced retrograde stasis of capillaries and impaired nutrient transport from the cerebrospinal fluid may lay the foundation for tissue changes responsible for pain genesis (Olmarker et al., 1990c; Rydevik et al., 1990). For example, compression may alter the permeability of the endoneurial capillaries supplying the nerve roots, resulting in intraneural edema, increased endoneurial fluid pressure, and impaired nutrition of the nerve roots (Low and Dyck, 1977; Low, Dyck, and Schmeizer, 1982; Lundborg, Myers, and Powell, 1983; Myers et al., 1982; Olmarker, Rydevik, and Holm, 1989a; Rydevik, Myers, and Powell, 1989).
The more rapid the onset of compression, the more significant the disturbance of nutritional transport, vascular permeability, and nerve impulse conduction that will occur at any given level of pressure (Olmarker et al., 1989a, 1990a, 1990c). In addition, it appears that nerve root compression at two levels ("double crush") increases the damage observed with a single site of compression. This scenario could occur in an individual with multilevel disc herniation or when both spinal stenosis and disc herniation contribute to multiple areas of compression. Once spinal nerve compression is present for a sufficient period of time, there may be sufficient edema formation to affect the nerve root after the compression is relieved. Furthermore, the persistent edema may contribute to the development of intraneural fibrosis and chronic nerve injury.
Symptoms experienced in individuals with low-back pain from disc herniation compressing a spinal nerve depend on the location of the compression, the speed and duration of compression, and the types of affected nerves. Neuromuscular hyperfunction could produce pain, hyperesthesias, and muscle fasiculations. Alternatively, there may be loss of motor (e.g., weakness), sensory (e.g., numbness), or reflex function.
Inflammatory and Chemical Mediators
Inflammatory and chemical mediators have also been implicated in the etiology for low-back pain (Bobechko and Hirsch, 1965; Diamant, Karlsson, and Nachemson, 1968; Marshall and Trethewie, 1973; Marshall, Trethewie, and Curtain, 1977; Nachemson, 1969). Proposed mediators include lactic acid, pH, substance P, bradykinin, cytokines, prostaglandins, and carageenan, among others. Signs of inflammation have been observed in compressed nerve roots (Lindahl and Rexed, 1950; Marshall and Trethewie, 1973), although human specimens are limited due to ethical constraints of obtaining tissue samples during interventional surgery. The generation of noxious agents could account for some circumstances where radicular low-back pain is noted with a lumbar disc herniation, yet there is an absence of disc material compressing the nerve root at the time of surgery. In this scenario, physical signs such as the straight leg raising test could result from sliding irritated meninges over a ruptured intervertebral disc. Epidural steroid injections have been utilized with some success to treat lumbar disc herniation with radiculopathy (Bigos et al., 1994; Bush and Hillier, 1991; Dilke et al., 1973; Mathews et al., 1987; Ridley et al., 1988), and reduction of inflammatory mediators may be the reason for improvement in symptoms. However, pain has also been noted to improve with injection of saline, perhaps from simple buffering effects (Snoek, Weber, and Jorgensen, 1977).
A.4.b Disc Anatomy and Biochemistry
The intervertebral disc is composed of two entities, the central nucleus pulposus and the surrounding annulus fibrosis. The nucleus pulposus is composed of water, collagen, and proteoglycans, and assists in the absorption and redistribution of compressive loads. The annulus fibrosus is a circular structure composed of collagen and hyaline cartilage. It contains alternating bands of angled fibers that resist tensile, shear, and torsion stresses (Chaffin and Andersson, 1991; White and Panjabi, 1990). Hyaline cartilage separates the intervertebral disc on both sides and anchors it to the adjacent vertebral bodies. The intervertebral disc is avascular, and the nutritional supply of the intervertebral disc is maintained via diffusion from blood vessels surrounding the annulus fibrosus and under the hyaline endplate cartilage.
Disc hydration is dependent on hydraulic permeability and mechanical pressure differentials (Chaffin and Andersson, 1991). Proteoglycans help the disc stiffen by absorbing water and holding it through osmotic pressure. Disc swelling is resisted by the tensile strength of the annular fibers, and by compressive forces resulting from body weight and muscle contraction. In response to loading that results from lifting or body segment motion, the disc adjusts its water content and becomes narrower. After the load is removed, hydraulic forces (osmotic force) permit rehydration (Chaffin and Andersson, 1991).
Solutes are transported to the disc through the cartilage endplates via molecular diffusion, assisted by the pumping action from spinal loading. The concentration of nutrients in the disc depends on diffusion characteristics of the disc matrix, disc thickness, contact area of the blood vessels, and cellular density. Damage to the cartilage endplates from repetitive loading can, therefore, result in abnormal diffusion of water and solutes with eventual mechanical implications for disc function (Erdil, Dickerson, and Chaffin, 1994). For example, loss of proteoglycans and degradation of proteoglycan molecules result in the loss of osmotic pressure in the disc with the eventual development of disc dessication and degeneration. This further compromises the capacity of the disc to withstand future loading (Erdil, Dickerson, and Chaffin, 1994). The lumbar intervertebral disc does normally weaken with age (Adams and Hutton, 1982; Perey, 1957). Early in life, the nucleus pulposus retains a water content as high as 85%. With aging, chondroitin sulfate is replaced with keratin, and the water content decreases to under 70% (Urban, 1996), thereby decreasing stiffness and ability to resist loading.
A.4.c Disc Biomechanics
Because of the lumbar spine anatomy, many manual materials-handling tasks (e.g., bending, twisting, reaching) require large spinal motions that are associated with small degrees of muscle shortening to move external loads. As a result, spinal structures (e.g., disc, muscle, ligament, and joint) are often exposed to relatively high forces (Chaffin and Moulis, 1969). To complicate matters, bending the lumbar spine in combination with lateral flexion or rotation involves additional action by antagonistic muscles, further increasing the compressive forces over bending without lateral flexion or rotation. Laboratory studies and biomechanical models have shown that most of the compressive, torsional, and shearing forces that the lumbar spine is subject to are transmitted through the intervertebral discs (Erdil, Dickerson, and Chaffin, 1994; Garg, 1992; Pope et al., 1991). These issues are discussed in Appendix II, but are briefly reviewed here in order to understand pathogenesis of lumbar disc disease.
Compressive force in the lumbar spine is directed in an axial direction through the spine and tends to flatten the intervertebral disc. It is primarily transmitted through the intervertebral disc, with the force dissipated in a radial direction through the nucleus pulposus and annulus fibrosus. Measurements of compression in the human lumbar spine using EGM and a direct pressure transducer demonstrate correlation with estimates from biomechanical models (Nachemson, 1969, 1981; Nachemson and Elfstrom, 1970; Nachemson and Morris, 1964). Lumbar facets bear as much as 20% to 25% of the compressive force in the lumbar spine (Garg, 1992), especially when the spine is loaded in extension or lordosis (e.g., lifting objects above shoulder height or carrying objects up a hill). Disc space narrowing from degenerative disc disease increases the distribution of compressive force on the facet joints as a result of the decrease in the distance between adjacent articulating surfaces.
Disc shear forces tend to pull adjacent vertebrae in opposite directions (e.g., one anteriorly, one posteriorly). It occurs when the lumbar spine is in flexion, extension, or lateral flexion, and is primarily resisted by the annulus fibrosis and facets (Fiorini and McCammond, 1976). Shear and compression during lateral bending also depends, in part, on speed of movement (Marras and Granata, 1997). Once again, disc narrowing will increase the distribution of shear force to the facet joints (Fiorini and McCammond, 1976; Garg, 1992).
Torsion occurs when there is twisting motion of adjacent vertebrae (e.g., one vertebra moves clockwise and the other counterclockwise as in a circumstance where an individual rotates while lifting). With torsional stress, one side of the annulus stretches and the opposite side relaxes. Resistance to torsion comes primarily from the annulus (40% to 50%) and facets (40%) (Farfan et al., 1970). Torsion produces the majority of its load concentration through the posterolateral aspect of the intervertebral disc, which, significantly, is the site of most disc herniations (Hickey and Hukins, 1980).
Different manual materials-handling tasks such as those often performed at work have unique characteristics, resulting in a variation in the nature and proportion of forces to which each spinal element is exposed. For example, handling loads distant from the lumbar spinal axis, and above and below hand height, increases compression. Lumbar flexion in the neutral plane, by itself, further increases disc loading. Lateral flexion and axial rotation of the lumbar spine increases antagonistic muscle activity, and likewise further increases disc compression. This is consistent with observations that the combination of lifting, twisting, and bending is one of the most frequent causes for low-back pain (Andersson, 1981; Kelsey et al., 1984; Rowe, 1983). As noted before, when the lumbar spine is loaded in an extended position, a higher proportion of compressive force is transmitted through the facet joints (Garg, 1992).
Dynamic lift characteristics are significant considerations for low-back pain pathogenesis. Sudden maximal lifting effort and unguarded movements appear to be risks for developing work-related low-back pain (Magora and Schwartz, 1976). Knowing the load weight before lifting appears to affect lifting technique and disc forces. In a laboratory setting, Butler et al. (1993) asked subjects to lift boxes containing weights from 0 to 30 kg with and without knowing the box weight prior to lifting. Lifting the unknown box with no weight resulted in a jerk-like motion and significantly increased peak flexion -- extension load moment at L5-S1 as compared to the known box. As the weight in the box increased, less difference was noted in lift technique. The authors suggested that box weights should be marked on the outside of containers to limit low-back injuries in lifting unknown weights.
Even static activities like sitting can cause increased intradisc pressure and increased posterolateral disc force distribution. Nachemson and Morris (1964) showed that intradiscal pressures in the lumbar spine of subjects was 35% greater than the pressure in the standing position. Nachemson and Elfstrom (1970) reported that intradiscal pressures with unsupported sitting equaled that with bending forward 20 degrees. When lumbar support is added to a chair, disc pressure decreases (Andersson et al., 1974). Chaffin and Andersson (1984) demonstrated increased myoelectric activity during sitting without a lumbar support as opposed to standing, suggesting that the load in the lumbar spine is greater in the unsupported sitting position. They postulated that lumbar supports decrease disc pressures in two ways. First, leaning back reduces the load on the lumbar spine when a portion of the body weight is transferred to the support. Second, lumbar supports help to maintain normal lordosis, thereby reducing deformation and corresponding disc pressure (Andersson and Marras, 1996; Chaffin and Andersson, 1991).
The pathogenesis of work-related lumbar disc disorders may be comprehended through an understanding of the effects of work activities on disc biochemistry and biomechanics. For ethical reasons the majority of observations on spinal tolerance have been derived from cadaver spines. However, in vitro and in vivo comparisons appear to validate these conclusions. There is a wide biologic variation in human disc and end plate tolerances (Brinckmann, Biggemann, and Hilweg, 1988) related to age, gender, genetics, prior injuries, and other factors. The maximum axial compressive force tolerated by the human cadaver lumbar spine has been measured by Brinckmann, Biggemann, and Hilweg (1988) to range from 2.1 to 8.8 kN (210 to 880 kg), with 30% fracturing at forces below 4 kN and 63% fracturing below 6 kN. Adams and Hutton (1982) studied cadaver discs from male subjects aged 22 to 46 years. The authors determined that most specimens could withstand an average of 10 kN on single loading prior to failure, usually at the end plate. In contrast, Bartelink (1957) noted that discs were fractured from forces ranging between 1.6 and 6.7 kN, with a mean of 3.1 kN. Characteristics of the disc and end plate appear to affect some of the strength of this unit. Biggemann, Hilweg, and Brinckmann (1988) and Brinckmann, Biggemann, and Hilweg (1989) performed a series of studies of compressive strength measurements on thoracolumbar vertebral spines. The authors observed that the ultimate strength of the vertebral segment was dependent on the density of the trabecular bone in the midplane as assessed by quantitative computed tomography (QCT) as well as the endplate area on CT. The lumbar intervertebral disc is generally weaker in older subjects (Adams and Hutton, 1982; Perey, 1957), and weaker in females than in males, in part due to the smaller force-bearing area (Kazarian, 1975). The wide inter-individual variation in tissue tolerance makes it difficult to assign a single value of compressive force against which to engineer jobs to prevent lumbar disc injury.
When mechanical failure occurs, it is generally through the cartilage endplates (Adams and Hutton, 1982; Armstrong, 1985; Brinckmann, Biggemann, and Hillweg, 1988; Erdil, Dickerson, and Chaffin, 1994) Disc height, spinal position, and frequency of bending appear to be risk factors. Creep results in loss of disc height, increased contact between load-bearing surfaces of the facet joints, diminished capacity to dissipate forces, and decreased ability of the spinal column to tolerate loading (Kazarian, 1975). Adams and Hutton (1982) observed maximal single loading tolerances of up to 10 kN; however, when the spines were flexed forward, 40% of discs prolapsed at an average of only 5.4 kN. Repeated lumbar spine loading can cause tissue fatigue with fracture at lower loads than the spine would tolerate for non-repetitive loading. Adams and Hutton (1985) determined that when repetitive loading was simulated, previously healthy discs failed at an average of 3.8 kN. Brinckmann, Biggemann, and Hilweg (1988) also noted fatigue and diminished tolerance with repeated loading of cadaver lumbar spine. The probability of fatigue fracture was related to both the number of load cycles and the compressive load used/ultimate compressive strength. This vulnerability may be due to progressive loss in height of the motion segment noted by the authors due to visoelastic deformation and creep resulting from repeated loading without sufficient periods of recovery. These studies support the clinical observation that the intervertebral disc is especially vulnerable when loaded in the flexed position or when subjected to repetitive loading. This becomes more significant when workers with lower tissue tolerance from prior injury, degenerative disc disease, or age lift at high rates for prolonged periods.
Intervertebral discs, if healthy, do not appear to fail (Erdil, Dickerson, and Chaffin, 1994; Garg, 1992). Cartilage end plate failure, commonly in the center of the vertebral body, is the apparent predecessor to failure of the disc itself (Armstrong, 1965; Hutton and Adams, 1982; Roaf, 1960). To demonstrate this, Brinckmann, Wilder, and Pope (1986) performed internal divisions on lumbar intervertebral discs from 25 human lumbar motion segments to simulate annular disease caused by a trauma or degenerative process. Under 1 kN axial compressive loading, a physiologic disc bulge was observed, amounting to less than 0.5 mm, but disc extrusion at the site of the annulus injury was not observed. This suggests that a radial injury to the annulus is not sufficient, by itself, to produce a clinically relevant disc herniation. Cartilage endplate damage and fragmentation of the disc material seem to be predecessors.
Armstrong (1985) noted that small microtears most often occur in the region of the posterior elements of the annulus fibrosus and cartilage end plates. As noted, these are the areas subject to the greatest spinal compressive forces (Gracovetsky and Farfan, 1986; Hickey and Hukins, 1980; Pope et al., 1991). With repeated lumbar spinal stresses and/or injuries, progressive microfractures in cartilage end plates and annular fibers (annulus fibrosus) may develop in the intervertebral discs (initially toward the center of vertebral bodies). This causes altered metabolism and fluid transfer with different mechanical behavior of the disc. Eventually radial tears result in the development of degenerative disc disease and/or bulging. As a result of this damage, the capacity of the lumbar intervertebral discs to tolerate further compressive loads during lifting is altered. When these smaller tears extend and form complete annular tears, the nucleous pulposis can protrude (disc herniation) (Farfan et al., 1970). Over time, sclerosis of cartilage endplates and altered disc loading can facilitate the development of facet arthropathy, osteophytic change, stenosis, or instability. Disc degeneration in combination with facet arthropathy may also lead to foraminal narrowing with resultant nerve compression and radicular pain. These observations are consistent with a cumulative trauma theory that could account for some types of low-back injuries and is supported by the research and opinions of other authorities (Erdil, Dickerson, and Chaffin, 1994; Pope et al., 1991; Yong-Hing and Kirkaldy-Willis, 1983).
While many individuals with degenerative disc disease are asymptomatic, individuals with greater degrees of degeneration are at risk for low-back pain. In one study (Vanharanta et al., 1987) 90% of subjects with severe disc degeneration experienced pain during discography, while only 23% of those without disc degeneration reported pain.
On the other hand, degenerative disc disease has been linked to aging effects, genetics, and cigarette smoking (Battié et al., 1995; Boden et al., 1990; Frymoyer, 1988). By ages 20 to 39, 34% of the asymptomatic population will have lumbar disc degenerative disease noted on MRI, and 56% of the asymptomatic population will have lumbar disc bulging on imaging, including CAT scan and myelography (Boden et al., 1990; Jensen et al., 1994; Modic et al., 1986; Wiesel et al., 1984). Nachemson, Schultz, and Berkson (1979) observed that disc degeneration does appear to increase with age; however, there may not be an association with mechanical property changes. Battié et al. (1995) performed an interesting retrospective cohort evaluation of lumbar spine magnetic resonance imaging in 115 male identical twins to assess the role of age and genetics in the manifestation of degenerative disc disease. Subjects completed an in-depth interview regarding occupational and leisure time physical loading, driving, and smoking. In the upper lumbar levels, heavier lifetime occupational and leisure physical loading was associated with greater disc degeneration (P = .055-.001), whereas sedentary work was associated with lesser degeneration (P = .006). Mean job code explained 7% of the variability, the addition of age explained 16%, and familial aggregation increased predictability to 77% of the variability. In the lower lumbar levels, univariate associations of lifetime occupational and leisure physical loading did not reach statistical significance. In the multivariate model, leisure time physical loading explained 2% of the variability, the addition of age explained 9%, and familial aggregation raised the explanation of variability to 43%.
Buckwalter (1995) suggested that age-related degeneration of intervertebral discs may result from declining nutrition, loss of viable cells and cell senescence, post-translational modification of matrix proteins and accumulation of degraded matrix molecules, as well as fatigue failure of the matrix. He feels that the most significant factor is decreasing central disc nutrition of the central disc with accumulation of degraded matrix molecules and cell waste products, which impairs cell nutrition, lowers pH, and further potentiates cell death.
Whole-body vibration, especially seated vibration, has been associated with the development of low-back disorders (Damkot et al., 1984; Frymoyer et al., 1983; Kelsey and Hardy, 1975; Bernard and Fine, 1997; Troup, 1988). Several mechanisms have been postulated. These include microfractures at vertebral endplates, vasospasm and decreased blood flow, tissue fatigue from mechanical overload and stretching of spinal structures, and ultrastructural changes in the spinal nerve root dorsal ganglion with biochemical alterations involving pain-inducing neuropeptides (Hansson, Kefler, and Holm, 1987; Hirano et al., 1988; Kazarian 1975; Keller, Spengler, and Hansson, 1987; McLain and Weinstein, 1994; Seidel and Heide, 1986; Seroussi, Wilder, and Pope, 1989).
Radiographic and pathologic changes have been noted in human subjects exposed to whole-body vibration (Frymoyer et al., 1980, 1983; Kelsey and Hardy, 1975; Kelsey et al., 1984; Pope et al., 1991; Tro Wilder et al., 1982). Christ and Dupuis (1966) evaluated radiographic lumbar spine findings in tractor operators. As the annual number of hours of operation increased, so did the prevalence of x-ray changes, with findings observed in 61% of operators driving under 700 hours per year, 68% of those who performed 700 to 1,200 hours of operation per year, and 94% of those driving over 1,200 hours per year. The study was weakened by the limited number of subjects, but other studies have reported similar associations of driving time, symptoms of low-back disorder and radiographic abnormalities of the lumbar spine (Fishbein and Salter, 1950; Seidel and Heide, 1986). Findings reported with increased frequency include reduced disc height, facet arthrosis, spondylosis, Schmorl's nodules, and spondylolisthesis. It has been pointed out that these studies have been retrospective, and some lack adequate controls (Hansson and Holm, 1991).
Unfortunately, many heavy equipment operators and fork truck drivers are exposed to a number of additional factors that increase disc stress, including seated postures, kyphotic postures, twisting, and whole-body vibration (Dupuis, 1994). This probably accounts for the premature onset of degenerative disc disease in these workers. The natural resonance frequency of the human lumbar spine in the seated position is in the range of 4 to 6.5 Hz (Wilder, Pope, and Frymoyer, 1982). This is similar to the vibration characteristic of many motor vehicles.
Whole-body vibration imposes several motions on the body and the spine, including impact, translation, and rotation. Within the natural frequency range, one animal in vivo study demonstrated that disc pressure and axial and shear strain from vibration can increase two to three times (Hansson, Kefler, and Holm, 1987). The significant increase of spinal loading from vibration in the natural frequency has the consequence of exacerbating the amount of disc shrinkage noted after simple sitting, and this has been demonstrated in human subjects using continuous measurement of the spine (Kazarian, 1975; Magnusson et al., 1990). As frequency increases within the range of 0 to 15 Hz, there is stiffening of the spinal structure noted in normal human subjects (Wilder et al., 1982). Shifting to positions of mild lateral spinal flexion transiently decreases stiffness, but this posture imposes other mechanical disadvantages, such as paraspinal and abdominal muscle fatigue (Wilder et al., 1982). Brinckmann et al. (1987) performed in vitro experiments and noted that repeated cyclic loading of vertebral bone reduced the strength of the material as opposed to single-load events. They suggested that the resulting endplate fractures were a possible mechanism of later disc injury and low-back pain. Vibration has additional effects upon the erector spinae muscles, with observations of greater myoelectric activity and fatigue (Seidel and Heide, 1986; Seroussi, Wilder, and Pope, 1989; Wilder et al., 1982). Johanning et al. (1991) observed that after 1 hour of exposure to whole-body vibration in subway operators, trunk muscle fatigue was experienced. Progressive muscle fatigue limits the ability of skeletal muscle to protect spinal structures. Additional spinal loading can also result when the muscle response diverges out of phase with the vibration input (Seroussi, Wilder, and Pope, 1989).
The physiologic result of vibration in the natural resonance frequency is structural failure that is first noted in the vertebral end plate, adjacent spongy bone of the vertebral body, and the intervertebral disc (Keller, Spengler, and Hansson, 1987). Hirano et al. (1988) demonstrated that blood flow decreased in the rabbit intervertebral disc exposed to in vivo vibration. Porcine intervertebral disc experiments have shown that solute transport is also disrupted (Holm and Nachemson, 1985). Both of these effects are likely to precipitate disc degeneration because of disturbed metabolic activity, as discussed earlier. McLain and Weinstein (1994) studied ultrastructural and neuropeptide changes in rabbit lumbar spine dorsal ganglion exposed to whole-body vibration similar to the amplitudes and frequencies of motor vehicles. On electron microscopy, the group exposed to vibration had more significant findings of nuclear clefting, mitochondrial, rough endoplasmic reticulum, and ribosomal changes relative to controls. The authors suggested that this may provide an anatomic link between the clinical observation of increased back pain and the biochemical alterations involving pain-related neuropeptides.
Information on the impact of controlling whole-body vibration in the workplace is limited. However, in a recent study, Johanning (1998) reported on a comparison between the subway systems in New York City and Munich, Germany. In Munich, an intervention program involving administrative reduction in operator cab time was combined with a behavioral program including exercise, back school, stress management, and diet. This resulted in a significant reduction in self-reported back symptoms. While one cannot attribute the entire reduction in low- back symptoms to the control of vibration, studies on the impact of back schools, stress management, and dietary counseling have not demonstrated conclusive findings regarding their ability to prevent low-back pain (Bigos et al., 1994).
Several studies have suggested a relationship between lumbar degenerative disease and work activities (e.g., heavy work, repetitive lifting, and vibration). This association has come from both radiographic and pathological evaluations in association with work histories. One difficulty in these evaluations is the observation that lumbar spine x-raychanges are common, occurring in about 40% of all low-back x-rays (Rowe, 1983). However, the relationship of many x-ray changes with symptoms of low-back pain is unclear (Andersson, 1981; Himmelstein et al., 1988; Magora and Schwartz, 1976; Rowe, 1963, 1969). Videman, Nurminen, and Troup (1990) noted an increase in vertebral osteophytosis in autopsy specimens from workers who performed heavy work. Of interest is that the heavier work exposures also were observed in association with increased rates of low-back disability. Riihimaki et al. (1991) performed a radiographic study of the lumbar spine in concrete workers and house painters. Lateral lumbar x-rays were obtained in 216 concrete reinforcement workers and 201 house painters aged 25 to 54 years. Disc space narrowing was noted 10 years earlier and spondylophytes 5 years earlier in the concrete workers. Risk ratios for the univariate effect of occupation on disc space narrowing was 1.8, and for spondylophytes it was 1.6. Potential cofounders such as age, prior back accidents, body mass index, and smoking had minimal effect. The authors concluded that heavy physical work with materials handling and postural loading enhances the degenerative process of the lumbar spine. Wickstrom, Nummi, and Nurminen (1978) evaluated degree of lumbar flexion, presence of pain, and x-ray findings of degenerative disc disease in 295 concrete reinforcement workers aged 19 to 64 years. These workers commonly perform work involving spinal loading in stooped postures. Radiographic evidence of degenerative disc disease was noted in two-thirds of the 110 individuals with restricted flexion and in one-third of those (n = 185) with normal flexion.
Kirkaldy-Willis (1983) described a pathophysiologic spectrum of changes that lead to the development of lumbar spine degenerative disease. In the first phase, there are early and mild changes in the posterior complex, with facet synovitis, joint effusion, capsular stretch, and thickening. Inflammed synovium may become entrapped in the joint between the cartilage surfaces and initiate cartilage damage. Meanwhile, the intervertebral disc develops some circumferential tears in the annulus fibrosus. Tears in the periphery have at least some potential to heal because of the proximity to vascularity, but these deeper tears lack this ability by virtue of their distance from blood flow or metabolic diffusion. As these circumferential tears enlarge, they develop into large radial tears. As a result, the nucleus pulposus begins to lose proteoglycan and exhibits structural changes with grade 1 or 2 degenerative disc disease. Loss of water and disc height as well as a decline in annular resistance can cause increased compression forces on the facets. Individuals may be asymptomatic or have vague low-back pain. However, due to the lack of nociceptors in the disc and facet joints (except the synovium), a significant degree of degenerative disease may occur before pain develops. Lumbar disc herniation may occur at this juncture with symptoms and signs or radiculopathy.
In the next phase, the posterior joint capsule and annulus fibrosus develops laxity and instability. The intervertebral disc progresses to grade 2 or 3 degenerative disease. It may be possible to detect instability on dynamic x-rays. Subperiosteal bone formation, calcification of the ligaments, and capsular fibers manifest as peripheral osteophytes and traction spurs (Dupuis, 1987) in an attempt to stabilize the motion complex (MacNab, 1977). If laxity predominates over repair processes, the degenerative spondylolisthesis (facet laxity) or retrolisthesis (disc laxity) may occur (Dupuis et al., 1985).
In the final phase, there is fibrosis of the posterior facet joints, loss of disc material (grade 3 or 4 degenerative disc disease), and progressive osteophyte formation (Wedge, 1983). This increases the load-bearing surface of the three-disc complex, although it decreases motion and results in increased stiffness. The repair process may create narrowing of the central canal (central spinal stenosis) from facet arthropathy, disc bulging, and hypertrophy of the ligamentum flavum. Lateral stenosis may also result from facet arthropathy and osteophyte formation adjacent to the neuroforamina. Spinal stenosis is a diagnostic entity that has only recently been described. A few patients have congenitally small spinal canals; however, most present with this type of acquired spinal stenosis secondary to longstanding degenerative disease. Most patients first become symptomatic after 50 years of age (Turner et al., 1992). By virtue of its long-term degenerative nature, spinal stenosis is not often considered a work-related disorder; however, patients with spinal stenosis may present with co-existing lumbar disc herniation or other degenerative changes that have been exacerbated by work factors.
B NECK DISORDERS
There are many similarities regarding the pathogenesis of neck and low-back disorders, although significant differences are present that reflect the different functions for these regions. As with the low back, neck disorders have been associated with several work factors, such as repetition, force, static loading, neck posture, and heavy work (Hales and Bernard, 1996; National Academy of Sciences, 1998; Bernard, 1997; Stock, 1991). While neck pain is not as frequent a cause of work absence as low-back pain, it does significantly contribute to morbidity in many working populations (Hales and Bernard, 1996; Bernard and Fine, 1997). To understand the mechanisms by which work causes or contributes to the genesis or expression of neck pain, a brief review of basic anatomy and observations regarding sources of neck pain is beneficial. Several reviews of cervical spinal anatomy, function, and pathology are available for additional information (Bland, 1994; Borenstein, Wiesel, and Boden, 1996; Jeffreys, 1993; Sherk et al., 1988; An and Simpson, 1994).
The majority of neck disorders involve soft tissues (muscle and ligament strains and sprains). More significant pathology results from disorders of the three-disc complex (the intervertebral disc and two facets). The latter may involve degenerative disc disease, disc herniation, osteoarthritic conditions, and cervical myelopathy. To understand how the performance of work causes cervical disc disease, cervical spine anatomy, disc biochemistry, and disc biomechanics will also be reviewed. With this foundation, pathogenic models are better appreciated.
Similar to the experience with low-back pain, neck pain is common. The lifetime prevalence of neck pain is estimated at 40% to 50%, with a 1-year prevalence of about 20% (Takala et al., 1982). Using a definition of 2 weeks of neck pain, the prevalence among men and women aged 25 to 74 years in the NHANES Survey II (1976 to 1980) was 8.2% (Praemer, Furner, and Rice, 1992). Chronic neck pain is estimated to be present in up to 9% to 10% of males and 12% to 14% of females (Makela et al., 1991; Revel et al., 1994). Individuals in the 4th to 6th decades of life have the greatest incidence of neck disorders (Makela et al., 1991; Praemer, Furner, and Rice, 1992).
With regard to work-related cervical spine disorders, the Quebec Spinal Study (1987) observed an annual incidence of over 0.1%. However, Bjorksten et al. (1996) reported a 68%, 3-month prevalence for neck pain in industrial workers performing unskilled tasks, more than double the rate in the general population. Certain jobs appear to have greater associations with neck pain than others, with the lifetime prevalence of neck and shoulder symptoms reaching 81% in machine operators, 73% in carpenters, and 57% in office workers (Tola et al., 1988). It must be understood that there may be an underestimation of work-relatedness of neck pain since the onset of pain may, at times, be delayed and the work relation uncertain.
It is estimated that 90% of patients with acute neck pain are improved within 2 months (Borenstein, Wiesel, and Boden., 1996). The Quebec Spinal Study (1987) series of individuals with work-related spinal disorders suggests that 74% recover by 7 weeks. A 10-year outcome study of patients with neck pain revealed that 79% had less pain and 43% were pain-free. However, 32% still experienced moderate or severe pain (Gore et al., 1987).
B.2 Anatomy and Sources of Neck Pain
The cervical spine is designed for less weight bearing than the lumbar spine (i.e., primarily the weight of the head), but mobility requirements are far greater. There are seven cervical vertebrae in the neck, which are bordered by intervertebral discs from the second space down to the thoracic spine, acting as shock absorbers and stabilizers. The posterior vertebral rings are composed of pedicles, laminae, spinous and transverse processes, and facet joints that enclose and protect the spinal cord and spinal nerve roots. The occiput (base of the skull) is at the superior (cephalad) end of the cervical spine, and the thoracic spine begins at the lower (caudad) end. Cervical vertebrae are smaller and more narrow than those in the dorsal and lumbar spine, due to the smaller load-bearing function. Vertebral body size increases progressively from the upper (C1 or first cervical vertebra) to lower (C7, or seventh cervical vertebra) end, as it does in the lumbar spine. The vertebral canal is widest at the atlantoaxial joint to accommodate the relatively large spinal cord at this level, and decreases in size to its narrowest dimension at the sixth vertebrae. In general, the size of the spinal canal is smaller in women than in men (Bland 1994). The transverse processes in the cervical spine, except at C7, are unique in having foramina traversed by the vertebral arteries on each side of the neck.
Anatomically, the two cephalad vertebrae (C1 and C2) are significantly different from the caudad vertebrae (C3 to C7). The first two vertebrae, the atlas and axis, have unique designs. The atlas consists of anterior and posterior arches with heavy lateral masses that bear the weight of the head and permit mechanical advantage to muscles that insert into the transverse processes. The atlantooccipital articulation permits neck flexion and extension but not rotation. There is no vertebral body at this level (C1), nor is there a groove in the transverse process for the spinal nerve. The axis (C2) has a long projection, called the odontoid, that is contiguous with the vertebral body and projects through the atlas. This arrangement permits the axis to pivot around the odontoid, with about 50% of cervical spine rotation occurring at the atlantoaxial articulation. Transverse cruciate, apical, and alar ligaments are the primary stabilizers at this level, and these structures resist further rotation.
The lower cervical vertebral (C3 to C7) are similar in design to each other, with a vertebral body width approximately 50% greater than the anterior-posterior distance. The upper surface of each vertebra has some concavity to it, and this geometry continues through to the uncinate processes, a bony protuberance at the posterolateral border of the vertebra, offering some resistance to disc herniation posterolaterally. The C7 vertebra is transitional between the cervical and thoracic spine. It contains a large spinous process and lacks a foramen in the transverse process for the vertebral artery. As noted, the spinal canal is at its most narrow dimension at about the C6 to C7 level. Pedicles in the lower cervical spine are short, and have superior and inferior articulations called the zygapophyseal joints. These facet joints in the cervical spine range from the C2 to C3 level to the C6 to C7 level. The joints have a surface area of about two-thirds of the intervertebral disc, and both their lax fibrous capsules and their orientations permit sliding movement in various planes. This arrangement, however, lacks the structural stability (resistance to displacement of one vertebra on the adjacent body) observed in the thoracic or lumbar spine. The fibrous capsules are lined with synovial tissue and the facet joints contain fibrocartilagenous menisci between the hyaline cartilage and articular bony surfaces. Joint capsules have greater innervation with pain and proprioceptive receptors than the thoracic spine or lumbar spine to assist in fine movement of the neck.
Cervical spine nerve roots are named for the pedicle above which they cross, so that the C6 nerve root exits at the C5 to C6 intervertebral discs. Dorsal nerve roots are generally much thicker than the ventral roots, due to the increased amount of sensory input. Intrathecal anastomoses exist, and may account for the dermatomal variations noted with nerve compression lesions in the neck. Caudal to the atlantoaxial articulation, the spinal nerve roots exit through an intervertebral foramen that is bordered by the vertebral body pedicles, facet joints; and posterolateral intervertebral disc. Neuroforamina generally decrease in size from C2 to C3 and from C6 to C7. Neck flexion tends to increase, and extension tends to decrease the dimensions of the neuroforaminae in the neck. Hypertrophic changes that develop in structures adjacent to the neuroforaminae may compress the nerve at these locations. Sympathetic nerve ganglia are located ventrally to the transverse processes.
The blood supply for the cervical spine is derived from the small central anterior spinal artery, collaterals from the vertebral arteries, and paired posterior spinal arteries. However, ischemia may contribute to symptoms and signs of cervical myelopathy and disc herniation.
In addition to the transverse cruciate, apical, and alar ligaments in the cephalad cord, there are other important ligaments in the cervical spine. Their major influence is probably at the end of range of motion (Monsey and Krag, 1994). The anterior longitudinal ligament (ALL) runs along the length of the anterior vertebrae down to the sacrum. It adheres to the vertebral bodies and loosely blends with the annulus fibrosus at each disc space. The biomechanical aspects of this anatomy probably account for the larger size of anterior osteophytes. The posterior longitudinal ligament (PLL) runs down the posterior surface of the cervical vertebrae to the level of the sacrum. In contrast to the ALL, it is firmly bound to the intervertebral disc and loosely adherent to each vertebrae. The PLL is three to five times thicker in the neck than in the lumbar spine and is also broader. The PLL to resist cervical disc herniation to some extent, although the lateral bands are weaker and more vulnerable than the central band. Thickening of the PLL in a neck with degenerative disease may contribute to compromise of the spinal canal. The ligamentum flavum assists in supporting the neck in the erect posture, and helps to limit motion of the zygoapophyseal joints. Supraspinous and interspinous ligaments traverse adjacent spinous processes, and assist with stability. Ligaments in the cervical spine are innervated with nociceptors, and may be a source of pain if deformed by postural abnormalities, excessive force, or loss of elasticity (Borenstein, Wiesel, and Boden, 1996; Konttinen et al., 1994).
The length and width of the cervical spinal canal varies with the position of the neck. As the neck moves from extension to flexion, the length of the anterior wall of the canal increases by 1.5 cm, and the posterior wall increases 5 cm (Bland, 1994). The spinal cord is displaced in a cephalad direction as the neck flexes, placing increased tension on the nerve roots. With extension of the cervical spine, there is mild narrowing of the spinal canal and thickening of the spinal cord. Narrowing results from two mechanisms. First, the PLL and ligamentum flavum are lax in extension, causing infolding of these structures. Second, in extension, the sliding of one vertebra on its adjacent body causes the posteroinferior margin of the cephalad vertebra to move 1 to 2 mm into the spinal canal.
Support for the head and movement of the neck are accomplished by paired lateral groups of muscles attached to the skull, spinous, and transverse processes. Balance of the skull results from counteracting deep anterior and posterior muscles. Anteriorly, these muscles are attached to the anterior arch of the atlas and the midline of the vertebral bodies. This provides resistance to sudden extension. Anteriolateral muscles primarily provide neck flexion and rotation. Posteriorly, these muscles attach to the occiput and provide extension and balance with smaller contributions to rotation and lateral flexion.
Specific neck muscles merit discussion. Anteriorly, the sternocleidomastoid muscles run from the sternum and clavicle to the mastoid, providing flexion and rotation. The paired longus colli muscles run from C1 to T3, with lateral attachments to the anterior tubercles that permit neck flexion. Paired scalene muscles assist in stabilizing the neck against lateral movement. The trapezius muscle is the most superficial posterior muscle, and is commonly divided into three different muscle portions (descending, transverse, and ascending), based on the direction of the fibers. This expansive muscle originates from the spinous processes of C2 to T12 and the occipital protuberance, and inserts on the scapula, acromion, and clavicle to provide neck extension and stabilization and elevation of the scapula. The trapezius muscle has been cited as a source of pain in many studies of work-related neck pain. The levator scapulae elevates and rotates the medial scapula. Spinal extension is accomplished by intermediate-level splenius muscles running from the spinous processes of the lower cervical and upper thoracic spine to the transverse process of the upper cervical spine and mastoid. Deep erector spinae muscles from the thoracolumbar spine also contribute to extension.
There are several potential sources of work-related neck pain. In addition to the muscles, ligaments, and joint capsules, sensory nerve innervation is present at the anterior and posterior longitudinal ligament, the outer third of the annulus fibrosus, and the anterior vertebral body (Bogduk, 1982; Bogduk, Windsor, and Inglis, 1988). These will be explored in the following sections.
B.3 Soft Tissue/Mechanical Neck Disorders
There is a high degree of coordination required to support the head while enabling the neck to make precise movements and permit visual, auditory, and vestibular systems to function adequately (Cailliet, 1991). Therefore, muscles in the neck are more innervated and have more proprioceptive receptors than muscles in the thoracic or lumbar spine. The adult head may weigh up to 10 to 15 pounds, and by itself, results in spinal loading. However, many hand-intensive jobs and tasks require static neck contraction to permit accuracy in task performance. Thus, significant muscle stress and fatigue may occur with maintenance of static neck postures required in many office and assembly workplace settings (Hales and Bernard, 1996; Bernard and Fine, 1997; Onishi, Sakai, and Kogi, 1982; Stock, 1991; Westgaard and Bjorklund, 1987). In confirmation of this postulate, several EMG studies have documented the increase in neck and upper back muscle activity from static work (Erdelyi et al., 1988; Onishi, Sakai, and Kogi, 1982; Schuldt et al., 1987). Postural extremes may also precipitate symptoms of neck pain in subjects exposed to this risk factor, and this has been observed epidemiologically and experimentally (Burastero et al., 1994; Chaffin, 1973; Hales and Bernard, 1996; Harms-Ringdahl and Ekholm, 1986; Harms-Ringdahl et al., 1986; Kumar, 1994). Some intervention studies have suggested that workplace modifications may decrease both symptoms of neck pain and/or muscle activity as recorded by EMG (Aarås, 1994a; Aarås et al., 1998; Schuldt et al., 1987). Nakanno (1994) and Bland (1994) estimate that the neck normally moves 600 times per hour, and therefore it is understandable how muscle fatigue may easily occur in individuals who perform highly repetitive work, or who do not have sufficient ability to control the pace of work (Hales and Bernard, 1996; Bernard and Fine, 1997; Putz-Anderson and Galinsky, 1993; Stock, 1991; Veiersted, Westgaard, and Andersen, 1993; Wærsted and Westgaard, 1991). Finally, while epidemiologic studies regarding vibration and non-discogenic neck pain have been inconclusive, there is some evidence that vibration may affect muscle activity, and therefore could be pathogenic for neck disorders (Viikari-Juntura et al., 1994).
B.3.a Static and Dynamic Loading
Abnormalities in muscle function have often been observed in workers with neck/shoulder disorders. Muscle force, as previously noted, is often characterized using markers of muscle activity such as EMG. These signals are often evaluated as a percentage of the amplitude measured at maximum voluntary contraction (MVC). Some studies have documented different patterns of EMG activity in subjects with symptoms of work-related neck pain. Hansson et al. (1992) evaluated trapezius and deltoid muscle endurance time for a group of women with and without diagnoses of neck/shoulder disorders who performed industrial work with repetitive short-cycled work tasks, as well as a group of controls. EMG was recorded with surface electrodes from the trapezius and deltoid muscles during a static endurance test at approximately 20% of maximal voluntary contraction. Individuals who were diagnosed with neck/shoulder disorders had significantly shorter endurance than the group with the same work but without a diagnosis of neck/shoulder disorder, as well as shorter endurance vs. controls. The most pronounced sign of fatigue for trapezius was an increase in the root mean square values. The study points to a difference in those with and without symptoms, but does not conclude causation.
Although hands and forearms perform repetitive work, this may often present static loading to the neck and shoulders. For example, sewing machine operators perform highly repetitive finger and hand motion while manipulating garments through the machine. Westgaard and Bjorklund (1987) estimated that static loading on the trapezius in these workers was around 5% MVC. Onishi et al. (1982) studied female office workers using typewriters, computers, and calculating machines. Almost 60% of this group reported shoulder/arm pain and stiffness, increasing as the day progressed. Trapezius muscle MVC ranged from 10% to 30%, and the significant elevation was attributed to high keyboard height and the speed of operation.
Hagberg (1984) postulated three pathophysiologic etiologies for tension neck syndrome. These involve transient high local stress with eccentric contractions of shoulder muscles in unaccustomed workers; decreased blood flow from inadequate rest breaks and frequent contractions exceeding 10% to 20% MVC; and altered metabolic activity from long-term static muscle contraction.
Histochemical and pathologic muscle changes in association with abnormal blood flow have been observed in symptomatic subjects with chronic, localized neck/shoulder pain exposed to static loading during repetitive assembly work. Larsson et al. (1990) performed bilateral open muscle biopsies from the painful upper part of the trapezius. Pain was assessed and graded as the difference between the two sides. Muscle blood flow was recorded in the exposed muscle before biopsy, using a laser-doppler flowmeter. Myalgia appeared to correlate with a reduction in blood flow. There was additional correlation between the presence of reduced muscle blood flow and pathologic changes. Isolated pathologic ragged red fibers were observed in subjects with complaints of myalgia, with findings confined to type I fibers. It was postulated that the biopsy changes were the result of disturbed mitochondrial function.
In a follow-up cross-sectional study of women with and without symptoms of neck tension syndrome who were engaged in assembly work with static muscle loading of the shoulder muscles, histochemical examination of the trapezius muscle revealed morphologic changes of type ragged red fibers in 8 of 11 neck-pain cases and in 7 of 11 exposed controls (Larsson, Libelius, and Ohlsson, 1992). However, similar changes were noted in 4 of 10 unexposed controls. The authors concluded that the pathologic and clinical importance of ragged red fibers in the trapezius muscle noted in this study was uncertain. More recently, Wharton, Chan, and Packard (1996) evaluated muscle biopsies from patients with severe cervical spine disorders (primarily cervical spondylosis or rheumatoid arthritis requiring surgery) and compared the biopsies to samples taken from a control necropsy group without a history of neck pain. Pathological findings of ragged red fibers and increased type I cells was noted with increasing age. The authors questioned whether the findings of muscle pathology were contributors to the development and symptomatology of cervical spine disease with increasing age.
Lindman et al. (1991a, 1991b) performed muscle biopsies of the descending portion of the trapezius muscle on female patients with chronic trapezius myalgia and from healthy women. Symptomatic subjects had larger type I fibers and a lower capillary:fiber area ratio for type I and type IIA fibers, as well as lower levels of ATP and phosphocreatine in both type I and type II fibers. The authors suggested that an imbalance between the capillary supply and the cross-sectional fiber area of type I and type IIA fibers could be a factor in the development of trapezius fatigue and pain. As discussed earlier in the section on skeletal muscle, slower and less fatiguable type I muscle fibers are selectively recruited for low-force work because of their lower thresholds (Henneman and Olson, 1965). Yet, the sustained recruitment of these limited motor units may result in energy depletion of these contracting fibers, with eventual fatigue and injury (Lieber and Friden, 1994). The capillary imbalance and ATP and phosphocreatine depletion noted by Lindman et al. (1991a) could potentially be the result of fatigue that results from abnormalities of skeletal muscle recruitment. In a second study, Lindman et al. (1991b) looked at muscle fiber makeup and size in the descending, transverse, and ascending portions of the trapezius muscle in men and women. While the fiber types appeared similar in both groups, the mean cross-sectional area of the fibers in the female muscle was considerably smaller than in men. The authors suggested that this finding may indicate a lower functional capacity in many women, and may be of importance in the development of neck and shoulder dysfunction in females.
Workplace interventions to mitigate static loading of neck muscles have been demonstrated to reduce pain, time out of work due to musculoskeletal problems, and EMG measured loading. Aarås (1994a, 1994b) evaluated users of video display terminals (VDTs) and assembly workers before and after ergonomic interventions consisting of changes in the workstations, tools, and work organization alterations. In assembly workers, mean static trapezius load decreased from 4.3% to 1.4% of MVC, and in VDT users, MVC declined from 2.7% to 1.6%. This was accomplished with more accessible tool placement and support for elevated arms. The median duration for sick leave resulting from MSDs dropped from 23 to 2 days per person/year. As a result of interventions, including the reduction in trapezius loading, the VDT operators also reported less intensity and duration of pain in the neck and shoulder region. The study design did not permit the determination of which intervention(s) were responsible for the decline in MVC and sick leave, but it does support the role of workplace ergonomics.
Schuldt et al. (1987) looked at the impact of arm supports on neck and shoulder muscular activity in seated workers. Ten skilled women workers performed simulated printed circuit board assembly in different sitting postures, with and without the use of loosely mounted, padded elbow supports or another device providing an adjustable, constant suspending force to the arm. Time-averaged and normalized surface EMG demonstrated a decline in neck and shoulder muscle activity with either aid. The authors suggested that elbow supports or arm suspension could be employed as adjunct technical aids in sedentary assembly work for individuals with cervical spine and/or shoulder pain.
There is a suggestion that once a clinical picture of chronic neck myalgia develops, abnromalities in physical exam and muscle function may persist despite long-term absence from the previous exposure to high static work load on the neck-shoulders. Alund, Larsson, and Lewin (1992) used electrogoniometric three-dimensional recordings of active neck motion to assess 21 female steel industry traverse crane operators with long-term sick-leave (range 1 to 8 years) due to chronic neck disability. The authors also considered case history and physical status. Controls consisted of working female crane operators having identical work posture and tasks and a group of working female clerks. Crane operators with chronic neck disability showed tenderness of the trapezius and levator scapulae muscles, short neck stature and impaired active neck motion range with reduced motion speed. The motion pattern, however, was unchanged.
B.3.b Piece Work and Pacing
As discussed earlier, skeletal muscle activity involves oxygen and energy consumption and metabolic end-product generation. Repeated damage from overuse without adequate recovery time for repair therefore has the potential to cause permanent structural damage to skeletal muscle (Armstrong et al., 1993). Thus, work pacing can reasonably be expected to affect muscle function in the neck. Froberg et al. (1979) compared female production workers performing piece work vs. salaried work. Piece work was associated with increased pain in the shoulders, arms, and back, accompanied by elevated excretion of adrenalin and noradrenalin. Unfortunately, financial incentives in piece workers may encourage workers to avoid pacing themselves in an effort to exceed production levels. Brisson et al. (1989) postulated that the biomechanical stressors involved with piece work performed by female garment workers in Quebec, and the time pressures imposed by their piece work, combined to account for observed disability from MSDs. The association was related to the number of years performing piece work, and was independent of age, smoking, education, and total length of employment. In addition, some researchers suggest that workers may ignore early warning symptoms of work-related MSDs (Arndt, 1985).
Veiersted, Westgaard, and Andersen (1993) noted fewer and shorter rest pauses (0.9 vs. 8.4 per minute) from trapezius muscle units in symptomatic subjects performing machine-paced repetitive packing work. It is reasonable to postulate that prolonged activation of small motor units at near maximal capacity may result in decreased blood flow, increased metabolite concentration, and pain.
Control of work pace by employees had a significant impact on the control of shoulder fatigue when tasks required repetitive arm elevation (Putz-Anderson and Galinsky, 1993). In this study, the ability to take unscheduled rest breaks limited the fatigue associated with high repetition and force output, and overall work capacity could be maintained without the development of musculoskeletal shoulder complaints.
Wærsted and Westgaard (1991) looked at the relationship between the length of the work day and the development of neck and back pain. Sick leave statistics of 408 sewing machine operators on full-time schedules (8-hour working day) were compared to those of 210 operators on part-time schedules (5-hour working day). The occurrence of sick leave due to musculoskeletal disorders was delayed by approximately 6 months in part-time workers, and the researchers recommended reorganization of work activities to counteract musculoskeletal injuries from repetitive work.
Posture has often been implicated as a factor in the development of work-related neck pain. Chaffin (1973) noted an increase in neck pain associated with the use of awkward neck postures even in the absence of additional external loads. This observation was confirmed by Harms-Ringdahl and Ekholm (1986). The authors evaluated ten healthy, seated individuals to determine whether maintained extreme flexion position of the lower-cervical, upper-thoracic spine would induce pain. These postures are adopted by some individuals in different work environments. Pain intensity and location were rated and recorded on a Visual Analogue Scale (VAS) and pain diagram. EMG activity was recorded for the splenius, thoracic erector spinae-rhomboid, and descending part of trapezius muscles. Neck and upper-back pain was experienced within 15 minutes, increased with time, disappeared within 15 minutes after the end of provocation, but was again experienced by nine subjects the same evening or next morning and lasted up to 4 days. EMG levels were low, but increased during provocation.
In a second study, Harms-Ringdahl et al. (1986) again observed neck pain persisting for 1 to 4 days after healthy subjects were exposed to prolonged extreme cervical spine postures (greater than 45 degrees flexion). Pain intensity related to both the duration of exposure and the calculated load moment induced by the weight of the head and neck, although muscle activity was generally low (mean of 2% to 4% of MVC). Using biomechanical and EMG evaluation, the author estimated a three-to four-fold increased load moment with flexion over 45 degrees. Neutral cervical spine postures were associated with lower extensor muscle activity. The author suggested that if these postures were maintained on a daily basis at work or in leisure time, it could account for some cervicobrachial disorders.
Thus, it appears that abnormal neck posture related to poorly designed work stations may promote persistent contractions of the posterior cervical muscles, resulting in fatigue. As a result, secondary muscles may be recruited, with greater potential for injury (Borenstein, Wiesel, and Boden, 1996).
Kumar (1994) observed increased neck pain and increased EMG activity in subjects using corrective lenses with raised computer monitors that required them to adopt postures with cervical spine extension. In another study, the introduction of intermediate focal length lenses to replace bifocals in VDT users reduced neck pain (Burastero et al., 1994). It was postulated that this resulted from less tilting of the back of the head to visualize the bottom of the screen through the lower portion of the bifocal lens. In addition, the level of visual and mental demand of VDT use may be an additional factor in the development of neck and shoulder MSDs. For instance, Wærsted, Bjorklund, and Westgaard (1991) indicated that VDT-based work tasks requiring higher levels of visual and mental demands, as opposed to pen and paper tasks, resulted in increases of upper trapezius activity. Eighteen subjects were evaluated while performing simple and complex reaction time tasks presented on a video display screen. Eight subjects consistently generated higher muscle tension in the complex tests, and the authors attributed this finding to increased mental effort required by the greater computational demands in the complex tasks.
Sauter, Schleifer, and Knutson (1991) noted increased arm discomfort with keyboard heights above the elbow. Bendix and Jessen (1986) demonstrated that lowering the placement of a keyboard resulted in a reduction of trapezius loading estimated by EMG. Erdelyi et al. (1988) studied the influence of elbow postural angle and arm supports on the electrical activity of upper trapezius muscle during keyboard work in healthy workers and subjects with shoulder pain. Trapezius muscle EMG activity (mean square root) declined with increased elbow angles. Electrical activity also decreased when subjects used arm supports (forearms at an angle of at least 100 degrees) while working. The authors concluded that while keyboard work consists mostly of dynamic contractions of the small muscles of the forearms and hands, continuous static muscle activity in the arm, shoulder, and neck muscles is required to maintain head-and-hand-adequate working postures. The two interventions evaluated were capable of decreasing trapezius muscle activity.
Winkel and Westgaard (1992) have estimated that optimal data entry positions are associated with loads in the 2% to 3% MVC range. The same authors (1992a) recommended that workers limit overhead or extended reach postures to 4 hours a day, with decreased times if higher levels of force are required. For continuous work, especially with high rates of repetition, low worker control, or limited task variation, the authors advised exposure times of 1 hour or less.
Tichauer (1966) looked at the impact of arm posture on trapezius stress. He noted that arm abduction to 40 degrees increased stress in the upper trapezius muscle eight times as much as when the arm was abducted to 20 degrees, and 64 times as much as at a 10 degrees angle.
As with the low back, whole-body vibration has potential to affect skeletal muscle and predispose an individual to work-related neck pain. Etiologies for this may include bursts of cyclic muscle contraction, muscle fatigue, decreased ability of fatigued muscles to protect spinal structures from loads, continuous compression and stretch of structures, decreased blood flow, and altered neuropeptides. However, epidemiologic studies to date are inconclusive regarding the relationship (Bernard and Fine, 1997). While studies by Magnusson et al. (1996) and Kelsey et al. (1985) suggest that driving is associated with neck disorders, it is uncertain whether vibration is the causative factor in their studies. Viikari-Juntura et al. (1994) observed an increased risk of cervical spine disorders in machine operators exposed to whole-body vibration from operation of heavy earthmoving equipment and longshoring. Odds ratios (OR), controlled for a variety of cofounders, were elevated in comparison to office workers when the authors looked at the development of moderate (OR 1.8) and severe (OR 3.9) neck problems over a 3-year follow-up.
B.4 Three-Joint Complex and Nerve Roots
B.4.a Brief Epidemiology and Theories on Etiologies of Pain
The age-specific annual incidence rate of cervical radiculopathy in the general population has been estimated to peak at 0.2% for the age group 50 to 54 years, with rates declining to approximately 0.1% in both the 35-to-39 and 60-to-64 year old age ranges (Radhakrishnan et al., 1994). Of these cases, 22% were due to disc herniation and 68% resulted from a combination of disc herniation and spondylosis.
Pain arising from cervical spine skeletal structures may potentially originate from many locations, since sensory nerve innervation is present in ligaments, joint capsules, the anterior and posterior longitudinal ligaments, the outer third of the annulus fibrosus, and the vertebral body (Bogduk, 1982; Bogduk et al., 1988; Hirsch, Inglemark, and Miller, 1963). Joint capsules, their synovium, and the adjacent vasculature have a high degree of innervation by both nociceptors and mechanoreceptors (Borenstein, Wiesel, and Boden, 1996; Konttinen et al., 1994). This assists in proprioceptive sensation and stabilization. There is an overlap in the innervation of these unmyelinated C nerve fibers from the posterior rami of many segments, and, therefore, pain localization after injury to these structures may not be precise (Borenstein, Wiesel, and Boden, 1996; Konttinen et al., 1994). However, in a study by Dwyer, Aprill, and Bogduk (1990), pain patterns from normal cervical zygapophyseal joints were determined in five volunteers by distending the joint capsule with injections of contrast medium. The authors reported that characteristic pain patterns were elicited that were of assistance in the segmental location of symptomatic cervical zygapophyseal joints. Ligaments also have nociceptive innervation, and experimental injection of hypertonic saline has assisted in the localization of pain (Kellgren, 1939). However, it is uncertain if pain from pure mechanical injury to zygoapophyseal joints or ligaments would be identical, since the experimental designs of these studies also introduced potential for pain to result from chemical irritation or the injection itself. The periosteum of the cervical vertebral body may be a source of pain, although some slowly progressive lesions may destroy a significant amount of bony tissue before they are recognized (Borenstein, Wiesel, and Boden, 1996). The anterior dura and the dural sleeves that surround the nerve roots as they enter the neuroforamina are richly innervated. Dural lesions may produce a deep, aching pain in the midline (Borenstein, Wiesel, and Boden, 1996). The annulus fibrosus only has innervation in the outer third of its fibers. Annular tears produce predominantly midline pain (Kuslich, Ulstrom, and Michael, 1991). The inner annulus fibrosus and nucleus pulposus have no nerve innervation, and, therefore, a significant degree of injury may occur without symptoms (Borenstein, Wiesel, and Boden, 1996; Pope et al., 1991). The spinal nerve roots are the source of pain when there is compression, ischemia, and inflammatory or chemical mediators that stimulate nociceptors. The reader is referred to the discussion in Section A.4 for further information.
B.4.b Disc Anatomy, Biochemistry, and Biomechanics
A review of lumbar spine disc anatomy, biochemistry, and biomechanics has been provided earlier. While there are many similarities between the lumbar and cervical spine, differences must be highlighted. Approximately one-fourth of the length of the cervical spine is composed of the intervertebral discs. In comparison to the lumbar spine, cervical discs are thinner, with relative thickening anteriorly accounting for the lordosis of the cervical spine. Cervical intervertebral discs are thickest at C6 to C7. There is no intervertebral disc between the atlas and axis (C1 to C2) interspace because of the unique anatomic design of this articulation. Each disc is bordered by cartilagenous end plates of the two vertebrae, and is contained more tightly than in the lumbar spine due to the concavity of the adjacent vertebrae. Historically, the annulus fibrosus has been reported to be composed of alternately slanting, concentric layers of fibrocartilagenous tissue and fibrous proteins that determine its biological properties in response to tension and loading (Bayliss and Johnstone, 1992; Bland, 1994; Borenstein, Wiesel, and Boden, 1996). These reports indicate that it is bound anteriorly and posteriorly by the ALL and PLL. Laterally, the annulus fibrosus blends with the periosteum. These anatomic characteristics, together with the bony resistance from the uncinate process and the lower loading of the cervical spine, make disc herniation less common than in the lumbar spine.
Recently, Mercer and Bogduk (1999) have questioned historical concepts of annulus fibrosus structure in the cervical spine. The authors studied cervical spinal columns from 12 human adult embalmed cadavers. Microdissection of the longitudinal ligaments and intervertebral discs was photographed to record the orientation, location, and attachments of collagen. The intervertebral disc appeared like a crescentic mass of collagen, anteriorly thick, and tapering laterally toward the uncinate processes. Posteriorly, a thin layer of paramedian, vertically orientated fibers was observed. The anterior longitudinal ligament appeared to cover the front of the disc, and the posterior longitudinal ligament appeared to reinforce posterior anulus fibrosus with longitudinal fibers. If confirmed, the biomechanical and pathophysiologic significance of this orientation will require additional investigation and consideration.
The annulus fibrosus is thicker anteriorly than posteriorly, and thins towards the internal nucleus pulposus (Borenstein, Wiesel, and Boden, 1996). The nucleus pulposus is located slightly anterior of center, and approximately 40% of the area of the intervertebral disc is taken up in it (Borenstein, Wiesel, and Boden, 1996). As with the lumbar spine, the nucleus pulposus in the cervical spine depends on its water-binding capacity to provide the ability to distribute compressive loads. The nucleus pulposus is composed of collagen fibrils in a mucoprotein gel. Proteoglycans are the major constituent of this mucoprotein gel, and are synthesized in chondrocytes. These proteoglycans consist of protein cores with attached chondroitin sulfates and keratin sulfate. Small glycoprotein links bind the glycoproteins to long hylauronic chains, providing the nucleus pulposus with water-binding properties (Bayliss and Johnstone, 1992). With age, there is a decline in proteoglycan synthesis in the nucleus pulposus (Bayliss and Johnstone, 1992). Proteoglycans lose their ability to bind with collagen, have a lower molecular weight, and have a greater amount of keratin (Borenstein, Wiesel, and Boden, 1996). By the age of 45 to 50 years, the nucleus pulposus becomes a fibrocartilagenous mass, similar to the inner layers of the annulus fibrosus (Borenstein, Wiesel, and Boden, 1996; Bland, 1994; Bland and Boushey, 1990). This affects the ability of the cervical intervertebral disc to imbibe water and dissipate compressive loads. Age-related disc changes appear to occur earlier in the cervical spine than in the lumbar spine. As such, patients with cervical radiculopathy due to disc herniation are somewhat younger than those with cervical spondylosis (Bland, 1994; Radhakrishnan et al., 1994).
The intervertebral disc is a relatively avascular structure, with no direct blood vessels capable of assisting in metabolic exchange after the age of 15 to 20 years (Borenstein, Wiesel, and Boden, 1996). Therefore, nutrition is via diffusion across the vertebral endplate. This limits diffusion of negatively charged sulfated molecules necessary for proteoglycan production. Decreased oxygen transport results in an increase in intradiscal lactate and lowered pH. The acidity of the environment negatively affects matrix synthesis and increases enzyme degradation. Overall, this leads to a lack of ability for the intervertebral disc to heal after injury (Eyre et al., 1988; Hampton et al., 1989).
Much of the current understanding of cervical spine biomechanics and stability comes from cadaver evaluations. Cervical spine function of the C1 to C2 complex differs from the C3 to C7 region. Approximately 23 degrees of flexion and extension, as well as 47 degrees of rotation occurs at the occipitoatlantoaxial complex (Dvorak et al., 1987; Penning, 1979; Werne, 1957). The remainder of flexion and extension as well as rotation and lateral flexion is distributed among the C2 to C3 to C7 to T1 intervertebral disc spaces (Monsey and Krag, 1994).
Cervical intervertebral discs assist in load displacement and sliding of adjacent vertebrae, and resist motion due to ligamentous and capsular attachments. As with the lumbar spine, disc pressures vary with posture. Additional biomechanical changes occur with changes in neck posture. During neck flexion, the anterior intervertebral disc is compressed, the posterior disc widens, force is displaced radially through the disc, there is separation and shear of the posterior elements, and the neuroforamina open (Monsey and Krag, 1994). The reverse occurs in extension. During lateral flexion, the neuroforamina closes on the side towards which the head bends. During flexion, extension, lateral flexion, and rotation, the load distribution in the neck is shared by the ALL and PLL, facets, and other ligamentous structures. Facets contribute a significant amount of resistance to shear and compression in the neutral position and to torsion in the flexed position (Borenstein, Wiesel, and Boden, 1996). Under pure compressive loads, the intervertebral disc is damaged prior to herniation of the nucleus pulposus. Abnormal torsional stresses applied to the neck have been proposed as the cause of radial and circumferential fissures in the annulus fibrosus that precede disc herniation. Asymmetry of the facets or intervertebral discs due to degenerative changes may intensify these torsional stresses, and, therefore, intervertebral discs may fail with lower degrees of loading and stress.
Several pathogenic mechanisms for disc herniation were reviewed in the previous sectionon the lumbar spine, and some of these may pertain to the cervical spine as well. However, as discussed, the cervical spine is significantly different from the lumbar spine in having greater mobility, but less mechanical loading. In addition, age-related changes in the nucleus pulposus appear accelerated in the cervical spine as opposed to the lumbar spine (Bland, 1994). The relationship between work exposures and cervical disc herniation is less certain than it is with lumbar disc herniation. Usually no clear antecedent history of trauma exists preceding the onset of symptoms of cervical radiculopathy. Radhakrishnan et al. (1994) observed an episode of trauma in 15% of their cases. Kelsey et al. (1984) attributed 23% of cases to a traumatic event. However, the absence of nociceptors in the nucleus pulposus and annulus fibrosus may permit a significant amount of damage to occur without the onset of pain, and, therefore, relatively minor amounts of trauma may permit a significantly damaged disc to herniate.
Extremes of neck posture are associated with other biomechanical changes in muscles, ligaments, and facets (Monsey and Krag, 1994). Therefore, biomechanical changes from excessive postural deviations and associated loading may be a mechanism of injury for the cervical intervertebral disc. Subsequent mechanical failure in the cartilage endplates could then occur as described by Adams and Hutton (1982), Armstrong (1985), and Brinckmann, Biggemann, and Hilweg (1988). Progressive microfractures in cartilage end plates and annular fibers could then cause altered metabolism and fluid transfer with different mechanical behavior of discs. Eventually radial tears could result in the development of degenerative disc disease and/or disc herniation in younger individuals (usually younger than 45 years old). Over time, sclerosis of cartilage endplates and altered disc loading can facilitate the development of facet arthropathy, osteophytic change, stenosis, or instability. Disc degeneration in combination with facet arthropathy may also lead to foraminal narrowing with resultant nerve compression and radicular pain. In addition, prolonged sitting or standing with abnormal postures, muscle atrophy in the neck, and abnormal disc motion resulting from intervertebral disc disease and narrowing has the potential to produce mechanical stress on joint capsules and trigger nociceptors in those structures (Borenstein, Wiesel, and Boden, 1996).
Wada et al. (1992) studied young rabbit spines to determine whether repetitive movement of the cervical spine could precipitate structural abnormalities similar to those associated with cervical spondylosis. The trapezius muscle was electrically stimulated to produce up to 200,000 cycles of repetitive flexion and extension. In comparison to controls, the repetitive loading resulted in more severe delamination of the annulus fibrosus in the lower cervical spine and early osteophyte formation at the same disc level. Of interest, significant degenerative changes were not observed in the nucleus pulposus. The study is significant, in that it provides some evidence that repetitive loading may play a role in the pathogenesis of cervical disc disease and spondylosis.
Another potential experimental animal model for cervical spondylosis was evaluated by Miyamoto, Yonenobu, and Ono (1991). Mechanical instability was surgically created in the mouse spine by detaching the posterior paravertebral muscles from the vertebrae, and resecting the spinous processes and supraspinous and interspinous ligaments. The researchers noted an acceleration of intervertebral disc degeneration, with varied pathologic findings in the cervical intervertebral discs of this experimental model: proliferation of cartilaginous tissue and fissures in the anulus fibrosus, shrinkage of the nucleus pulposus, herniation of disc material, and osteophyte formation.
Of significance, a few studies have observed an association between cervical and lumbar radiculopathy (Lawrence, 1969; Henderson et al., 1983; Radhakrishnan et al., 1994). In the population-based study of 561 patients from the Mayo Clinic, 41% had a prior history of lumbar radiculopathy (Radhakrishnan et al., 1994). Henderson et al. (1983) noted that 33% of the 736 patients surgically treated for cervical disc herniation had a prior history of lumbar disc operations. While occupation and estimates of spinal loading, postural deviations, or vibration were not studied, these associations raise the question of individual predisposition toward disc pathology.
Whole-body vibration, especially seated vibration, has been associated with the development of low-back disorders, (Damkot et al., 1984; Frymoyer et al., 1983; Kelsey and Hardy, 1975; Bernard and Fine, 1997; Troup, 1988). The role of vibration in the pathogenesis of cervical disc disease or spondylosis is uncertain, although some studies have suggested an association (Kelsey et al., 1984; Magnusson et al., 1996). Several mechanisms have been postulated, and potentially some or all may play a role in cervical spine disorders related to vibration. These include microfractures at vertebral endplates, vasospasm and decreased blood flow, tissue fatigue from mechanical overload and stretching of spinal structures, ultrastructural changes in the spinal nerve root dorsal ganglion with biochemical alterations involving pain-inducing neuropeptides, tissue fatigue from repetitive loading, and increased spinal loading from muscle fatigue (Brinckmann et al., 1987; Hansson, Kefler, and Holm, 1987; Hirano et al., 1988; Kazarian, 1975; Keller et al., 1987; McLain and Weinstein, 1994; Pope et al., 1984; Seidel and Heide, 1986; Seroussi, Wilder, and Pope, 1989; Wilder et al., 1982).
The relationship between performing work and developing cervical spine arthritis or spondylosis has not been clarified. In part, this is because there have been few studies of this subject. Furthermore, there is a lack of universal acceptance for the criteria (e.g., symptoms, signs, imaging) used to make this diagnosis. Finally, cervical spine degenerative changes are common. Schmorl and Jungham (#) have noted that 90% of males over age 50 years and 90% of females over age 60 years have radiologic evidence of cervical spine degenerative disease. The most commonly noted levels are C6 to C7 and C5 to C6. Boden et al. (1990) observed cervical spine MRI abnormalities in 19% of asymptomatic subjects: 14% of those who were younger than 40 years old and 28% of those who were older than 40. Of the subjects who were younger than 40, 10% had a herniated nucleus pulposus and 4% had foraminal stenosis. Of the subjects who were older than 40, 5% had a herniated nucleus pulposus, 3%, bulging of the disc, and 20% had foraminal stenosis. Narrowing of a disc space, degeneration of a disc, spurs, or compression of the cord were also recorded. The disc was degenerated or narrowed at one level or more in 25% of the subjects who were younger than 40 and in almost 60% of those who were older than 40. These data further support age as a contributing factor in cervical spine degenerative disease.
Two studies have looked at cervical spine x-ray changes in workers. Alund, Larsson, and Lewin (1994) looked at relatively young, male steelworkers who used grinding machines and who developed cervical spine impairment or required a job change because of neck pain. The workers were compared to other age- and sex-matched white collar workers from the same plant. High static loading and impact trauma to the neck and shoulders in steelworkers were associated with cervical spine disorders, including limited range of motion, speed of motion, and foraminal encroachment from cervical spondylosis. In contrast, Andersen and Gaardboe (1993) evaluated sewing machine operators, including a history, physical exam, and x-ray study. There was a poor correlation between the diagnosis of cervical syndrome and the presence of degenerative changes on cervical spine x-rays.
Pathogenesis of cervical spine degenerative disease has similarities to many other joint structures, although there are important differences. As stated, the cervical spine has a great deal more movement than the remainder of the spine. Rather than being subject to repetitive and impulsive loading, zygoapophyseal joints achieve much of their motion via gliding and sliding on adjacent structures (Bland, 1994). However, these zygoapophyseal joints in the cervical spine have fibrocartilagenous, meniscus-like structures that are capable of responding with proliferative changes (Bland et al., 1988). As with other joints, aging, repetitive motion, and some loading result in fissuring of the hyaline cartilage surfaces. This may be the result of a decrease in proteoglycan synthesis or enzymatic degradation. Gradually, the hyaline cartilage develops deeper and downward fissuring, larger erosions, and general thinning. In the cervical spine, the chondrocytes mitose and proliferate in areas of fibrillation or loosely textured matrix (Bland, 1994). The matrix may demonstrate some attempts at repair from the mitotic chondrocytes, but the repair is generally disorderly. Subchondral bone increases in density, followed by microfracturing and callus formation. New bone, called osteophytes, appear at the margins of the articular cartilage, and may protrude into the joint space or neuroforamen. If large enough, this may cause nerve compression. Unlike other weight-bearing joints, cystic rarefaction is uncommon (Bland, 1994). Similar osteophytic changes may occur as spondylotic bars either anteriorly, due to degenerative changes in the ALL, or degenerative posteriorly, due to changes in the PLL. Posterior spondylotic bars, especially if combined with hypertrophy of the ligamentum flavum, have the potential to compress the spinal cord, causing symptoms of cervical myelopathy. Anatomically, the C4 to C5, C5 to C6, and C6 to C7 intervertebral disc spaces are most commonly affected by osteoarthritis and degenerative disc disease.
C UPPER EXTREMITY
There has been a significant increase in the number of work-related MSDs of the upper extremity reported over the past two decades (Bureau of Labor Statistics, 199#). These include cases of tendinitis, tenosynovitis, epicondylitis, carpal and cubital tunnel syndrome, and other nerve entrapments, as well as sprains, strains, and other conditions. Several epidemiologic reviews have concluded that there is evidence that certain work factors or combinations of factors appear to cause or significantly contribute to the manifestation of upper-extremity MSDs (Hales and Bernard, 1996; National Academy of Sciences, 1998; NIOSH, 1997; Stock, 1991). These factors have been reviewed elsewhere in this document. Since a comprehensive review of pathogenic and pathophysiologic evidence associated with the multitude of upper-extremity work-related MSDs is beyond the scope of this document, a limited number of specific diagnoses are presented for discussion in the subsequent sections. These conditions have been chosen because of the significant body of cohesive epidemiologic, pathogenic, and biomechanical evidence that is available. The inclusion of these conditions in this document by no means suggests that they are the only upper-extremity conditions that appear to have associations with work activities, or that every case is work-related. Nor does the exclusion of any other conditions insinuate that there is no relationship between these disorders and work. When evaluating work-relatedness of MSDs, physicians and other qualified health professionals must make an accurate diagnosis, and consider epidemiological information, pertinent exposure data, and other relevant factors to arrive at an appropriate conclusion on causation. While pathogenic and pathophysiologic information is contained in the following sections, the reader is advised to consider other sources of information for conditions that are not included in the scope of this document.
C.2 Rotator Cuff Disorders
C.2.a Theories of Pathogenesis
There are multiple plausible theories for the pathogenesis of disorders of the rotator cuff. For purposes of this review, it is assumed that supraspinatus tendon tears and calcification represent endpoints of one pathological process as opposed to separate and unique endpoints. Mechanisms related to disorders of the rotator cuff complex with acute onset are excluded (e.g., strains, falls, dislocations). Comprehensive consideration of all potentially relevant factors (e.g., prior traumatic injury, congenital or acquired deformity, variations in normal anatomy, and work versus non-work physical activities) is beyond the scope of this review. It is possible, and probably likely, that combinations of these mechanisms are often relevant. In particular, compromised or inadequate repair of damaged collagen fibers within the avascular zone of the tendon is probably a factor in all cases.
The presence of a watershed or avascular zone in the supraspinatus tendon has been described and demonstrated by several investigators (Moseley and Goldie, 1963; Rothman and Parke, 1965; Rathbun and Macnab, 1970). It is believed that the avascular zone compromises the ability of the tenocytes within this portion of the tendon to repair damage to collagen fibers or their matrix. This impaired ability to repair the tendon implies that degenerative changes within this portion of the tendon will accumulate over time; therefore, the degree and progression of tendon degeneration will increase with increasing exposure to potential sources of injury, age, or both. Potential sources of injury to the tendon's collagen fibers or matrix may be ischemic, mechanical (impingement), or physiological (contractile load).
According to the ischemia theory, the function and viability of the tenocytes within the supraspinatus tendon are compromised because they are in an avascular zone; therefore, they are unable to sustain the normal structure of the tendon over one's lifetime. This lack of maintenance manifests itself as degenerative changes within the substance of the tendon. The positive correlation between the prevalence of spuraspinatus tendon degeneration and tears with age is consistent with this theory. It is not clear that task variables related to work are necessary in this pathogenetic model; however, Rothman and Macnab (1970) postulated that shoulder adduction with neutral rotation would subject this avascular portion of the tendon to pressure from the humeral head, thus "wringing out" the blood from this already avascular area. If this were true, the duration of shoulder adduction would probably be more important than the number of shoulder adductions.
Neer (1983) estimated that 95% of rotator cuff tears were the end result of impingement. Neer (1972) proposed that the subacromial bursa and supraspinatus tendon were mechanically impinged on the underside of the anterior aspect of the acromion process or coracoacromial ligament as the shoulder approached 80 degrees abduction or flexion when internally or externally rotated. Below 80 degrees flexion or abduction, the greater tuberosity of the humerus is generally not in immediate contact with the acromion process or the coracoacromial ligament. Beyond this degree of elevation, the humeral head is displaced down and away from the acromion and the ligament, thus relieving these structures of this contact stress. This contact stress is postulated to cause disruption of collagen fibers within the tendon mechanically. This mechanism of collagen disruption may (or may not) be combined with the phenomenon of impaired healing related to the avascular zone. The critical relationship between this proposed model of supraspinatus tendon disease and biomechanical task variables is the passage of the shoulder through the 80 degrees abduction or flexion arc. Since this biomechanical stress occurs in a limited portion of these arcs, it is anticipated that the number of times the shoulder performs this task (per unit time) is more relevant than the duration of time the shoulder is in this position. Anatomical variations in the size and shape of the acromion (particularly type II [curved] and type III [hooked]) as well as hypertrophy of tissues related to the coracoacromial arch are also important factors. (Bigliani et al., 1991; Fu, Harner, and Klein, 1991)
Static Tensile Loading
Using EMG, several investigators have demonstrated that the supraspinatus muscle is activated throughout most of the range of motion of the shoulder. Herberts and Kadefors (1976) and Herberts et al. (1984) postulated that the level of tension in the supraspinatus muscle during arm elevation (with or without holding an object in the hands) was sufficiently high to increase intramuscular pressure to a point sufficient to compromise intramuscular circulation. As reported by Edwards, Hill, and McDonell (1972), intramuscular pressures of 20 mm Hg may be sufficient to prevent muscular perfusion. Since many of the blood vessels within the tendon are longitudinal extensions of the blood vessels in the muscle belly, reduced perfusion of the intramuscular blood vessels implies reduced perfusion of the intratendinous blood vessels. If this reduced perfusion is sustained for sufficient durations of time, the tenocytes or other tendon components are susceptible to ischemic injury. In terms of biomechanical task variables, experimental data suggest that overhead work may cause intramuscular pressures capable of reducing intramuscular perfusion. Lifting combined with arm elevation (shoulder load) also contributes to the magnitude of supraspinatus muscle activation. From a temporal perspective, this proposed model is more related to the duration of the intramuscular pressure than to its frequency.
C.3 Cubital Tunnel Syndrome
In general, Panas is credited with reporting the first case of tardy ulnar palsy at a presentation before the French Academy of Medicine in 1878. Murphy is credited for the first publication on this topic in the American literature in 1914 (Gay and Love, 1947; Feindel and Stratford, 1958a). These initial cases usually occurred in the context ofpost-traumatic complications, especially fractures in and near the elbow. In 1958, Feindel and Stratford reported the occurrence on ulnar nerve disorders at the elbow among three patients without distortion of the elbow joint or ulnar groove. These cases were unique for two reasons: sparing of the motor function of the flexor carpi ulnaris (FCU) and deformity of the ulnar nerve just beneath the aponeurosis joining the two heads of the FCU. This location was just distal to the ulnar groove at the medial epicondyle. Feindel and Stratford (1958a) coined the phrase "cubital tunnel" to describe this anatomical arrangement and "cubital tunnel syndrome" to describe the clinical condition. Buzzard and Osborner also described compression of the ulnar nerve at the aponeurosis joining the two heads of the FCU in this same time frame (Campbell et al., 1991).
According to Campbell et al. (1991), "cubital tunnel syndrome" was meant to refer to compression of the ulnar nerve by the humeroulnar arcade, but its use degenerated into a generic label for almost any ulnar neuropathy at the elbow. Campbell et al. no longer use the term cubital tunnel syndrome, but instead describe ulnar nerve lesions about the elbow as "retroepicondylar compression" or "humeroulnar arcade compression." They note, however, that distinguishing retrocondylar compression from humeroulnar arcade compression is not straightforward.
Some authors feel that cubital tunnel syndrome is the most common form of ulnar neuropathy at the elbow (Eisen and Danon, 1974; Miller, 1979). Others report that retroepicondylar compression is more common (Campbell et al., 1991).
The ulnar nerve originates from the medial cord of the brachial plexus (C8 and T1 nerve roots). It travels adjacent to the brachial artery and vein in the upper arm between the coracobrachialis laterally and the triceps posteriorly. At the insertion of the coracobrachialis near the middle third of the humerus, it separates from the neurovascular bundle, pierces the intermuscular septum, and travels posteriorly along the medial head of the triceps. According to Spinner and Kaplan (1976), the arcade of Struthers is present in 70% of the population and crosses over the ulnar nerve 8 to 10 cm proximal to the medial epicondyle. At the medial epicondyle, the ulnar nerve enters a fibro-osseous canal formed by the ulnar groove, the ulnohumeral ligament, and the FCU aponeurosis extending from the olecranon to the medial epicondyle. At or just proximal to the FCU aponeurosis, the ulnar nerve gives off its branch for the FCU. Further distally, the ulnar nerve gives off branches to the medial half of the flexor digitorum profundus (FDP) (to digits IV and V). At the elbow, the motor fibers for the intrinsic muscles of the hand and the sensory fibers are most vulnerable to compression because they lie superficial in relation to the FCU and FDP motor fibers (Wadsworth, 1977; Sunderland, 1978).
Campbell et al. (1991) dissected 130 cadaver elbows and explored 14 surgical cases to describe relationships between the ulnar nerves, medial epicondyles, olecranon processes, the humeral and ulnar heads of the origin of the FCUs, and the humeroulnar arcades. They measured the distance from a line joining the medial epicondyle and olecranon (called the epicondylar level) to the point where the ulnar nerve disappeared under the huneroulnar arcade and where the nerve exited the FCU distally. Typically, the humerulnar arcade was 1.0 cm to 1.5 cm distal to the medial epicondyle (range from 0.3 cm to 2.0 cm) for both cases and cadavers. In several specimens, it was noted to span directly between the medial epicondyle and olecranon as a straight line. The arcade was usually 1 cm to 2 cm in length (proximal to distal) with the fibers gradually merging with the muscle fibers of the FCU distally. The average thickness of the arcade was 1 mm to 3 mm. After passing beneath the humeroulnar arcade, the nerve traversed the substance of the FCU, exited the FCU muscle belly, then passed through the deep flexor pronator aponeurosis. The flexor-pronator aponeurosis lines the deep surface of the FCU and separates the FCU from the FDP and flexor digitorum superficialis (FDS).
Anterior subluxation has been reported to be present in 10% to 16% of the population (Apfelberg and Larson, 1973; Childress, 1975; Rayan, Jensen, and Duke, 1992).
Osborne (1957) noted that the aponeurotic band was slack with elbow extension, but taut with elbow flexion. According to Apfelberg and Larson (1973), the capacity of the cubital tunnel is greatest when the elbow is in full extension. Its capacity is reduced by 45% with flexion secondary to bulging of the medial collateral ligament (the floor of the tunnel) and stretching of the FCU aponeurosis (the roof of the tunnel). Campbell et al. (1991) confirmed the "dynamic anatomy" of the ulnar nerve reported by Apfelberg and Larson (1973) and Vanderpool, Chalmers, and Lamb (1968). They noted that the olecranon process moved forward during elbow flexion (approximately 5 mm of separation for each 45 degrees of elbow flexion) and that this increasing separation tightened the humeroulnar arcade, thus narrowing the cubital tunnel. Werner, Ohlin, and Elmqvist (1985) measured pressure at the cubital tunnel in 10 patients. On average, the pressure was 9 mm Hg (range: 0 mm Hg to 19 mm Hg) with elbow extension and 63 mm Hg (range: 2 mm Hg to 187 mm Hg) with elbow flexion. With concomitant electrical activation of the FCU, the mean pressure was 92 (range from 28 to 238) with elbow extension and 209 (range from 52 to 413) with flexion.
According to Abrams, Fenichel, and Callahan (1998), intact nerves, including the ulnar nerve, have a longitudinal in situ tension. In animals, blood flow is severely compromised when this strain exceeds 8% to 15% (Clark et al., 1992; Lundborg and Rydevik, 1973). Toby and Hanesworth (1998) used a microstrain gauge to measure strain at five locations along the ulnar nerve in relation to elbow posture in 20 cadavers. The five locations were 5 cm proximal and distal to the medial epicondyle; 2.5 cm proximal and distal to the medial epicondyle; and at the medial epicondyle. The strain gauge was inserted with the elbow at 60 degrees (0% strain). Elbow postures were 90 degrees, 120 degrees, and maximum flexion (approximately 150 degrees to 160 degrees). At the medial epicondyle, the average strains at 90 degrees, 120 degrees, and maximum flexion was 1.50%, 3.69%, and 5.77%, respectively. The strain at 90 degrees, but not 120 degrees, was significantly different from maximum flexion. When compared at maximum elbow flexion, the average strains at the five locations (from 5 cm proximal to 5 cm distal) along the ulnar nerve were 0.65%, 1.17%, 5.77%, 1.62%, and 0.22%. Compared to the average strain at the medial epicondyle, both proximal locations and the most distal location (5 cm) were significantly different. Based on maximum recorded strains at the medial epicondyle with maximum elbow flexion, cadaver specimens were sorted into three groups. The first group (n = 6, 30%) had no ulnar nerve strain under this circumstance. The second group (n = 9; 45%) had strains less than 10%. The third group (n = 5; 25%) had strains greater than 10%. Four of the specimens (20%) manifested subluxation of the ulnar nerve over the medial epicondyle with elbow flexion. Three of these four specimens exhibited no strain through the entire range of motion. The fourth specimen had a strain of 5% at the medial epicondyle at maximum elbow flexion.
Classically, four sites of compression have been described: the arcade of Struthers, the medial intermsucular septum, the cubital tunnel, and the deep flexor-pronator aponeurosis. Compression by the arcade of Struthers usually occurs 8 cm proximal to the medial epicondyle. Compression at the cubital tunnel is approximately 5 cm distal to the medial epicondyle.
Among surgical cases, the ulnar nerve is often reported to demonstrate gross deformities, such as the presence of a fusiform neuroma; swelling, edema, and hyperemia proximal to the cubital tunnel; and pale, narrowed, or flattened under the tunnel (Gay and Love, 1947; Osborne, 1957; Miller and Hummel, 1980; Chan, Paine, and Varughese, 1980).
The most common anatomical finding reported to be the source of compression has been the FCU aponeurosis at the entry of the cubital tunnel (Feindel and Stratford, 1958a, b; Osborne, 1957; Miller and Hummel, 1980; Macnicol, 1979). Ho and Marmor (1971) reported compression by a fibrous band proximal to the FCU aponeurosis.
In Macnicol's series of 110 nerves, 50 (46%) appeared constricted at the aponeurosis of the FCU ("Osborne's lesion"); 19 (17%) by a muscle (either the anconeus epitrochlearis or the hypertrophied medial head of the triceps); and 4 (4%) by a ganglion (Macnicol, 1979.) He also noted adhesions in 20 (18%); nerve dislocation in 8 (7%); and apparent stretching of the nerve over a post-traumatic deformity in 2 (2%). More than one lesion was considered significant in 20 (18%). No lesion was found in 25 (23%).
Brooks (1952) also reported five cases of ulnar nerve symptoms originating from the elbow related to ganglia arising from the medial aspect of the elbow joint.
Chan, Paine, and Varughese (1980) reported operative findings for their 235 cases: 141 (60%) reported constriction and swelling of the nerve; 61 (26%) had significant adhesions; 13 (6%) had no abnormalities; 3 had a ganglion cyst (1%); 5 (2%) had a stretched nerve over a deformity; 3 (1%) had loose bodies; and 3 had osteophytes (1%).
Gilliatt and Thomas (1960) reported that operative findings included thickened nerve with ganglio-form swelling behind medial epicondyle, constriction of nerve by fibrous origin of FCU with proximal neuromatous thickening, nerve broad and firmly adherent to the ulnar groove, neuromatous thickening, nerve surrounded by fibrous tissue, local constriction of nerve by deep fascia between olecranon and medial epicondyle.
Entrapment of the ulnar nerve by the deep flexor pronator aponeurosis investing the FCU distally was described by Amadio and Beckenbough (1986) and Campbell, Shani, and Pridgeon (1988). Compression at the FCU exit occurs approximately 4 cm to 6 cm distal to the epicondylar level and may be confused with cubital tunnel syndrome (humeroulnar arcade compression) (Campbell et al., 1991).
Epitrochleoanconeus muscle is an anomalous slip of triceps that runs directly from the medial epicondyle to the olecranon process. It may compress the ulnar nerve (Campbell et al., 1991). This muscle was present in 10.8% of 130 cadaver specimens and 7.1% of 14 surgical cases. Compression by epitrochleoanconeus ligaments was also reported by Feindel and Stratford (1958a), Lavyne and Bell (1982), and Shi-qing, De-hao, and Quan-shi (1986). Campbell et al. (1991) observed dense epitrochleoanconeus ligaments bridging directly from the medial epicondyle to the olecranon process in 4.6% of cadaver specimens.
Kojima, Kurihara, and Nagano (1979) reported marked constriction by the tendinous arch in 28 cases, mild constriction in 7 cases, and no compression by this arch in nine cases. Eight of the 44 cases manifested dislocation of the ulnar nerve. Anconeus epitrochlearis was present in three of nine cases. Ligament epitrochleoanconeus was noted in one. Pseudoneuroma was noted in 18 cases: proximal to tendinous in 15, proximal to postcondylar groove in 2, and both in 2.
C.3.d Descriptive Epidemiology
Based on a surgical case series, ulnar nerve entrapment at the elbow is generally more common among males than females (Gay and Love, 1947; Miller and Hummel, 1980; Chan, Paine, and Varughese, 1980; Gilliatt and Thomas, 1960; Kojima, Kurihara, and Nagano, 1979; Miller, 1979; Robinson, Aghasi, and Halperin, 1992; Seror, 1994; Kaempffe and Farbach, 1998; Seradage and Owen, 1998). Tsai et al. (1999) reported that 38% of their cases were male. Nathan et al. (1992) reported that 29% of their cases of ulnar neuropathy at the elbow (based solely on electrodiagnostic criteria) were male.
The mean age of cases varies from 38 to 59 years (range from 16 to 73 years) (Gay and Love, 1947; Chan, Paine, and Varughese, 1980; Macnicol, 1979; Gilliatt and Thomas, 1960; Miller, 1979; Robinson, Aghasi, and Halperin, 1992; Kaempffe and Farbach, 1998; Seradge and Owen, 1998; Tsai et al., 1999; Nathan et al., 1992; Buehler and Thayer, 1988; Stuffer et al., 1991). The minimum and maximum ages reported were 10 years and 84 years, respectively (Macnicol, 1979; Seradge and Owen, 1998).
Two authors have reported that the dominant arm is involved more than the non-dominant arm (Macnicol, 1979; Robinson, Aghasi, and Halperin, 1992); however, most have reported no such predominance (Gay and Love, 1947; Chan, Paine, and Varughese, 1980; Kaempffe and Farbach, 1998; Nathan et al., 1992). Seradge and Owen (1998) and Tsai et al. (1999) reported that the left limb was involved in approximately 50% of cases even though approximately 90% of cases were right-hand dominant. The condition is bilateral in 10% to 23% of cases (Gay and Love, 1947; Chan, Paine, and Varughese, 1980; Robinson, Aghasi, and Halperin, 1992; Nathan et al., 1992).
Concomitant orthopedic conditions are relatively common among patients with ulnar neruropathy at the elbow. Seradge and Owen (1998) reported the presence of ipsilateral thoracic outlet syndrome in 58 (36%) of their patients and concomitant ipsilateral carpal tunnel syndrome (CTS) in 71 (44%).
Tsai et al. (1999) reported that 97% of their cases had associated diseases of the upper extremities. Sixty-eight (89%) had CTS; 48 (63%) had pronator teres syndrome; 11 (14%) had shoulder impingement; and eight (10%) had thoracic outlet syndrome.
C.3.e Clinical Observations on Etiology
A significant percentage of cases have been reported to have no apparent etiology (idiopathic or spontaneous) (Macnicol, 1979; Folberg, Weiss, and Akelman, 1994). Estimates of this percentage include 12% (Gay and Love, 1947), 27% (Robinson, Aghasi, and Halperin, 1992), 59% (Stuffer et al., 1991), and 97% (Seror, 1994).
Occupations, Occupational Activites, and Workers' Compensation Benefits
Gay and Love (1947) reported the occupations of their 100 patients with tardy ulnar palsy. They reported that 24 (24%) were employed in agriculture, fishing, forestry, or mining; 21 (21%) in clerical and sales; 21 (21%) in service; 17 (17%) in professional and managerial; 12 (12%) in skilled labor; 5 (5%) in unskilled labor; and none in semiskilled labor. They concluded that the condition was not likely to develop in any particular occupational group. They reported one case postulated to be solely related to occupational trauma. It was an accountant who habitually rested his elbow on his desk. Protection of the ulnar nerve from this trauma and restorative exercises for the ulnar-innervated muscles facilitated recovery without surgery.
Robinson, Aghasi, and Halperin (1992) reported that 10 (45%) of their 22 patients were manual laborers. Gay and Love (1947) reported that four (4%) of their 100 cases involved occupational trauma of the elbow. Kaempffe and Farbach (1998) noted that 11 of their 27 patients (41%) received workers' compensation benefits. Seradge and Owen (1998) noted that 120 (75%) of their 160 surgical cases filed for workers' compensation benefits. Of these, 86 were "assembly line" workers and 11 had "intensely physical" jobs. Sixteen were employed in jobs that required less repetition, but lengthy periods of work with the elbows acutely flexed, such as dental hygienist or hair dresser. The age distribution among those filing for workers' compensation benefits was noted to be the same as non-workers' compensation group. In the series reported by Tsai et al. (1999), 28 (37%) were manual assembly line workers, 16 (21%) were heavy manual laborers; 18 (24%) were homemakers or office workers, 5 (7%) were retired or disabled, and work was undetermined in 9 (12%). The condition was considered work-related in 47 (62%). Nathan et al. (1992) reported that 62% of their cases had applied for workers' compensation benefits. In the series of 13 male cases reported by Buehler and Thayer (1988), 8 (62%) were white collar workers, 2 (15%) were heavy laborers, 1 (8%) was a dentist, and 2 (15%) were unemployed.
The list of etiologic conditions among the 100 cases reported by Gay and Love (1947) included old fracture of the elbow (57%); elbow arthritis (20%); unknown (12%); occupational trauma of the elbow (4%); congenital anomalies (3%); adhesions secondary to elbow injury (2%); elbow cyst (1%); and recurrent dislocation of elbow (1%). Among those with elbow arthritis, the arthritis was perceived to obliterate the ulnar groove, thus stretching and displacing the ulnar nerve, or directly irritating the nerve by spurs or loose bodies.
Stuffer et al. (1991) reported that the condition was idiopathic in 30 of 51 patients (59%); post-traumatic in 17 (33%), related to nerve subluxation in 3 (6%); and related to faulty positioning during surgery in 1 (2%).
Seror (1994) stated that 29 of his 30 cases (97%) had an idiopathic etiology and 1 (3%) had late-onset ulnar palsy. Six of his cases (20%) occurred after general anesthesia and 3 (10%) had undergone unsuccessful prior surgeries.
Robinson, Aghasi, and Halperin (1992) reported that 6 (27%) of their 22 patients were diabetic.
Miller (1979) noted the presence of a generalized polyneuropathy in 2 of his 9 cases (22%). He considered polyneuropathy a definite predisposing condition. In another case series, 2 of 12 patients (17%) had mild underlying neuropathy (one familial, the other idiopathic).
Of the 13 male patients reported by Buehler and Thayer (1988), 3 had a history of injury to the involved elbow, but none had clinical or radiographic evidence of arthritis. None had rheumatoid arthritis. Two had adult-onset diabetes mellitus, but no evidence of peripheral neuropathy. Four had a significant history of alcohol abuse. Two of these cases had bilateral disease.
No precipitating etiology occurred in over half of Macnicol's cases (1979). Childhood fracture was noted in 14 (supracondylar: 5; posterolateral fracture-dislocation: 1). Osteoarthritis was evident radiographically in 15, including 5 with history of previous fracture. Pressure on the elbow accounted for symptoms in 17 (15%). This included pressure during recumbency, after operation, or from prolonged leaning on the elbow. 4 in this group had subluxation of the ulnar nerve at the elbow. Another 4 with subluxation had no apparent cause. Definite cervical spondylosis was noted in 6; CTS in 4; and tennis elbow in 4. There was a vague collection of trauma in 6.
None of Miller's 9 patients (1979) had a history of leaning on their elbows, any history of trauma, or a history of recurrent elbow swelling or arthritis. Six were reported to be engaged in occupations such as assembly line worker, chef, carpenter, and sawyer that were perceived to require repetitive movements of the hands with the elbows flexed. One patient was a traveling salesman who noted that symptoms increased with prolonged elbow flexion.
According to Campbell et al. (1991), the relationship between subluxation of the ulnar nerve at the ulnar groove remains uncertain. Sunderland (1978) reported that the incidence of ulnar nerve subluxation was 17%. Campbell et al. (1991) reported subluxation in 18% of their cadavers and cases. They also noted that the observed difference in distance between the actual vs. the presumed normal course of the ulnar nerve was 15% to 20%. As a result, subluxation could result in under diagnosis of the ulnar neuropathy at the elbow.
Chan, Paine, and Varughese (1980) sorted etiologies by pattern of onset (acute, subacute, and chronic). Direct trauma was the only identified etiology for acute onset (n = 11; 6.5%). Subacute onset etiologies included anesthesia (n = 17; 8.5%); bedrest/bedridden (n = 17; 8.5%); occupational trauma (N = 6; 3%); elbow leaning (n = 6; 3%). For chronic set, there were 30 cases (15%) that were post-traumatic. Of these, 12 (6%) had arthritis, 12 (6%) had cubitus valgus deformity, and 6 (3%) had a fixed flexion deformity. 20 (10%) cases had gross osteoarthritic changes; 3 (1.5%) had rheumatoid arthritis; 3 (1.5%) had ganglion cysts; 4 (2%) had recurrent subluxation of the ulnar nerve; 5 (2.5%) had diabetes mellitus; 3 (1.5%) had chronic alcoholism; 9 (4.5%) had other etiologies, and 66 (33%) were idiopathic.
Seradge and Owen (1998) reported 1 case among 160 related to supracondylar fracture and "a few" reported hitting their elbows on a hard surface.
C.3.f Analytic Epidemiological Studies
No analytic epidemiological studies report evidence of association between work in general or workplace task variables in particular with ulnar nerve entrapment at the elbow.
C.3.g Historical Observations on Pathogenesis
Cubital Tunnel Compression
In the first half of this century, ulnar neuropathy at the elbow was generally believed to arise from traction and tensile forces in the nerve. This started to change in the 1950s. Osborne (1957) believed that tardy ulnar palsy was caused by compression, not traction or tension. This theory was supported by the observations of Apfelberg and Larson (1973). They postulated that the volume in the cubital tunnel decreased with elbow flexion and that this decreased volume caused compression and restriction of normal movement. Pechan and Juliš (1975) demonstrated that elbow flexion combined with wrist extension increased pressure in the ulnar nerve threefold. Fronek (1971) demonstrated that placing the hand behind the head also resulted in intraneural pressure six times higher than the pressure in the relaxed nerve.
Traction or Tension from an Altered Ulnar Groove
The ulnar nerve normally elongates 5 mm at the postcondylar groove during elbow flexion and is able to glide freely (Apfelberg and Larson, 1973). If the mechanics at the groove are altered, either after fracture or because of adhesions, then the nerve is no longer free to alter shape or position (Macnicol, 1979). Lundborg (1992) stated that compression of the ulnar nerve at the elbow can be the end result of a pathological process of chronic irritation due to its superficial position and its sliding through tight anatomical spaces (blunt trauma and traction). He postulated that inflammation and edema might result and, as a consequence, impair normal longitudinal excursion with elbow flexion, thus forming a vicious cycle eventually leading to chronic compression of the nerve.
The nerve may also be compressed at the FCU aponeurosis, by nearby fibrous bands, by hypertrophied muscle, or by ganglia or osteophytes (Macnicol, 1979).
Ulnar Nerve Dislocation
Kojima, Kurihara, and Nagano (1979) noted that dislocation of the ulnar nerve followed by friction neuritis was reported historically, but did not appear to be common. They argued against this theory of pathogenesis based on the facts that (1) dislocation is as uncommon among cases as in the general population and (2) dislocation typically occurs bilaterally, but ulnar neuropathy is generally unilateral.
Recurrent direct trauma or repetitive elbow flexion/extension may cause compression, traction, or friction of the ulnar nerve, as seen in baseball pitchers (Eaton, Crowe, and Parkes, 1980; Godshall and Hansen, 1971; Zemel, Jobe, and Yocum, 1991) or assembly line workers (James, 1956).
C.3.h Proposed Mechanisms of Pathogenesis
Several plausible pathogenetic models relate ulnar nerve entrapment at the elbow to acquired or congenital anatomical variations, systemic diseases, and other factors unrelated to physical activity of the upper limb.
In terms of physical activities, the clinical observations, pathology, and physiology suggest that ulnar nerve compression at the level of the cubital tunnel may be related to flexion of the elbow, with or without concomitant wrist extension. Physiological data suggest that the degree of elbow flexion to generate meaningful physiological or biomechanical stresses must be near maximal. At this time, there are no data on which to estimate the duration of time spent in elbow flexion or the number of times the nerve must be compressed secondary to elbow flexion to place individuals at increased risk of cubital tunnel syndrome.
Compression of the ulnar nerve at the cubital tunnel by hypertrophied FCU muscle-tendon units has been suggested in the context of athletes. The theory postulates that repeated forceful activity with the arm leads to FCU hypertrophy, which, secondarily, reduces the volume of the cubital tunnel and thus leads to cubital tunnel syndrome. The intensity, frequency, and duration of physical activity necessary to elicit this training effect is unknown.
The ulnar nerve may be compressed at the elbow in response to a single traumatic event.
C.4 Epicondylitis ("Tennis Elbow")
C.4.a Normal Anatomy and Kinesiology
There are three muscle-tendon units that primarily extend the wrist. They also contribute to deviation of the wrist. The extensor carpi radialis longus (ECRL) originates on the lateral supracondylar ridge of the humerus, the lateral intermuscular septum, and sometimes from the upper portion of the lateral epicondyle. It inserts on the dorsal surface of the base of the second metacarpal. The ECRL also contributes to forearm supination when the elbow is extended. The extensor carpi radialis brevis (ECRB) originates from the lateral epicondyle, from the common extensor tendon, and from the lateral intermuscular septum (often fused with the ECRL). It inserts on the dorsal surface of the base of the third metacarpal. Both the ECRL and ECRB also contribute to radial deviation moments about the wrist. The extensor carpi ulnaris (ECU) originates on the lower pole of the lateral epicondyle as part of the common extensor tendon and inserts on the medial side of the base of the fifth metacarpal. The ECU also contributes to ulnar deviation of the wrist. The aponeuroses of these tendons are located near, and perhaps in contact with, the orbicular ligament and the radial head.
There has been only one comprehensive description of the pathology of epicondylitis.
All other papers were derived from surgical case series that may or may not have included controls. No visible pathological process was noted in 6 (7%) (Nirschl and Pettrone, 1979). Among the 88 surgical elbows reported by Nirschl and Pettrone, a pathological lesion was noted in 82 (93%).
Spencer and Herndon (1953) reported that the deep fascia just distal to the epicondyle and the tendinous origin frequently appeared thicker and denser than normal, but noted no real gross abnormality. Nirschl and Pettrone (1979) described the gross appearance of the affected ECRB origin as grayish, immature scar tissue that appeared shiny, edematous, and friable; they also observed a lack of firm attachment of the ECRB to the epicondyle. They noted the presence of a tear or marked changes in the ECRB origin. Goldberg, Abraham, and Siegel (1988) reported no gross findings in 14 (41%) elbows; fibrous granulation tissue in 19 (56%); a bursa-like structure in 5 (15%); and an extra-articular loose body in 1 (3%).
Among studies that included controls, specimens were generally obtained from cadavers with no known history of tennis elbow (Doran et al., 1990; Regan et al., 1992). These specimens exhibited normal cortical bone, a clear interface with the fibrocartilagenous zone, and a smooth transition to tendon. In addition, these findings were generally consistent throughout the age range, i.e., there was no evidence of age-related degeneration. Isolated findings among controls included the presence of mucopolysaccharides in older specimens plus mild vascular proliferation (Doran et al., 1990; Regan et al., 1992). The most characteristic histological findings are:
Cyriax (1936) compiled a list of published opinions on the pathology of tennis elbow. His list included the following:
Cyriax (1936) compared his list of proposed pathologies to eight clinical aspects of lateral epicondylitis and narrowed the list to three possible etiologies. These included affections of bursae; nipped or inflamed synovial fringes; and tears of the extensor tendon from the bone and consequent periostitis. Overall, he favored periostitis as the most probable pathology. In particular, he stated that epicondylitis was primarily caused by a tear of the ECRB at its tendinous origin at the anterior aspect of the lateral epicondyle.
Meherin and Cooper (1950) stated that the etiology of tennis elbow was unknown except in cases explained by a bursa or an abnormality of the synovial fringe. They found no evidence of inflammation among cases and no evidence of tendon degeneration among controls. Histologically, they only reported increased ovoid or spindle-shaped cells and increased small blood vessels among cases compared to controls.
Wall (1960) believed that the condition involved the periosteum over the lateral epicondyle and the inserting fibers of the common extensor tendon, i.e. a fascioperiostitis with local edema and perhaps adhesion formation.
Goldie reported on a total of 58 surgical specimens obtained for studying the patho-morphology of the condition (Goldie, 1964). Gross observations at surgery revealed no bursae in any case; white floccular masses of amorphous material in 8 patients who had received cortisone injections; and aponeuroses that appeared to have a glossy surface and were richly vascularized, but had no ruptures, longitudinal splits, hematomas, or signs of necrosis. The subtendinous space was filled with granulomatous or fibrotic tissue. Pulling or nipping this tissue during surgery elicited the spontaneous mention of pain. An arthrotomy was performed in 5; none had an abnormality. Histologically, age appeared to have no bearing on the findings. Osseous structure was normal. The blue line appeared hazy and irregular in 35, but variability in its width was similar to controls. The tendinous insertion appeared smooth with collagen fibrils arranged in normal fashion. Staining for mucin, glycoproteins, and mucopolysaccharides failed to reveal positive findings. Splits between collagen fibrils, with occasional granulation tissue, were seen in 20 cases. The fibrocartilagenous zone near the cortical bone showed no abnormalities. There were no significant differences between cases and controls related to the appearance and number of cells in the tendon insertion zone. The most marked changes were noted in the aponeurosis, including fibrinoid degeneration (n = 11), suspected but not proven hyaline degeneration; granulation tissue within the tendinous tissue from the undersurface of the ECRB (n = 49). Collagen fibers had variable appearances -- some normal and some broken, coiled, swollen, and separated from each other -- and the myotendinous junction appeared normal. Free nerve endings were noted in the aponeurosis and granulation tissue. Assessment of the dry weight of aponeuroses from cases and controls suggested that the aponeuroses of controls were edematous. Overall, Goldie felt that hypervascularization of the aponeurosis, the presence of granulation tissue in the subtendinous space and aponeurosis, cellular invasion, and probably interfibrillar edema were the characteristic histologic features of lateral epicondylitis. Less constant findings included fibrinoid degeneration, calcium deposition, and fraying and fragmenting of collagen fibrils.
Newman and Goodfellow (1975) believed that fibrillation of the radial head was a major cause of the symptoms of tennis elbow. The term "fibrillation" denoted the appearance of the fibrous framework of the cartilage due to loss of ground substance. The term "chondromalacia" meant softening of the articular cartilage. When the orbicular ligament was excised and examined, it generally revealed degenerative changes with abnormal nuclei and mucoid degeneration.
Coonrad and Hooper (1973) described their series of 339 patients treated between 1952 and 1972. A tear of the extensor or flexor origin was observed in 28 (72%) cases. 22 (79%) of these were superficial; 6 (15%) were deep with a normal superficial surface. In 4 (10%), there were extensive avulsions. In 11 (28%), an actual tear was not demonstrated, but 9 of these had scar tissue replacement of tendon (by observation). In 2, there was no definite lesion other than minute calcareous deposits. Microscopic studies of the grossly torn margins of tendon were made (n = 28). The researchers noted round cell infiltration, scattered foci of fine calcification, scar tissue with areas of cystic degeneration, and fibrinoid degeneration. In the 9 cases without macroscopic evidence of a tear, the abnormal tissue in the aponeurosis adjacent to the epicondyle contained scar tissue similar to that seen for those with gross tears. In the 2 patients with no gross evidence of aponeurotic tear, there were macroscopic and microscopic foci of calcification at the epicondylar origin.
Hyperplastic synovium (Goldberg, Abraham, and Siegel, 1988), new bone formation at the bone-tendon junction (Doran et al., 1990; Chard et al., 1994), and degenerative changes with areas of fibrofatty change and elastosis have been reported in a minority of cases (Doran et al., 1990; Chard et al., 1994).
There has been no evidence of correlation between histologic appearances and history of prior steroid injections or outcomes from surgical treatment (Doran et al., 1990).
Doran et al. (1990) felt that their findings were consistent with microavulsion fractures at the lateral epicondyle and possibly tendon tears. They felt that the symptoms were due to a repair response rather than degenerative changes. Among the epicondylitis cases, 13 (65%) had glycosaminoglycan infiltration within the tendon close to the insertion; 6 (30%) had new bone formation at the site tendon insertion, but distinct from the normal transitional area of tendon insertion to bone; 4 (20%) had fibrofatty change; 4 (20%) had partial rupture of the tendon; and 2 (10%) had fibrocartilage formation within the tendon ± calcification. One (5%) specimen showed changes at the tendon attachment. Mild lymphocyte infiltration was noted for 1 (5%) case. Similar changes were noted in the cadaveric rotator cuff specimens, but the percentage of specimens exhibiting these changes were generally lower (7% to 18%). The researchers felt that the histological picture seen among patients with lateral epicondylitis was similar to the age-related changes seen in the rotator cuffs of cadavers with no known history of shoulder pain, e.g., fibrocartilagenous change with minimal to no inflammation. They postulated that the progression of these changes might start with blood vessel and fibroblast abnormalities, progress to deposition of glycosaminoglycan infiltration as the fibroblasts are unable to repair and replace tendon collagen, and continue with transformation of the fibroblasts to chondrocyte-like cells, with subsequent cartilage formation and attempted calcification. Wittenberg, Schaal, and Muhr (1992) described histopathological changes noted in 19 synovial specimens obtained from surgery for resistant cases of medial and lateral epicondylitis. Twelve (63%) demonstrated fibrosis, chronic irritation, and foreign-body reactions. Seven cases undergoing the Wilhelm procedure had scar formation, degenerative tissue changes, and reactive necrosis in the connective tissues and tendons. In no case was there active inflammation.
Maffulli et al. (1990) reported diagnostic ultrasonographic findings for 41 tennis players with tennis elbow. They determined the following lesions: enthesiopathy (5 cases; enlargement and altered echogenicity affecting the proximal part of the ECRB); tendinitis (15 cases; enlargement and loss of normal waveform structure of the main tendon of the ECRB with areas of dishomogeneous hypoechogenicity); peritendinitis (4 cases; thickening of the peritenon); bursitis (5 cases; a well-defined ovoid hypoechoic area located on the inferior surface of the ECRB tendon); intramuscular haematoma (7 cases; some circular or ovoid hypoechogenic areas within the muscular substance of the ECRB); mixed lesions (7 cases); and no ultrasonographic abnormality (3 cases). In 14 cases, the tendon of the ECRB appeared as a distinct anatomical structure.
Commandre and Valdener (1983) reported a single case of sudden onset of lateral elbow symptoms. Echotomography demonstrated a gap in the muscle(s) near the lateral epicondyle. They interpreted this as evidence of a tear within the muscle(s).
Coel, Yamada, and Ko (1993) studied 7 patients (5 males and 2 females ages 36 to 51 years) diagnosed by orthopedic surgeons as having chronic lateral epicondylitis and 3 controls using axial short tau inversion-recovery magnetic resonance (MR) images. Signal intensities were measured at the tomographic levels of the medial and lateral epicondyles and the olecranon. Three muscles, the anconeus (posterior compartment), pronator teres (medial compartment), and brachioradialis (lateral compartment), were studied visually and with computer analysis (measurement of their signal intensities) by two independent observers. Among controls, there was no substantial difference in signal intensity for the three muscles, but the anconeus muscle never had the most prominent signal intensity. The signal intensities of the pronator teres and brachioradialis muscles were -0.2% to 0.7% of the signal intensity for the anconeus muscle. In the 7 patients with chronic lateral epicondylitis, the anconeus had the most intense signal intensity by both visual and computer analysis. The signal intensity of the anconeus was, on average, 3.1% greater than the brachioradialis (range 1.5% to 5.8%), and 2.8% greater than that of the pronator teres (range 1.5% to 5.4%). Four patients (57%) had increased signal intensity about the proximal radial head and 2 (29%) had fluid adjacent to the lateral epicondyle. The anconeus muscle arises from the back part of the lateral epicondyle and inserts into the side of the olecranon and the posterior surface of the proximal portion of the ulna. Its function is uncertain, but it may contribute to elbow extension and ulnar abduction when the forearm is pronated. It is unknown if any abnormality of this muscle is primary and related to abnormal posture or motion, or secondary in response to compensating for problems with the ECRB. High-signal intensity is usually attributed to inflammation, edema, or granulation tissue. The significance of these findings is unclear.
Based on their ultrasonographic observations of the lesions related to tennis elbow, Maffulli et al. (1990) felt that the provocative movements that caused increased elbow pain produced pain via compression of an underlying inflamed bursa or production of microtears in muscle or tendon incapable of further lengthening.
Coonrad and Hooper (1973) believed that the syndrome, initiated by tears in degenerated or aged origins of the flexor or extensor groups by undue stress or trauma, secondarily irritated the subtendinous fat pad and radiohumeral synovial membrane by continued muscle action. When the extensors were involved, the supinator muscle tightened the annular ligament, thus placing traction on the collateral ligament. Free nerve endings in the collateral ligament may be the source of pain as well as reflex synovitis by involvement of the articular branch of the radial nerve by the subtendinous granulation tissue.
C.4.d Clinical Observations on Etiology
Approximately 5% of patients with epicondylitis are golf or tennis players (Goldberg, Abraham, and Siegel, 1988; Coonrad and Hooper, 1973; Wadsworth, 1987). Repetitive use related to employment or recreation is commonly noted as a precipitating factor. Goldberg, Abraham, and Siegel (1988) observed this factor in 70% of their 37 elbows, with the largest number of cases related to secretarial and housework. (Direct blunt trauma accounted for 30% of cases.)
Osgood (1922) reported cases related to tennis (including himself), painting (as an occupation), and strenuous cranking of an automobile. He also mentioned 15 cases related to lead poisoning he had seen at the Industrial Medicine Clinic at Massachusetts General Hospital with Dr. Wade Wright. He observed that the right arm was more often affected than the left and men more often than women, even though both could be affected. The most characteristic cause was strenuous or repeated extension of the arm in a flexed position, meeting a sudden opposition to further extension, e.g., a backhand stroke in tennis, striking blows with a hammer with the arm in a cramped position, punching and lasting (shoemaker), or slinging mortar (mason).
Hannson and Norwich (1930) believed there were two forms of lateral epicondylitis: acute and chronic. The acute form was believed to be related to 1 or more repeated severe sudden strains in the extensors that insert at the lateral epicondyle. The chronic form was considered occupational. They mentioned presser's elbow as a typical example. Of their 16 reported cases, 4 (25%) were related to sports (tennis -- 1; squash -- 2; and polo -- 1). Of the remaining 12, 4 were pressers, 2 were factory workers, 1 performed delivery work, 2 did housework, 1 made braces, 1 a was a cutter, and 1 was a waiter.
Carp (1932) presented 8 cases. One was an American housewife who worked as a cutter. Apparently, she frequently struck her lateral epicondyle on the edge of a table. Others included an American merchant who played squash-tennis; an executive who struck his elbow on a piece of iron; a lawyer who had repeatedly lifted a 35-lb sewing machine from the floor to a table with his right hand; a tinsmith; a telephone operator who suddenly flexed and extended her elbow to plug in the wire; a corset-fitter who had struck the outer surface of her elbow on an iron gate; and an executive who repeatedly struck his arm against the wall while playing squash. Blunt trauma alone was a factor in 2, indirect trauma in 3, and a combination in 2.
Cyriax (1936) stated that work or play that entailed repeated pronation/supination movements with the elbow almost fully extended was essential for the development of tennis elbow. Patients who could not remember any special overexertion would be found working at screwing, lifting, hammering, ironing, etc., or to be violinists, surgeons, masseurs, etc. He also felt that a cubitus valgus deformity was important, if present, because the smaller carrying angle on the outer elbow placed greater strain when the elbow was extended and the forearm vigorously supinated and carrying an object with the forearm supinated. Cyriax also identified four varieties of tennis elbow. Type I (acute -- following indirect trauma) usually started with sensation of something giving way at the elbow during performance of a violent action. The lesion is believed to be a muscle rupture. Type II (subacute -- following indirect trauma) was considered the typical variety usually found in younger patients. Onset was gradual following vigorous exercise with the arm. Symptoms subsided with rest, but reappeared with increased activity until the patient could hardly turn a door handle or lift a tea pot. Type III (chronic occupational) was usually found in older patients and required 1 or more months for full development. Often there was no history of injury, but the patient's occupation provided the clue to the etiology. He felt that this type was less prone to spontaneous cure than Type II. Type IV (following direct trauma) was said to resemble Type III.
Meherin and Cooper (1950) stated that, among their 56 cases, direct violence was the dominant mechanism of injury (> 2:1), They stated that, in cases related to direct injury, the history was of one or more minor blows to the lateral epicondyle. In cases due to indirect trauma, there was usually a history of persistent repetition of certain movements, especially movements done for the first time, greatly increased in frequency, or resumed after lengthy rest (unaccustomed work).
Spencer and Herndon (1953) noted few tennis players among their cases and observed that the condition appeared to be more common among people whose occupations involved repetitive flexion and supination. Some cases followed direct trauma.
Quin and Binks (1954) noted a history of onset immediately after trauma in 2 of their 31 cases. Three others reported onset following falls in which they knocked their elbows, but not severely. Repetitive movements associated with occupation or recreation might have had a bearing on disability in 3 cases. Two recalled minor injury around the time of onset, but they were of a nature experienced by most people on any day of their lives. Twenty-one patients could not associate the onset of their symptoms with any form of trauma. Of these, 4 said that recent unaccustomed work worsened their symptoms and forced them to seek medical attention. They also noted that tennis elbow may be a manifestation of a more generalized disturbance, with trauma being merely a precipitating or aggravating factor.
Murley (1954) noted that the condition typically affects individuals over 30 years of age who undertake unaccustomed activities involving repeated pronation and supination of the forearm while the hand maintains a grip. He mentioned the case related to excessive tennis playing in a man out of training and in an accountant who celebrated the acquisition of a new house with a burst of cabinet-making.
Bosworth (1955) stated that the occupations represented by his cases "practically cover the employable personnel in our metropolis." These included dentist, nurse, carpenter, bricklayer, presser, and bookkeeper. Only nurses (n = 3) and dentists (n = 2) were listed more than once. In terms of types of injury, 15 had a blow to the side of the elbow; 6 had a twisting strain; 1 stated that the condition resulted from overuse of the hand and forearm; and no known cause was identified for 5.
Paul (1957) reported on 314 cases of radiohumeral bursitis. Of these, 137 had no history of trauma, 56 had a history of sprain, and 101 a history of contusion. He felt there was no occupational predilection.
Wall, a physician at the General Electric Company, discussed his company's experience treating tennis elbow among the workers of the River Works plant (Wall, 1960). He stated that the condition was "common" among the plant's workers. He stated that the condition usually occurred in individuals whose occupation required frequent pronation/supination movements, especially against some form of resistance. He stated the condition was not uncommon among carpenters or among those who used heavy wrenches repeatedly and in those who use the elbow for repetitive actions such as pulling on levers. Some cases arise in people who do not perform such activities. In Wall's series of 95 cases, 50 gave a history of blunt trauma to the elbow with subsequent development of a pain at the lateral elbow aggravated by twisting motions in a supinating direction against resistance, by attempting to lift objects with the forearm in a pronated position, and often by merely shaking hands. In the other 45 cases, the condition followed a single straining type of injury or development in the course of repeated motions of the elbow related to work.
Miller (1960) reported a case of right medial elbow pain in a right-handed javelin thrower. The onset of this condition, termed "javelin thrower's elbow," was usually insidious and the intensity of pain was related to the intensity and duration of practice. It was most commonly seen in unskilled or untrained throwers, but any caliber of athlete could be affected. Miller described two types of this condition, both related to the style of throw. One was related to a side-arm throwing technique where the arm would be abducted parallel to the ground with the elbow flexed at 90 degrees. Internal rotation of the shoulder transmitted force to the javelin, but also to the medial aspect of the elbow. In this case, damage was reported to be cumulative rather than from a single accident. The lesion was postulated to be a strain to the medial ligament of the elbow. The second type is related to the more common method of throwing. In this technique, the shoulder is almost fully abducted and the arm is led by the elbow. The force is generated by elbow extension. This method is believed to prevent stress to the medial elbow but may occasionally create problems at the olecranon secondary to hyperextension.
Garden (1961) reported information on 50 surgical cases. The list of occupations included: houseworker (n = 11); carpenter (n = 1); crane driver (n = 1); weaver (n = 3); brick burner (n = 1); company director (n = 1); farmer (n = 1); teacher (n = 1); painter (n = 1); butcher (n = 1); shoemaker (n = 1); bookkeeper (n = 1); representative (n = 1); laborer (n = 3); salesman (n = 1); fireman (n = 1); cook (n = 1); mechanic (n = 1); police officer (n = 2); electrician (n = 2); overlooker (n = 1); clerk (n = 2); domestic help (n = 1); molder (n = 1); planer (n = 1); foundry worker (n = 1); chemist (n = 1); packer (n = 1); typist (n = 1); shop assistant (n = 1); local government officer (n = 1); and motor engineer (n = 1).
Hohl (1961) reported on 66 elbows in 64 patients. The symptoms developed gradually in 51 and suddenly in 15. No trauma was reported by 34 patients; 10 had direct injury; 8 related onset to participation in athletics; and 14 gave a history of muscular strain, e.g., digging, pulling, or twisting, with gradual onset thereafter. Thirty were sedentary workers; 7 were laborers; 12 were housewives; and 12 had unrecorded occupations.
According to Goldie (1964), overexertion was often cited as an etiologic factor. The term "overexertion" included forced extension of the wrist as well as repeated pronation-supination movements of the forearm. Some of the occupations related to this condition included masons, gardeners, builders, waiters, printers, surgeons, housewives, and painters. Among his 113 cases, Goldie noted onset following three circumstances: as a sequelae of unaccustomed movements involving the extensors in a forced and monotonous way; spontaneously in someone accustomed to such repeated movements involving the forearm extensors; and secondary to trauma. For those with onset related to unaccustomed work (n = 33; 29%), onset occurred within 2 to 3 weeks. This was especially noted among piece-workers, builders, stevedores, waiters, masons, gardeners, and housewives. Onset related to accustomed work was noted for 50 cases (44%). Most of these cases worked in highly automated industries with their grip patterns being monotonous, e.g., rotating bands and carrying wheels. Other circumstances included a boxmaker who hammered 4,000 nails per day, typewriting secretaries, and mechanics tightening screws. Trauma was related to onset in 29 (26%) cases. Trauma included a direct blow to the lateral epicondyle as well as sudden direct strain as with a pull of forceful extension of the elbow. Sports activities were related for 3 (3%). All were traumatic in nature. Etiology was unknown for 1 (1%). There were 67 males (59%) and 46 females (41%). The dominant extremity was affected in 110 (97%) cases, with 103 (91%) in the working extremity. In terms of age, there were only 18 cases aged 20 to 39 years (16%) and only 5 cases aged 60 years or greater (4%). The vast majority of cases were in the 40 to 59 year age range (n = 90; 80%) with a peak number of cases around 50 years.
Carroll and Jorgensen (1968) reported 16 cases treated by the Garden procedure. Occupations included lab technician (n = 1); carpenter (n = 1); cook (n = 1); housewife (n = 7); deckhand (n = 1); hairdresser (n = 1); janitor (n = 1); mechanic (n = 1); electrician (n = 1); and clerk (n = 1).
Stovell and Beinfeld (1979) reported on 18 of the their 21 cases who underwent surgery with the Garden procedure. Occupations included housewives, executives, laborers, and marine mechanics.
Price (1982) reported 2 cases of lateral epicondylitis in a police officer and warrant officer. Both developed the condition in the arm used to open and close cell doors up to or more than 80 times per day. The cell doors of one particular magistrate's court were changed toward the end of 1979. The first case developed symptoms within 6 months and ultimately underwent surgery. The second case working in the same court reported elbow pain in December 1981. He responded to an initial steroid injection, but had a recurrence that was especially noted when opening and closing cell doors. He responded to a second injection plus avoidance of further cell duties. The offending activity was believed to be the repetitive gripping and twisting movements related to locking and unlocking the cell doors. Problems disappeared after attention to the locks.
Binder et al. (1985) reported that 39 (51%) of their 76 patients attributed their symptoms to a specific cause or activity. These included housework (n = 11); working with tools (n = 9); lifting or carrying heavy weights (n = 8); and sports or hobbies (n = 7). Thirty (40%) of their cases were housewives or domestic workers; 25 (33%) were sedentary workers or unemployed; and 21 (28%) were manual or tool workers. Four cases (5%) followed blunt trauma.
Lundeberg, Haker, and Thomas (1987) noted that among the 82 cases evaluated for inclusion in their study, 62 (76%) attributed their symptoms to sport; 18 (22%) to housework; and 2 (2%) to trauma. Lundeberg, Abrahamsson, and Haker (1988) noted that 52 of their 99 patients (53%) attributed their symptoms to sport; 43 (43%) to housework; and five (4%) to elbow trauma. Haker and Lundeberg (1990) noted that 42 (86%) of their cases affected the dominant extremity (all right-handed). Nineteen (39%) attributed their symptoms to sport; 14 (29%) to work; 10 (20%) to other activities; and 6 (12%) did not know of a possible cause. Haker and Lunderberg (1991) recorded that the self-reported causes among their 43 cases include work (n = 14; 33%); sport (n = 14; 33%); other activities (n = 24; 56%); and unknown (n = 7; 16%). In another study reported by these authors, work was reported as the cause in 23 (40%); sport in 21 (36%); other activities in 19 (33%); and unknown in 4 (7%) (Haker and Lundeberg, 1991b).
Dimberg (1987), noting that most white-collar workers contracted their elbow problems while working on their house or gardening, suggested that unaccustomed work may be an important factor.
Murley (1987), based on personal experience, mentioned the favorable effect of enlarging the grip circumference of his tennis racquet in alleviating his symptoms. He felt that small grips decreased wrist extension, thus increasing tension in the extensors, while large grips increased wrist extension, thus reducing tension in the extensor.
Mitchell and Reid (1983) reported 2 cases of lateral epicondylitis related to concurrent neurological problems. Their first case occurred in an engineer who gripped a pen with excessive force and hyperflexion of the thumb. His symptoms decreased after treatment for "writer's cramp." Their second case arose in an individual with dystonic posturing and athetotic movements of the left arm. Her elbow pain decreased upon treatment of the underlying movement disorder. Mitchell and Reid felt that these observations were consistent with the prevalent notion that repetitive movements resulted in small tears in the common extensor origin.
Shapiro (1990) reported that karate practitioners may be at increased risk of developing tennis elbow because their movements involved forceful pronation and supination combined with elbow extension.
Taylor and Bender (1991) reported 2 cases of lateral epicondylitis among computer users. One was the hospital chief of service; the other performed data entry. According to the authors, both cases appeared to be related to the use of standard keyboards at non-standard heights plus unaccustomed work.
Koval (1993) reported a case that followed an attack by an octopus that squeezed the patient's arm in the region of the elbow. Klimek (1984) reported a case of bilateral tenderness over the muscle bellies proximal to the wrist flexor tendons (perhaps analogous to medial epicondylitis) in an otherwise unemployed woman who picked out unsuitable potatoes from a conveyor belt for 2 days prior.
Kivi (1982) reported on the etiology and types of occupations of 88 cases seen at a large occupational health center in Finland between 1977 and 1979. All patients were questioned about their history of illness, work, and hobbies. The etiology of each patient's condition was established on the basis of history, clinical examination, and acquaintance with the workplace. The condition was judged to be occupational in 64 (73%), and related to spare time activities in 24 (27%). In terms of specific etiologies: 14 (16%) were related to direct trauma; 3 (3%) to repeated microtrauma (strain); 17 (19%) to unaccustomed movements engaging the forearm in a forced and monotonous way; 48 (55%) to accustomed repeated monotonous movements at work; 6 (7%) to accustomed isometric overexertion of the forearm; and none from other causes (C5 to C6 cervical radiculopathy; posterior interosseous nerve syndrome (PINS); underlying rheumatic disease; anxiety or depression). As for types of occupations among the 64 occupational cases, 19 (30%) were metal workers; 13 (20%) were packers; 7 (11%) were shop assistants; 3 (5%) were industrial cleaners; 3 (5%) were office employees; 3 (5%) were shoemakers; and 16 (25%) had miscellaneous jobs. Forty-seven (73%) of these jobs involved a pinching-squeezing grip; 53 (83%) involved repetitive rotation of the forearm. The number of daily working movements of the occupational cases was stated to be statistically significantly increased compared to the number of working movements for the non-occupational cases (p < .001). The tools used or the weights moved weighed between 1 kg to 20 kg in 43 (67%) of occupational cases compared to 4 (17%) for the non-occupational cases (p < .001). Heavy continuous turning of nuts was related to 10 (16%) cases. Three sheet-metal workers developed the condition in their non-dominant hand -- used to statically hold dented sheets of metal while the other hand was used to hammer on them. All of the occupational cases had performed their jobs for more than 1 year and 50 (78%) for more than 5 years. Among office employees, the condition was due to some spare time occupation. As for the occupations of the 24 cases with epicondylitis due to hobby, 17 (71%) were office workers and 7 (29%) had miscellaneous jobs.
Farr (1982) reported 3 cases of lateral epicondylitis among aviators. In 1 case, the aviator rested his forearm on his thigh, thus operating his control stick by flexing and extending the wrist of his dominant hand. The second case reported jerking his briefcase up into the aircraft by abducting the shoulder and extending the wrist. The etiology of the third case was not clear. All cases responded to conservative treatment.
Baumgard and Schwartz (1982) noted that 9 (27%) of their 34 patients with medial or lateral epicondylitis reported a history of direct trauma.
Vasseljen et al. (1992) noted that, among their 30 patients, 15 (50%) identified work as the etiology; 4 (13%) identified leisure; and 11 (37%) had unknown etiology.
Newman and Goodfellow (1975) believed that the fibrillation of the radial head was related to repeated pronation and supination of the forearm.
C.4.e Descriptive Epidemiology
Lateral epicondylitis is far more common that medial epicondylitis (Spencer and Herndon, 1953; Wall, 1960; Coonrad and Hooper, 1973; Wadsworth, 1987; Hohl, 1961; Kivi, 1982; Kilroy, 1955). Among cases of lateral epicondylitis, the ECRB is the most commonly involved muscle-tendon unit (Nirschl and Pettrone, 1979; Doran et al., 1990; Chard et al., 1994). Among cases of lateral epicondylitis affecting one arm, the right side is affected in approximately 70% of cases (Doran et al., 1990; Spencer and Herndon, 1953; Cyriax, 1936; Meherin and Cooper, 1950; Wall, 1960; Coonrad and Hooper, 1973; Wadsworth, 1987; Quin and Binks, 1954; Bosworth, 1955; Bosworth, 1965; Carroll and Jorgensen, 1968; Stowell and Beinfeld, 1979; Haker and Lundeberg, 1991b; Kivi, 1982; Vasseljen et al., 1992; Kilroy, 1955). Bilateral lateral epicondylitis is relatively uncommon (<10%) (Spencer and Herndon, 1953; Coonrad and Hooper, 1973; Wadsworth, 1987; Garden, 1961; Stowell and Beinfeld, 1979; Kilroy, 1955). The mean age was 42 years (range 30 to 70 years) (Spencer and Herndon, 1953; Cyriax, 1936; Meherin and Cooper, 1950; Coonrad and Hooper, 1973; Quin and Binks, 1954; Bosworth, 1955; Garden, 1961; Hohl, 1961; Carroll and Jorgensen, 1968; Stowell and Beinfeld, 1979; Kivi, 1982; Calvert et al., 1985; Kilroy, 1955). In most series, the number of male cases is approximately equal to the number of female cases (Doran et al., 1990; Spencer and Herndon, 1953; Coonrad and Hooper, 1973; Quin and Binks, 1954; Carroll and Jorgensen, 1968; Stowell and Beinfeld, 1979; Kivi, 1982; Calvert et al., 1985).
Allander (1947) reported that the prevalence of tennis elbow among a sample of 15,000 Swedes aged 34 to 74 years was approximately 1% to 3%, except among females aged 42 to 46 years, whose prevalence was 10%. Incidence and prevalence fell while spontaneous remission rose with increasing age. This was in contrast to other age-related degenerative conditions, such as arthrosis of the hips and knees.
The condition appears to predominantly affect Caucasians (Coonrad and Hooper, 1973; Wadsworth, 1987).
In general, tennis or golf players represent less than 5% of epicondylitis cases (Coonrad and Hooper, 1973; Wadsworth, 1987). Among tennis players, the prevalence of lateral epicondylitis was reported to be 39.7% (Gruchow and Pelletier, 1979).
C.4.f Analytic Epidemiological Studies
Roto and Kivi (1984)
Roto and Kivi compared the prevalence of epicondylitis and tenosynovitis among 90 male meatcutters to 77 construction foremen. All participants completed a self-administered questionnaire, part of the Nordic questionnaire, that inquired about symptoms in the upper extremities and located the painful part with a diagram. Physical examinations were performed by physicians blinded to the questionnaire responses. The case definition of epicondylitis included local tenderness, pain during resisted extension/flexion of the wrist and fingers, and decreased hand grip power compared to the opposite side. The case definition for tenosynovitis required local pain during movement, swelling, and weakness of finger movements. Eight (9%) meatcutters met the case definition for epicondylitis compared to 1 (1%) construction foreman. The odds ratio was 6.4 (p 0.05; 95% CI:0.99-40.9). For the meatcutters, 2 cases were aged 31 to 40 years (6% of workers in that age range); 2 were 41 to 50 years (11% of that age range); and 4 were 51 to 65 years (25% of that age range). The affected foreman was in the 51-65 year age range (12.5% of workers on that age range). All meatcutter cases had worked more than 15 years in their current occupation. In addition to the 8 cases among meatcutters, 7 (8%) additional meatcutters had positive physical signs of epicondylitis. During the week prior to completing the questionnaire, 26 (29%) meatcutters and 5 (7%) of foremen reported pain in the region of the medial or lateral epicondyles. During the prior 12 months, 39 (43%) meatcutters and 12 (16%) foremen reported pain in the region of either epicondyle. During the week prior to the study, 27 (30%) meatcutters and 8 (10%) foremen reported discomfort or pain in the wrists of hands. During the prior 12 months, 49 (54%) meatcutters and 13 (17%) foremen reported pain in their wrists or hands. All reported symptoms were associated with increasing age. For the meatcutters, reported symptoms were also associated with the dominant hand.
Given the nature of hand use associated with meatcutting, Roto and Kivi postulated that the etiology epicondylitis might be associated with local muscle-tendon load, especially when cutting frozen meat. They did not perceive a relationship with repetitive or monotonous work movements (unlike tenosynovitis). Epicondylitis was more associated with aging than tenosynovitis. Citing data from another study, they noted that the prevalence of pain and discomfort symptoms among normal male Finnish workers ages 40 to 64 years was approximately 9% for the upper extremities and 11% for the hands and wrists. For the same age group of foremen, the prevalence from this study was 10% for both circumstances. The prevalence was higher for the meatcutters of that age.
Luopajarvi et al. (1979)
In this cross-sectional evaluation, 152 assembly line packers were compared to 133 shop assistants. There were 4 cases of lateral epicondylitis among the former group (prevalence = 3%) and 3 cases among the latter group (prevalence = 2%).
Dimberg (1987) distributed a questionnaire that contained questions about elbow pain to every fifth person in the personnel file of Volvo Aircraft Engine Division (Volvo Flygmotor). The sample targeted 571 workers. After exclusions, there were 546 subjects (494 males and 52 females). Questionnaires were returned by 540 (98.9% response rate). The 6 who refused to participate had not been sicklisted for elbow pain. The questionnaire included items related to age, gender, suspected causal factors, present job, tennis playing, and physician visits for the elbow problem. All workers ever reporting an elbow problem were examined by a physician. Only those with a confirmed diagnosis of lateral epicondylitis were included in the analysis. The case definition included lateral elbow pain, pain on palpation, and pain increase on wrist extension against resistance.
The main products developed and manufactured by the company included jet engines, hydraulic pumps, and car components. Among the 200 white-collar workers, the most common job categories were production technologists, designers, typists, and computer operators. Among 340 blue-collar workers, the most common job activities involved operating numerically controlled machines, burring, welding, and grinding. Jobs were classified by the safety officer, a physiotherapist, and the company physician into three categories with respect to elbow stress: low, moderate, and high.
Of the 540 responders, 83 (15%) had lateral elbow pain. Lateral humeral epicondylitis was verified by the physician in 40 cases (48%), thus yielding an estimated point prevalence of 7.4%. Epicondylitis occurred in the dominant arm in 38 (95%) and bilaterally in 2 (5%). The prevalence among white-collar workers was 11.0% compared to 5.3% for blue-collar workers, but the difference was not statistically significant. The prevalence among blue-and white-collar workers less than 40 years of age was 4.6% and 6.1%, respectively, compared to 8.9% and 13.9% among those aged 40 or more years, but these differences were not statistically significant. Based on the job classifications, blue-collar and younger workers were exposed to greater elbow stress than white-collar or older workers. There was no evidence that employees with epicondylitis were exposed to greater elbow stress than the totality of employees. The proportion of workers who had consulted a physician for their elbow problems was significantly greater (p < .05) among workers exposed to increasing elbow stress. The prevalence among older individuals in high-stress jobs was 17.9%.
Half of the affected workers had not sought medical advice, but there was no indication of a difference in severity between those that did and those that did not seek medical advice. Multiple regression using the presence or absence of epicondylitis as the dependent variable and gender, employee category, age, and degree of exposure to elbow stress as independent variables revealed that only age was significantly related to prevalence. Twenty-eight (70%) of the epicondylitis cases identified overexertion of the extensor muscles due to gripping and twisting movements as the activity preceding onset of symptoms. Onset was sudden in 27 of these 28 cases and all affected the dominant arm. Fourteen (35%) were considered to be related to work; 3 (8%) related to playing tennis; 11 (27%) related to other leisure activities (house building and gardening); and 12 (30%) reported no related activity. No particular job dominated among cases. Comparison of the leisure-related group, no-known-cause group, and work-related group according to degree of exposure to elbow stress revealed a greater percentage of those in the work-related group in the moderate and high categories.
Moore and Garg (1994)
Moore and Garg performed a retrospective cohort morbidity study that compared the incidence and spectrum of upper-extremity disorders associated with 37 job categories in a pork processing plant with the ergonomic task requirements of the jobs.
Jobs were first described according to intensity of effort, exertional cycle time, duration of exertion per cycle, duration of recovery per cycle, frequency of exertion, wrist posture, pinch vs. power grasp, presence vs. absence of vibration, speed of work, and presence vs. absence of localized compression at the palm. Intensity of effort was estimated as percent maximal strength by comparing reported weights of objects with estimated average maximal strengths for the observed worker. Exertional cycle time, duration of exertion per cycle, and duration of recovery per cycle were measured with a stopwatch. Wrist flexion and extension angles were estimated from the videotape and classified as neutral (< 25 degrees), non-neutral (25 degrees to 45 degrees), and extreme (> 45 degrees). Wrist ulnar deviation was classified as neutral (< 10 degrees), non-neutral (10 degrees to 20 degrees), and extreme (> 20 degrees). Radial deviation was classified only as neutral and non-neutral. Pinch grasp, localized mechanical compression, vibration, and cold temperature were noted for their presence or absence.
Second, the investigators relied on the exposure data as well as their knowledge and experience to predict which jobs would pose an increased risk of distal upper-extremity morbidity and which would not. These jobs were called hazardous and safe, respectively.
Musculoskeletal morbidity was ascertained from employee medical records. "Elbow" included medial epicondylitis and lateral epicondylitis. The case definition was localized pain about the medial or lateral aspect of the elbow that increased with tension of the attached muscle-tendon units and direct palpation.
The exposure factors of the 15 jobs associated with any distal upper-extremity disorder ("positive" jobs) were compared to the 17 jobs not associated with such disorders ("negative" jobs). Intensity of effort was significantly different when evaluated with and without log-transformation of the data. Wrist posture was only significantly different when evaluated with log-transformation. None of the other exposure factors were significantly different, regardless of transformation. Stepwise regression revealed that the job category incidence rates (for all disorders) were best predicted by the intensity of effort (to the second power) divided by the percentage of time available for recovery during the cycle (to the 0.6 power). Wrist posture failed to be a significant predictor of the incidence rates.
Of the 104 observed conditions, non-specific hand/wrist pain was the most common condition (n = 41; 39%). There were 24 (23%) cases of epicondylitis. There were more female cases than male cases for epicondylitis. Twenty (83%) of the cases of epicondylitis were unilateral. Among cases with multiple conditions, the most common association was trigger finger affecting two digits (IV and V), followed by epicondylitis plus a more distal hand/wrist disorder on the same side.
The relative risk for epicondylitis was 10.7 (p < .01) when comparing "hazardous" jobs to "safe" jobs.
C.4.g Experimental Results
Goldie (1964) performed the most comprehensive investigation related to lateral epicondylitis. His investigation involved three parts. Part I dealt with characterizing the normal anatomy and evaluating age-related structural variations. Part II dealt with the clinical picture of lateral epicondylitis. Part III dealt with the pathology of epicondylitis (presented earlier).
In Part I of his monograph, Goldie reported macroscopic and microscopic observations from 31 control cadaveric specimens. These specimens varied according to age and results were presented for different age groups (0-10 = 5; 11-20 = 3; 21-50 = 18; 51-60 = 5). Even though there were some moderate differences observed with increasing age, he found no evidence of age-related degeneration.
In Part II, he discussed the evaluation of 176 patients referred for orthopedic evaluation at a hospital in Göteborg, Sweden. Of these 176, 154 had lateral epicondylitis and 20 had medial epicondylitis (ratio 7.7:1). Forty-one (27%) of the lateral epicondylitis cases were treated conservatively and not described any further. The other 113 (73%) underwent surgery. These 113 cases represented 114 elbows. Of the 114, 24 (21%) reported a sudden onset of pain and of these 24, 17 (71%) were related to trauma and 7 (29%) to overexertion. Of the 90 reporting an insidious onset, 12 (13%) reported onset related to trauma compared to 77 (86%) related to overexertion, and 1 (1%) of unknown origin.
C.4.h Historical Theories of Pathogenesis
Hannson and Norwich (1930) believed that the lateral epicondyle was a source of specific morbidity because it gave origin to phylogenetically young muscle, especially compared to the medial epicondyle. They felt that sport and work activities that involved sudden feats of strength or long continued work caused these structures to "give way." Using a rabbit, they determined that the locus minoris resistentiae of an intact muscle-tendon unit was at its insertion site into bone. They postulated that lateral epicondylitis represented a form of an avulsion fracture with accompanying myositis; however, review of several cases with x-rays was disappointing. Bosworth's theory (1955) emphasized the role of the radial head and the orbicular ligament. He noted that the radial collateral ligament, the orbicular ligament, and the radio-humeral joint capsule fibers merged with one another. He also noted several attributes of the radial head: it is not quite circular; it is not concentric with the radial shaft (it is slightly offset); one margin of the radial head is considerably elevated above the opposite margin; its peripheral border varies considerably in width; and the lateral border is not smoothly molded throughout its circumference (it is irregular). He believed that the rotation of this distorted radial head in a changing plane, on a changing stress axis, inside a sensitive membrane, or compressed by powerful muscles and tendinous structures was capable of producing the pain of tennis elbow.
Goldie (1964) outlined a summary for the pathogenesis of lateral epicondylitis. He proposed that a space filled with areolar tissue is normally underneath the aponeurosis. In epicondylitis, this space becomes filled with granulation tissue. This granulation tissue contains free nerve endings assumed to mediate pain. At surgery, pain could be elicited from this granulation tissue. Edema was present in the tendinous structures. Long-standing cases tended to have the granulation tissue replaced by fibrotic tissue. Goldie postulated that hyperfunction of the forearm extensor muscles, especially the ECRB, might induce edema in the aponeurosis, followed by fibrinous exhudation in the subtendinous space with beginning hypervascularization and formation of adhesions. Further muscular actions might break these adhesions and contribute to the development of granulation tissue. The granulation tissue would fill the sub-aponeurotic space, thus making it more susceptible to mechanical irritation, which would then give rise to symptoms.
According to Goldberg, Abraham, and Siegel (1988), the pathology, age distribution, and temporal relationship between repetitive stress and onset of symptoms supported the concept that lateral epicondylitis is a degenerative process in which repetitive stress precipitates symptoms, e.g., repetitive stress is superimposed on a degenerative condition.
According to Dimberg (1987), the sudden onset of symptoms, predominance of cases affecting the dominant extremity, and association with specific causal activities among cases in his study favored the theory of overexertion of the wrist extensors due to gripping and twisting movements. According to Kivi (1982), the occurrence of the condition most commonly in middle age plus the observed relationship with overexertion was consistent with the theory that degeneration of the connective tissue combined with overexertion are significant factors in the pathogenesis of the condition. Wadsworth (1987) held the same opinion.Based on ultrasound findings that the tendon of the ECRB was a distinct structure, as opposed to part of the common extensor tendon, Maffulli et al. (1990) postulated that such an independent tendon may be less able to tolerate repeated stresses because of its reduced area of attachment (cross-sectional area). This might represent a predisposing factor.
C.4.i Models of Pathogenesis
A significant portion of cases of lateral epicondylitis occur in the context of acute, blunt trauma. In this context, external forces transmitted through the skin to the external surface of the ECRB aponeurosis are postulated to disrupt the collagen fibers within the tendon. The ensuing repair response accounts for the pathological and clinical manifestations of the condition.
A Non-Traumatic Model
There is limited information with which to develop a definitive non-traumatic theory for lateral epicondylitis. However, the following theory appears to be consistent with the observed patterns of pathology, plausible anatomical relationships, and some of the clinical and epidemiological studies of this condition.
It is proposed that tensile loading of the ECRB (via muscular action, elbow extension, or both) combined with elbow extension creates compression between the underside of the ECRB aponeurosis and the orbicular ligament and radial head. Pronation and supination of the forearm might contribute to this process given the asymmetric axis of rotation of the radial head on the end of the radius. Under temporal circumstances not yet defined (e.g., prolonged duration or repeated loading), this contact pressure between the orbicular ligament or radial head and the underside of the ECRB tendon might cause fraying or fibrocartilagenous metaplasia of the ECRB tendon or the adjacent orbicular ligament. The natural repair response contributes to the accumulation of granulation tissue, including the influx of nociceptors, and the clinical and pathological manifestations of lateral epicondylitis.
C.5.a Normal Anatomy
The myotendinous junction is a specialized anatomical structure characterized by extensive folding (Garrett and Tidball, 1988). This decreases the loading angle of the tensile forces on the cell membrane (Garrett and Tidball, 1988; Tidball and Daniel, 1986). Maintenance of this extensive folding requires significant energy, as evidenced by increased mitochondria near the myotendinous junction (Garrett and Tidball, 1988). The distal upper-extremity muscle-tendon units most commonly affected are the ECRL, the ECRB, the abductor pollicis longus (APL), and the extensor pollicis brevis (EPB) (Tidball and Daniel, 1986; Howard, 1937; Lipscomb, 1944; Flowerdew and Bode, 1942; Thompson, Plewes, and Shaw, 1951).
In peritendinitis, gross observations of the myotendinous junction have revealed the presence of highly vascularized subcutaneous tissue with edema; clear, jelly-like edema of the areolar tissue about the tendon; thickened deep fascia with outward bulging of underlying structures on incision; edema of the perimysium and peritenon associated with dilated blood vessels and straw-colored serous fluid; fibrin deposition; dark-colored muscle that may lack voluntary contractible power, but no evidence of a tear; and normal-appearing tendons and tendon sheaths distal to the involved areas (Howard, 1937; Howard, 1938). There may be increased cellularity due to fibroblasts or histiocytes, with a few plasma cells or lymphocytes (Howard, 1937).
Microscopically, there is muscle fiber lysis and destruction with hyaline changes; interstitial hemorrhage in muscle and areolar tissue; venular thrombosis; interstitial fibrin deposition; loss of muscle glycogen; and a relatively acidic pH associated with the presence of lactic acid (Howard, 1937). There may be increased cellularity due to fibroblasts or histiocytes, with a few plasma cells or lymphocytes (Thompson, Plewes, and Shaw, 1951).
Crepitation is a clinical manifestation of fibrin deposition on the surface of the muscle and/or tendon near the myotendinous junction (Howard, 1937, 1938). The weakness of the muscle may be associated with glycogen depletion (Howard, 1937, 1938). Pain probably arises from sensitized or stimulated nociceptors associated with the local tissue changes.
C.5.d Clinical Observations on Etiology
According to Howard (1937), some early theories were that peritendinitis was a metastatic form of bacterial infection, a toxic manifestation of an infection, or a rheumatic disorder, such as gout.
Approximately half of Howard's cases were associated with blunt trauma (contusion), followed by performance of usual and accustomed work, then onset of symptoms within 1 to14 days (Howard 1937, 1938). Objective evidence of trauma is usually present, e.g. ecchymosis, laceration, or abrasion (Howard, 1937). The blunt trauma may occur in the course of employment, followed by customary exertions while pursuing a sport or hobby (Howard, 1937, 1938). The opposite sequence may also occur.
Most cases occur in association with unaccustomed work, e.g., renewed previous employment after long lay-offs or assignment to unfamiliar tasks involving repeated and rapid movements of particular muscle groups (Howard, 1937, 1938; Flowerdew and Bode, 1942). Howard (1938) stated, "In the normal sedentary adult, the prolonged and continued muscular effort of a certain task, sports, or hobby may be followed by the onset of mild or severe forms of crepitating peritendinitis in the muscular groups subjected to unaccustomed exertion." He cited an example of a professor who weeded a garden, trimmed a hedge, and spaded a flower border one morning, then developed peritendinitis in the forearm within days. Another example was an executive who went deer hunting. Several days of climbing hills produced fatigue of the calf muscles. Upon his return home, his spouse insisted on going dancing. He awoke the following morning with peritendinitis in his calf. Howard (1938) also noted instances where a change from normal and accustomed work precipitated small epidemics of peritendinitis. He conveyed a story of a flashlight battery manufacturing plant that had a history of few cases of peritendinitis in the years prior to 1931. During 1931, demand for their product increased, so the employees worked longer and faster, and also had to modify their usual work method to accommodate the non-standard size of the batteries. This modification increased the degree of "wrist movement excursion." Within 1 week, 15 employees developed peritendinitis.
Flowerdew and Bode (1942) noted, as did Howard, that their cases seemed to occur in association with work that required repeated, stereotypical movements. Individuals inexperienced with such work usually utilized "incorrect and uneconomic" muscular effort. Most, however, adapted with continued practice.
Thompson, Plewes, and Shaw (1951) observed that 144 of their cases (26.5%) arose in the context of an occupational change necessitating performance of unaccustomed work. One hundred fourteen (21%) cases occurred after return to work following an absence. Repetitive or single episodes of localized strain (defined as unusually heavy work requiring strength, dexterity, and speed) were associated with 79 cases (14.5%). A single, sudden wrenching movement appeared responsible in many cases, while simple repetitive movement, such as filing, hammering, or assembly work accounted for 32% of the cases in this strain category. The acute strains were suggested as causing injury to the myotendinous junction. Direct local blunt trauma was associated with 76 cases (14%). Simple stereotyped movements associated with intensity of effort and speed accounted for 53 cases (9.7%). No cause was identified for 78 cases (14.3%). Combinations of factors were evident for 169 cases (31.1%).
C.5.e Descriptive Epidemiology
The most commonly involved muscle-tendon units are the ECRL, the ECRB, the APL, and the EPB (Howard, 1937, 1938; Flowerdew and Bode, 1942; Thompson, Plewes, and Shaw, 1951; Blood, 1942; Rais, 1961; Taylor-Jones, 1942). Typically, more than one muscle-tendon unit is affected (Howard, 1937, 1938; Flowerdew and Bode, 1942). More than half of cases involve the APL and EPB (Howard, 1937, 1938; Thompson, Plewes, and Shaw, 1951; Rais, 1961). Flexor tendon involvement is relatively uncommon, but there are reports of peritendinitis of the flexor carpi radialis (FCR) and FCU (Howard, 1937, 1938; Rais, 1961).
Unlike de Quervain's tenosynovitis, peritendinitis appears to affect males more than females (Howard, 1938; Thompson, Plewes, and Shaw, 1951).
Flowerdew and Bode (1942) discussed the occurrence of "tenosynovitis crepitans" within a farm camp. None of their 16 cases had performed manual work within the preceding 4 months, and 14 of the 16 performed office or other non-manual work during their normal life. These 16 cases arose among a cohort of 52 total workers; therefore, 23.1% of the total cohort were affected. The ECRL and EDC were affected. They also noted that no cases arose among workers who currently or previously participated in sports, suggesting personal predisposition.
Taylor-Jones (1942) noted the occurrence of at least a half a dozen cases of tenosynovitis within days after the onset of hop-picking. Taylor-Jones also noted that most cases occurred among experienced pickers "out to do a little better this year," rather than novices picking only a few bushels per day.
Blood (1942) published another similar experience. He noted a 50% increase in cases in 1941 compared to 1940. Even though the total number of employees and the work processes were essentially unchanged, the number of new workers had increased. In his experience, both new workers as well as experienced workers returning after holiday or sick leave were at risk when their work involved repetitive, stereotyped movements.
In 1951, Thompson, Plewes, and Shaw described 544 cases of peritendinitis and tenosynovitis that occurred in varied industrial settings. Approximately 90% of their cases were males. Manual workers represented approximately 80% of cases. They noted that the incidence increased significantly in 1945 in association with a dramatic influx of new employees. Peritendinitis of the ECRB, ECRL, APL, or EPB accounted for 419 cases in their entire series (77%). The other 125 cases involved the tendon sheaths, i.e., tenosynovitis.
C.5.f Historical Models of Pathogenesis
It has been generally accepted that peritendinitis develops via fatigue and exhaustion of selected muscle groups (Howard, 1937, 1938; Flowerdew and Bode, 1942; Thompson, Plewes, and Shaw, 1951; Blood, 1942; Rais, 1961; Taylor-Jones, 1942). Howard (1938) felt that peritendinitis probably developed initially in the muscle via exhaustion caused by "continued and unremitting unaccustomed toil." Such use of a particular muscle group created friction between adjacent tendons that were unprotected by synovial sheaths. This friction, as well as direct external trauma, could cause thrombosis of the blood vessels in the peritenon and perimysium. This impairment of circulation caused accumulation of lactic acid, edema, and hemorrhage in areolar and muscle tissue, followed by fibrin deposition, then crepitation.
Blood (1942) believed that the condition was an inflammatory response to excessive fatigue of various muscle groups, especially those crossing the dorsum of the wrist (Taylor-Jones, 1942).
Rais (1961) postulated the following course for peritendinitis:
"As a result of muscular fatigue or direct violence to the muscles, circulatory disturbances and edema of the muscles and its paratenon develops. Depending on the severity of the damage, degenerative changes develop in the muscles; these undergo disintegration followed by the formation of connective tissue, and regeneration by the formation of new muscle fibers. Fibrin is deposited in the edematous peritenon and interstitially in the muscles leading to organization of the edema with formation of connective tissue and capillaries."
C.5.g Experimental Results
Rais (1961) performed two experiments using rabbits. In the first study, the exercised legs of seven rabbits performed passive movements combined with active contractions at a rate of 150 per minute. Duration of exercise varied from 30 minutes to 6 hours. Observations on the exercised limb were compared to the unexercised control limb. On gross examination, findings included adhesions between the skin and underlying tissue, and clouding of the mesotendons after 3 hours of exercise. Histological findings were edema in the peritenon, mesotendon, and muscle interstitium after 4 hours of exercise. After 6 hours of exercise, there was also a slight perivascular round-cell infiltrate. There was no fibrinous exudate. In the muscles, edema was evident after 1 hour of exercise. After 2 hours, the edema was more marked and a paucity of nuclei was noted. After 3 hours, a few muscle fibers had undergone hyaline degeneration with pyknotic nuclei, and after 4 hours, regenerative changes were noted.
In the second experiment, the exercised leg performed 150 movements per minute for 4, 5, or 6 hours. Animals were then sacrificed between 1 and 6 days post-exercise. As the interval after exercise increased, the degree of adhesions of the skin to underlying tissues increased. During the first 3 days post-exercise, there was more or less marked edema of the peritenon and mesotendon. On the fourth day, increasing numbers of fibroblasts were noted. By the fifth day, there was marked proliferation of fibroblasts, marked collagen and new capillary formation, and perivascular neutrophils about the peritenon and mesotendon. By the thirteenth day, there were few inflammatory cells, but marked fibrinous exudation in the peritenon, mesotendon, and muscle interstitium.
Regarding the muscles, marked hyalinization of fibers and a pronounced cellular reaction was noted after 6 hours of exercise as early as the first day. By the fourth day, the muscle fibers were necrotic. Hyaline degeneration was pronounced, as was marked invasion of neutrophils and monocytes. These latter changes were paralleled by marked increases in the number of muscle nuclei wi thin intact sarcomeres, marked fibroblastic proliferation, and interstitial round-cell infiltration. By the seventh day, fibroblastic proliferation with collagen formation was prominent. By the thirteenth day, regeneration and remodeling were essentially complete.
Overall, Rais concluded that the morphological changes associated with peritendinitis were localized to the peritenon and muscles, both near the myotendinous junction. The primary changes of the paratenon consisted of edema with fibrinous exhudation, followed by reabsorption and organization. In the muscles, one observed degeneration of varying degree, fibrin deposition, then regeneration.
C.5.h Proposed Models of Pathogenesis
Peritendinitis appears to have two distinct etiologies: blunt trauma or "strain" followed by repetitive stereotyped exertions to which the person is accustomed, and repeated, stereotyped exertions to which the person is unaccustomed.
A single traumatic event followed by accustomed activity has been reported to account for up to 50% of cases. A direct mechanical insult that injured and compromised the integrity of a myotendinous junction, when followed by usage of the affected muscle-tendon unit, might lead to the manifestation of peritendinitis.
The other 50% of cases of peritendinitis have been reported to occur in the context of unaccustomed hand activity. Fatigue appears to be the critical factor. According to the fatigue theory, the metabolic demands to maintain the exertions consume or deplete available energy supplies within the muscle. As a result, the myotendinous junction is not able to maintain its extensive folding of the muscle cell membrane. When the loading angle on the membrane increases, the cell membrane is susceptible to rupture by the shear forces transmitted across it. This could initiate a sequence of events, such as loss of intracellular homoeostasis of calcium or potassium, that might lead to the tissue changes characteristic of peritendinitis.
C.6 First Dorsal Compartment Tendon Entrapment
This discussion of de Quervain's disease is adapted from a recent comprehensive review (Moore, 1997).
C.6.a Normal Anatomy and Kinesiology
On the dorsum of the wrist (the extensor side), there are six fibro-osseous compartments. On this side of the wrist, the ligamentous structure covering these six compartments is usually called the extensor retinaculum.
Finkelstein (1930), using cadaver dissection, described the normal anatomy of the first dorsal compartment. The first dorsal compartment is located on the thumb side of the wrist (at the radial styloid) just proximal to the wrist joint. In most circumstances, the first dorsal compartment is a single compartment that contains the tendons and synovial sheaths of the APL and the EPB. The synovial sheaths are approximately 2.25 inches long. The extensor retinaculum at the first dorsal compartment is approximately 5/8 inches long and 1/32 inches thick. Normally, the tendons glide freely and a probe passes easily through the fibro-osseous canal. De Quervain's tenosynovitis involves thickening of the extensor retinaculum of the first dorsal compartment and narrowing (stenosis) of the fibro-osseous canal.
The APL and EPB originate on the shaft of the radius near the beginning of its distal third. The APL inserts on the base of the dorsum of the first metacarpal. The EPB inserts on the base of the dorsum of the first phalanx of the thumb. Both muscle-tendon units control the position and orientation of the thumb so that it will be in proper position to apply force. As a result, the APL and EPB may be active even though the distal phalanx of the thumb is involved with application of force via its flexors.
The term "tenosynovitis" means inflammation of the tendon sheath; however, there are many potential forms of tenosynovitis. Classical acute inflammatory changes are characteristic of tenosynovitis related to certain systemic diseases, e.g., rheumatoid arthritis or gout. Tenosynovial disorders may also be related to infections of tendon sheaths by micro organisms, e.g., mycobacterium tuberculosis or nisseria gonorrhea. The form of tenosynovitis related to de Quervain's tenosynovitis is called stenosing tenosynovitis.
Despite the strict meaning of tenosynovitis mentioned above, the pathology of de Quervain's tenosynovitis does not generally involve inflammation. Instead, the primary pathological change is thickening of the extensor retinaculum that covers the first dorsal compartment of the wrist (Cotton, Morrison, and Bradford, 1938; de Quervain, 1912a, 1912b; Finkelstein, 1930; Schneider, 1928; Stein, 1927; Patterson, 1936; Lipscomb, 1944; Griffiths, 1952; Diack and Trommald, 1939; Younghusband and Black, 1963; Muckart, 1964; Troell, 1921; Conklin and White, 1960; Kelly and Jacobsen, 1964; Welti, 1896; Michaelis, 1912; Flörcken, 1912; Nussbaum, 1917; Keppler, 1917; Reschke, 1919; Eichoff, 1927). Mild cases may be associated with a retinaculum that is only twice normal thickness while more severe cases are associated with thickening three to four times normal (Finkelstein, 1930; Schneider, 1928; Patterson, 1936; Lamphier, Crooker, and Crooker, 1965; Conklin and White, 1960; Nussbaum, 1917). The retinaculum may appear non-translucent, densely fibrous or even cartilaginous, and it may cut like gristle (Finkelstein, 1930; de Quervain, 1912a, 1912b; Stein, 1927; Schneider, 1928; Patterson, 1936; Diack and Trommald, 1939; Welti, 1896; Nussbaum, 1917). The side of the retinaculum facing the tendon may demonstrate fibrocartilagenous metaplasia (Lamphier, Crooker, and Crooker, 1965; Huber, 1933). The cross-sectional area of the fibro-osseous canal is decreased (Finkelstein, 1930; de Quervain, 1912a, 1912b; Stein, 1927; Schneider, 1928; Patterson, 1936; Younghusband and Black, 1963; Michaelis, 1912; Flörcken, 1912).
Mild cases are microscopically characterized by thickened synovial layers (except at the site of constriction where they may be thinned or absent); a thickened and vascularized loose connective tissue layer; and a slightly thickened, but less vascularized, extensor retinaculum (Finkelstein, 1930; Patterson, 1936; Diack and Trommald, 1939; Younghusband and Black, 1963). In more severe cases, the synovial layers are completely destroyed; the loose connective tissue layer is compressed and thinned out; and the extensor retinaculum is markedly thickened with fibrous tissue, fibrocartilagenous metaplasia, or hyaline and cartilaginous degeneration (Finkelstein, 1930; Stein, 1927; Schneider, 1928; Patterson, 1936; Diack and Trommald, 1939; Younghusband and Black, 1963; Michaelis, 1912; Keppler, 1917).
In general, the tendons appear normal (Schneider, 1928; Patterson, 1936; Lipscomb, 1944; Younghusband and Black, 1963; Muckart, 1964; Lamphier, Crooker, and Crooker, 1965; Michaelis, 1912; Eichoff, 1927). In some cases, the tendons may be thinned at the point of constriction (fusiform); covered with granulation tissue secondary to compression at the site of stenosis; and fail to glide freely in the fibro-osseous canal (Finkelstein, 1930; Stein, 1927; Diack and Trommald, 1939; Younghusband and Black, 1963; Muckart, 1964; Reschke, 1919; Eichoff, 1927; Eschle, 1924). There may be adhesions between the tendon and its sheath or between tendons (Finkelstein, 1930; Schneider, 1928; Muckart, 1964; Lamphier, Crooker, and Crooker, 1965; Keppler, 1917; Reschke, 1919).
Anatomical variations are important. Partitioning of the first dorsal compartment and its tendons into several sub-compartments and tendon strands has been observed more commonly among individuals with de Quervain's tenosynovitis than controls (Finkelstein, 1930; Younghusband and Black, 1963; Muckart, 1964; Lamphier, Crooker, and Crooker, 1965; Lipscomb, 1959; Kelly and Jacobsen, 1964; Bunnell, 1951; Lacey, Goldstein, and Tobin, 1951; Loomis, 1951).
Mechanically, functional impairment is believed to be caused by impaired gliding of the APL or EPB tendons because of anarrowed fibro-osseous canal and, in some cases, alterations in the tendons, i.e., gross physical deformity or granulation tissue deposited on their surfaces (Finkelstein, 1930; Patterson, 1936; Cotton, Morrison, and Bradford, 1938; Wood, 1941; Reschke, 1919; Eichoff, 1927; Eschle, 1924). An explanation for the symptoms is less clear. Attempted use of a thumb with stenosing tenosynovitis of the first dorsal compartment probably causes mechanical impingement (compression) between the tendon and its narrowed fibro-osseous canal (de Quervain, 1895; de Quervain, 1912a, 1912b; Michaelis, 1912; Flörcken, 1912). This compression might cause increased tensile loading of the abnormal retinaculum. The increased tensile loading might elicit pain via stimulation of nociceptors. This pathophysiological model provides one way to explain why splinting with a thumb spica is an effective way to manage symptoms, i.e., it inhibits gliding of the tendon through the abnormal fibro-osseous canal and mechanical impingement of the tendon against the retinaculum.
C.6.d Clinical Observations on Etiology
Several authors have noted traumatic etiologies, including being struck on the forearm, falling down stairs, carrying an 8-year old boy for 10 to 15 minutes, drying dishes, sudden wrenching of the hand during a quarrel, and falling on the tip of the thumb (Finkelstein, 1930; Hoffmann, 1898; Stein, 1927; Hanson, 1926). Six (25%) of Finkelstein's 24 cases were associated with acute trauma (1930).
One of the more prevalent etiologic themes emphasizes overexertion of the thumb (Welti, 1896). Hoffman reported that 7 (58%) of his 12 cases had no history of acute trauma (1898). One woman used a bread knife 4 to 5 hours daily which "greatly tired her hand" and another wrung clothes, but was apparently accustomed to the task. One of the male cases caught 7- to 10-lb packages thrown from a wagon for 8 to 9 hours daily. de Quervain (de Quervain, 1912a, 1912b) noted that the most frequent "exciting cause" was overexertion from household duties. Troell postulated that "monotonous and tiring work" may have an etiologic role (1921). Schneider (1928) stated that the exact etiology was not clear, but that there was "more or less agreement that excessively monotonous use of the involved tendons is the most commonly evident cause." Finkelstein (1930) stated "the general impression prevails that the inciting factor must be attributed to chronic trauma" and noted relationships with varying activities: prolonged piano-playing; working at a typewriter or adding machine; excessive writing, washing, or wringing out clothes; chopping wood; carrying heavy objects; farm labor; and cutting cloth with heavy scissors. Patterson (1936) stated that the etiologic factor was "undoubtedly" trauma. His 10 cases were all engaged in occupations that required pressure by the thumb while in a partially abducted position and the hand in ulnar deviation, such as when working on a grinding or buffing machine. One case involved fitting rubber rings over a pipe. This task required firm thumb pressure and the individual developed severe pain in both thumbs the evening after performing this task 500 times. Many others have agreed with these observations on etiology (Lipscomb, 1944; Diack and Trommald, 1939; Wood, 1941; Conklin and White, 1960).
Griffiths (1952) stated that the most common provoking cause was repeated unaccustomed movement. He noted that many patients start to have symptoms on the second day of taking a new job or on resuming an old one after a holiday or illness and that the thumb tendons were especially affected by repeated full movements of the thumb and wrist, as in picking up and laying bricks. He also noted that some cases seem to be due to persistent repetition of an accustomed task continued beyond the point of fatigue. This observation was shared by Kelly and Jacobson (1964).
Muckart (1964) specifically excluded friction as an important part in the production of stenosing tendovaginitis. He emphasized firm grasp combined with movement of the hand in a radial direction, as in wringing clothes. In addition, he noted that the angle of the tendon at the distal edge of the retinaculum may be 105 degrees.
Other etiologies have been mentioned, but without affirmative reports by others. Poulson (1911) suggested that the condition was a periostitis due to traction by the tendon sheath. Burke (1912) attributed the cause to habitual subluxation of the first carpal-metacarpal (CMC) joint.
C.6.e Experimental Results
Finkelstein (1930) performed seven animal experiments designed to determine what kind of stimuli could reproduce the pathological changes at the radial styloid of the rabbit. Based on his experiements, he concluded that "stenosing tenosynovitis in rabbits can be produced by thermal, chemical, and mechanical irritation. When the skin remains intact, injury to the tendon sheath is possible, but to the tendon itself, improbable."
The experimental work reviewed in the section on flexor tendon entrapment of the digits (Section C.8) is relevant to this disorder as well, but will not be repeated here.
C.6.f Historical Theories of Pathogenesis
Early in the history of this disorder, chronic inflammation was considered the most likely mechanism for the development of the pathological changes associated with stenosing tenosynovitis (Michaelis, 1912; Keppler, 1917; Vischer, 1919). However, histological evidence of this inflammation is generally lacking.
Some cases appear to arise primarily from an altered tendon (Troell, 1921; Hanson, 1926). Hanson (1926) reported a single case of stenosing tenosynovitis caused by blunt direct trauma to the tendon. The trauma apparently caused incomplete rupture of the tendon and, therefore, a localized repair response on the tendon. The retinaculum was normal in this case. While plausible, this mechanism appears to be uncommon.
Increased friction has been postulated as a pathogenetic mechanism (Schneider, 1928; Eschle, 1924). In the context of a fracture of the radial styloid, Eschle (1924) believed that increased friction of the two tendons over the callous formation at the distal radius produced thickening of the retinaculum. He also noted that friction was quantitatively related to exertion. He stated "the friction may be increased qualitatively if the normal smooth osseous base is changed by trauma."
Eschle (1924) also introduced the concept of stenosing tenosynovitis being a vicious cycle. He stated, "one may assume that the tendon sheath [retinaculum] becomes edematous, which further increases friction...a vicious cycle is formed the ultimate result of which is a thickening of the tendon sheath [retinaculum]."
Several have discussed the role of biomechanical compression in the pathogenesis of de Quervain's tenosynovitis (Griffiths, 1952; Cotton, Morrison, and Bradford, 1938; Wood, 1941; Eichoff, 1927). The compression forces arise from the taut tendons changing direction at the fibro-osseous canal ("loaded tendons turning corners"). The tendons are taut because of thumb exertions; the tendons change direction because of a non-neutral wrist or thumb posture. According to Eichoff (1927):
The role of predisposing factors has been discussed (Lipscomb, 1944; Welch, 1972). According to Welch (1972): "In most instances, it appears that tenosynovitis will only occur if the worker has a predisposition to the disease." The main predisposing factor was postulated to be small muscles with inadequate blood supply. He speculated that training the muscles would increase their blood supply, thus decreasing the degree of predisposition. Emotional upset was a secondary predisposing factor because it was believed to cause the worker to work with tensed muscles, resulting in jerky movements and unnecessary grip forces. Working with tired muscles, perhaps due to a second job or housework, was also considered a predisposing factor. Welch offered no data to substantiate any of these opinions. Lipscomb (1944) speculated that individuals at "early middle life are not as active as in earlier years, but most likely to overexert themselves without realizing decreasing ability to stand physical activity as formerly."
Welch (1972) also discussed movements and posture as precipitating causes of tenosynovitis. He characterized movements by their force, direction, speed, frequency, and number. He considered force the single greatest precipitating factor, accounting for 30% of 500 investigated cases. Factors that could increase force included inexperienced or untrained workers, aggressive work methods (maybe related to emotional state), unsuitable tools, operation of controls, and poor quality control of components for assembly. Welch noted that force must be considered in relation to frequency. Regarding direction, Welch stated that movements away from or across the body, especially if substantial force were involved, should be avoided. Speed and high-frequency movements were often related to incentive production. Fast movements of the fingers, hands, and arms required greater muscular force and, if repeated without adequate rest, may cause tenosynovitis. Similarly, high-frequency tasks may not allow sufficient rest periods for muscles to recover from fatigue. For posture, Welch recommended avoiding static loading of musculature and working in favorable body postures. None of these factors were tied directly to the pathogenesis of de Quervain's tenosynovitis.
C.6.g Proposed Theories of Pathogenesis
The proposed theories to follow are limited to describing plausible mechanisms for the development of de Quervain's tenosynovitis in the context of acute trauma and hand usage. The potential roles of two "non-occupational" factors, anatomical variability and unaccustomed hand usage, have been included because they have also been mentioned as having potentially significant roles in the context of hand usage. The potential roles of personal factors, such as age and gender, have not been included at this time.
As summarized earlier, observations by clinicians suggest that de Quervain's tenosynovitis is related to repeated, prolonged, or unaccustomed exertions that involve the thumb in combination with non-neutral wrist or thumb postures. Thumb exertions are associated with tensile loading of the APL and EPB (they position the thumb to apply force and prevent collapse of the first metacarpal bone). Postural deviation of the wrist or CMC joint of the thumb makes the APL or EPB turn a corner at the extensor retinaculum. Tensile loading of these tendons in combination with their turning a corner creates a compressive force between the tendons and the distal end of the retinaculum. Based on the experimental data discussed in the section on flexor tendon entrapment of the digits (Section C.8), the retinaculum may respond to this compressive stimulus with functional hypertrophy or fibrocartilagenous metaplasia. The fibrocartilagenous changes in the retinaculum and the granulomatous changes on the surface of the tendon (secondary to collagen fibril disruption) are consistent with compression being the critical mechanism.
A simple biomechanical analysis of the static situation predicts that the magnitude of the compressive force on the distal end of the extensor retinaculum (FC) would be proportional to the tensile load of the tendons passing through the compartment (FT) and the sine of the angle () between the course of the deviated tendon(s) compared to the neutral position of the tendon(s).
Static Compression (Shear)
In the static compression model, it is assumed that the total duration of loading during a period of activity (of duration T) is most critical. Mathematically, this can be described by equation 1.
Accumulated Compressive Force =
In this model, the duration of compression (as a fraction of the job cycle) is more important than the repetition (number) of compressions, e.g., one prolonged exertion at relatively moderate levels of compressive load could be more significant than a series of brief and intermittent exertions at the same or higher levels of compressive load.
Repeated Compression (Shear)
This theory relies on the same biomechanical argument as the static compression theory, except the number of episodes of loading (n) during a period of activity is considered more critical than the accumulated duration of loading. Mathematically, this can be described by equation 2.
Accumulated Compressive Force =
Acute Trauma ("One-Hit")
A single episode of acute trauma involving the first dorsal compartment, such as a contusion, has been reported to be related to up to 25% of cases of de Quervain's tenosynovitis (de Quervain, 1912; Hoffmann, 1898; Stein, 1927; Schneider, 1928; Hanson, 1926). It should be acknowledged, however, that not all episodes of such trauma necessarily lead to de Quervain's tenosynovitis and that qualitative and quantitative descriptions of such stimuli are lacking.
This proposed theory begins with a single episode of blunt trauma targeted directly over the region of the first dorsal compartment. Three subsequent pathways appear plausible. The first pathway involves disruption of the collagen fibers within the extensor retinaculum, followed by a repair response that leads to thickening of the retinaculum and stenosis of the fibro-osseous canal. The second pathway involves disruption of collagen fibers within the tendon(s) of the APL or EPB, followed by a repair response that leads to a nodular lesion on the tendon. This nodular lesion leads to a "relative" stenosis of the fibro-osseous canal even though the extensor retinaculum is otherwise unaffected. The third pathway involves hemorrhage and edema in the general region that increases compressive or shear forces between the otherwise normal APL or EPB tendons and the extensor retinaculum (see previous models). Since there is little information upon which to base this theory of pathogenesis, the proposed mechanism should be considered quite tentative.
C.7 Carpal Tunnel Syndrome (CTS)
The carpal tunnel is a fibro-osseous canal located on the palmar aspect of the hand. Normal contents of the carpal tunnel include the flexor tendon pairs for digits II-V, the flexor pollicis longus, and the median nerve. The tendons within the carpal tunnel are covered by tendon sheaths. For some individuals, the proximal ends of the lumbrical muscles enter the distal end of the carpal tunnel, especially with digital flexion (Yii and Elliot, 1994; Cobb et al., 1994; Tanzer, 1959). CTS is usually defined as symptomatic compression of the median nerve at the wrist.
C.7.a : Pathology
Indentation of the median nerve at the site of compression was not uncommon historically, but the most commonly reported gross anatomic change was thickening of the flexor tendon synovium (Tanzer, 1959; Yamaguchi, Lipscomb, and Soule, 1965; Phalen, 1966; Phalen and Kendrick, 1957; Lipscomb, 1959; Cseuz, Thomas, and Lambert, 1966). Histopathological studies have almost uniformly demonstrated a lack of inflammation (Faithfull, Moir, and Ireland, 1986; Neal, McManners, and Stirling, 1987; Schuind, Ventura, and Pasteels, 1990; Fuchs, Nathan, and Myers, 1991). Instead, they usually report edema, collagen bundle thickening, hyaline degradation of the synovial membrane, fibrous hyperplasia of the synovial membrane, or vascular sclerosis (Faithfull, Moir, and Ireland, 1986; Neal, McManners, and Stirling, 1987; Schuind, Ventura, and Pasteels, 1990; Fuchs, Nathan, and Myers, 1991). The origin of these tendon sheath changes have not been identified. They are characteristic of degenerative changes, but their cause(s) are generally unknown.
Ultrastructural studies related to chronic nerve entrapment models have demonstrated invagination and retraction of myelin lamellae on axons exposed to mechanical pressure (Ochoa and Marotte, 1973).
The symptoms of CTS are usually explained on the basis of ischemia that is related to increased intracarpal pressure (Gilliatt and Wilson, 1953; Fullerton, 1963; Thomas and Fullerton, 1963; Szabo and Gelberman, 1987; Cailliet, 1988; Lundborg and Dahlin, 1989; Dawson, Haillet, and Millender, 1990; Dahlin and Rydevic,1991). An explanation for the characteristic electrodiagnostic abnormalities is less clear. Delayed conduction of the motor or sensory fibers of the median nerve are believed to be secondary to a reduction in the diameter of the larger axons, focal demyelination of selected axons, or both (Ochoa and Marotte, 1973; Fullerton, 1963; Thomas and Fullerton, 1963). The reduction in nerve fiber diameter is believed to be a response to increased pressure (mechanical) (Thomas and Fullerton, 1963). The cause of the demyelination, however, may be mechanical or physiological. The mechanical theory is based on physical deformation of myelin sheaths in areas of contact pressure. The physiological theory is based on the notion that focal ischemia of a nerve segment may also cause demyelination. The physiological theory does not explain the tadpole deformity.
C.7.c Proposed Models of Pathogenesis
Several models are plausible and consistent with the reported observations. At this time, there are probably insufficient data to reject any of the proposed models outright. Similarly, there may be insufficient data to affirm any one of the proposed models. It is possible that none of them are correct.
Proposed CTS Model #1: Tendon Sheath Thickening
Perhaps the most popular model is based on the assumption that thickening of the flexor tendon sheath(s) causes increased intracarpal fluid pressure and mechanical contact pressure on the median nerve. The observations from surgical case series and biomechanical theory are consistent with this model (Tanzer, 1959; Yamaguchi, Lipscomb, and Soule, 1965; Phalen, 1966; Phalen and Kendrick, 1957; Lipscomb, 1959; Cseuz, Thomas, and Lambert, 1966; Faithfull, Moir, and Ireland, 1986; Neal, McManners, and Stirling, 1987; Schuind, Ventura, and Pasteels, 1990; Fuchs, Nathan, and Myers, 1991; Ochoa and Marotte, 1973; Armstrong et al., 1987; Goldstein et al., 1987). It is possible, however, that the tendon sheaths are merely responding to the same stressor affecting the median nerve, such as increased intracarpal pressure, and their thickening has no effect whatsoever on the median nerve.
In this model, repeated movements or exertions of the digital flexor tendons combined with non-neutral wrist posture lead to increased contact pressure or friction on the flexor tendon sheaths. The increased contact pressure, under some circumstance of duration or repetition, might lead to edema or degenerative changes within the tendon sheaths. Long-standing edema or degenerative changes might lead to thickening of the flexor tendon sheaths. The thickened tendon sheaths would contribute to increased intracarpal pressure and contact pressure on the median nerve, leading to symptoms and electrodiagnostic test abnormalities characteristic of CTS. Note that the temporal aspects of this model are undefined.
Proposed CTS Model #2: Tendon Hypertrophy
The second proposed model assumes that the digital flexor tendons, like their associated muscles, have the capability to hypertrophy in response to repeated exertions. Animal experiment data support the biological plausibility of this model (Woo et al., 1980). A case-control study using computed tomography (CT) supports the plausibility of this theory in humans (Jessurun et al., 1987). It is unknown, however, if the digital flexor tendons are exposed to tensile loads sufficient to cause this adaptive response.
In this model, repeated or prolonged forceful exertions of the digital flexor tendons are postulated to lead to their hypertrophy. The enlarged flexor tendons lead to increased intracarpal pressure and contact pressure on the median nerve. These changes contribute to the manifestation of the symptoms and electrodiagnostic test abnormalities characteristic of CTS. Again, the temporal aspects of this model are unknown.
Proposed CTS Model #3: Tendon Compression
The third proposed model assumes that the median nerve can be trapped and compressed between loaded digital flexor tendons and the transverse carpal ligament. This model is supported by the results of the cadaver experiments (Smith, Sonstegard, and Anderson, 1977). It is currently unclear whether such exertions also cause increased intracarpal fluid pressure, increased intraneural pressure, both, or neither.
In this model, repeated or prolonged forceful exertions of the digital flexor tendons combined with wrist flexion are postulated to lead to increased contact pressure on the median nerve from the flexor tendons. These changes are postulated to contribute to increased intracarpal pressure and contact pressure on the median nerve and, therefore, manifestation of the symptoms and electrodiagnostic test abnormalities characteristic of CTS. The temporal aspects of this model are unknown.
Proposed CTS Model #4: Lumbrical Retraction
The fourth proposed model assumes that the proximal ends of the lumbrical muscles may enter the distal end of the carpal tunnel as the flexor tendons upon which they originate move within the carpal tunnel in response to finger flexion (Yii and Elliot, 1994; Cobb et al., 1994; Cobb, An, and Cooney, 1995). The increased contents within the carpal tunnel would increase intracarpal pressure and create mechanical contact pressure on the median nerve.
In this model, repeated or prolonged digital flexion is postulated to cause retraction of the proximal ends of the lumbricals into the distal carpal tunnel. This change is postulated to lead to increased intracarpal pressure and contact pressure on the median nerve and, therefore, the manifestation of symptoms and electrodiagnostic test abnormalities characteristic of CST. The temporal aspects of this model are unknown.
Proposed CTS Model #5: Transverse Carpal Ligament Hypertrophy
The fifth proposed model relies on the assumption that the transverse carpal ligament (TCL) has the ability to respond to mechanical loading in a manner analogous to stenosing tenosynovitis at other sites. Very few observations support this proposed model. Tanzer (1959) observed no differences in the thickness of the TCL when comparing cases to controls. Surgeons rarely mention this as a finding in their case series.
In this model, it is postulated that repeated or prolonged exertions of the digital flexor tendons in combination with wrist flexion create compressive force between these tendons and the TCL. This leads to increased tension in the TCL and, in response, passive functional hypertrophy and/or fibrocartilagenous metaplasia of the TCL. The thickening of the ligament is postulated to cause increased intracarpal pressure and contact pressure on the median nerve. These changes lead to manifestation of symptoms and electrodiagnostic test abnormalities characteristic of CTS. The temporal aspects of this model are unknown.
Proposed CTS Model #6: Ischemia
The sixth proposed model assumes that prolonged or repeated increases in intracarpal pressure related to non-neutral wrist postures, independent of the flexor tendons, cause intraneural ischemia that leads to symptoms and myelin degeneration (Yamaguchi, Lipscomb, and Soule, 1965; Dawson, Haillet, and Millender, 1990; Dahlin and Rydevic, 1991; Phalen, 1970; Brain, Wright, and Wilkinson, 1947; Gelberman et al., 1981). There is a question as to whether the magnitude or duration of such increases in intracarpal pressure leads to physiologically meaningful episodes of ischemia.
In this model, repeated or prolonged non-neutral wrist postures are postulated to lead to increased intracarpal pressure. If sustained for sufficient durations of time, this leads to intraneural ischemia. Repeated episodes of intraneural ischemia are postulated to lead to intraneural fibrosis and demyelination, which the lead to the manifestation of symptoms and electrodiagnostic test abnormalities characteristic of CTS. This model requires prolonged durations of increased intracarpal pressure.
Proposed CTS Model #7: Blunt Trauma
There is some evidence that direct, blunt trauma over the carpal tunnel might lead to direct injury to the median nerve. In this circumstance, forecful contact stress to the palm of the hand, such as using the hand as a hammer, would transmit contact forces through the skin, subcutaneous tissue, through the TCL, and create traumatic injury to the nerve itself. It is plausible that one notably forceful event could lead to adverse consequences. It is also plausible that repeated, but less forceful, events might also be plausible.
C.8 Digital Flexor Tendon Entrapment
C.8.a Normal Anatomy
Detailed descriptions of the anatomy and function of the digital flexor tendon sheaths have been reported (Doyle and Blythe, 1974, 1975; Lundborg and Myrhage, 1977; Zancolli, 1979; Hunter and Cook, 1982; Delattre et al., 1983; Idler, 1985; Strauch and deMoura, 1985; Doyle, 1988; Lin et al., 1989; Hoving and Hillen, 1989). These tendon sheaths are usually described as having two components: a membranous synovial component and a ligamentous retinacular component (Lundborg and Myrhage, 1977; Delattre et al., 1983; Idler, 1985; Strauch and deMoura, 1985; Doyle, 1988; Hoving and Hillen, 1989; Bunnell, 1944). The synovial component was initially described as a double-walled hollow tube sealed at both ends (Doyle and Blythe, 1974; 1975; Lundborg and Myrhage, 1977; Idler, 1985; Strauch and deMoura, 1985; Bunnell, 1944). The interior of the synovial component contains synovial fluid. Along the flexor side of the digit, the synovial component appears to be covered by a series of intermittent ligamentous structures, called pulleys (Doyle and Blythe, 1975; Lundborg and Myrhage, 1977; Hunter and Cook, 1982; Delattre et al., 1983; Idler, 1985; Doyle, 1988, 1989; Lin et al., 1989; Hoving and Hillen, 1989; Bunnell, 1944; Cohen and Kaplan, 1987; Jones and Amis, 1988; Amis and Jones, 1988). The pulleys represent the retinacular or ligamentous component of the tendon sheath. There are two types of pulleys, annular and cruciate (Doyle and Blythe, 1975; Doyle, 1988, 1989; Lin et al., 1989; Hoving and Hillen, 1989). Two annular pulleys cover the flexor tendons over the shafts of the proximal and middle phalanges (A2 and A4, respectively) (Lin et al., 1989). Three annular pulleys are related to the palmar plates of the MP, PIP, and DIP joints (A1, A3, and A5, respectively). The cruciate pulleys usually cover the tendons as they cross joints. This configuration and arrangement of the retinacular system permits flexion of the digit without buckling the pulleys or impinging on the underlying tendon(s) (Doyle, 1988; Hoving and Hillen, 1989).
Annular pulleys are present at areas of greatest biomechanical stress from the flexor tendons. The most proximal pulley, called the palmar aponeurosis (PA) pulley, begins in the palm (Doyle, 1988; 1989; Manske and Lesker, 1983).The first annular pulley, A1, begins about 5 mm proximal to the MP joint line (Doyle and Blythe, 1974, 1975; Hoving and Hillen, 1989). It is made up of one to three bands, is approximately 0.5 mm thick, and, depending on the finger, is 5 mm to 10 mm long (Doyle and Blythe, 1975; Idler, 1985; Doyle, 1988, 1989).
Histologically, A1 pulleys are composed of two layers (Sampson et al., 1991). The outer vascular layer is a dense capillary network. The inner friction layer is composed mainly of dense collagen bundles with spindle-shaped fibroblasts interspersed throughout and ovoid cells near the friction surface (Sampson et al., 1991). These ovoid cells have characteristics of chondrocytes (Lundborg and Myrhage, 1977; Sampson et al., 1991; Eskeland et al., 1977). The synovial component has visceral and parietal layers that are most apparent between the pulleys and do not appear to be subject to the same mechanical forces as the pulleys (Lundborg and Myrhage, 1977; Doyle, 1989). The avascular surface of the pulleys appears to be nourished by diffusion from the synovial fluid (Lundborg and Myrhage, 1977). Chondrocyte-like cells have been observed on the friction surface of the distal end of the A2 pulley (Doyle, 1988; Knott and Schmidt, 1986).
Several authors have published reviews or studies related to biomechanical models of the hand (Landsmeer, 1961; Armstrong and Chaffin, 1978; An et al., 1979, 1983a, 1983b, 1985; Weightman and Amis, 1982; Hamman et al., 1997; Buchner, Hines, and Hemami, 1988; Thompson and Giurintano, 1989). Most of these models describe relationships between tendon shortening relative to joint rotation or applied fingertip force relative to tendon tensile load. Biomechanically, the pulleys deflect the flexor tendons at their point of contact. Goldstein et al. (1987) demonstrated that the magnitude of the shear force between the flexor tendons and the TCL (a more proximal retinaculum) varied with the magnitude of the tendon load and the degree of tendon deflection (wrist posture). Hume et al. (1991) developed and validated a mathematical model to estimate tension on a pulley based on applied fingertip force, tendon tension, tendon excursion, joint range of motion, pulley position, and pulley geometry at a generic joint. Their simplified model (equation 3) included terms related to tendon tension, tendon deflection, and pulley geometry.
For a constant fingertip force, maximum pulley tension was predicted to occur at the more extreme joint flexion angles (70 to 90 degrees) despite decreased tendon tension at these angles (Hume et al., 1991). For a fingertip force of 3 N with a moment arm of 50 mm and joint flexion angles between 0 degrees and 30 degrees, tension at the proximal and distal ends of the pulley were predicted to be relatively constant at 11.0 N and 11.5 N, respectively. At 90 degrees joint flexion, the pulley tension values increased to 12.9 N at the proximal end of the pulley and 28.3 N at the distal end of the pulley.
Since pulley tension is proportional to joint posture, understanding the full active and functional ranges of motion of the joints of the hands is relevant. Hume et al., reported these ranges of motion of the joints of the hands of 35 right-handed males, aged 26 to 28 years, who had no history of hand injury (Hume et al., 1990). The functional ranges of motion were measured during a series of activities of daily living (holding a telephone, holding a can, using a zipper, holding a toothbrush, turning a key, using a comb, printing with a pen, holding a fork, holding scissors, unscrewing a jar, and holding a hammer). The normal range of motion for the metacarpophalangeal (MP) joint of the thumb was 0 degrees to 56 degrees for 85% of the population and 0 degrees to 27 degrees for 15% of the population. Flexion of the MP joint of the thumb contributed to 60% of the total arc of motion for the thumb. The normal ranges of motion for the MP joints of the fingers were not significantly different and, as a group, were 0 degrees to 100 degrees. Finger MP joint flexion contributed to 33% of the total arc of motion for the fingers. The functional range of motion for the MP joint of the thumb was 10 degrees to 32 degrees (mean 21 degrees; median 22 degrees). The functional ranges of motion for the MP joint of the fingers were 33 degrees to 73 degrees (mean 61 degrees; median 62 degrees). For key pinch, the MP joint of the thumb was 20 degrees (± 15 degrees) and the MP joints of the fingers were 62 degrees (± 15 degrees). For tip pinch, the MP joint of the thumb was 22 degrees (± 19 degrees) and the MP joints of the fingers were 58 degrees (± 7 degrees). For precision grasp, the MP joint of the thumb was 10 degrees (± 9 degrees) and the MP joints of the fingers was 33 degrees (± 6 degrees). For power grasp, the MP joint of the thumb was 23 degrees (± 9 degrees) and the MP joints of the fingers was 72 degrees (± 12 degrees).
Based on cadaver experiments, it is estimated that a normal A1 pulley ruptures when the pulley tension is around 250 to 300 N (its ultimate strength) (Hume et al., 1991; Manske and Lesker, 1977). The average ultimate strength of the A2 pulley is 400 N (Lin et al., 1989). Hume et al. (1991), estimated that a 3 N force applied with the fingertip would correspond to 107 N of tension in the A1 pulley. A fingertip force of 12 N would correspond to 428 N of tension, thus placing the pulley at risk of mechanical failure. Using S-shaped force transducers applied to the flexor pollicis longus (FPL), FDS, and FDP tendons of thumb and index finger of patients undergoing carpal tunnel release surgery, Schuind et al. (1992) measured tendon forces during active and passive wrist and digit motion, tip pinch, lateral pinch, and grasp. Active and passive motion of the wrist resulted in similar mean tendon forces that ranged between 0.0 to 2.9 N. Higher forces were observed during wrist hyperextension compared to passive flexion-extension. Passive flexion-extension or hyperextension of the interphalangeal (IP) joint of the thumb resulted in mean FPL forces of 2.9 and 5.9 N, respectively. Active IP flexion and extension resulted in mean FPL forces of 17.6 and 3.9 N, respectively. Passive distal interphalangeal (DIP) flexion-extension of the index finger resulted in a mean force of 0.1 N in the FDP tendon (no forces were measured in the FPL or FDS tendons). Active DIP flexion resulted in no FPL force, but a mean of 18.6 N in the FDP and 0.2 N in the FDS. Passive proximal interphalangeal (PIP) flexion-extension of the index finger resulted in a mean force of 1.0 N in the FPL and FDP tendons and 2.0 N in the FDS tendon. Active PIP finger flexion resulted in mean forces of 1.0 N in the FPL and FDP tendons and 8.8 N in the FDS tendon. During tip pinch (with applied force up to 34.3 N), the maximum forces in the FPL, FDP, and FDS were 58.8, 117.6, and 34.3 N, respectively (means 26.5, 81.3, and 18.6 N). For lateral pinch (with applied forces up to 46.1 N), the maximum forces for the FPL, FDP, and FDS were 70.6, 64.7, and 30.4 N, respectively (means: 37.2, 34.3, and 13.7 N). For grasp, the maximum forces for the FPL, FDP, and FDS were 41.6, 62.7, and 8.8 N, respectively (means: 19.5, 39.2, and 5.9 N). The means of the ratios between tendon forces and applied forces for tip pinch was 3.6 for the FPL, 7.92 for the FDP, and 1.73 for the FDS. For lateral pinch, these mean ratios were 3.05, 2.90, and 0.71, respectively. These values were noted to be consistent with predicted values from other studies.
Azar et al. measured pressure on the A1 pulley (Wilson, 1983). In the neutral position, pressures ranged from 0 mm Hg to 50 mm Hg. With full finger flexion, pressures increased to 500 mm Hg to 700 mm Hg.
Other than a difference in location, the pathology of flexor tendon entrapment of the digits is essentially identical to tendon entrapment at the first dorsal compartment (de Quervain's tenosynovitis) (Lipscomb, 1944; Sprecher, 1949; Conklin and White, 1960; Sampson, Wisch, and Badalamente, 1994; Zelle and Schnepp, 1936; Kalms and Højgard, 1991). The A1 pulley of the tendon sheath is thick and fibrous, thus compromising the cross-sectional area of the fibro-osseous canal (Kamhin, Sampson et al., 1991; Lipscomb, 1944; Sprecher, 1949; Conklin and White, 1960; Sampson, Wisch, and Badalamente, 1994; Zelle and Schnepp, 1936; Kalms and Højgard, 1991; Compere, 1933; Sperling, 1951; Nasca, 1980; Lapidus and Fenton, 1952; Fahey and Bollinger, 1954; Lipscomb, 1959; Kolind-Sørensen, 1970; Boyes, 1970; Wilson, 1983; Ametewee, 1983; Thompson and Phelps, 1990; Jahss, 1936; Hueston, 1972 ).The underlying flexor tendons may exhibit a nodular or fusiform swelling and may be covered with granulation tissue, both believed to be secondary to the stenosis caused by the thickened tendon sheath (Sampson et al., 1991; Lipscomb, 1944; Sprecher, 1949; Conklin and White, 1960; Zelle and Schnepp, 1936; Nasca, 1980; Lapidus and Fenton, 1952; Fahey and Bollinger, 1954; Lipscomb, 1959; Kolind-Sørensen, 1970; Boyes, 1970; Ametewee, 1983; Thompson and Phelps, 1990; Jahss, 1936; Hueston and Wilson, 1972; Griffiths, 1952; Lapidus, 1953; Hodgins and Lipscomb, 1956; Medl, 1970; Lorthioir, 1958; Laing, 1986).
Histologically, the A1 pulleys and, in some cases, the adjacent surfaces of the flexor tendons demonstrate findings consistent with fibrocartilagenous metaplasia, including more chondrocytes and increased glycosaminoglycan compared to controls (1991; Kalms and Højgard, 1991; Compere, 1933; Lapidus and Fenton, 1952; Huber, 1933). These changes are believed to represent adaptations to shear (compressive) load. They also demonstrate degenerative changes and proliferation of fibrous tissue (Lipscomb, 1944; Kalms and Højgard, 1991; Sperling, 1951; Fahey and Bollinger, 1954). Several authors noted the absence of inflammatory changes (Kalms and Højgard, 1991; Fahey and Bollinger, 1954). The synovial portion of the tendon sheath was reported to be comparable to controls (Kalms and Højgard, 1991). Lipscomb (1944) reported that marked fibrosis combined with hemosiderin deposits (changes he considered indicative of a traumatic origin) were present in only one of his cases.
In flexor tendon entrapment, snapping or triggering is caused by disproportion between the diameter of the flexor tendons compared to the diameter of the fibro-osseous canal formed by the A1 pulley (Sprecher, 1949; Conklin and White, 1960; Sampson, Wisch, and Badalamente, 1994; Compere, 1933; Sperling, 1951; Fahey and Bollinger, 1954; Lipscomb, 1959; Kolind-Sørensen, 1970; Wilson, 1983; Ametewee, 1983; Jahss, 1936; Griffiths, 1952; Lapidus, 1953; Hodgins and Lipscomb, 1956; Medl, 1970; Lorthioir, 1958; Rosenthal, 1987; Creighton, Idler, and Strickland, 1990). Since the digital flexors are stronger than the digital extensors, patients are usually able to flex the digit, but have difficulties extending it (Sprecher, 1949; Jahss, 1936; Griffiths, 1952; Hodgins and Lipscomb, 1956).
C.8.e Clinical Observations on Etiology
Observations made by clinicians who have evaluated or treated patients may be helpful in identifying factors that might be relevant to pathogenesis; however, the limitations of such data sources should be appreciated. In particular, these observations are anecdotal and subject to referral bias, observer bias, and respondent bias. In addition, these reports do not incorporate control or comparison groups.
Some authors considered the etiology of many cases of flexor tendon entrapment of the digits unknown (idiopathic) or doubtful (Sprecher, 1949; Compere, 1933; Fahey and Bollinger, 1954; Kolind-Sørensen, 1970; Wilson, 1983; Ametewee, 1983; Creighton, Idler, and Strickland, 1990; Quinnell, 1980; Buch-Jaeger et al., 1992; Chammas et al., 1995; Bartell and Shehadi, 1991; Gray and Gottlieb, 1976). Fahey and Bollinger (1954) stated that there was no apparent relationship between use of the thumb and the origin of the condition. Freiberg et al. (1989), reported that 58 (62.4%) of their 93 patients were idiopathic.
Compere (1933) noted that the occurrence of the condition in children suggested a congenital etiology and hypothesized that constant use of the thumb may have contributed to irritation, thickening, and narrowing of the tendon sheath and further enlargement of the nodule on the tendon. Wilson (1983) stated that some patients may report a history of excessive use of the hand but, more often than not, most patients are at a loss to explain it. Weber (1979) suggested the importance of trauma and heredity. Fahey and Bollinger (1954) noted the occurrence in fraternal twins. Hudson (1924) Weber (1979), Van Genechten (1982), and McCarroll (n.d.) independently reported cases suggesting heredity as a factor for trigger thumb in children. A few cases have been related to anatomical variations of lumbrical muscles (Matricali and Verstreken, 1993). Some cases are related to tumors (Robb, 1978; Rankin and Reid, 1985).
Many have considered chronic trauma or repetitive strain to be the primary etiologic factor (Lipscomb, 1944; Zelle and Schnepp, 1936; Compere, 1933; Sperling, 1951; Thompson and Phelps, 1990; Medl, 1970). Zelle and Schnepp (1936) observed cases occurring among occupations perceived to involve prolonged, frequent, vigorous movements of the involved tendons, including pianists, typists, bookkeepers, maids, factory workers, tailors, and clerks. Lapidus and Fenton (1952)specifically mentioned continuous use of the limb to perform activities such as hammering, sewing, wringing clothes, and stretching leather. In a subsequent publication, Lapidus (1953) offered his impression that "...in a majority of our patients, cumulative irritation of the sheath by forceful back and forth gliding of the tendon during repeatedly performed identical operations, often several times a minute and for 7 to 8 hours a day, was the producing factor of this lesion rather than direct trauma." Fahey and Bollinger (1954) reported three cases from one assembly line where the workers applied pressure with their thumbs to insert plastic tubes into a round plastic cap.
Rosenthal (1987) stated that pinching placed greater forces on the pulley system than grasping because all of the forces were concentrated on the finger tip during pinch, but dissipated across the skin and other phalanges during grasp. He postulated that this might explain the occurrence of flexor tendon entrapment of the digits among workers who continually crimp or cut with small, narrow-handled tools. He stated that use of palmar pads to distribute forces over a larger area and the use of broader tool handles to reduce the degree of finger flexion reduced the incidence of flexor tendon entrapment of the digits.
Localized compression of the pulley against hard objects, such as scissor handles, pruning shears, or a bowling ball, perhaps combined with repeated movements of the tendons, has also been postulated as contributing to the development of flexor tendon entrapment (Lipscomb, 1959; Lenggenhager, 1969; Rayan, 1990).
Several authors have mentioned the role of unaccustomed activity (Lapidus and Fenton, 1952; Fahey and Bollinger, 1954; Rayan, 1990; Kelly and Jacobson, 1954). Specifically, they frequently noted a history of recent job change to one involving repetitive motor tasks or increased speed in an accustomed form of work. Medl (1970) reported that patients in downtown Manhattan sought treatment at years' end and April, times of increased activity with overtime and moonlighting. Rayan (1990) reported a case of trigger thumb that occurred several months after increased bowling.
Sperling (1951) reported that a single episode of trauma was observed for 5 patients; the remaining 21 were believed related to "prolonged overstraining of the flexor apparatus." Ettelson and Weeks (1984) reported a case related to primary injury to the flexor tendon caused by a penetrating wound with a thorn. Others have mentioned the lack of acute trauma in the majority of cases (Lapidus and Fenton, 1952; Quinnell, 1980). Ametewee (1983) reported three cases following hyperextension injury of the thumb.
Hand disorders among rock climbers is common (Shea, Shea, and Meals, 1991). Shea et al. (1991), reported that approximately 50% of rock climbers in their survey reported DIP or PIP pain with climbing, especially with a cling grip (pads of distal phalanges on a lip of rock, PIP joints flexed, and DIP joints hyperextended). Apparently, climbers frequently trust the support of their entire body weight to this form of grip. Both chronic and acute injury to the A2 pulley was reported by Bollen (1990). Many climbers circumferentially wrap their proximal and middle phalanges with tape to support their flexor tendons, but the effectiveness of this technique is unknown (Shea, Shea, and Meals, 1991).
C.8.f Experimental Results
Sperling (1951) conducted a series of experiments using himself as a test subject. Initially, he flexed the right 5th digit at the MP, PIP, and DIP joints 9,000 times in a 72-hour span of time against the resistance of a spring. He noted generalized swelling and tenderness on the flexor side of the finger immediately after completing the task. Within weeks, he developed snapping and palpable thickenings over the proximal and middle phalanges. Two months later, these thickenings were still present and the digit still snapped. In a second experiment, Sperling overexerted the tendons of the left EPB and APL, the tendons involved with de Quervain's tenosynovitis, with an extension-abduction movement against a spring. He selected this site because these muscle-tendon units rarely work against resistance and snapping was rarely reported in this area. He performed approximately 8,000 movements and noted results immediately. He noted generalized swelling, redness, and tenderness over the dorsum of the proximal phalanx of the thumb, intense pain with movement (even when not against resistance), visible jerks on extension of the MP joint and abduction of the CMC joint of the thumb, and audible snaps. Two months later, the symptoms persisted although the pain and tenderness decreased. In his third experiment, he performed 9,000 flexions of the right thumb, but tried to limit motion to only the MP joint. He noted pronounced fatigue of the muscles, but no other symptoms. After 1 month, he performed a combination of flexion and inward rotation of the MP joint against a spring attached to the IP joint of the thumb. He performed approximately 40 movements per minute for a total of approximately 1,000 movements per hour. After 8,000 movements, he noted tenderness on the volar aspect of the proximal phalanx and discontinued the experiment. After 48 hours, he had swelling, pain, and snapping of the thumb. In conclusion, he stated ". . . these experiments show that a single trauma to the flexor apparatus of the fingers is not necessary for the production of snapping fingers, and that numerous small movements, which individually are neither abnormal or strenuous, may lead to the condition."
According to Vogel and Koob (1989), Ploetz (1938) first reported a region of cartilage-like material in the tendon of a rabbit at a site corresponding to the application of compressive loads. Alexander and Dimery (1985) reported that such changes were a characteristic of tendons that change direction as they wrap around a joint. Vogel and Koob (1989) reviewed the differences in general histology, collagen fibril diameter and periodicity, cellular characteristics, water content, collagen amount and type, glycosaminoglycan (GAG) content, and proteoglycan content between the pressure-bearing and tension-bearing portions of tendons. The tension-bearing portions of tendons have characteristics typical of dense connective tissue, while the pressure-bearing portions are more like cartilage along the surface subjected to compressive load. Subsequent experiments demonstrated that these characteristics change in response to alterations of the mechanical forces on the tendons (Gillard et al., 1979; Koob and Vogel, 1987). Gillard et al. (1977) determined the amount of GAG in the tension-bearing and pressure-bearing portions of the flexor digitorum tendon of the rabbit. This tendon originates from its muscle belly in the calf, turns at a pulley located on the medial surface of the talus and calcaneous, then continues under the sole of the foot. This arrangement places different sections of this tendon under different mechanical influences. The pressure-bearing section is that portion in closest contact to the pulley (along the inner portion of the curve). The tension-bearing section is that portion under greatest tension (along the outer portion of the curve). The third portion is the main body of the tendon between these two sections. The tension-bearing section of the tendon had thick collagen fibres of high tensile strength with less than 0.2% GAG, of which 60% was dermatan sulphate. The pressure-bearing section had a significantly greater GAG content (3.5%), of which 65% was chondroitin sulphate. The investigators felt that the observed differences were directly related to the functional needs of the tissues. In a subsequent paper, Gillard et al. (1979) demonstrated that altering these mechanical forces by surgical manipulation led to changes in the GAG type and content of these sections of the tendon. Others have confirmed these observations in other species and tendons (Koob and Vogel, 1987; Merrilees and Flint, 1980; Okuda et al., 1987).
C.8.g Descriptive Epidemiology
The age distribution for flexor tendon entrapment of the digits is bimodal with one group below 6 years of age and the other above 40 years of age (Sprecher, 1949; Compere, 1933; Sperling, 1951; Nasca, 1980; Lapidus and Fenton, 1952; Fahey and Bollinger, 1954; Jahss, 1936; Griffiths, 1952; Quinnell, 1980; Hudson, 1924; Poulson, 1911; Weilby, 1970; Tsuyuguchi, Tada, and Kawaii, 1983; McArthur et al., 1969; Zadek, 1942; Miller, 1950; Blower, 1966; Otto and Wehbe, 1986; Kraemer, Young, and Arfken, 1990; Eyres and McLaren, 1990; Ger, Kupcha, and Ger; Wood and Sicilia, 1992; Kasdan, Leis, and Kasdan, 1996; Steenwerckx, De Smet, and Fabry, 1996).
Strom (1977) reported that the lifetime prevalence of trigger digit among a group of non-diabetics above age 30 was 2.2%. Among adults, flexor tendon entrapment of the digits is generally more common among females than males and usually affects individuals in the fifth or sixth decades of life (Compere, 1933; Sperling, 1951; Nasca, 1980; Lapidus and Fenton, 1952; Fahey and Bollinger, 1954; Lipscomb, 1959; Creighton, Idler, and Strickland, 1990; Quinnell, 1980; Freiberg, Mulholland, and Levine, 1989; Buch-Jaeger et al., 1992; Chammas et al., 1995; Weilby, 1970; Miller, 1950; Blower, 1966; Otto and Wehbe, 1986; Kraemer, Young, and Arfken, 1990; Eyres and McLaren, 1990; Kasdan, Leis, and Kasdan, 1996; Tanaka et al., 1990; Anderson and Kaye, 1991; Eastwood, Gupta, and Johnson, 1992; Griggs et al., 1995; Lapidus and Guidotti, 1972; Clark, Ricker, and MacCollum, 1973; Gray and Gottlieb, 1977; Bonnici and Spencer, 1988; Faunø, Andersen, and Simonsen, 1989; Panayotopoulos et al., 1992; Lambert, Morton, and Sloan, 1992; Benson and Ptaszek, 1997; Turowski, Zdankiewicz, and Thompson, 1997; Patel and Moradia, 1997).
Nasca (1980) reported that, in his experience, cases among blacks were rare. Even though most cases involve a single digit, some patients have multiple affected digits (Sampson, Wisch, and Badalamente, 1994; Compere, 1933; Sperling, 1951; Lapidus and Fenton, 1952; Creighton, Idler, and Strickland, 1990; Freiberg, Mulholland, and Levine, 1989; Buch-Jaeger et al., 1992; Chammas et al., 1995; Miller, 1950; Blower, 1966; Otto and Wehbe, 1986; Kraemer, Young, and Arfken, 1990; Kasdan, Leis, and Kasdan, 1996; Griggs et al., 1995; Gray and Gottlieb, 1977; Bonnici and Spencer, 1988; Faunø, Andersen, and Simonsen, 1989; Patel and Moradia, 1997; Rhoades, Gelberman, and Manjarris, 1984; Gottlieb, 1991; Howard, Pratt, and Bunnell, 1953; Patel and Bassini, 1992).
According to Blower (1966), patients with multiple affected digits at presentation were three times more likely to have a subsequent digit affected compared to patients with isolated affected digits at presentation (45% vs. 16%). Among patients without concurrent disease, the thumb (digit I) is the most commonly affected digit, followed by III and IV (Lipscomb, 1944; Conklin and White, 1960; Compere, 1933; Nasca, 1980; Lapidus and Fenton, 1952; Fahey and Bollinger, 1954; Lapidus, 1953; Rosenthal, 1987; Creighton, Idler, and Strickland, 1990; Quinnell, 1980; Freiberg, Mulholland, and Levine, 1989; Buch-Jaeger et al., 1992; Chammas et al., 1995; Weilby, 1970; Zadek, 1942; Miller, 1950; Blower, 1966; Otto and Wehbe, 1986; Kraemer, Young, and Arfken, 1990; Tanaka et al., 1990; Anderson and Kaye, 1991; Eastwood, Gupta, and Johnson, 1992; Lapidus and Guidotti, 1972; Clark, Ricker, and MacCollum, 1973; Bonnici and Spencer, 1988; Panayotopoulos et al., 1992; Lambert, Morton, and Sloan, 1992; Benson and Ptaszek, 1997; Turowski, Zdankiewicz, and Thompson, 1997; Patel and Moradia, 1997; Rhoades, Gelberman, and Manjarris, 1984; Howard, Pratt, and Bunnell, 1953).
Some cases with flexor tendon entrapment of the digits have co-morbidity, e.g., epicondylitis, peritendinitis, Dupuytren's contractures, de Quervain's tenosynovitis, and wrist fractures, among others.
Several studies have reported a relationship between flexor tendon entrapment of the digits and diabetes mellitus (Sperling, 1951; Kolind-Sørensen, 1970; Buch-Jaeger et al., 1992; Chammas et al., 1995; Gray and Gottlieb, 1976; Otto and Wehbe, 1986; Kasdan, Leis, and Kasdan, 1996; Griggs et al., 1995; Bonnici and Spencer, 1988; Faunø, Andersen, and Simonsen, 1989; Benson and Ptaszek, 1997; Turowski, Zdankiewicz, and Thompson, 1997; Rhoades, Gelberman, and Manjarris, 1984; Yosipovich et al., 1990; Gamstedt et al., 1993; Benedetti et al., 1982); rheumatoid arthritis (Lispcomb, 1959; Kolind-Sørensen, 1970; Creighton, Idler, and Strickland, 1990; Quinnell, 1980; Chammas et al., 1995; Blower, 1966; Clark, Ricker, and MacCollum, 1973; Gray and Gottlieb, 1977; Bonnici and Spencer, 1988; Faunø, Andersen, and Simonsen, 1989; Panayotopoulos et al., 1992; Benson and Ptaszek, 1997; Rhoades, Gelberman, and Manjarris, 1984; Gottlieb, 1991; Meachim and Roberts, 1969; Jacobs, Hess, and Beswick, 1957; Marmor, 1963; Nalebuff and Potter, 1968);carpal tunnel syndrome (Lipscomb, 1959; Kolind-Sørensen, 1970; Buch-Jaeger et al., 1992; Chammas et al., 1995; McArthur et al., 1969; Griggs et al., 1995; Gray and Gottlieb, 1977; Bonnici and Spencer, 1988; Benson and Ptaszek, 1997; Turowski, Zdankiewicz, and Thompson, 1997; Rhoades, Gelberman, and Manjarris, 1984; Gottlieb, 1991; Yamaguchi, Lipscomb, and Soule, 1965; Cseuz et al., 1966; Phalen, 1972; Inglis, Straub, and Williams, 1972); Dupuytren's disease (Sperling, 1951; Buch-Jaeger et al., 1992; Griggs et al., 1995; Parker, 1979); arthritic changes in the digits (Sperling, 1951; Griggs et al., 1995; Turowski, Zdankiewicz, and Thompson, 1997; Rhoades, Gelberman, and Manjarris, 1984); amyloidosis (Young and Holtmann, 1980); mucopolysaccharidoses (MacDougal, Weeks, and Wray, 1977); hypothyroidism (Griggs et al., 1995; Rhoades, Gelberman, and Manjarris, 1984; Gottlieb, 1991); and congestive heart failure (Rhoades, Gelberman, and Manjarris, 1984). No relationship to pregnancy has been reported (Heckman and Sassard, 1994).
C.8.h Epidemiological Studies
No publications in the current literature focus specifically on the epidemiology of flexor tendon entrapment of the digits, especially in an occupational context. Many epidemiological studies of upper-extremity musculoskeletal morbidity in the workplace either did not include or did not find flexor tendon entrapment of the digits among their health outcomes (Luopajarvi et al., 1979; Kuorinka and Koskinen, 1979; Armstrong et al., 1982; Viikari-Juntura, 1983; Roto and Kivi, 1984; Viikari-Juntura, 1984; Kivi, 1984; Punnett et al., 1985; Silverstein, Fine, and Stetson, 1987; Tanaka et al., 1988; Thompson, Plewes, and Shaw, 1951; Armstrong et al., 1987).
Several case series provide insights or estimates of the percentage of cases attributable to work activities or occupations. Thompson, Plewes, and Shaw (1951) reported on 544 cases of tenosynovitis between 1941 and 1950. Most of the cases were employed at the Vauxhall Motors factory. The majority of their tenosynovitis cases were classified as peritendinitis. They reported no cases of trigger finger or trigger thumb. Of the 334 adult cases reported by Lapidus and Fenton, (1952) there were 149 housewives (45%), 34 sewing machine operators (10%); 32 needle workers (10%); 27 clerks (8%); 13 domestic workers; 7 each of physicians, managers, and furriers; 5 secretaries; 4 each of writers/waitresses, pressers, bookeepers; 3 each of leather workers, beauticians, metal workers, nurses, packers, and laundreses; 2 each of peddlers, laborers, and barbers; and 1 each of dentist, elevator operator, teacher, painter, porter, social worker, broker, designer, cigar roller, photographer, artist, lawyer, telephone operator, candy maker, advertising man, driver, and dish washer. Nasca (1980) reported that housewives, manual workers, and white collar workers were equally affected. Anderson and Kaye (1991) reported that most of their 58 patients were housewives, retirees, or others with sedentary types of work as opposed to occupations involving repetitious use of the hand. Kasdan et al. (1996), reported that 155 of their 516 cases (30%) were not employed at the time of treatment. Of the 361 employed cases, 178 cases (49% of employed and 34.5% overall) were felt to be work-related. In this case series, the decision of work-relatedness was based on whether the patients performed jobs that involved heavy lifting or high-force gripping activities.
Armstrong et al. (1987) studied the relationship between the prevalence of symptoms or physical findings of hand and wrist tendinitis with force, repetitiveness, and hand and wrist posture. Hand and wrist tendinitis included de Quervain's tenosynovitis, trigger finger and trigger thumb, and tendinitis/tenosynovitis. They observed a statistically significant increased odds ratio for the prevalence of hand and wrist tendinitis only among workers performing high-force, high-repetition jobs (odds ratio:29.4; p < .001). There were no associations with percentage of work time spent in wrist flexion, ulnar deviation, wrist flexion and ulnar deviation, pinching, or pinching and wrist flexion. The specific clinical conditions were not evaluated separately.
Moore and Garg (1994) performed a retrospective cohort morbidity study that compared the incidence and spectrum of distal upper-extremity disorders associated with 37 job categories in a pork processing plant with the ergonomic task requirements of the jobs. "Specific distal upper extremity disorders" included de Quervain's tenosynovitis, flexor tendon entrapment affecting the fingers (trigger finger), flexor tendon entrapment affecting the thumbs (trigger thumb), epicondylitis (medial and lateral), and CTS. The case definition for flexor tendon entrapment of the digits included a subjective sensation of locking or impaired extension of the affected digit combined with either objective demonstration of triggering or palpation of a nodule along the flexor tendon that would be consistent with stenosis at the A1 pulley. Of the 104 observed conditions, there were 15 cases of flexor tendon entrapment of the digits. Twelve cases involved the fingers and 3 cases involved the thumb. The 12 cases of trigger finger occurred among 8 males and 2 females. The 3 cases of trigger thumb occurred among 3 females. All 15 cases were unilateral and involved workers performing "hazardous" jobs. No cases occurred among workers performing "safe" jobs. Among cases with multiple conditions, the most common association was trigger finger affecting multiple digits (IV and V). The 9 cases of trigger finger among males occurred in one job category (Whizard Knife Operator,) and affected digits IV or V of the right hand. This job involved constant grasping of the tool with the right hand with a "light" amount of force plus use of the tool approximately 11.6 times per minute. The tool was held with a power grip; wrist posture was neutral; speed of work was "high"; localized mechanical compression was not observed (but the hand-tool interface could not be assessed directly); and hand-arm vibration was present. The 3 cases of trigger finger among females and 2 of the 3 cases of trigger thumb occurred in one job category (Scaler/Grader/ Downgrader). This job involved pinching with both hands to lift and hold one or more pieces of paper containing sliced bacon (weight approximately 1 pound each). There were approximately 25.6 efforts per minute, "negligible" intensity of effort, applied effort for 39% of the time, pinch grasp, non-neutral wrist posture, "high" speed of work, no localized compression, and no hand-arm vibration. When comparing morbidity on "hazardous" jobs to "safe" jobs, the relative risk for developing a "specific distal upper extremity disorder" (excluding CTS) was 19.4 (p = .02). Since there were no cases of flexor tendon entrapment of the digits among workers performing the "safe" jobs, relative risk for this specific condition was not estimated in the original manuscript. If a single case were assigned to the "safe" group of jobs, the relative risk among workers performing "hazardous" jobs would be 7.0 (p < 0. -- ). If one compared the Whizard Knife job alone to the "safe" jobs, the relative risk was 83.3 (p < 0. -- ). This study did not control for non-occupational factors.
Ranney et al. (1995) examined 146 female workers in five industries for the presence of MSDs in the upper limbs as part of a cross-sectional study. The industries and job activities included electronics assembly, packaging, medium weight assembly, food retail cashiers, and garment and automotive sewing. The case definition for tenosynovitis of the finger or thumb included symptoms of clicking or catching the affected digit on movement plus possible complaints of pain or a lump in the palm, and physical examination findings that demonstrated the clicking, catching, or lump with tenderness to palpation anterior to the metacarpal of the affected digit. Clinical problems about the upper limb were detected in 82 persons (56%). No cases of flexor tendon entrapment of the fingers or thumb were observed.
C.8.i Models of Pathogenesis
The following discussion related to the pathogenesis of flexor tendon entrapment of the digits is limited in that it addresses only one biomechanical mechanism related to hand usage. The first section reviews the biomechanical basis of the model. The second section discusses the temporal aspect of this mechanism. The potential contribution of personal or non-biomechanical factors have not been considered. It is beyond the scope of this manuscript to address other potentially relevant pathogenetic pathways.
Biomechanical Loading (Shear)
Clinical observations have suggested that flexor tendon entrapment of the digits may be related to repeated, prolonged, or unaccustomed exertions. Gripping, pinching, or pressing with the fingers or thumb involve exertions that require tensile loading of the flexor tendons of the digits. Flexion of the MP joint of the digit makes the flexor tendons turn a corner at the A1 pulley. Tensile loading of these tendons in combination with a marked change in direction creates shear (compressive) force between the tendons and the A1 pulley. As suggested by the available experimental data, the A1 pulley may respond to this compressive stimulus with functional hypertrophy, fibrocartilagenous metaplasia, or both. The pathological changes characteristically observed in affected pulleys are consistent with these relationships.
The biomechanical model proposed by Hume et al. (1991) predicts that the magnitude of the pulley tension at the A1 pulley would be proportional to the tensile load of the tendons passing through the pulley (FFT*RMA) and the sine of the total deflection angle (+) between the course of the deviated tendon(s) compared to the neutral position of the tendon(s). For simplicity, the pulley geometry term will be ignored. The shear force on the pulley is proportional to the pulley tension. The magnitude of MP joint flexion of the fingers is greater with grasping than any other form of prehension (Hume et al., 1990). No particular form of prehension was reported to create large deviations of the MP joint of the thumb.
Temporal Patterns of Biomechanical Loading
There are two plausible patterns of temporal loading that might be relevant to a pathogenetic theory for flexor tendon entrapment of the digits. The first model assumes that the duration of biomechanical loading during a period of activity (of duration T) is most critical. Mathematically, this is represented by equation 4.
Accumulated Shear Force =
In this model, the duration (expressed as a fraction of cycle time) of pulley loading is more important than the repetition (number) of loadings, e.g., one prolonged exertion at relatively moderate levels of shear could be more significant than a series of brief and intermittent exertions at the same or higher levels of shear.
The second model assumes that the number of episodes of pulley loading (n) during a period of activity (of duration T) is more important than the duration of pulley loading. Mathematically, this can be described by equation 3.
Accumulated Shear Force =
At this time, there is no experimental evidence to establish one theory's superiority over the other. Epidemiologically, there is evidence favoring the duration model over the repetition model. Moore and Garg (1994) observed a cluster of cases of trigger finger among workers who statically grasped a hand-held tool.
D LOWER-EXTREMITY DISORDERS
Work-related disorders of the lower extremities have not received the same degree of scientific scrutiny as disorders of the upper extremities or spine. However, Bureau of Labor Statistics (1999) data indicate that there were 375,000 lost time work-related injuries and illnesses involving the lower extremities out of a total of 1,833,400 total reported cases. Of these, 129,900 involved the knee; 69,300 involved the foot; and 21,300 involved the toes. While many of these cases are the result of acute trauma, work-related activites that involve repetitive impact loading, static loading, loading in abnormal postures, or vibrational exposure have potential to cause non-acute lower-extremity disorders. Epidemiologic studies suggest that factors such as kneeling more than 30 minutes a day, prolonged squatting, climbing more than 10 flights of stairs a day, and repetitive heavy lifting are all risk factors for knee osteoarthritis (Cooper et al., 1994; Vingaard et al., 1996). For hip disorders, frequent stair climbing, large amounts of walking on the job (> 2 miles per day), heavy work, significant jumping, and stair climbing appear to be associated with osteoarthritis of the hip (Coggon et al., 1998; Cooper et al., 1988; Croft et al., 1992; Felson et al., 1988). While osteoarthritis and tarsal tunnel are reviewed in this document, the absence of other disorders does not imply that additional conditions do not have the potential to be related to work factors.
Although the specific details may differ, in general, osteoarthritis is considered to be a "non-inflammatory disorder of movable joints characterized by functional deterioration, abrasion of articular cartilage, and formation of new bone at and around the joint surfaces" (Meisel, 1984). This definition appears to rule out the possibility of an inflammatory basis to osteoarthritis; this does not preclude the potential for an osteoarthritic lesion to be accompanied by an inflammatory component. However, atrophic (rheumatoid) arthritis and hypertrophic degenerative joint disease or osteoarthritis are two separate diseases (Moskowitz, 1992).
Some authors suggest that the term "osteoarthrosis" be used to represent an "organ-level failure of a diarthrodial joint in which mechanical factors play the primary role in initiation and progression (Radin, 1994). This would contrast with arthritis where the etiological factor would be other than mechanical.
Osteoarthritis has recently been classified using a combination of anatomic and etiologic mechanisms to characterize the variety and number of arthritic illnesses that exist. This classification separates degenerative joint disease into two broad groups -- primary or idiopathic osteoarthritis, and secondary osteoarthritis, or a disease that has an identifiable underlying condition contributing to its occurrence.
Osteoarthritis, osteoarthrosis, degenerative joint disease, and arthrosis are used in this discussion to refer to the same disease entity or process. The term osteoarthritis will be used to refer to these conditions in this text.
D.2.a Characteristics of Osteoarthritis
Although commonly thought to be a disease of old age or an illness most commonly associated with the aging process, it is probably not the case that osteoarthritis is only the result of wear and tear on joints (Moskowitz, 1992). The prevalence of osteoarthritis is thought to increase in older age groups -- by age 75, almost everyone has some degenerative joint disease. Although some authors disagree, in general males and females have similar prevalence of osteoarthritis, although the prevalence is greater in men younger than 45 years and in women older than 55 years (Moskowitz, 1992).
D.2.b Signs and Symptoms of Osteoarthritis
Patients presenting with osteoarthritis tend to develop gross and visible anatomic joint abnormalities. The joints most commonly affected include the fingers, hips, knees, and spine. Osteoarthritic changes usually occur in only one or a few joints, although systemic disease does occur. Clinically, persons with osteoarthritis typically notice the onset in one or more joints of pain, stiffness, redness, and deforming changes of the joint (Meisel 1984). Patients may complain of mild aching pain associated with movement, limitation of motion, or stiffness after periods of rest.
D.2.c Pathophysiology of Osteoarthritis
The Normal Joint
The normal joint is made up of three key structural features: the geometry of the articulating surfaces of the joint; the supportive structures, including ligaments, tendons, and muscles; and the material characteristics of the joint components, including the strength, resilience, and elasticity of the articular cartilage and the subchondral bone that underlies the cartilage (Meisel, 1984). In a healthy, properly functioning joint, the opposing structures and surfaces are matched in such a way as to allow transmission of expected loads at the lowest and most uniform pressure (Meisel, 1984). Loads are transmitted from one surface to another almost entirely by compression. The ends of the bones that carry out this function are composed of cancellous bone, an expanded and more flexible component ofbone.
Attached to this cancellous bone is articular cartilage (Meisel, 1984). This articular cartilage surface is the key to understanding the pathophysiology of osteoarthritis. The articular cartilage bears the brunt of alterations in shape and supporting structure, and is the key to understanding osteoarthritis (Meisel, 1984). In general, articular surfaces are uniform and move upon one another with ease (Meisel, 1984). They have soft, smooth, and slippery surfaces and are flexible and elastic. This allows for friction to be minimized and diffused over the whole of the joint surface, shock to be minimized, and abrasion to be prevented (Meisel, 1984).
The cartilage making up the articular surfaces in the joint is made of three substances: collagen, proteoglycans, and water, which makes up approximately 80% of the weight of the cartilage (Meisel, 1984). The cellular component of cartilage is called the chondrocyte.
Gross Changes in the Evolution of Osteoarthritis
Osteoarthritis begins with the breakdown of the collagen meshwork at the surface of the joint. This gives the cartilage a rough and shaggy appearance and is termed fibrillation (Meisel, 1984). The cartilage may become softened. The next step in the progression of the disease involves the disruption of the thin surface overlying the load-bearing cartilage. The cartilage is damaged with flaking and pitting, leading ultimately to progressive erosion and ulceration (Meisel, 1984). Fissures extend into the base of the cartilage and chondrocytes proliferate and cluster around the margins of these fissures. Cellular injury occurs and focal or generalized necrosis or death of the chondrocytes may be seen (Meisel, 1984). Once cellular necrosis occurs, the cartilage is no longer viable and disappears.
Repair or regeneration takes place along with this cartilaginous breakdown. Cellular proliferation occurs and is seen in clumping of chondrocytes. This results in identifiable reparative but disordered collagen (Meisel, 1984).
There are thought to be two sources of reparative tissue in the joint: the damaged cartilage itself may create new and reparative cartilage (intrinsic repair); or the synovial membrane or subchondral bone may generate reparative structures (extrinsic repair). In most cases of osteoarthritis, both intrinsic and extrinsic mechanisms exist (Meisel, 1984).
As the cartilage becomes increasingly damaged and deteriorated, the articular surface may entirely lose its cartilaginous surface. The underlying bone takes on a polished appearance and is said to be eburnated. This loss of cartilage necessitates the application of force to a surface less able to sustain those forces. As a result, the bone becomes misshapen and is subjected to increasingly greater stresses. This increased loading leads to necrosis of the surface of the bone, which may cause bone resorption and the formation of subchondral bone cysts, as well as the bony sclerosis (Meisel, 1984).
The synovial membrane surrounding the joint cooperates in these processes of erosion and repair. The breakdown of bone and cartilage results in increased amounts of debris in the joint cavity. The synovial membrane takes an active role in removing these bits of cartilage and bone. The synovium may hypertrophy and extend onto the articular surface of the joint. This may lead to chronic inflammation and scarring, which renders it incapable of further nourishing the cartilage (Meisel, 1984).
The morphologic repair of the joint occurs consequent to the breakdown of the cartilaginous and bony surfaces. The repair is achieved with the production of new bone along the joint surface, especially at the margins of the joint. This results in the formation of marginal new bone in the shape of spurs, called osteophytes. In the advanced stages of osteoarthritis, the structural integrity of the joint is lost and overall deformities such as subluxation may occur. Joints may become unstable and loose bodies are seen within the joint space. When the disease is advanced, there is bone-on-bone contact (Meisel, 1984).
Biochemical Characteristics of Osteoarthritis
It is not entirely clear how the biochemical function of the cells within the osteoarthritic joint are disordered. Collagen synthesis within the osteorarthritic joint is greater than in normal joints and increases with the severity of the disease (Meisel, 1984). There is less proteoglycan component in the articular cartilage matrix. This is thought to be due to degradation or loss from the cartilage (due to altered enzymatic degradation) because proteoglycan syntheseis actually increases in early osteoarthritis and continues to increase throughout the course of the disease until the chondrocytes fail and matrix production ceases. Because the newly synthesized cartilage does not contain the normal amount and type of proteoglycans, the result is a less resilient cartilage (Meisel, 1984).
Etiologic Features of Osteoarthritis
According to Felson, the prevalence of osteoarthritis correlates with age. Studies have noted an incidence of osteoarthritis of the hand at age 35 of less than 5% to over 70% at age 65 or older (Felson, 1994). Osteoarthritis of the hip or knee is seen in 1% of the population at age 60 and in approximately 0.1% at ate 40 to 49 (Felson, 1994). This age-related prevalence is not confounded by sex, race, or regional considerations (Meisel, 1984).
One explanation for these age-related changes is that as the joint ages, changes in joint symmetry occur which result in greater congruity in the articulating surfaces. This is thought to interfere with cartilage nutrition and alter the distribution of the load, putting abnormal stress on previously non-loaded or less loaded cartilage and leading to more generalized cartilage breakdown.
There appears to be a role for genetic influences in the development of some types of osteoarthritis, especially for those types that occur because of systemic metabolic derangements such as hemochromatosis or chondrocalcinosis. The role of genetics in the development of primary osteoarthritis is difficult to define (Meisel, 1984).
There is evidence that certain familial forms of osteoarthritis are characterized by an abnormality in the genetic coding of type II collagen, the major component of cartilage and the component that lends the tensile strength to cartilage (Bleasel, et al., 1995). It is unclear what the role of genetic mutation might be in the nonfamilial forms of osteoarthritis.
Women develop osteoarthritis more commonly than men, especially in the age group over 55 (Meisel 1984). The only exception is in disease in the hip (Felson, 1994).
Until age 65, prevalence of osteoarthritis is similar between white and black Americans. After age 65, the prevalence increases for whites (Meisel, 1984). In general, Caucasian populations from developed nations have similar rates of osteoarthritis in the hands and knees (Felson, 1994). There are remarkable differences in the rates of hip osteoarthritis separated by race. Rates among Hong Kong residents is very low while rates seen in Caucasian populations are as much as 7- to 25-fold higher. This is thought to result from the increased prevalence of congenital and developmental hip disorders in Caucasian populations compared with Chinese populations (Felson, 1994). This suggests a different etiology for hip arthritis than for arthritides of other joints.
It is postulated that excessive body weight increases the load on weight-bearing joints and may cause changes in posture and gait that change the mechanical function of the joint. There is an association between obesity and symptomatic osteoarthritis of the knee, but not of the hip. This raises a question about these presumed causal theories. There is also the theory that a hormonal or other biologic factor associated with obesity is the cause of osteoarthritis in the obese individual. At this time, no specific biological marker has been found to explain the relationship. However, findings such as the linkage between arthritis in the hand and obesity suggest a humoral factor (Felson, 1994).
Acute Joint Injury
Factors such as sudden joint injuries, including cruciate ligament tears, meniscal tears, and other knee-deranging injuries, are known to cause osteoarthritis in humans. This is most predictable among men (Felson, 1994). Men with major knee injuries were noted to have a greater than threefold relative risk for the development of osteoarthritis and women had a greater than double relative risk in the Framingham study (Felson, 1994).
Repetitive Joint Injury
Epidemiological studies of farmers, jackhammer operators, shipyard and dockyard workers, and miners suggested that workers who engaged in certain repetitive activities had an increased risk for osteoarthritis (Anderson and Felson, 1988; Coggon et al., 1998; Cooper et al., 1998; Croft et al., 1992; Vingard et al., 1991). For farmers, for example, these activities included standing, bending, walking long distances on rough surfaces, lifting or moving heavy objects, and tractor driving. Jackhammer operators had an increased risk of osteoarthritis of the upper-extremity joints, presumably because the repetitive impact loads on these joints made them vulnerable to the degree of the forces. In one study, women required to use persistent pinch grip developed osteoarthritis at a rate greater than those required to utilize a power grip. Jobs requiring knee bending and lifting greater than 25 pounds are associated with increased rates of osteoarthritis of the knee (Felson, 1994). Other occupational groups have also been found to be at higher risk for the development of osteoarthritis.
Mechanical stress has been shown to predispose to osteoarthritis. A single major impact, minor impacts, and protracted overuse have all been associated with increased risk for developing osteoarthritis. In addition, structural abnormalities have also been shown to increase this risk. Protracted overloading tends to be more pivotal in the development of osteoarthritic disease, however. Apparently, sclerotic changes in the subchondral bone, a result of accumulated microtrauma, affect the ability of articular cartilage to withstand the stress of joint loading and may lead to cartilage degeneration.
The major factors that attenuate a load delivered to a joint are the joint motion, the associated lengthening of muscles under tension, and the deformation of the subchondral bone under load. Even minor but unanticipated impulse loading such as slipping on a stair may be a major factor in primary joint degeneration. Unexpected falls of only 1 inch allow insufficient time to bring protective reflexes to play and are thus associated with transmission of excessive loads to articular cartilage. Factors that lead to muscle fatigue also tend to impair the shock-absorbing mechanism and contribute to the development of cartilage damage.
There are various levels of understanding of the relationship between other risk factors and osteoarthritis, including diabetes and hypertension (Felson, 1994).
D.2.d Proposed Models of Osteoarthritis Development
The literature contains several proposed models to explain the development of osteoarthritis in humans. These are well described and delineated by Moskowitz (1992). These models propose a series of alternate explanations for the development of osteoarthritis, none of which consider it an inevitable outcome of the aging process. Although the understanding of the models varies, none appear to be well documented from the perspective of biochemical understanding of the etiologic framework of the disease (Moskowitz, 1992).
Metabolic and Endocrine Manipulation
When cartilage is introduced to certain hormones or other biological materials (somatotropin -- a growth hormone -- or corticosteroids), changes are noted in the integrity of the cartilage, especially affecting the chondrocytes. These can include hypertrophic changes as well as degradation (Moskowitz, 1992).
Foreign Bodies in Joint Spaces
Experiments involving the introduction of cartilage and bone fragments, polyethylene, papain, vitamin A, Filipin (a polyene), and sodium iodoacetate all were shown to generate changes in the intrinsic character of the joint resembling those changes known to occur in the development of osteoarthritis. These changes involved the cartilage, the chondrocytes, and the synovial membrane as well as the subchondral bone, depending on the various materials used (Moskowitz, 1992).
Focal Cartilage Defects
Small lesions in cartilage have been shown in animal models to lead to several of the changes characteristic in the development of osteoarthritis. These include fibrillation, the clustering and proliferation of chondrocytes, and evidence of repair, including generation of fibrous tissue and cartilage (Moskowitz, 1992).
Primary Alteration of Joint Forces
This model may be most relevant to the consideration of work-related stresses contibuting to the development of osteoarthritis. This model suggests that osteoarthritis may result from forces and stresses exerted on a joint that are different in type and amount than those typically applied to the joint. When stresses become excessive, the joint is unable to adequately distribute those forces and becomes damaged (Moskowitz, 1992).
Animal models subjecting animals to repetitive impact loading of one or more limbs identified processes similar to those thought key to the development of osteoarthritis: increased bone formation, increased bone stiffening, and damage to the cartilage involving both fibrillation and splitting of the cartilage. In addition, chondrocyte activity increased and cartilage makeup changed. It is theorized that the combination of a stiffened bony endplate with increased joint loading causes the cartilage to fracture and subsequently degenerate (Moskowitz, 1992).
Additional evidence suggesting that altered or increased loading of the joint leads to changes characteristic of osteoarthritis in humans has been shown in several types of animal models. In one experiment, single blows to the patella of the rabbit led to damage in the knee joint, including fibrillation, erosions, and chondrocyte clusters and the development of osteophytes (Moskowitz, 1992).
Experiments changing the load bearing of animal joints to increase either the valgus or varus direction of the forces via the use of wedge osteotomy led to histologic and other evidence of classic degenerative changes. These included changes such as cartilage fibrillation and clefts. In other studies, degenerative changes in the cartilage included findings such as osteophyte formation, surface fibrillation, cellular derangement, and cloning; occasionally complete cartilage erosion to subchondral bone was seen on the portion of the knee joint that had increased loading. In general, the changes occurred in areas of the knee covered by meniscus, but not in the central weight-bearing regions (Moskowitz, 1992).
This model suggests that neurologic capacity in the limb is necessary for maintenance of normal joint health. Rabbit models using animals with degeneration of the hind limb revealed degenerative changes in the chondrocytes, especially in the more central layers (Moskowitz, 1992).
Certain strains of laboratory mice, hamsters, and guinea pigs have been shown to spontaneously develop evidence of osteoarthritic joint changes, including fraying and ulceration of cartilage, subchondral bony sclerosis, and proliferative osteophyte changes. These changes have been noted to be associated with the genetic type of the animal, the diet characteristics of the animal, the sex of the animal, and certain increased susceptibility to other illnesses. Domestic animals such as cattle and dogs are susceptible to the development of osteoarthritis. Etiologic findings, including joint laxity and hip dysplasia, are thought to be predisposing characteristics. In the laboratory setting, rats are noted to be relatively resistant to the development of osteoarthritis (Moskowitz, 1992).
Degenerative Changes Following Release of Joint Contact
There is speculation that the absence of weight bearing is a factor in the development of osteoarthritic joint changes. These theories hold that cartilage apposition and associated weight bearing are necessary for the development and maintenance of healthy cartilage. Surgical procedures designed to modify joints so that normal weight-bearing contact was not maintained led to development of degenerative changes (Moskowitz, 1992).
Immobilization and Compression - Immobilization Models
Models in animals have been studied to evaluate the impact of both compression and immobilization in animal joints on the development of osteoarthritis. In general, cartilage destruction occurs as a result of prolonged joint immobilization. This occurs because of damage due to the pressure of extrinsic tissues encroaching on the joint and the lack of synovial fluid to nourish the cartilage (Moskowitz, 1992).
Patellectomy and Patellar Dislocation Models
Patellectomy may lead to degenerative arthritis of the knee. In rabbits, these degenerative changes in the cartilage were accompanied by chondrocyte proliferation, fibrillation and cartilage irregularity, and erosions and cartilage denudation. These changes are thought to be caused by several factors, including synovial inflammation, the mechanical effect of a rough surgical surface, altered biomechanics, and lack of adequate nutrition to the cartilage (Moskowitz, 1992).
Models Based on Surgical Repair of Internal Derangements
In humans, osteoarthritis may develop when anterior cruciate ligament injuries occur and lead to joint instability, as well as when meniscus resections occur. Efforts to develop animal models have been partially successful. In dogs, damage to the anterior cruciate ligament led to cartilaginous softening, fibrillation, and erosions. Joint instability was considered to be the major etiologic agent in inducing degenerative changes in these experiments, but, in addition, the amount of bleeding in the joint was noted to lead to more significant changes, with excessive bleeding resulting in worse disease (Moskowitz, 1992).
Meniscectomy was noted to lead to degenerative joint disease in humans; this has been confirmed in models with rabbits and dogs (Moskowitz, 1992).
Models Based on Major Surgical Manipulation
Major surgical procedures such as ligament resections and meniscectomies in the same joint were shown in rabbits and in guinea pigs to lead to the deterioration of cartilage including the development of fissures and fibrillation, focal erosions and ulceration, and osteophyte growth.
D.2.e Repetitive Trauma and the Joint
As discussed in many of the models above, gross trauma to the joint often leads to the development of osteoarthritic changes, often relatively soon after the traumatic insult. There is evidence, as well, that repetitive trauma associated with smaller forces and with less gross derangement of the joint may also lead to the development of osteoarthritis (Radin et al., 1994). The theory explaining the damage caused by repetition of less substantial forces follows.
As noted above, the key processes involved in the development of osteoarthritis include loss of cartilage, subchondral sclerosis caused by bone remodeling, increase in metaphyseal bone, and the formation of osteophytes (Radin, 1994). Limited but persistent forces are thought to cause microfractures in the cartilage and subchondral bone. The microfractures and submicrofractures induce bone remodeling in the joint and the onset of degenerative changes. This repetitive impulsive loading causes loss of proteoglycans, fibrillations, and chondrocyte cloning. With time, cartilage damage leads to cartilage thinning and progressive deterioration (Radin, 1994).
The concept of tidemark is critical to the theory behind repetitive trauma and degenerative disease. Tidemark refers to the junction between the articular cartilage and the calcific cartilaginous base (Radin, 1994). Changes occurring in the calcified cartilage represent early evidence of damage after repetitive impulse loading.
In animal and other models, changes in the calcified bed are shown to be the earliest signs of the development of osteoarthritis.
Evidence of osteoarthritis resulting from repetitive impact loading has been developed in models of rabbits subjected to repetitive forces. Even 6 weeks of repetitive impulsive loading lead to thickness of the calcific cartilage and remodeling of the subchondral bed. As the calcific cartilage thickens and fibrillations and cartilage loss occur, significant changes occur in the relative stresses and forces exerted upon the components of the joint. These stresses lead to the development of fissures and subsequent cartilage loss (Radin, 1994).
Damage to the calcified cartilage layer in the form of microfractures has been observed in models of dogs' knees after an impact load was sustained. Similarly, autopsy studies confirm that microfractures are seen in the calcified cartilage layer of human hips at autopsy and in the knees of rabbits after repetitive impulsive loading (Radin, 1994).
Osteoarthritis of the Hip
The hip represents a ball and socket joint with the femur (ball) articulating with the acetabulum (socket). The cartilaginous integrity of the joint is designed so that weight-bearing characteristics of the hip increase as the forces increase. The cartilage surface deforms as additional force is absorbed until the maximum tolerance is achieved. As the joint ages, the capacity to absorb increasing forces declines (Wilson, 1992).
Osteoarthritis develops when the load on the cartilage is greater than the limits of the chondrocyte and osteocyte. This may occur because of mechanical failure in the hip such as a change in the shape of the joint surfaces, a decrease in joint surface area, or a biologic or physiologic failure, such as a decrease in the cellular capacity to respond to normal stress levels (Wilson, 1992). Mechanical failure typically results from the residual deformities associated with congenital or other hip diseases. Biologic or physiologic failures are caused by metabolic diseases and diseases such as inflammatory arthritis (Wilson, 1992). The overwhelming proportion of cases of hip osteoarthritis (up to 80% to 85%) are caused by a mechanical deforming of the hip usually occurring during childhood or by trauma to the joint.
Osteoarthritis of the Knee
Osteoarthritis of the knee is common, ranking third behind osteoarthritis of the spine and hip in frequency (Goldberg, 1992). Acute injuries, including meniscal damage, ligamentous injuries, surgical procedures such as meniscectomy, joint instability, articular surface irregularities such as those following tibial plateau fractures, and angular deformities, are predictable forerunners to osteoarthritis. The common etiologic factor is thought to be the increase of stress on the articular cartilaginous surfaces (Goldberg, 1992). In each of these acute injury situations, it is possible to identify increases in stresses on the cartilaginous surfaces that lead to cartilage degeneration.
The overload on the joint is greater than the joint's ability to withstand the stress and damage occurs. For example, in the setting of meniscectomy, the loss of the medial meniscus decreases the area of contact between the femur and tibia by approximately one-half. The remaining cartilage transmits substantially more force during activity. As a result, up to 85% of persons with meniscectomy subsequently develop osteoarthritis of the knee over time (Goldberg, 1992).
Tarsal Tunnel Syndrome
Tarsal tunnel syndrome (TTS) is a relatively newly identified nerve impingement syndrome, having been described as recently as 1962 (Turan, 1997). TTS is the lower extremity analogy to CTS. That is, the tibial nerve is entrapped by the flexor retinaculum or laciniate ligament (Day, 1996). This ligament is composed of fascial tissue and is attached to the medial malleolus and calcaneus (Day, 1996). The posterior tibial artery, vein, and nerve course deep to the ligament and compose a neurovascular bundle (Day, 1996). TTS may involve compression of the posterior tibial nerve or one of its branches.
Signs and Symptoms
Individuals with TTS complain of diffuse burning pain and paresthesia -- or "pins and needles" sensation -- at the medial plantar surface of the foot. The pain is exacerbated by activity and is usually noted to be more prominent at the end of the work day. Pain at rest is usually not a characteristic of TTS. Cramps may accompany the pain and paresthesia. Additional symptoms include throbbing, aching, and electric shock-like sensations in the foot (Mahan, 1996).
Treatment of TTS may be conservative, such as the application of orthotics or ankle immobilization, anti-inflammatory medications, and shoe modification. Surgery may be required to decompress the entrapped nerve by releasing the laciniate ligament.
Etiology of Tarsal Tunnel Syndrome
TTS is thought to have multiple causes. Some authors have likened the risk factors to those for CTS, a possibly etiologically similar upper-extremity nerve entrapment. Turan describes three broad causal categories, including posttraumatic, neoplastic, or inflammatory (Turan, 1997). However, in his own series of 18 cases of TTS decompressions described in 1997, fully 15 of them had an unknown etiology (Turan, 1997). The remaining 3 were associated with trauma or fracture. Other authors describe multiple etiologies, including biomechanical, congenital, idiopathic, soft tissue and bony masses, metabolic disorders, neoplasms, and trauma (Mahan, 1996) .
Pathophysiology of Tarsal Tunnel Syndrome
At least one component of the pathophysiology of TTS may be related to the biomechanical type of foot. Hyperpronation in the setting of the pes planus foot occurs because the foot is hyperpronated. Hyperpronation describes the anatomic abnormality seen in the classic flat foot. The calcaneus is everted, the subtalar and midtarsal joints are pronated, and the medial column of the arch is collapsed while the forefoot is abducted (Mahan, 1996). Joint hypermobility, squatting position, and rapid weight gain are associated with TTS caused by hyperpronation (Mahan, 1996).
Pes cavus feet are also prone to TTS for different biomechanical reasons. In the pes cavus foot, the compression of the nerve is caused by a rearfoot varus deformity (Mahan, 1996).
Neoplastic or other space-occupying lesions compress the tarsal tunnel due to a competition for the limited available space. Ganglions, talo-calcaneal joint cysts, hypertrophy of the flexor retinaculum, talonavicular osteophytes, and talar exostoses are a few of the space- occupying lesions that have been associated with TTS (Mahan, 1996). In addition, many metabolic disorders such as rheumatoid arthritis, diabetes, and hyperthyroidism are also associated with TTS (Mahan, 1996).
Traumatic injuries most frequently associated with TTS include ankle sprains (both medial and lateral), fracture of the bony components within the tarsal tunnel, and fracture of the fibula secondary to ankle valgus deformity (Mahan, 1996). In general, any traumatic injury that leads to swelling, inflammation, or fibrous tissue in the tarsal tunnel region can lead to the development of the syndrome (Mahan, 1996).