Case Definitions and Diagnostic Criteria: Disorders of the Muscle-Tendon Units of the Distal Upper Extremity

J. Steven Moore

University of Texas Health Center at Tyler
P.O. Box 2003
Tyler, TX 74710

ABSTRACT

This paper is concerned with describing and discussing the most common disorders that affect the muscle-tendon units of the distal upper extremity (defined as the elbow, forearm, wrist, and hand). For each disorder, there is a brief review of normal anatomy and function; a description of the abnormal changes in the affected tissues (pathology); historical or current thoughts on factors that may contribute to the development of these tissue changes (pathogenesis); and typical symptoms, signs, and physical examination maneuvers related to their clinical assessment. Recommendations for case definitions and diagnostic criteria developed at a workshop sponsored by the Center for VDT and Health Research (Johns Hopkins University) in November 1996 are presented (see acknowledgment). Several problems are research issues related to case definitions and diagnostic criteria are mentioned.

TRIGGER FINGER AND TRIGGER THUMB

The formal medical label for trigger finger or trigger thumb is stenosing tenosynovitis of the digits. 'Stenosing' means that a structure is abnormally narrowed. Even though 'tenosynovitis' technically implies inflammation of a tendon sheath, the actual change thickening. Taken together, 'stenosing tenosynovitis' means that a tendon sheath is narrowed secondary to thickening. There are many tendon sheaths located throughout the body that are susceptible to stenosing tenosynovitis. When stenosing tenosynovitis affects the tendon sheath of one of the fingers, the condition is called trigger finger. When it affects the thumb, it is called trigger thumb.

Anatomy and Function

The muscles that bend or flex the fingers and one of the muscles that flex the thumb are located on the palm (volar) side of the forearm. The tendons that connect the ends of these muscles to the bones in the fingers are shaped like cords. For each finger, there are two flexor tendons that run together along the palm side of the finger. The anatomy for the thumb is similar. A synovial sheath is like a tubular balloon-like structure filled with a low viscosity fluid (synovial fluid) that reduces friction. Imagine the cords (tendons) pressed into the balloon (the tendon sheath) so that the balloon wraps around the cords. When the cords move back and forth, the fluid inside the balloon reduces friction. In addition to this balloon-like structure, the synovial sheath, there is also a series of ligaments, called pulleys, that loop around the tendons and their synovial sheaths. These pulleys hold the tendons close to the bones and joints. If you were on the tendon looking toward the pulley, you would see a tunnel. The underlying bone is the floor of the tunnel. The pulley makes up the walls and the roof of the tunnel. Stenosing tenosynovitis is a disorder that affects one of these tunnels. In particular, it affects the tunnel formed by the A1 pulley. The finger A1 pulleys are approximately at the level of the distal crease in the palm.

Pathology

With trigger finger or trigger thumb, the A1 pulley appears thick and fibrous. As the pulley thickens, it reduces the cross-sectional area of the tunnel (stenosis). When the tunnel becomes too narrow, the tendons no longer move freely through the tunnel and may develop a nodular deformity. Fibrocartilagenous metaplasia has been observed. Since the flexor muscles are stronger than the extensor muscles, people are usually able to flex the digit, but have difficulty extending it. The result is snapping or locking (called 'triggering') that occurs when the flexed finger or thumb is straightened.

Pathogenesis

Current theory suggests that the thickening of the A1 pulley is an adaptation to repeated or prolonged tension on the A1 pulley by the flexor tendons. According to biomechanical theory, this tension is primarily related to the degree of bending of the joint and the degree of tension (also called loading) in the tendon, e.g. 'loaded tendons turning corners.' Maximum tensions in the A1 pulley appear to occur with extreme bending of the joint at the base of the finger. At this time, it is unknown how high this pulley tension must be, how many times it must be experienced, or how long it must last before thickening of the A1 pulley begins.

Presentation, Symptoms, and Signs

For most people, trigger finger or trigger thumb develops gradually, but some cases may follow acute trauma. Snapping, locking, or difficulty extending a flexed finger or thumb, often with discomfort or pain, are the most prominent symptoms. The snapping sensation may be barely perceptible without any actual triggering; or it may be painful, especially when a triggered digit is forcefully extended. The triggering and pain are localized to an area in the palm where the digit joins the hand. Some people report more difficulties in the morning compared to other times. It may be possible for an examiner to feel a nodule on the tendon in the region of the A1 pulley as well as a clicking or snapping sensation with movement of the digit.

DEQUERVAIN'S TENOSYNOVITIS

DeQuervain's tenosynovitis is a disorder that is very similar to trigger finger and trigger thumb. It is also a form of stenosing tenosynovitis, but it occurs along the thumb side of the wrist instead of the palm side of the finger or thumb.
Anatomy and Function

Most of the muscles that control the wrist and fingers anchor at the elbow or on the forearm bones. The tendons that connect these muscles to the bones out in the wrist and fingers are, like the finger flexor tendons, shaped like cords. As these tendons cross the wrist joint, they enter tunnels. On the back side of the wrist (the same side as the back of your hand), the tendons crossing the wrist pass through six tunnels. These are called the six dorsal compartments. The first dorsal compartment is on the thumb side of the wrist. DeQuervain's tenosynovitis is stenosing tenosynovitis of the first dorsal compartment.

The tendon sheath for the first dorsal compartment is located at the end of the radius - the forearm bone on the thumb side. Two muscles that control the thumb, the abductor pollicis longus (APL) and extensor pollicis brevis (EPB), originate on the shaft of the radius in the forearm. The APL inserts on the back side of the first metacarpal bone (the bone that runs between the wrist and the thumb) just beyond the wrist. The EPB inserts on the back side of the proximal phalanx of the thumb (the first bone forming the shaft of the thumb) just beyond the MP joint (at the base of the thumb). These two muscles control the position and orientation of the thumb so the thumb can be used to grip, pinch, or press. These tendons normally glide freely through the tunnel of the first dorsal compartment.

Pathology

The primary change is thickening of the roof of the tunnel (the extensor retinaculum) that results in narrowing of the tunnel. Fibrocartilagenous metaplasia has also been observed. Functional impairment is believed to be caused by impaired gliding of the tendons within the tunnel.

Pathogenesis

Like trigger finger and trigger thumb, it is generally believed that the changes related to DeQuervain's tenosynovitis are a result of 'loaded tendons turning corners.' The APL and EPB tendons are loaded whenever the thumb is used. These tendons turn a corner when the wrist or the thumb are bent.

Presentation, Symptoms, and Signs

The onset of DeQuervain's tenosynovitis is usually gradual. The most common symptom is pain localized to the thumb side of the wrist. The intensity of the pain varies, but it may be severe enough to keep a person awake at night. It also increases with pinching, grasping, sticking the thumb out to the side (the hitch-hiking signal), and bending the wrist toward the little finger. The pain may be severe enough to render the hand useless. There may be slight swelling at the thumb side of the wrist, and full, but sometimes painful, ranges of motion of the wrist and thumb. Firm touching may result in tenderness at the thumb side of the wrist. There should be no sensation of creaking (called crepitus) because it suggests a different disorder (called peritendinitis). Stretching or contraction of the APL or EPB muscles increases the pain. A maneuver called Finkelstein's test is the most characteristic physical sign. This test involves a health care provider grasping the patient's thumb, then bending the wrist toward the little finger. Exquisite pain along at the first dorsal compartment indicates a positive test.

PERITENDINITIS

The myotendinous junction is where a muscle joins its tendons. It is a specialized anatomical structure whose purpose is to transmit a muscle's tension to its tendons when it contracts. There is a myotendinous junction at each end of each muscle cell. Each end of the muscle cell has numerous finger-like projections that match up to similar projections from the tendon. This structure reduces stresses to the cell membrane of the muscle cells while maximizing the transmission of tension from the muscle to the tendon.

The myotendinous junction appears to be the structure involved in two types of conditions: muscle strains and peritendinitis. Muscle strains will not be discussed further here. Peritendinitis is a condition that is widely recognized in other parts of the world, but it has not been discussed in the United States much since the 1940s. It appears that most cases of peritendinitis in the United States are mis-labeled as 'tendinitis' or 'tenosynovitis.'

More than half of cases of peritendinitis affect the same muscles involved in DeQuervain's tenosynovitis, the APL and EPB, but the location of the problem is more in the forearm (an inch or two toward the elbow) rather than at the wrist. Other commonly affected muscles are wrist extensors (also located on the back of the forearm).

Pathology

The problem is localized to the myotendinous junction. There is usually swelling (edema), hyperemia and inflammation. The surface of the muscle and tendon may be covered with a sticky substance called fibrin. The tendons and tendon sheaths beyond the myotendinous junction appear normal.

Pathogenesis

It is generally accepted that peritendinitis develops via fatigue and exhaustion of selected muscle groups or direct trauma. Both factors lead to swelling, inflammation, and the deposition of fibrin around the myotendinous junction.

Presentation, Symptoms, and Signs

Pain, aching, soreness, and tenderness, sometimes severe, are the dominant symptoms. These symptoms are localized to the mid-forearm or a few inches above the wrist. Some patients may report crepitation in this area. Crepitation is a 'creaking gate' noise or sensation associated with movement of the affected structures. The affected area may be swollen, red, warm, or tender to touch. The affected muscle is usually painful when stretched or contracted.

LATERAL EPICONDYLITIS

The medical term for 'tennis elbow' is lateral epicondylitis. The lateral epicondyle is the bony prominence located on the outer (lateral) side of the elbow when the arm is held along the side of the body and the palm facing forward. There is also a bony prominence on the inner (medial) side of the elbow, called the medial epicondyle. When someone has pain localized to the medial epicondyle, the condition is called medial epicondylitis (also called 'golfer's elbow'). Lateral epicondylitis is far more common than medial epicondylitis and there is much less published information about medial epicondylitis. As a result, this section will focus on lateral epicondylitis.

Anatomy and Function

There are two muscles that primarily stabilize, extend, and deviate the wrist from side to side. The extensor carpi radialis longus (ECRL) originates just above the elbow and inserts on the back side of the base of the second metacarpal bone (just beyond the wrist). The extensor carpi radialis brevis (ECRB) originates primarily from the bony prominence on the outside of the elbow, called the lateral epicondyle, and inserts on the back side of the base of the third metacarpal bone (also just beyond the wrist). Whenever the fingers are used to grasp or pinch something, there is simultaneous contraction of the wrist extensor muscles. This stabilizes the wrist joint so that the wrist does not flex when the fingers forcefully grip or press on something.

Pathology

The pathology of lateral epicondylitis is not precisely known. The ECRB appears to be the most commonly involved structure. The tendon near the origin of the ECRB may appear normal from the outside, but usually has some abnormal tissue on the underside. A tear of the tendon is sometimes observed. The nature of these changes as well as those observed under a microscope suggest that something rubbed the underside of this tendon, frayed some of the tendon's fibers, and that the body is trying to repair this damage.

Pathogenesis

Why lateral epicondylitis develops is generally unknown. For cases that occur after blunt trauma to the elbow, it is believed that the trauma injured some of the fibers in the ECRB tendon. For non-traumatic cases, several have postulated microtears within the ECRB tendon following repeated forceful exertions. It has also been suggested that one of the forearm bones (the radial head) may rub the underside of the ECRB tendon. This would most likely occur when the hand grasps an object; the elbow is extended; and the forearm rotates (pronates and supinates) as when using a screwdriver. Lateral epicondylitis does not appear to be a degenerative condition related to aging.

Presentation, Symptoms, and Signs

Lateral epicondylitis usually presents as pain at the lateral side of the elbow. The onset may be sudden or gradual. The intensity of the pain varies. Relatively minor levels may be described as 'discomfort' while more intense levels may be described as 'sharp', 'severe', or 'lightning-like.' The pain often limits activities of daily living (such as lifting a coffee cup or jar), leisure pursuits (gardening or sports), and work (both heavy and sedentary). There is usually tenderness localized at or near the lateral epicondyle. Gripping forcefully, pulling the wrist or long finger back against resistance (extension); having the elbow straight (extension) with the forearm turned inward (pronation) and wrist bent forward (flexion); or resisted rotation of the forearm inward (pronation) and outward (supination) increases the pain. Elbow extension or forearm pronation may be limited. Grip strength and wrist extension strength may be reduced.

CARPAL TUNNEL SYNDROME

Carpal tunnel syndrome is the most complex and controversial of the distal upper extremity disorders.

Anatomy & Function

The carpal tunnel is located on the palm side of the hand. The floor and walls are formed by the carpal bones; the roof is formed by the transverse carpal ligament. Normal contents of the carpal tunnel include a total of 8 finger flexor tendons; one flexor tendon for the thumb; and the median nerve. As in other tunnels, there are tendon sheaths. When the fingers are flexed, the flexor tendons move farther than the median nerve. In addition, the lumbrical muscles (attached to the profundus flexor tendons in the hand) retract into the carpal tunnel with finger flexion.

Pathology

The tendon sheaths covering the nine tendons are often reported to be thickened. The thickening appears to be related to swelling (edema) or scarring (fibrosis) within the tendon sheaths. Even though described as 'tenosynovitis', inflammation does not appear to be involved.

The median nerve often looks normal, but individual nerve fibers inside the nerve may be affected. Most of the individual nerve fibers are covered by an insulation-like material (called myelin sheaths). At the site of compression, this 'insulation' appears pushed off the nerve fiber under the area of compression. Since this 'insulation' is necessary for fast conduction of nerve impulses, its loss contributes to slow (or delayed) nerve conduction as measured during an electrodiagnostic test.

The symptoms of carpal tunnel syndrome are usually explained on the basis of impaired circulation to the median nerve inside the carpal tunnel when intracarpal pressure is elevated. When intracarpal pressure is elevated to a relatively high level for a sufficient period of time, circulation inside the nerve is stopped. Individual nerve fibers begin to spontaneously discharge and produce unusual sensations of numbness and tingling (called paresthesias). When intracarpal pressure is lowered, blood flow returns, spontaneous nerve discharges end, and the paresthesias end.

Pathogenesis

At this time, it is not possible to reliably state why carpal tunnel syndrome develops in a given person. There are several possible mechanisms that might be related to hand usage and numerous others that would include factors unrelated to hand usage. Some of the possible hand usage models include: (1) thickening of the tendon sheaths inside the carpal tunnel; (2) hypertrophy (enlargement) of the tendons that pass through the carpal tunnel; (3) direct pressure on the median nerve by the flexor tendons when using the fingers with a flexed wrist; (4) retraction of some small hand muscles (lumbricals) into the carpal tunnel when forming a tight fist; (5) thickening of the transverse carpal ligament in response to tension from 'loaded flexor tendons turning a corner' at the wrist (wrist flexion); (6) alterations within the nerve secondary to repeated or prolonged episodes of elevated intracarpal pressure; (7) traction or friction related to disproportionate movement of the tendons relative to the median nerve; and (8) bruising the median nerve within the carpal tunnel secondary to direct trauma or using the palm of the hand as a hammer. Which one(s) of these models are correct, if any, is currently unknown.

Presentation, Symptoms, and Signs

Excluding acute trauma, symptom onset is usually gradual and often related to unaccustomed activity. The dominant symptoms are numbness or tingling (called paresthesias). Pain or weakness are uncommon, although intense paresthesias may be reported as 'painful.' Typically, the paresthesias affect the thumb, index, long, and part of the ring finger, but should spare the little finger and occur at night or with static grasp. Symptoms may radiate into the forearm, elbow, arm, or shoulder. There are no reliable physical findings. Electrodiagnostic studies, often called nerve conduction studies or EMGs, are the best way to confirm the presence of carpal tunnel syndrome.

RECOMMENDED DIAGNOSTIC CRITERIA FOR EPIDEMIOLOGICAL STUDIES

The diagnostic criteria for disorders of the muscle-tendon units of the distal upper extremity primarily rely on the quality and location of symptoms, response to palpation, and response to provocative maneuvers. Pain is the most dominant symptom quality for these disorders, but burning may also be characteristic for some disorders. The location of the dominant symptom is expected to correspond to the site of involvement. Palpation of the site of involvement is expected to increase pain. Provocative maneuvers generally increase the tensile load of the affected muscle-tendon unit via passive elongation, active contraction, or both. Provocative maneuvers targeting the affected muscle-tendon are expected to increase pain.

The distal upper extremity can be conveniently divided into five anatomical categories (elbow, proximal forearm, distal forearm, wrist, and hand) that roughly correspond to the tissues that make up the muscle-tendon units (tendon, muscle, myotendinous junction, and tendon sheath). Most categories can be further divided according to anatomical side (volar versus dorsal). The working group's proposed anatomical categories and corresponding nosology are in Table I. There may be circumstances where it would be desirable or necessary to combine some of these categories.

The working group also developed proposed diagnostic certainty categories (Table II). There are three certainty categories, 'definite', 'probable', and 'possible.' The presence of symptoms is an absolute requirement for all categories. 'Probable' requires the presence of tenderness to palpation or a positive response to provocative testing. 'Definite' requires the presence of tenderness to palpation and a positive response to provocative testing.

Proposed case definitions for common distal upper extremity conditions are outlined in Table III.

Table I. Proposed anatomical categories and nosology for the distal upper extremity.

^A Specification of the dorsal compartments (I-VI) is recommended.
^B Specification of the digits (I-V) is recommended.

Table II. Proposed diagnostic certainty categories.

^A Symptoms are characterized by their quality and their location.
^B The location of the tenderness to palpation should correspond to the location of the symptoms.
^C Provocative testing should correspond to the location of the symptoms and the location of the tenderness to palpation.

Table III. Proposed case definitions for the distal upper extremity.

PROBLEMS RELATED TO CASE DEFINITIONS AND DIAGNOSTIC CRITERIA

The are several factors related to case definitions and diagnostic criteria that have contributed to misunderstanding the relationship between work and distal upper extremity disorders.

1. The use of generic disease categories, such as cumulative trauma disorders or repetitive motion disorders, is inappropriate for epidemiological and clinical applications.
   1. Several 'lists' of cumulative trauma disorders has been published. Many of the conditions included on such 'lists' of are based on anecdotal comments or reports (opinions, case reports, or case series) rather than epidemiological evidence. Examples of such conditions include ganglion cysts; ulnar nerve compression about the elbow (supracondylar, retrocondylar, and cubital tunnel); avascular necrosis of the carpal bones (Keinbock's disease or Preiser's disease); and osteoarthritis.
   2. Generic categories lump distinct disorders into a single morbidity category without consideration of unique factors, e.g. anatomy, pathology, and theories of pathogenesis. For example, the are few such similarities for lateral epicondylitis and DeQuervain's tenosynovitis (see earlier sections in this paper).
   3. Generic categories imply mechanisms of pathogenesis are poorly substantiated. For example, the pathogenesis of stenosing tenosynovitis (DeQuervain's tenosynovitis, trigger finger, and trigger thumb) is probably more adaptative than traumatic.
   4. Generic categories fail to effectively communicate the multifactorial etiology of many of the conditions. Decisions about work-relatedness may be based on the presence of the condition on a 'list' rather than assessment of exposure.
   5. Generic categories imply epidemiological characteristics that are either unknown or unsubstantiated in the current literature. For example, the term cumulative trauma disorders implies that risk of disease increases with duration of exposure. There are epidemiological studies that are inconsistent with this assumption. In addition, such an assumption fails to consider the importance of unaccustomed activity.
   6. A generic label should never be accepted as a clinical diagnosis. This is akin to saying "I don't know what you have, but I know it is related to work."
2. Diagnostic misclassification of carpal tunnel syndrome is a problem. According to recent BLS data, carpal tunnel syndrome is the most common occupational illness; however, according to epidemiological data from multiple studies in the workplace, disorders of the muscle-tendon units are far more common than carpal tunnel syndrome. In my case series, approximately 33% of workers' compensation cases with a diagnosis of carpal tunnel syndrome could not be confirmed using a generous case definition. Several companies have observed a reduction in the number of cases of carpal tunnel syndrome and the number of carpal tunnel release surgeries following implementation of only a medical management program.
3. Establishing the work-relatedness of a condition involves more than making a diagnosis of a distal upper extremity disorder in a person that works. Determining work-relatedness begins with accurate diagnosis. Review and consideration of the medical and epidemiological literature is used as a second step to establish the disorder's relationship to work and to define the context (exposure circumstances) within which it occurs. Assessment of exposure determines whether the disorder developed within the recognized context. Misclassification of work-relatedness (and therefore exposure) also appears to be a problem. The BLS criteria for recording entries on the OSHA 200 log favors misclassification. In my case series, the magnitude of exposure misclassification among treating physicians was approximately 50%.

RESEARCH ISSUES

From a research perspective, there are several issues related to the "disease" side of the equation that should be addressed in future research.

1. If the primary goal is to prevent the development of musculoskeletal disorders, we should focus on discovering the relationship between exposure factors and the incidence of such disorders.
   1. A longitudinal study design is necessary to measure the incidence of a condition. Few studies in this arena have been longitudinal.
   2. Many epidemiological studies utilize the prevalence of one or more conditions as the measure of health outcome. Extrapolation of prevalence to incidence generally requires some insight into the duration of the condition. The durations of the distal upper conditions are generally unknown.
2. Many epidemiological studies utilize the prevalence of symptoms, as opposed to the incidence or prevalence of clinical conditions, as the measured health outcome. Factors related to the occurrence of symptoms may not be related to the development of the condition. Strategies to prevent symptoms may be important for medical management, but may not contribute to disease prevention.
3. Knowledge about the latent period for these disorders would be useful. Does the risk of developing these disorders increase progressively with accumulated exposure (long latencies) or do these disorders primarily occur in the context of unaccustomed activity (short latencies).
4. Research in this arena should be conducted in a manner that tests theories of pathogenesis.

ACKNOWLEDGMENT

Members of the working group (listed alphabetically) included Jacqueline Agnew, Dorcas Beaton, Cindy Ensor, Glenn Haughie, Steve Moore, Glenn Pransky, Laura Punnett, and Frank Rooney.