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Repetitive Motion Hand Disorders

effectively treated and often dramatically improved using traditional surgical procedures directed at the component clinical entity. The characteristic of cumulative trauma disorder, however, is a tendency toward either recurrent problems or the development of additional symptoms following treatment for one entity. Therefore, long-term relief is possibly best accomplished through thoughtful modifications in upper extremity use habits or careful redesign of workplace conditions.
Hands

Repetitive Motion Hand Disorders

By Douglas H.C.L. Chin, MD, and Neil F. Jones, MD

Copyright 2002 Journal of the California Dental Association.

 


The clinical management of cumulative trauma disorder is based upon the identification and treatment of individual component pathologies and, frequently, referral to a knowledgeable occupational therapist with an understanding of ergonomic behavioral, postural, and workspace modification. Most commonly, these individual pathologic entities are carpal tunnel syndrome, cubital tunnel syndrome, trigger finger, and De Quervain’s tenosynovitis. In this article, the anatomy, diagnosis, and treatment of each of these disorders will be considered separately. In addition, since these clinical entities are often use-related, special attention should be directed toward biomechanical and ergonomic considerations.

 

The various names given to the clinical disorder known as cumulative trauma disorder, repetitive strain injury, repetitive motion injury, overuse syndrome, work-related musculoskeletal syndrome, and repetitive stress injury reflects the poor understanding of the pathophysiology of this entity. The currently favored designation is cumulative trauma disorder, but even this name betrays a great misunderstanding of the pathophysiologic influences underlying the disorder. Contrary to the implications of its name, cumulative trauma disorder is typically characterized by a lack of antecedent trauma. Even the notion of an additive effect of many minor but repetitive "microinjuries" as a result of repetitive motions is unsubstantiated and probably false. Conversely, cumulative trauma disorder of the upper extremity is characteristically associated with a history of repetitive stereotyped behaviors that require prolonged static posturing of the upper extremity, not repetitive traumas. Moderate or high-energy repetitive maneuvers are notably absent from the typical history. Interestingly, symptoms often relate not to the tendon and muscle groups involved in repetitive motions, but to the stabilizing or antagonistic tendon and muscle groups used to position and stabilize the extremity in space during the repetitive motion.

Clinically, the symptomatology of cumulative trauma disorder is as ill-defined as its pathophysiology. There are no established criteria for determining its diagnosis. Clinically, most hand surgeons will designate the term cumulative trauma disorder to an ill-defined, inconsistent, widely variable but often debilitating constellation of weakness, paresthesias, pain, and tenderness of the upper extremity in the presence of a significant history of repetitive stereotyped upper extremity activity. Hand surgeons attempt to reduce this perplexing array of symptoms into a compilation of well-understood clinical entities, such as carpal tunnel syndrome and trigger finger, for example. This tendency to reduce the complex and poorly understood aggregate of cumulative trauma disorder into individual well-understood component entities has some practical clinical importance, because many of the symptoms of cumulative trauma disorder are effectively treated and often dramatically improved using traditional surgical procedures directed at the component clinical entity. The characteristic of cumulative trauma disorder, however, is a tendency toward either recurrent problems or the development of additional symptoms following treatment for one entity. Therefore, long-term relief is possibly best accomplished through thoughtful modifications in upper extremity use habits or careful redesign of workplace conditions.

As poorly understood as cumulative trauma disorder may be pathophysiologically, it is clear clinically that it tends to be over diagnosed. Properly applied, cumulative trauma disorder should be designated when a constellation of refractory or recurrent symptoms are present in association with a history of repetitive or prolonged stereotyped use, or when such symptoms and history are associated with the development of additional symptoms following treatment. Isolated clinical entities such as carpal tunnel syndrome do not alone constitute cumulative trauma disorder, even when associated with a significant history of repetitive stereotyped behavior, such as keyboard use or dental handpiece use.

For the hand surgeon, the clinical management of cumulative trauma disorder is based upon the identification and treatment of individual component pathologies and, frequently, referral to a knowledgeable occupational therapist with an understanding of ergonomic behavioral, postural, and workspace modification. Most commonly, these individual pathologic entities are carpal tunnel syndrome, cubital tunnel syndrome, trigger finger, and De Quervain’s tenosynovitis. In this article, the anatomy, diagnosis, and treatment of each of these disorders will be considered separately. In addition, since these clinical entities are often use-related, special attention should be directed toward biomechanical and ergonomic considerations.

Carpal Tunnel Syndrome

The median nerve arises from the anterior cord of the brachial plexus and emerges anteriorly below the cubital fossa at the elbow, passing from beneath the aponeurosis of the flexor digitorum superficialis and pronator teres muscles, and coursing distally into the wrist. At the level of the wrist, the median nerve enters a quadrangular fibro-osseous tunnel, known as the carpal tunnel.

The carpal tunnel is bordered on three sides by bone and on one side by a fibrous ligament. In the anatomic position, with the palms facing upwards, the carpal tunnel is bounded laterally, dorsally, and medially by the carpal bones. The "roof" consists of a thick, dense fibrous band, the transverse carpal ligament. The carpal tunnel is a hard, nonexpansile structure that houses the median nerve, along with the nine flexor tendons to the fingers and thumb. After exiting distally from the carpal tunnel, the median nerve divides into common digital nerves, which in turn bifurcate, providing sensibility to the palmar aspects of the thumb, index finger, middle finger, and typically the radial aspect of the ring finger. After entering the carpal tunnel, the median nerve also gives rise to its motor branch, which supplies most of the thenar muscles of the thumb.

Because of the low mechanical compliance of the carpal tunnel, swelling within the carpal tunnel will lead to increased hydrostatic pressure within the carpal tunnel. A variety of factors may contribute to swelling within the carpal tunnel. Tenosynovitis,1,2 amyloid deposition,3 fibrosis,4,5 and hyalinosis4,5 of the flexor tenosynovium within the carpal tunnel have all been widely speculated to be etiologic factors in the development of compression neuropathy of the median nerve.

Regardless of specific pathologic findings within the flexor tenosynovium, swelling of this tissue from longstanding edema, vascular stasis, and inflammation seems to be a final common final pathway resulting in increased carpal tunnel pressures. Small, highly repetitive movements requiring minimal amplitudes of tendon excursion may engender the development of interstitial edema and venous and lymphatic stasis. These low-energy movements are thought to be of insufficient force and excursion to allow the development of contractive forces necessary to generate venous and lymphatic drainage of the carpal tunnel and hand (R.W. Beasley; personal communication). Thus, carpal tunnel syndrome seems to be seen more commonly among users of low-force keyboards, such as computer keyboards, than among users of the higher-force keyboards of manual typewriters (R.W. Beasley, personal communication). The nature of finger motion is also subtly but significantly different between these two keyboard types. Higher-force keyboards may require the recruitment of the intrinsic muscles of the hand (interossei and lumbricals) to bring about the simultaneous interphalangeal joint extension and metacarpophalangeal joint flexion necessary to forcefully press a typewriter key. In contrast, with the low-force keyboards of computer workstations, most finger motion is generated within the extrinsic flexor muscles of the forearm, and far less intrinsically motored interphalangeal joint extension is required. Thus, the relative exclusion of intrinsic muscle use with low-force keyboards may result in significantly increased interstitial edema and vascular stasis.

Carpal tunnel pressures are a well-studied function of wrist position. Carpal tunnel dimensions decrease with both wrist flexion and wrist extension.6 Thus, carpal tunnel pressures are elevated with either wrist flexion or wrist extension.7,8 Rojviroj and colleagues9 demonstrated carpal tunnel pressures to be the lowest with the wrist in neutral position, highest in 90 degrees of dorsiflexion, and significantly elevated with wrist palmar flexion. Thus, sustained static flexion of the wrist, as might be required to operate a dental drill, particularly working in the "clock" position about the dental chair,10 may result in an increased incidence of carpal tunnel syndrome among dental health care workers. In addition, the sustained fine but firm posturing of the hand required for dental procedures, with minimal amplitudes of intrinsic muscle excursion, may contribute to the development of edema and vascular congestion within the hand and carpal tunnel. It is well-established in the literature that musculoskeletal complaints occur with high frequency among dental personnel10,11 In one study, dental hygienists were found to be 5.2 times more likely to be told they had carpal tunnel syndrome, and 3.7 times more likely to meet accepted criteria for its diagnosis.10

When carpal tunnel pressures become sufficiently elevated, ischaemic neuropathy of the median nerve may occur, clinically manifesting as carpal tunnel syndrome. Patients with carpal tunnel syndrome have significantly elevated carpal tunnel pressures compared to patients without carpal tunnel syndrome.9 Carpal tunnel pressures in excess of 30 to 60 mmHg result in paresthesias in the median nerve distribution,12 the signature feature of carpal tunnel syndrome. Because of the orientation of the sensory fibers of the median nerve at the level of the carpal tunnel, sensory abnormalities typically affect the middle and index fingers more than the thumb. Any sensory disturbances in the distribution of the median nerve may reflect compression neuropathy within the carpal tunnel. Patients usually present with paresthesias, hyperesthesias or even dysesthesias of the radial three and one-half digits. Other patterns of sensory disturbances in carpal tunnel syndrome may relate to normal anatomic variations in median innervation or to segmental compression or ischaemia of the nerve. Hence, patients may present with numbness or paresthesias of the middle finger only, the thumb only, or, rarely, all of the fingers.

Because the motor branch of the median nerve generally originates from the main trunk of the nerve within or distal to the carpal tunnel, elevated carpal tunnel pressures may also result in weakness of the thenar muscles of the thumb supplied by the motor branch. Thus, weakness, clumsiness, an increasing tendency to drop objects, and difficulty with fine manipulation, such as required for buttoning clothes or sewing, may be the presenting motor complaints in patients with carpal tunnel syndrome.

Clinical experience suggests that carpal tunnel syndrome is accurately diagnosed by the presence of any two of three criteria:

* Symptoms strongly suggestive of carpal tunnel syndrome;

* Physical signs that strongly implicate compression of the median nerve within the carpal tunnel; and

* Electrodiagnostic studies demonstrating significant slowing of median nerve conduction velocities across the wrist.

Therefore, in the absence of either a convincing history or strongly persuasive physical findings to suggest carpal tunnel syndrome, nerve conduction studies may be necessary to confirm or exclude such a diagnosis. In patients with a classic history for carpal tunnel syndrome supported by highly suggestive physical findings, confirmatory nerve conduction studies may be unnecessary (and uncomfortable). However, even with a strongly suggestive history and a convincing physical examination, nerve conduction studies may be useful in providing objective measurements to document the severity and reversibility of nerve and thenar muscle damage.

The patient’s history is the single most predictive factor in establishing the diagnosis of carpal tunnel syndrome. Patients complain of painful paresthesias in the median nerve distribution that are usually worse at night, but significantly improved during the course of the day. Classically, patients are awakened with painful paresthesias. The frequency of nocturnal wakening may be related to the severity of the condition.

Physical examination may be quite variable but is most supportive of a diagnosis of carpal tunnel syndrome when sensibility is subjectively and objectively diminished in the thumb, index finger, middle finger, and ring finger (Figure 1). "Splitting" of the ring finger, in which the radial aspect of the ring finger (supplied by the median nerve) exhibits decreased sensibility but the ulnar aspect (supplied by the ulnar nerve) exhibits normal sensibility, is particularly suggestive of carpal tunnel syndrome. Sensibility should be normal over the thenar eminence of the thumb. This area is supplied by the palmar cutaneous branch of the median nerve, which originates proximal to the carpal tunnel and is therefore unaffected by the compression. Other highly suggestive physical findings include the subjective report of "electrical" shooting sensations to the middle finger, index finger, or thumb when the base of the palm is tapped (Tinel’s sign) or when sustained deliberate pressure is applied over the carpal tunnel (Durkan’s sign). Phalen’s test is a quantitative test, which roughly correlates with the level of irritability of the median nerve at the carpal tunnel. The patient’s wrist is passively flexed, and the number of seconds after which the patients reports the onset of paresthesias to one or all of the radial 3ฝ digits is recorded. Paresthesias within 60 seconds of wrist flexion are considered diagnostic of carpal tunnel syndrome. Phalen’s test is positive in 66 percent to 88 percent of patients with carpal tunnel syndrome,13-15 whereas Tinel’s sign has been shown to have a positive predictive value of only 56 percent to 67 percent.13,14 However, a positive Tinel’s sign associated with a positive Phalen’s sign has a positive predictive value of 88 percent. Durkan’s sign is independently positive in 87 percent13 to 100 percent14 of patients with carpal tunnel syndrome. Therefore, a highly "positive" physical examination combined with a history of symptoms classic for carpal tunnel syndrome may accurately establish the diagnosis of carpal tunnel syndrome without the need for confirmatory nerve conduction studies. Some of the common symptoms and signs of carpal tunnel syndrome are shown in Table 1.

Nerve conduction studies measure the conduction velocity of the median nerve across the carpal tunnel. Electromyelography records patterns of electrical potentials (positive sharp waves and fibrillation potentials) within the abductor pollicis brevis muscle of the thumb, which may indicate the presence of muscular denervation seen in severe neuropathy. The clinical utility of electrodiagnostic testing is threefold. If the patient has either a nonclassical history or a poorly defined physical examination, the demonstration of slowing of nerve conduction or denervation on electromyelography may confirm or support an otherwise uncertain diagnosis. Even if there is little doubt of carpal tunnel syndrome on clinical grounds, electrodiagnostic studies may be useful in two ways. Associated compression neuropathies of the ulnar nerve or of the median nerve more proximally may be evaluated. In addition, the severity of carpal tunnel compression may be inferred from the presence or absence of positive sharp waves and fibrillation potentials and from the degree of slowing of conduction velocity. Fibrillations or positive sharp waves on electromyelography indicate that muscular denervation is present. Irreversible atrophy of the thenar muscles may result from the less than timely resolution of carpal tunnel syndrome in such severe cases.

Conservative treatment for mild to moderate cases of carpal tunnel syndrome includes splintage and steroid injections. A wrist splint will support the wrist in a neutral or slightly extended position so that the carpal tunnel maintains a geometry with maximum volume and minimum intraneural pressure.9 Splinting of the wrist is particularly helpful at night, when patients tend to sleep with the wrist flexed and when carpal tunnel swelling may be increased due to inactivity. Steroid injections are directed toward decreasing the volume of the carpal tunnel contents by exerting a powerful anti-inflammatory effect upon the flexor tenosynovium. Both of these conservative measures serve to minimize the volumetric discrepancy between the carpal tunnel itself and the carpal tunnel contents -- i.e. the median nerve and flexor tendons -- thus lowering intraneural hydrostatic pressures.

For patients with moderate to severe carpal tunnel syndrome or for those who fail to improve with conservative measures, surgical release of the carpal tunnel may be indicated. Division of the transverse carpal ligament, which forms the roof of the tunnel, increases the anteroposterior and transverse dimensions of the carpal tunnel, resulting in a 24 percent increase in the volume of the carpal tunnel.16 Increased intraneural blood flow is observed within 60 seconds following release of the transverse carpal ligament.17 Carpal tunnel release may be performed either through a single 2 to 4 cm long incision placed longitudinally over the palm (open carpal tunnel release) or, more recently, with the assistance of a small endoscope (endoscopic carpal tunnel release).18,19 Either procedure is generally performed as a short outpatient procedure, usually requiring only local or regional anesthesia. Patients are generally discharged 60 to 90 minutes after surgery with a small dressing splint that leaves the fingers free to move. Relief from preoperative symptoms of carpal tunnel syndrome is variable, depending on the severity and duration of the carpal tunnel syndrome. However, generally patients note significant improvement immediately following surgery. Clinical improvement then continues several months afterward, as the chronically compressed and ischemic median nerve slowly recovers within its new carpal tunnel environment.

Recurrence of carpal tunnel syndrome following adequate surgical release of the transverse carpal ligament is uncommon. Recurrent symptoms following carpal tunnel release are generally due either to incomplete surgical release of the transverse carpal ligament or to accompanying proximal compression neuropathy at the level of the proximal forearm or in brachial plexus or cervical spine.

Cubital Tunnel Syndrome

The ulnar nerve passes behind the medial epicondyle at the elbow and enters the forearm between the two heads of the flexor carpi ulnaris muscle. The cubital tunnel is a fibro-osseous space bounded laterally by the olecranon and medially by the medial epicondyle with the aponeurosis of the flexor carpi ulnaris forming a fibrous roof. Compression of the ulnar nerve at the level of the elbow was first described by Panas20 in 1878. Although cubital tunnel syndrome was originally used to describe ulnar nerve compression specifically within the anatomic confines of the cubital tunnel,12 the term is currently used to describe compression neuropathy of the ulnar nerve at any of several different anatomic sites around the elbow. In addition to the fibro-osseous cubital tunnel itself, other common sites of ulnar nerve impingement include the medial intermuscular septum; the Arcade of Struthers (a consistent fascial band extending from the medial intermuscular septum to the medial head of the triceps); the medial epicondyle of the humerus; and Osborne’s ligament (a thickened band of the flexor carpi ulnaris aponeurosis).

Increased interstitial pressures within the soft tissues surrounding the ulnar nerve may result in neural ischemia. Elevated interstitial pressures may be further exacerbated by elbow and wrist motion. Elbow flexion, wrist extension, and/or shoulder abduction synergistically elevate intraneural pressure.22,23 With elbow flexion, the cubital tunnel narrows in caliber by 55 percent,23,24 thus increasing cubital tunnel and intraneural pressures. In addition, with elbow flexion the ulnar nerve is subject to longitudinal traction. Wrist extension, independent of elbow flexion, also stretches the ulnar nerve and passively tightens the origin of the flexor carpi ulnaris over the ulnar nerve. Active wrist flexion may also directly compress the ulnar nerve at the origin of the contracting flexor carpi ulnaris. Together, these dynamic changes with elbow flexion and wrist extension or flexion result in decreased perfusion and oxygenation of the ulnar nerve, resulting in cubital tunnel syndrome.25

These dynamic anatomic factors are important when considering the ergonomic factors contributing to the development of cubital tunnel syndrome. Static posturing of the elbow in flexion and the wrist in extension, such as might be required with some computer workstations, may have the dual effect of narrowing the confines of the cubital tunnel while tightening the origin of the flexor carpi ulnaris against the ulnar nerve. In addition, wrist extension places the ulnar nerve in traction.23 Similar upper extremity posturing may be required in the operation of dental handpieces, surgical drills and other instrumentation. Drilling in a "clock" position around the patient, with the wrist and elbows flexed, may have the combined effects of decreasing the volume of the cubital tunnel, placing the ulnar nerve in traction at the medial epicondyle, and directly compressing the ulnar nerve against the contracting flexor carpi ulnaris. Some dentists and surgeons with cubital tunnel syndrome clearly identify the operation of handheld handpieces or drills and other power tools as exacerbating activities. Other repetitive or sustained activities, particularly those combining elbow flexion with passive wrist extension or active wrist flexion could be predicted to precipitate or exacerbate symptoms of cubital tunnel syndrome. Racket sports, cycling, weight lifting, driving, blow-drying hair, and holding a telephone are frequently identified activities, which tend to aggravate cubital tunnel syndrome.

Unlike the median nerve which supplies sensibility to the radial three and one-half digits of the hand, the ulnar nerve typically supplies sensibility to the small finger and medial half of the ring finger, as well as the remainder of the medial aspect of the hand (Figure 2). Motor contributions of the ulnar nerve include innervation of the adductor pollicis and the first dorsal interosseous, which serve to enable pinch grip of the thumb against the radial side of the index finger, as might be required, for example, to turn a key. In addition, the ulnar nerve supplies the flexor of the small finger’s distal interphalangeal joint, as well as most of the intrinsic muscles of the hand. As a result, compression neuropathy of the ulnar nerve potentially results in a variety of clinical manifestations (Table 2). Patients typically present with intermittent paresthesias of the ulnar two digits, exacerbated by elbow flexion. Patients frequently report nocturnal wakening. Often, such patients report a habit of sleeping with their elbows flexed or their hands behind their pillow. Not infrequently, patients present with pain or aching feeling over the medial aspect of their elbow or forearm. Motor symptoms generally occur later in the course of cubital tunnel syndrome, although subtle objective motor findings may be present on careful physical examination. Difficulties referable to intrinsic muscle weakness are the earliest motor symptoms. Patients may relate a history of difficulty with writing, turning keys, or opening jars. In severe cases of cubital tunnel syndrome, the strong median-innervated flexors of the interphalangeal joints and radial innervated extensors of the metacarpophalangeal joints are unopposed or weakly opposed by the intrinsic muscles that normally exert the opposite effect. A classic ulnar "claw" deformity may result (Figure 3).

The clinical evaluation of cubital tunnel syndrome is similar to that of carpal tunnel syndrome. The most consistent clinical finding is a sensibility deficit in the distribution of the ulnar nerve, particularly affecting the small finger. Splitting of the ring finger, with deficient or otherwise abnormal sensibility of its ulnar aspect but normal sensibility over its radial half, is nearly pathognomonic of an ulnar sensory neuropathy. The detection of subtle sensory deficits may be enhanced by first performing provocative tests, such as sustained acute elbow flexion. If the ulnar nerve already is marginally ischaemic or irritable at the level of the elbow, then transient longitudinal traction on the nerve engendered by acute elbow flexion will make the nerve incrementally more ischaemic. An increase in paresthesias and sensibility deficits is noted in the distal ulnar distribution. Acute elbow flexion is the provocative test for cubital tunnel syndrome equivalent to Phalen’s test for carpal tunnel syndrome. A Tinel sign at the elbow, wherein the patients reports shooting electrical sensations or paresthesias in the ring and small finger upon tapping of the medial epicondyle, is nearly pathognomonic of cubital tunnel syndrome. Motor involvement is assessed quantitatively as a weakness in lateral (key) pinch, which measures the opposing forces of the adductor pollicis of the thumb and the first dorsal interosseous muscle of the index finger. Qualitatively, this weakness of lateral pinch is manifested as Froment’s sign: The patient is asked to play tug-of-war with a piece of paper gripped in opposition between the lateral pinch of one hand and the lateral pinch of the other. A hand significantly affected by an ulnar motor neuropathy attempts to compensate for its inability to adduct the thumb and abduct the index finger in opposition. Abduction of the thumb and flexion at its interphalangeal joint occurs instead (Figure 4).

Conservative treatment for mild to moderate cases of cubital tunnel syndrome are directed at preventing flexion of the elbow and the significant biomechanical effects of such motion. A splint may be used to immobilize the elbow in extension, particularly at night. However, occasionally the splint itself becomes a source of compression or irritation of the nerve at the level of the elbow. Accordingly, simply wrapping the elbow region with a bulky towel may accomplish the same goals of immobilization and may be more comfortable to the patient. Other measures of conservative therapy are directed at avoiding or at least modifying activities, which tend to aggravate cubital tunnel syndrome. Simply moving a computer keyboard inward on the desk away from the user may accomplish the desired goal of decreasing sustained elbow flexion and wrist extension. Use of certain ergonomic keyboards may allow the maintenance of a neutral wrist position while alleviating flexor carpi ulnaris strain. Lowering the level of a keyboard may also accomplish the above goals.

The surgical management of cubital tunnel syndrome is currently an area of active debate among hand surgeons. Common to all treatment plans is an adequate exploration and release of the common sites of nerve compression, such as the arcade of Struthers, the cubital tunnel, the medial epicondyle, and the leading fascial edge of the flexor carpi ulnaris. However, in addition to thorough decompression of the nerve in situ, several authors advocate transposition of the entire nerve segment anteriorly, so that the nerve no longer passes posterior to the elbow.25-27 Theoretically, by transposing the nerve anterior to the axis of elbow flexion, the ulnar nerve is no longer placed in longitudinal traction with elbow flexion. However, nerve transposition procedures require skeletonization of the nerve for sufficient lengths to permit transposition. Theoretically, this dissection results in devascularization of a nerve that is already intermittently ischaemic.28 More recently, considerable attention has been paid to the option of medial epicondylectomy, without formal transposition of the nerve.29-31 This operation has the benefit of accomplishing release of the nerve, allowing anterior subluxation of the ulnar nerve, thus eliminating the fulcrum effect of the medial epicondyle so that elbow flexion no longer places the nerve on stretch. Finally, and arguably most importantly, medial epicondylectomy accomplishes the above without the need to excessively devascularize portions of an already ischemic ulnar nerve.

Stenosing Flexor Tenosynovitis (Trigger Finger)

There are no muscles within the hand which flex the interphalangeal joints of the fingers or thumb. Rather, muscular contractions within the forearm are transmitted to the fingers of the hand by way of the flexor digitorum profundus, flexor digitorum superficialis, and flexor pollicis longus tendons to produce flexion of the fingers and thumb.

A series of transversely oriented fibrous pulleys maintains the position of the flexor tendons along the phalangeal bones, preventing the tendons from subluxing anteriorly away from the digits, which would cause "bow stringing" across the palmar aspect of the hand. For smooth painless finger flexion to occur, there must be free gliding of the flexor tendons within the fibro-osseous tendon sheaths formed by these pulleys.

Volume discrepancies between the flexor tendon sheath and the flexor tendons may lead to impingement of this free gliding mechanism by causing actual mechanical abrasion between the two gliding surfaces. As a result, progressive inflammation develops between the tendons and the sheath. "Trigger finger" is the colloquial term given to this condition, stenosing flexor tenosynovitis. A vicious cycle perpetuates and exacerbates the condition, because increased inflammation causes increased mechanical resistance to gliding (stenosis), which again produces increased inflammation. Early descriptions of stenosing flexor tenosynovitis attributed the high incidence of this entity in middle-aged women to the half-flexed position the fingers adopt for carrying shopping bags. Furthermore, because the pulleys maintain the flexor tendon in close apposition to the metacarpal head and proximal phalanx, an extremely small moment arm across the metacarpophalangeal joint results. Consequently, very large forces are must be generated within the forearm to allow finger flexion distally, and the transmission of these forces across the joints results in large sheer forces across the pulleys. Activities requiring sustained or repetitive finger flexion over a limited range of excursion engender significant sustained or recurrent sheer forces across a small segment of the flexor tendons and pulleys, resulting in flexor tenosynovitis. Such activities could include carrying heavy bags or briefcases, prolonged writing, rock climbing, or strenuously grasping certain dental instruments.

The most proximal of the palmar pulleys is the A1 pulley, located at the base of each finger overlying the metacarpal head. The A1 pulley is the site is most frequently involved in stenosing flexor tenosynovitis. Patients usually complain of a finger or thumb "catching," "clicking," or locking in a flexed position. They may require using their other hand to extend the affected digit. Patients may also complain of pain in the palm at the base of the affected finger or thumb. On physical examination, the patient generally has point tenderness over the A1 pulley at the base of the affected finger. Occasionally patients present with pain in the proximal interphalangeal or distal interphalangeal joint or in the entire finger. This is because inflammation at the A1 pulley may involve the digital nerves immediately adjacent to the flexor tendon sheath, resulting in referred pain more distally. Not uncommonly, patients complain of painful "arthritis" at the proximal interphalangeal joint; however, physical examination reveals point tenderness over the A1 pulley but no tenderness of the proximal interphalangeal joint. Similarly, patients may report numbness or paresthesias on one side of the finger due to irritation of the digital nerve more proximally.

In most cases, a tender nodule may be palpated at the level of the A1 pulley. This nodularity represents inflammation within the flexor tendon itself. The nodule moves proximally with flexion and distally with extension of the finger. When the finger is flexed, the flexor tendon nodule is proximal to the A1 pulley. As the patient attempts to extend the finger, the nodule is forced beneath the A1 pulley. At this point, extension of the finger may temporarily be prevented; the finger becomes "stuck" in a semi-flexed position (Figure 5). With increased force of extension, this impingement to gliding of the flexor tendon beneath the A1 pulley is overcome, resulting in a sudden acceleration in finger extension. A characteristic "snapping" of the finger results. In more severe cases of stenosing flexor tenosynovitis, it may be impossible to overcome this impingement, and the finger becomes "locked" in the flexed position. Failure to release such a "locked" trigger finger and restore a full range of extension to the finger may result in stiffness or even a permanent flexion contracture of the affected finger.

Because stenosing flexor tenosynovitis represents a volume discrepancy between the flexor tendons and the flexor tendon sheath, treatment may be directed at either decreasing the volume of the two flexor tendons or increasing the size of the tendon sheath. The former is generally attempted first by injecting the flexor tendon sheath with a small volume of a corticosteroid preparation, usually betamethasone or triamcinolone. Relief of pain with this injection is immediate and diagnostic, because it is typically delivered with a small amount of local anesthetic, such as lidocaine. The lidocaine is eliminated within hours and the pain recurs. Sustained and significant relief of the stenosing flexor tenosynovitis usually begins to occur one to three weeks following the injection. Maximal therapeutic effect is not realized for at least four to six weeks following injection.

Significant clinical improvement in stenosing flexor tenosynovitis has been observed in approximately 73 percent of patients following one corticosteroid injection.32 A second injection is usually given if the first injection is not successful, and the rate of clinical improvement after a second injection is approximately 82 percent.32 Overall, steroid injections are effective in approximately 90 percent of patients with trigger finger.33 The administration of more than two steroid injections is considered by some to be ill-advised because of the cumulative local effects of the steroid on tendon strength. Spontaneous ruptures of the flexor tendons following steroid injection have been reported, although this complication is extremely rare.33 However, this potential complication should be considered when deciding between repeat injections or surgical release.

Surgery for stenosing flexor tenosynovitis increases the volume of the flexor tendon sheath at the A1 pulley. A transverse or longitudinal incision is performed over the palmar aspect of the metacarpal head, midway between the radial and ulnar neurovascular bundles. The digital nerves and arteries are protected as the A1 pulley is incised longitudinally. Upon release, the divided A1 pulley tends to splay apart, allowing the distal flexor tendon sheath to accommodate the inflamed portion of the flexor tendon without impingement during full extension of the proximal interphalangeal and distal interphalangeal joints. Inflammation within the flexor tendon spontaneously defervesces following the creation of this funnel-type geometry.

Indications for the surgical release of trigger fingers include failure of steroid injections, bilateral trigger fingers, "locked" trigger fingers, and trigger fingers in the setting of diabetes mellitus. Failure to improve after multiple steroid injections is an indication for surgical release because the poor probability of sustained improvement is outweighed by the potential risks of repeated steroid use. In general, patients with trigger fingers for more than one year ultimately require surgical release.32 Recurrent tenosynovitis in the same finger is also likely to require surgical release. Bilaterally symmetric trigger fingers are at increased risk of requiring surgical release eventually, although injection is usually attempted initially. Patients with "locked" flexion deformities due to trigger finger should be advised to consider release earlier rather than later, because steroid injection is less likely to release a locked digit and because the development of fixed flexion contractures may be a significant concern. Over half of all diabetic patients with trigger finger eventually require surgical release.34

DeQuervain’s Tenosynovitis

Inflammation of the first dorsal extensor tendon compartment bears the name of the Swiss surgeon who reported five cases in 1895.35 Finkelstein, whose name is given to the classic diagnostic sign, provided a comprehensive discussion of the disorder in 1930.36

This condition is analogous to stenosing flexor tenosynovitis of the digits, but involves the extrinsic extensors of the thumb carpometacarpal and metacarpophalangeal joints. The abductor pollicis longus and the extensor pollicis brevis muscles are connected to the thumb by tendons that pass through fibrous tendon sheaths along the radial aspect of the wrist. These tendon sheaths constitute the first dorsal extensor tendon compartment of the wrist, passing over the radial styloid. Just as in stenosing flexor tenosynovitis of the fingers, volume discrepancies due to inflammation may cause stenosis of the first dorsal compartment and result in impingement of the smooth gliding of abductor pollicis longus and extensor pollicis brevis tendons within the first dorsal compartment. The resulting inflammation between these tendons and the first dorsal compartment is known as De Quervain’s tenosynovitis.

Patients typically complain of sharp pain over the radial styloid process of the wrist, the bony prominence just proximal to the wrist joint over the radial aspect of the distal forearm. Pain can be extreme, even excruciating. With severe tenosynovitis, a hard, tender nodule may be palpable within the first dorsal compartment. "Snapping" and "locking" may occur with attempts to actively extend the thumb. A diagnosis of De Quervain’s tenosynovitis is seldom mistaken when there is point tenderness over the first dorsal compartment and pain with passive excursion of the abductor pollicis longus and extensor pollicis brevis tendons. This is best elicited by passively flexing the thumb carpometacarpal and metacarpophalangeal joints in succession, while maintaining the wrist in ulnar deviation (Figures 6a through c). This test can potentially localize the site of inflammation to the abductor pollicis longus or extensor pollicis brevis tendon or both. Originally described by Eichhoff, this test is frequently erroneously referred to as Finkelstein’s sign.37,38 Finkelstein’s sign is elicited when the patient experiences increased pain when the wrist is deviated ulnarly with the thumb clenched tightly within the fist. Eichhoff’s maneuver rather than Finkelstein’s is more commonly performed by hand surgeons to establish a diagnosis of De Quervain’s tenosynovitis. Finkelstein’s and Eichhoff’s tests may be positive and tenderness may be elicited over the first dorsal compartment in other conditions, such as degenerative arthritis of the carpometacarpal joint of the thumb. Therefore, the gold standard for the diagnosis of De Quervain’s tenosynovitis is the total relief of pain following the precise injection of a small quantity of local anesthetic into the first dorsal compartment.

Predisposing activities include postures that maintain the thumb in abduction and extension. In addition, ulnar deviation places traction on the tendons of the abductor pollicis longus and extensor pollicis brevis tendons. Nursing mothers and, more recently, fathers of newborn babies, seem to be at some risk for the development of De Quervain’s disease. This is probably due to the need to support the head of the infant with a flexed ulnarly deviated wrist and an extended abducted thumb. De Quervain’s tenosynovitis also frequently affects computer users who utilize a mouse or trackball. It appears to be less frequent among glide pad users and laptop users who navigate by means of a small rubber button located between the G, H, and B keys. The reason for this predisposition may lie in the postural requirements for mouse and trackball use in which the thumb is typically maintained abducted and extended as the hand is held in a hovering position over the mouse or trackball.

Also at some risk for developing De Quervain’s tenosynovitis are dentists and surgeons, who utilize instruments such as wide-handled dental handpieces that require posturing the thumb in an extended and slightly abducted position to stabilize and activate the instrument. At the same time, patient positioning may necessitate some degree of wrist flexion and ulnar deviation by the operator.

As with tenosynovitis of the digital flexor tendon sheaths, De Quervain’s tenosynovitis is initially treated with injection of a corticosteroid preparation followed by splint immobilization. Anecdotally, the experience of many physicians is that steroid injections for De Quervain’s are less effective than for trigger fingers. However, when administered by a skilled hand surgeon, the efficacy of corticosteroid injection for DeQuervain’s disease is approximately 71 percent following one injection and 83 percent following two injections.39 The poor reputation of steroid injections for De Quervain’s disease is probably due to the failure of many treating physicians to recognize the existence of two or even several anatomically separate sheaths within the first dorsal compartment. An "extra" slip of abductor pollicis longus tendon was originally regarded as an "aberrant tendon,"40 but it is now accepted that several slips of abductor pollicis longus tendon may be quite common and that they may be separated anatomically by significant septation. Among Western populations, the existence of independent abductor pollicis longus and extensor pollicis brevis tendon sheaths occurs with a prevalence ranging between 26 percent to 34 percent.41 Among Asians, independent compartments for the abductor pollicis longus and extensor pollicis brevis tendons occur in approximately 80 percent of wrists.42 Therefore, De Quervain’s tenosynovitis differs quite distinctly from stenosing flexor tenosynovitis in that the existence of a multiply septated first dorsal extensor tendon compartment is more the rule than the exception. Multiple injections may be required to adequately treat all subcompartments of the first dorsal compartments. With proper injection of all compartments, steroid injection should result in complete and lasting relief of De Quervain’s disease in 80 percent of cases.39 When surgery was required following failure of multiple steroid injections, a separate extensor pollicis brevis compartment is found in 91 percent of cases, suggesting that injection may be ineffective due to the presence of the septation.39

Surgery for De Quervain’s tenosynovitis, when indicated after failure of conservative treatment, consists of division of the roof of the first dorsal compartment in order to allow smooth gliding of the abductor pollicis longus and extensor pollicis brevis tendons. It is imperative that the surgeon look for and release any separate compartments containing the extensor pollicis brevis tendon or accessory slips of the abductor pollicis longus tendon. Otherwise, incomplete release will not relieve the patient’s symptoms.

Summary

Cumulative trauma disorder represents a wide array of tendonitides, neuropathies, and other conditions in association with repetitive stereotyped activities. In the upper extremity, the most common manifestations of cumulative trauma disorder are carpal tunnel syndrome, cubital tunnel syndrome, flexor tenosynovitis, De Quervain’s tenosynovitis, lateral epicondylitis, and generalized tendonitis. While the pathophysiology of cumulative trauma disorder is poorly understood, clinical management is directed at the identification and treatment of individual component pathologies, such as carpal tunnel syndrome. Long-term relief, however, may be best achieved by means of careful and well-considered modifications in work environment and in upper extremity use habits.

Authors

Douglas H.C.L. Chin, MD, is a clinical instructor at Alta Bates Summit Medical Center in Oakland, Calif.

Neil F. Jones, MD, is a professor in the Department of Orthopaedic Surgery and Division of Plastic and Reconstructive Surgery at the University of California at Los Angeles.

References

1. Phalen G, Spontaneous compression of the median nerve at the wrist. JAMA 145:1128, 1951.

2. Lipscomb P, Tenosynovitis of the hand and wrist: Carpal tunnel syndrome, de Quervain's disease, trigger digit. Clin Orthop 13:164, 1959.

3. Kyle R, Eilers S, et al, Amyloid localized to tenosynovium at carpal tunnel release: Natural history of 124 cases. Am J Clin Pathol 91:393, 1989.

4. Phalen G, Seventeen years experience in diagnosis and treatment of 654 hands. J Bone Joint Surg (Am) 48:211, 1966.

5. Scelsi R, Zanllungo M, et al, Carpal tunnel syndrome. Anatomical and clinical correlations and morphological and ultrastructural aspects of the tenosynovial sheath. Ital J Orthop Traumatol 15:75, 1989.

6. Garcia-Elias M, Sanchez-Freijo S, et al, Dynamic changes of the transverse carpal arch during flexion-extension of the wrist: Effects of sectioning the transverse carpal ligament. J Hand Surg (Am) 17:1017, 1992.

7. Tanzer R, The carpal tunnel syndrome: a clinical and anatomical study. J Bone Joint Surg (Am) 41:626, 1959.

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9. Rojviroj S, Sirichativapee W, et al, Pressures in the carpal tunnel. A comparison between patients with carpal tunnel syndrome and normal subjects. J Bone Joint Surg (Br) 72:516-8, 1990.

10. Liss GM, Jesin, E, et al, Musculoskeletal problems among Ontario dental hygienists. Am J Indust Med 28:521-40, 1995.

11. Akesson I, Schutz A, et al, Musculoskeletal symptoms among dental personnel -- lack of association with mercury and selenium status, overweight and smoking. Swed Dent J 24:23-38, 2000.

12. Lundborg G, Gelberman R., et al, Median nerve compression in the carpal tunnel: Functional response to experimentally induced controlled pressure. J Hand Surg (Am) 7:252, 1982.

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23. Osterman AL, and Kitay GS, Compression neuropathies: Ulnar. In, Peimer CA, ed, Surgery of the Hand and Upper Extremity. McGraw-Hill, New York, 1994.

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To request a printed copy of this article, please contact/Neil F. Jones, MD, UCLA Hand Center, 200 UCLA Medical Plaza, Suite 140, Los Angeles, CA 90095

Table 1. Symptoms and Signs of Carpal Tunnel Syndrome.

Table 2. Symptoms and Signs of Cubital Tunnel Syndrome

Legends

Figure 1. The classic pattern of diminished sensibility in carpal tunnel syndrome -- "splitting" of the ring finger occurs because sensibility over the ulnar aspect of the ring finger is provided by the ulnar nerve.

Figure 2. The classic pattern of diminished sensibility in cubital tunnel syndrome -- both the volar and dorsal aspects of the ring and small fingers are innervated by the ulnar nerve. "Splitting" of the ring finger classically occurs, because sensibility over the palmar radial aspect of the ring finger is provided by the median nerve.

Figure 3. Ulnar claw hand deformity. Flexion of the interphalangeal joints (by the flexor muscles innervated by the median nerve) and extension of the metacarpophalangeal joints (by the extensor muscles supplied by the radial nerve) are unopposed or weakly opposed by the intrinsic muscles of the ring and small fingers (innervated by the ulnar nerve), which normally extend the interphalangeal joints and flex the metacarpophalangeal joints.

Figure 4. Froment’s sign: Weakness of the adductor pollicis and first dorsal interosseous muscles results in weakness of lateral (key) pinch. The affected hand attempts to compensate for this weakness by recruiting the flexor pollicis longus muscle, resulting in pronounced flexion of the interphalangeal joint of the thumb.

Figure 5. Trigger finger. Impingement of the flexor tendons beneath a relatively stenotic portion of the flexor tendon sheath (A1 pulley) results in "locking" of the affected digit in a partially flexed position.

Figures 6a through c. Eichhoff’s test for De Quervain’s tenosynovitis. The wrist is positioned in ulnar deviation, placing the abductor pollicis longus and extensor pollicis brevis tendons on stretch (Figure 6a). This maneuver alone may elicit significant pain. Inflammation within the abductor pollicis longus tendon sheath is indicated by pain on passive flexion of the thumb carpometacarpal joint (Figure 6b). Similarly, inflammation within the extensor pollicis brevis tendon sheath is suggested by pain on passive flexion of the thumb metacarpophalangeal joint (Figure 6c).



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