Work-related upper extremity disorders associated

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1 Nerve entrapments of the wrist Early treatment preserves function Nerve entrapment syndromes may affect as many as one in four office workers. Prompt diagnosis is critical to the selection of an appropriate and effective treatment. Capt. Gina M. Wellik, MPAS, PA-C Work-related upper extremity disorders associated with repetitive motion have a price tag of $2.1 billion in annual workers compensation costs. 1 Prevalence rates based on symptom surveys along with a physical examination indicate that 25% of office employees in selected workplaces report workrelated upper extremity disorders. 1 These disorders are associated with the longest absences from work for any reason. A Washington state study indicated that carpal tunnel syndrome (CTS) was associated with a significantly longer time to return to work than were back and neck sprains, fractures, and all other injuries. 1 This article reviews the relevant structures (see Anatomy of nerve entrapment syndromes of the wrist ) and discusses the etiology, clinical presentation, and treatment of nerve entrapments of the wrist. The CME Earn Category I CME credit by reading this article and the article beginning on page 25 and successfully completing the post-test on page 31. Successful completion is defined as a cumulative score of at least 70% correct. This material has been reviewed and is approved for 1 hour of clinical Category I (Preapproved) CME credit by the AAPA. The term of approval is for 1 year from the publication date of April Learning objectives Review the anatomy and cause of common nerve entrapment syndromes of the wrist Describe the presentation, diagnosis, and treatment of carpal tunnel syndrome and ulnar tunnel syndrome Discuss the role of acute presentations that develop secondary to trauma discussion will include overuse syndromes such as CTS and ulnar tunnel syndrome (UTS), as well as acute presentations. The degree of damage due to the nerve entrapment seen at presentation to the primary care clinician guides the choice for appropriate treatment. Prevention, prompt recognition, and appropriate intervention can help to preserve function of the affected extremity. Etiology Nerve entrapments of the wrist have three main causes: systemic conditions, ischemia and mechanical compression, and double crush syndrome. Another separate but contributing factor is overuse syndrome. Systemic conditions Systemic conditions affect nerve function at the wrist by way of systemic depression of peripheral nerve function or alteration of interstitial fluid equilibrium. 2 Diabetes, alcoholism, hypothyroidism, and aging can cause systemic depression of peripheral nerve function, which lowers the threshold for manifestation of a compression neuropathy. Pregnancy, myxedema, and rheumatoid arthritis are conditions that alter interstitial fluid equilibrium. Compression neuropathies may occur from the increased contents in a limited space. Ischemia and mechanical compression Nerves have a predictable response to progressing compression. At 20 to 30 mm Hg of compression, epineural blood flow is reduced. At 30 mm Hg of compression, axonal transport is impaired, while at 30 to 40 mm Hg of compression, symptoms of paresthesias appear. Greater The author is stationed at Minot Air Force Base, ND. She has indicated no relationships to disclose relating to the content of this article. 18 JAAPA VOL.18, NO. 4 APRIL

2 Anatomy of nerve entrapment syndromes of the wrist Synovial sheath of tendons Median nerve Transverse carpal ligament Ulnar nerve Deep and superficial flexor tendons Pathway of the median nerve The median nerve derives from the brachial plexus with a contribution from both the lateral and medial cords. C6 to C7 sensory fibers from the lateral cord supply sensation to the thenar eminence, thumb, and index and middle fingers. These same levels supply the majority of motor fibers to the median nerve-innervated muscles in the proximal forearm. C8 to T1 fibers from the medial cord supply the majority of motor fibers to the distal median-innervated muscles of the forearm and hand as well as sensory fibers to the lateral half of the ring finger. The median nerve crosses from the distal forearm to the hand through the carpal tunnel. Thus, the sensory fibers of the median nerve that pass through the carpal tunnel supply sensation to the index and middle fingers in addition to the medial thumb and lateral half of the ring finger. Pathway of the ulnar nerve The ulnar nerve arises from the medial cord C8 to T1. It passes superficial to the transverse carpal ligament (also known as the flexor retinaculum) and to the radial side of the pisiform, then to the ulnar side of the hamulus (hook of the hamate) through the ulnar tunnel, and bifurcates within the ulnar tunnel into superficial and deep branches. The superficial branch continues subcutaneously to provide sensation to the palmar surface of the medial ring finger and little finger. Carpal tunnel anatomy The walls and floor of the carpal tunnel are formed by the carpal bones and the roof by the transverse carpal ligament. This ligament evolves from the antebrachial fascia at about the level of the wrist crease and extends 4 to 6 cm into the palm. The passageway is narrowest 2 to 2.5 cm distal to its origin, which corresponds to the usual site of median nerve compression. 1 Lying with the median nerve in the tunnel are the eight tendons of the deep and superficial flexor tendons, and the tendon of the flexor pollicis longus surrounded by a complex synovial sheath. Ulnar tunnel anatomy The palmar carpal ligament, palmaris brevis, and hypothenar fat and fibrous tissue comprise the roof of the ulnar tunnel. The tunnel s floor is composed of the deep and superficial flexor tendons, the transverse carpal ligament, the pisohamate and the pisometacarpal ligaments, and the opponens digiti minimi. The flexor carpi ulnaris, the pisiform, and the abductor digiti minimi create the medial wall, while the lateral wall is comprised of the tendons of the extrinsic flexors, the transverse carpal ligament, and the hook of the hamate. The tunnel is 4 to 4.5 cm long and begins at the proximal edge of the palmar carpal ligament and extends to the fibrous arch of the hypothenar muscles. The ulnar tunnel is a narrow, oblique canal that contains the ulnar nerve, artery, and vein with some fatty tissue. The distal section is called Guyon s canal and is the common area where the ulnar nerve is vulnerable to compression from surrounding structures Campbell WW. Diagnosis and management of common compression and entrapment neuropathies. Neurol Clin. 1997;15: Kothari MJ. Ulnar neuropathy at the wrist. Neurol Clin. 1999;17: Here and on the cover: Kevin Somerville JAAPA VOL.18, NO. 4 APRIL

3 Entrapment syndromes than 60 mm Hg of compression leads to total intraneural ischemia with complete sensory and motor block. 2 Compression is classified into early, intermediate, and late stages. Early, low-grade compression responds favorably to conservative measures. Intermediate-stage compression, which is defined by constant paresthesias and numbness, is best treated with surgical decompression. In late-stage compression, which is defined as permanent sensory loss and muscle atrophy, endoneural fibrosis has been induced and surgical decompression may not eliminate all the symptoms. Pathologic changes involving the myelin sheath are the earliest indications of pressure applied to a nerve. Greater forces cause myelin loss along a longer section of the nerve; this is termed segmental demyelination. After nerve compression is relieved, nerve repair takes place. With lesions involving only myelin, repair can occur rapidly over days to weeks. If there is axonal damage, recovery is much more protracted, with the regenerating axons covering 1 to 3 mm per day from the site to the target muscle. 3 Double crush syndrome Peripheral fibers are more vulnerable to pressure injury than are central ones. Nerve compression can occur at two levels. Double crush syndrome suggests that proximal compression may decrease the ability of the nerve to tolerate a second, more distal compression. 4 Thus, when a proximal cervical lesion is present, less compression of the median nerve at the carpal tunnel level is necessary to produce symptoms. Overuse syndromes The wrist is a common site of overuse syndromes, and 15% of workers at risk can develop CTS. 5 Overuse syndromes are some of the most common occupational illnesses treated by primary care providers. 5 Most cases of nerve compression begin gradually and then become chronic, so relationships to activity are not always obvious. At the pathophysiologic level, overuse is defined as the level of repetitive microtrauma sufficient to overwhelm the tissues ability to adapt. Microtrauma results from repetitive loading episodes at a force or elongation KEY POINTS in this article Nerve entrapment syndromes of the wrist are both common diagnoses and common causes for missed work hours. A working knowledge of wrist anatomy is crucial for making the correct diagnosis. Asking about the patient s occupation, as well as the symptoms, can aid the evaluation. The primary care clinician can do much to help the patient prevent further injury and preserve function. level well within the physiologic range. Fibrosis results from continued or repeated release of inflammatory products leading to thick, unyielding, restrictive tendon sheaths or retinacular tunnels. 5 Clinically, overuse syndromes have three stages. The first is characterized by fatigue, often described as increased aching and tiredness during work or activity that subsides with overnight rest. In the second stage, the discomfort continues into the next day, with earlier onset of fatigue during the workday. This fatigue is a sign that injury is developing, and the worker should immediately reduce the strain inflicted on the affected part and take frequent rests. The person should also modify work or sports activities to avoid the offending motion. The third stage is marked by chronic aching, fatigue, and weakness that persist despite resting the affected part. This is a warning sign of incipient fibrosis. Key occupational risk factors for overuse syndromes include repetition, high force, awkward joint posture, direct pressure, vibration, and prolonged constrained posture. 5 A study conducted by Uniformed Services University of the Health Sciences demonstrated that computer keyboard operators generate significantly higher levels of force four to five times higher than required to operate the computer. 1 Participants who were symptomatic used even higher levels of force across the keyboard. Nerve entrapments can occur in athletes because of repetitive, vigorous use of the upper extremities; athletes are especially susceptible to compression of the peripheral nerves. Thus, the clinician must take a thorough history to evaluate any stresses due to work or hobbies that may be contributing to overuse injuries. Treatment of overuse syndromes The goal of treatment for overuse syndromes is to prevent fibrosis. The affected body part should be rested for 2 weeks. Treatment must involve identifying the conditions that cause or aggravate the illness; thus evaluation of the workplace, including the patient s work posture and use of tools, is essential. For optimal hand and arm strength and skill, work should be placed 10 to 12 inches in front of the eyes, and elbows should be at an 85- to 100-degree angle. The shoulder should be in the vertical position, with abduction no greater than 20 degrees. The wrist should be in the neutral position, without ulnar or radial deviation and with minimal flexion or extension. 5 Biofeedback and future keyboard design may aid in decreasing the force used while typing. 1 Carpal tunnel syndrome Distal median neuropathy is the most common compression neuropathy of the upper extremity, 6 with CTS 20 JAAPA VOL.18, NO. 4 APRIL

4 carrying a 10% lifetime risk. 7 Flexor tenosynovitis is the most common cause of this condition, which is usually associated with repeated forced hand movements such as those used by typists, cashiers, electronic assembly workers, musicians, cooks, and carpenters. 5 In idiopathic CTS, the transverse carpal ligament is the point of compression. The typical progression begins as the wrist is subjected to a repeated mechanical stress. Local necrosis then develops, with subsequent edema and collagen fragmentation. Fibrous hypertrophy of the flexor tendon synovium results in compression occurring at the transverse carpal ligament. Biopsies on specimens of this ligament from patients undergoing surgical decompression demonstrated findings of edema, vascular sclerosis, and fibrosis that are consistent with repeated stress to connective tissue. 6 Lack of evidence of frank inflammation further supports this claim. Clinical presentation The median nerve at the wrist is 94% sensory and only 6% motor; therefore, dysfunction at the wrist usually manifests first as sensory changes; motor changes develop with severe compression. 5 Pain and paresthesias are present on the palmarradial aspect of the hand, while the little finger is spared. CTS is usually bilateral, but in idiopathic CTS the dominant hand is usually more severely affected. 6,7 The symptoms are exacerbated by extreme flexed or extended wrist positions during activities such as driving or typing, which increase the pressure within the carpal tunnel. Repetitive, forceful use of the hand also exacerbates the condition. In mild CTS, the findings on physical examination may be normal or show trivial sensory loss. Earliest sensory loss seems to occur over the volar tip of the middle finger. 3 Patients with advanced cases may drop items because of altered sensibility or thenar weakness. In these patients, impaired dexterity is due to the weakness of thumb abduction and opposition resulting from the motor fibers clinically involved. 6 Symptoms often seem worse at night. Flexion and extension positions during sleep lead to increased carpal tunnel pressure, nerve ischemia, and subsequent painful paresthesias that awaken patients and cause them to shake or wring their hands. 6 Another theory is that the same pathway is followed, but fluid redistribution caused by being in a supine position is to blame rather than hand posture. 8 Diagnosis CTS is diagnosed based on clinical findings and neurophysiologic evaluation. 7 Plain radiographs in two planes will rule out posttrauma deformity. Although MRI and CT are helpful in visualizing certain anatomic factors responsible for compression, they are not useful for specifically diagnosing entrapment neuropathy at the wrist unless a mass or other lesion is suspected. 2 Fullness in the wrist or palm, or a history of a slowly progressing deficit without intermittent fluctuations, are indications for MRI and CT. 6 Physical examination should include the Phalen s test, Tinel s sign, and compression testing. Phalen s test involves holding the wrist in 90 degrees of flexion for 60 seconds. Numbness or tingling in median nerve distribution suggests CTS. Tinel s sign is considered positive if percussion of the median nerve at the site of compression causes tingling in the fingers. Compression testing requires the examiner to apply direct compression on the median nerve for 30 seconds. Presence of paresthesias suggests CTS. Patients with moderately severe symptoms should not labor unduly long with conservative treatment before having surgery. Electrophysiology localizes and aids in assessing the location, severity, and prognosis and also helps guide subsequent treatment. Two types of electrophysiology testing are used: nerve conduction studies and electromyography (EMG). Nerve conduction studies test for latency or asymmetry of stimulus across the wrist and represent the only completely objective evaluation for CTS. Lack of an abnormal nerve conduction test result does not exclude a diagnosis of CTS, especially early in the course of the process. EMG measures denervation of the thenar muscles in advanced motor median nerve compression. Clinicians must take into account that both nerve conduction studies and EMG are operator dependent. Differential diagnosis The most common alternate diagnosis is cervical radiculopathy, most often at the level of C6, but clinicians should remember that CTS and cervical radiculopathy can coexist. The presence of neck and shoulder pain, weakness in C6 innervated muscles, reflex changes, sensory loss restricted to the thumb, the absence of nocturnal paresthesias, and the ability to reproduce the paresthesias with root compression maneuvers all favor cervical radiculopathy. 3 Proximal median neuropathy is another alternate diagnosis. The palmar cutaneous branch of the median nerve leaves the main trunk 5 to 8 cm proximal to the wrist crease. Thus, loss of sensation over the thenar eminence is not part of CTS and suggests a lesion proximal to the wrist. 3 Look for sensory disturbances over the thenar eminence and weakness of median muscles proximal to the wrist, especially distal thumb JAAPA VOL.18, NO. 4 APRIL

5 Entrapment syndromes flexion due to the flexor pollicis longus, arm pronation (pronator teres and pronator quadratus), and wrist flexion (flexor carpi radialis). 6 Other possibilities are neurogenic thoracic outlet syndrome, upper brachial plexopathy, flexor tenosynovitis, and de Quervain s tendinitis. Conservative treatment Splinting the wrist in a neutral position is the mainstay of conservative treatment. Initially, most patients achieve the best response with initial round-the-clock splinting. As symptoms improve, the patient may cut back to just wearing the splints at night. Nocturnal splinting alone may be enough for very mild symptoms. 3 A 2- to 3-week course of oral anti-inflammatory agents should be tried to reduce synovitis. If CTS is due to a systemic condition, that condition should be treated. Ulnar nerve compression is often of acute onset and may not be amenable to conservative treatment. Corticosteroid injections are indicated for transient relief for persistent symptoms of less than 6 months duration. 5 The injection consists of 40 to 80 mg of methylprednisolone acetate instilled adjacent to the carpal tunnel. 6 Although 80% of patients will have transient relief, only 22% will be symptom-free 12 months after injection. 2 A maximum of two to three injections may be performed; more might cause local tendon damage. The patients who will benefit the most from corticosteroid injections and splinting are those whose symptoms have been present for less than 1 year, who are experiencing only mild or intermittent paresthesias, who have normal two-point discrimination, and who demonstrate no weakness or thenar atrophy on physical examination. Forty percent of this group will be symptom-free after 1 year. 2 Surgical treatment Surgical decompression is indicated when a mass or other lesion is present, conservative measures have failed to relieve symptoms, or distal median neuropathy is severe and associated with axonal loss that manifests as thenar atrophy. Patients with moderately severe symptoms should not labor unduly long with conservative treatment before having surgery. The operation releases the transverse carpal ligament via a longitudinal incision from the wrist into the palm. Surgery may be open or endoscopic, although the open technique is preferred because limited exposure invites incomplete release. Surgical decompression of the carpal tunnel is safe and highly effective, with a response rate of 85% to 90%. Outcomes are best in patients without advanced disease. Prognosis The prognosis for CTS is very good. The pain and paresthesias bring most patients to seek medical treatment before significant axonal loss has occurred. Remyelination is complete within several weeks, and axonal loss recovers slowly over several months. Persistent or recurrent symptoms may be due to inadequate surgical release of the transverse carpal ligament, a recurrent compression due to scar formation, significant axonal damage, or the wrong initial diagnosis. Interestingly, a study of workers compensation cases found that patients involved in a claim were more likely to have a prolonged postoperative disability. The study suggests that before deciding whether to proceed with carpal tunnel release, the practitioner should take a detailed history to ascertain the worker s attitude about his or her current or previous jobs and to determine the patient s motivation to improve. 9 CTS remains a clinical diagnosis. If the findings on both Phalen s test and Tinel s sign are positive and the history is suggestive, the diagnosis is 85% certain. 8 Patients who have no clinical symptoms and whose nerve conduction tests show slowing of the median nerve do not have CTS and do not require directed therapy. This distinction is important, as treatment with splinting, injection, or surgery is not appropriate in patients who lack signs or symptoms. 6 Ulnar tunnel syndrome Approximately 25% of patients with work-related CTS have an accompanying disorder such as ulnar neuropathy at the wrist, trigger finger, de Quervain s tendinitis, or arthritis of the basal joint of the thumb. 5 UTS occurs when the ulnar nerve is compressed when passing through the canal of Guyon. Athletes who cycle, participate in racket sports, or use wheelchairs are vulnerable to compression injuries of the ulnar nerve because of its superficial location and sparse soft tissue coverage. 10 Clinical presentation The patient with UTS experiences numbness along the little finger and the ulnar half of the ring finger, with or without weakness of grip. When grip is affected, it is because ulnar nerve musculature contributes to 40% of grip strength. 10 The patient usually describes motor symptoms as a cramping weakness on grasping and pinching, 11 although pain is usually less significant than it is in CTS; symptoms may be purely sensory, purely motor, or mixed, depending on the site of the lesion. There are three types of lesions. Type I lesions are located proximal to Guyon s canal and involve motor and sensory nerves; type II lesions occur in the distal part of the canal, sparing all sensory nerves; and type 22 JAAPA VOL.18, NO. 4 APRIL

6 III lesions are distal to Guyon s canal and involve only the superficial sensory branch of the ulnar nerve. 10 Diagnosis Ganglia and other soft-tissue masses comprise 32% to 48% of UTS cases, while 16% are due to muscle abnormalities. 2 Fractures of the distal radius and ulna and hook of the hamate can also cause UTS. Plain radiographs, including carpal tunnel and oblique views, are often diagnostic. CT and MRI are extremely useful diagnostic tools for UTS, but not for CTS. Hamate fractures are most clearly visible on CT. 12 If the patient has any history of smoking or shoulder pain, a chest film should be obtained to rule out a Pancoast s tumor. On physical examination, Tinel s sign may be present over Guyon s canal. Ulnar neuropathy at the wrist is rare and often difficult to diagnose electrophysiologically. However, because it may be the initial manifestation of a generalized neuropathy, careful clinical and electrophysiologic evaluation using EMG, along with standard motor and sensory studies of the other nerves, are important to exclude a more generalized neuropathy. 12 Differential diagnosis Ulnar nerve compression at the elbow the most common site for this condition should be considered. Sensory involvement on the ulnar dorsal aspect of the hand suggests compression proximal to the wrist, because the dorsal cutaneous branch of the ulnar nerve originates in the forearm. Cervical root compression is another possibility, but splitting of the ring finger usually excludes plexopathy and radiculopathy. 3 The practitioner should also be wary of mistaking cubital tunnel syndrome and thoracic outlet syndrome for UTS. Treatment Conservative treatment is initially the same as for CTS. If radiologic studies have been performed and no lesion is present, a regimen of altering repetitive activities, splinting in neutral position, and anti-inflammatory medications may alleviate the symptoms. However, ulnar nerve compression is often of more acute onset than CTS, and for this reason it is often not amenable to conservative treatment. 11 Surgery is indicated when an anatomic lesion is documented or the condition is refractory to conservative care. At that point, surgical release of Guyon s canal may be performed. Prognosis If UTS is due to occupational trauma, behavioral modification improves function. 12 If a surgical lesion is identified and resected, ulnar nerve function gradually improves. Athletes can return to their sport 4 to 8 weeks after surgical decompression, depending on the activity involved. 13 As with CTS, persistent or recurrent symptoms may be due to inadequate surgical decompression of Guyon s canal, a recurrent compression due to scar formation, significant axonal damage, or the wrong initial diagnosis. Acute presentations Acute presentations, such as fractures, develop rapidly secondary to trauma and may manifest as either an acute CTS or an acute UTS. The first step is to reduce the fractured bone. If the neuropathy is not immediately resolved, the situation is analogous to a compartment syndrome and constitutes a surgical emergency. Acute CTS Fractures or dislocations of the lunate, distal radius fracture, or bleeding from a malfunctioning radial arterial line may cause an acute CTS. Lunate dislocation into the carpal tunnel results from a hyperextension mechanism and dislocates in a palmar direction. 8 Significant swelling over the carpal tunnel will be seen, and progressive deterioration in median nerve function will be noted. If reduction of the fracture is unsuccessful, carpal tunnel pressure must be measured. Urgent decompression is indicated if the result exceeds 40 mm Hg. Acute UTS A fractured pisiform or hamate may cause an acute UTS. The pisiform, superficially palpable at the hypothenar base, is usually injured by a fall on an outstretched hand. Hook of the hamate fractures occur more commonly in athletes who use a racket or club: Forceful wrist flexion and ulnar deviation can force the base of the racket into the hypothenar region. 10 Fractures can impinge on Guyon s canal, resulting in ulnar nerve injury. 8 As with acute CTS, an urgent decompression of Guyon s canal is indicated if reduction of the fracture is unsuccessful. Conclusion Prompt diagnosis, which relies heavily on the history and physical examination, is critical to selecting an appropriate treatment. Counseling regarding behavior modification and prevention can help the patient be a partner in achieving the goal of preserving function in the affected extremity. Whether the presentation is chronic or acute, the primary care clinician must be empowered with the modalities or treatments critical to abating nerve entrapments of the wrist. REFERENCES 1. Feuerstein M, Armstrong T, Hickey P, Lincoln A. Computer keyboard force and upper extremity symptoms. J Occup Environ Med. 1997;39: Szabo RM, Steinberg DR. Nerve entrapment syndromes in the wrist. J Am Acad Orthop Surg. 1994;2(2): Campbell WW. Diagnosis and management of common compression and entrapment neuropathies. Neurol Clin. 1997;15: Mercier LR. Practical Orthopedics. 4th ed. St. Louis, Mo: Mosby; Verdon ME. Overuse syndromes of the hand and wrist. Prim Care. 1996;23: Preston DC. 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