Nerve Entrapment Syndromes in the Wrist

Nerve Entrapment Syndromes in the Wrist Robert M. Szabo, MD, and David R. Steinberg, MD Abstract The patient with compression neuropathies of the median and ulnar nerves at the stresses, posture, vibration, and tem- wrist commonly presents with pain, paresthesias, and weakness in the hand and perature. However, the relative digits. Diagnosis of these conditions is becoming more widespread with the importance of these factors and the increased attention given to “cumulative trauma disorders” during the past mechanisms by which they produce decade. Successful management requires a thorough understanding of the patho- neuropathy are poorly understood. physiology of compression neuropathy and how it relates to the various diagnos- The growing importance of work- tic tests available today. The authors review the epidemiology, etiology, and related factors has required a com- evaluation of compression neuropathy and discuss common clinical presenta- pensatory change in the physician’s tions, treatment recommendations, and controversies surrounding carpal and approach to managing these condi- ulnar tunnel syndromes. tions. The surgeon must treat the J Am Acad Orthop Surg 1994;2:115-123 patient, rather than focus on the injured extremity. This may best be accomplished with a team approach, Compression neuropathy at the wrist This syndrome is one of a group of with contributions by a physical ther- is not a single disease, but rather a nonspecific conditions termed apist, an occupational therapist, a constellation of symptoms resulting “cumulative trauma disorders.” psychologist, a kinesiologist, and, from compression of either the Workers’ compensation litigation most important, the patient. A suc- median or the ulnar nerve caused by and labor-management hostilities, as cessful outcome is more likely if the a disparity between the size of the cor- well as psychological and economic patient becomes an active participant responding tunnel and its contents. factors, are often an important part of in his or her own rehabilitation. History and physical examination the picture. Workstation and task- Progress toward correction of obe- will localize the site of compression related modifications should be sity, alcohol abuse, or tobacco abuse and direct further diagnostic studies. undertaken first, as these may obvi- is good evidence of the patient’s com- Once the cause is determined, appro- ate the need for surgical treatment. mitment. If specific objective evi- priate therapy can, in most cases, Objective evidence of a specific nerve dence of a compression neuropathy is yield a successful outcome. disorder should be demonstrated lacking, it is best to institute a trial of before surgical intervention is rec- nonoperative management and to let Epidemiology ommended. It also should be empha- other members of the team assume sized that a large number of patients the primary role in treatment. Upper-extremity compression neu- who obtain relief of symptoms after ropathy remains one of the most fre- surgical decompression ultimately quently encountered disorders seen will require job retraining.1,2 Dr. Szabo is Associate Professor of Orthopaedic by orthopaedists and hand surgeons. Industry continues to seek a Surgery and Chief, Hand and Microvascular Classically, these syndromes have screening tool for identifying patients Surgery, University of California, Davis. Dr. Steinberg is Assistant Professor of Orthopaedic presented as either posttraumatic at risk for upper-extremity compres- Surgery, University of California, Davis. conditions or the gradual onset of sion neuropathies. Preemployment paresthesias and pain in a patient, screening is controversial and can Reprint requests: Dr. Szabo, Department of typically female, in late middle age. lead to discriminatory practices. The Orthopaedic Surgery, University of California, In the past decade, these two forms only clearly documented intrinsic risk Davis, 2230 Stockton Boulevard, Sacramento, CA 95817. have been surpassed by another pre- factors appear to be female sex, preg- sentation—symptoms developed in nancy, diabetes, and rheumatoid Copyright 1994 by the American Academy of the younger industrial worker in arthritis. Occupational factors include Orthopaedic Surgeons. relation to repetitive motions. task repetition, force, mechanical Vol 2, No 2, Mar/Apr 1994 115 Nerve Entrapment Syndromes in the Wrist Etiology of idiopathic carpal tunnel syndrome term hemodialysis, and rheuma- has also been challenged. Only 4% to toid arthritis), extreme wrist posi- Between the cervical spine and the 10% of biopsy specimens of tenosyn- tions, and proliferation of flexor wrist there are a number of specific ovium from over 800 wrists that tendon tenosynovium also may sites where nerve compression is underwent carpal tunnel release cause nerve compression. common, giving rise to various revealed the presence of inflamma- well-known nerve compression tory cells, while edema and vascular Ischemia and Mechanical syndromes. The most common site sclerosis were consistently observed Compression for compression is at the wrist in (98% of cases).3,4 Recently, two inves- Experimental and clinical studies the region of the carpal and ulnar tigative groups examined tenosyn- and intraoperative observations sug- tunnels. Here both median and ovium specimens from patients with gest ischemic causation for many ulnar nerves may be entrapped in idiopathic carpal tunnel syndrome compression neuropathies.7 Re- their anatomic compartments and found amyloid deposition in an duced epineural blood flow is the (Fig. 1). overwhelming majority.5,6 earliest manifestation of low-grade Some of the factors associated with peripheral nerve compression and the development of carpal tunnel and Systemic Conditions can occur experimentally at com- ulnar tunnel syndromes are listed in Diabetes, alcoholism, hypothy- pression pressures as low as 20 to 30 Tables 1 and 2, respectively. A careful roidism, and exposure to chemical mm Hg. Axonal transport becomes history and physical examination can toxins may cause systemic depres- impaired at 30 mm Hg, with a subse- usually identify the specific causative sion of peripheral nerve function, quent increase in endoneural fluid factor. In most cases, the appropriate which lowers the threshold for man- pressure. Neurophysiologic changes surgical procedure to decompress the ifestation of a compression neuropa- and symptoms of paresthesias have involved nerve has been established. thy. Aging may have a similar been induced in human volunteers However, the concept that a static systemic effect. The importance of with 30 to 40 mm Hg of compression anatomic structure is the sole cause of systemic conditions may be reflected on the median nerve. Experimental a nerve compression syndrome is too in the high prevalence of bilateral compression at 50 mm Hg for 2 hours simple; other factors enter into the clin- occurrence and multiple-nerve caused epineural edema and axonal ical picture. For example, in idiopathic involvement, even if only one transport block in animal studies. carpal tunnel syndrome, the point of extremity is used in the activity that Pressures greater than 60 mm Hg compression is the flexor retinaculum. provokes symptoms. cause total intraneural ischemia with The pathologic changes, however, are Children with mucopolysaccha- a complete sensory block followed related to fibrous hypertrophy of the ridosis or mucolipidosis, a rare by complete motor block. flexor tendon synovium, probably sec- group of disorders, frequently In chronic cases of nerve com- ondary to repeated mechanical have carpal tunnel syndrome and pression, recovery following decom- stresses that induce local necrosis with benefit from early carpal tunnel pression may be very slow, or edema and collagen fragmentation. release. Systemic conditions that progression of the condition may The principle that chronic in- alter interstitial fluid equilibrium halt without improvement of symp- flammation is the underlying cause (e.g., pregnancy, myxedema, long- toms. In these cases, the initial vascular causation is superseded by other processes, particularly fibrosis of the nerve, that diminish potential Fig. 1 Cross-section of the for recovery. wrist demonstrating the relationship of the carpal Recognition of these physiologic tunnel (CT) and the ulnar changes in peripheral nerves sec- tunnel (UT). A = ulnar ondary to progressive ischemia has artery, C = capitate, H = hamate, M = median nerve, led to the classification of nerve P = pisiform, PCL = palmar compression lesions into early, carpal ligament, S = intermediate, and late stages. Early, scaphoid, t = flexor tendon, T = triquetrum, TCL = trans- low-grade compression responds verse carpal ligament, U = most favorably to conservative ulnar nerve. management, such as splinting and modification of activities and limb position. Intermediate-stage nerve 116 Journal of the American Academy of Orthopaedic Surgeons Robert M. Szabo, MD, and David R. Steinberg, MD Table 1 Factors in the Pathogenesis of Carpal Tunnel Syndrome* Anatomy Physiology (continued) Decreased size of carpal tunnel Alterations of fluid balance Abnormalities of the carpal bones Pregnancy Thickened transverse carpal ligament Eclampsia Acromegaly Myxedema Increased contents of canal Long-term hemodialysis Neuroma Horizontal position and musle relaxation (sleep) Lipoma Raynaud’s disease Myeloma Obesity Abnormal muscle bellies Congenital Persistent median artery (thrombosed or patent) Mucopolysaccharidosis Hypertrophic synovium Mucolipidosis

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