4.2 Article Proceedings Paper

Biomechanical models for the pathogenesis of specific distal upper extremity disorders

Journal

AMERICAN JOURNAL OF INDUSTRIAL MEDICINE
Volume 41, Issue 5, Pages 353-369

Publisher

WILEY
DOI: 10.1002/ajim.10037

Keywords

pathogenesis; distal upper extremity neuromusculoskeletal disorders; biomechanical models; tendon entrapment at the wrist; peritendinitis; lateral epicondylitis; carpal tunnel syndrome

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Background Knowledge of the pathogenesis of most disorders that occur in the distal upper extremity is generally lacking. The individual roles of postulated etiologic factors, such as biomechanical or psychosocial exposures, are poorly understood and their potential interactions even less so. This article proposes biomechanical or physiological models of pathogenesis for specific distal upper extremity, disorders. Methods Tendon entrapment of the dorsal wrist compartments (tenosynovitis), peritendinitis, lateral epicondylitis, and carpal tunnel syndrome are common specific neuromusculoskeletal disorders of the upper extremities observed among workers. The normal anatomy and function of the targeted structures is considered the initial state; their pathology, is considered the final state. Using biomechanical or physiological principles combined with clinical observations and experimental studies, pathways leading from the initial state to the final state are proposed. Each model defined a critical biomechanical or physiological attribute that was considered to best characterize 'dose.' Two temporal patterns of exposure (duration vs. repetition) were used to characterize 'dosage.' The roles of long-term exposure vs. unaccustomed work were mentioned, but not incorporated into the models. Results Compressive force transmitted to the extensor retinaculum was considered the critical factor in the model for tendon entrapment at the dorsal wrist compartments. Two models were proposed for lateral epicondylitis. One emphasized the role of eccentric exertions; the other emphasized contact pressure from the radial head. The model for peritendinitis relied on localized muscle fatigue. Seven plausible models were presented for carpal tunnel syndrome. Conclusions It is possible to propose biologically plausible models of pathogenesis that are both coherent with current knowledge of tissue responses and consistent with clinical observations; however more than one model was plausible for some conditions. Additional research is needed to determine which, if any, of the proposed models might be correct. Such models may be useful to health care providers and ergonomists in the context of primary, secondary, or tertiary prevention. (C) 2002 Wiley-Liss, Inc.

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