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“Do not let what you cannot do interfere with what you can do.”

John Wooden

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Objectives

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On completion of this chapter, the student/practitioner will be able to:

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  • Identify common peripheral neuropathies associated with sports.

  • Relate specific neuropathy to a specific sport.

  • Identify the biomechanical etiologies of sports-related neuropathies.

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Key Terms

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  • Burner

  • Inflammation

  • Neuropathy

  • Repetitive and overuse athletic movements

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Introduction

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The last three decades have witnessed a tremendous increase in sports participation at all levels. However, increased sports participation has also increased the numbers, and perhaps the incidence, of sport-related injuries. Injuries can be due to either acute trauma or overuse. Acute injuries are defined as a high-force, low-repetition tissue stress resulting in a wide spectrum of injury severity—from a simple strain or sprain to trauma affecting multiple body systems—the complications of which may include shock, respiratory failure, or death. Overuse injuries may be defined as a low-force, high-repetition tissue stress that subsequently leads to an inflammatory cascade–initiated impairment in tissue reparative mechanisms. Peripheral nerve injury may result from high-force, low-repetition and low-force, high-repetition athletic injuries.

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In recent years, a rich literature has significantly contributed to the understanding of the etiologies, types, assessment, intervention, and prevention of peripheral nerve injury related to athletic participation. This chapter reviews the most frequent peripheral nerve injuries encountered by athletes. For organizational purposes and ease of reader understanding, we discuss the possible neural injuries in the context specific to types of athletic participation and, to a lesser extent, gender, age, and psychological variables that may affect injury.

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Background

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The pathophysiology of nerve injuries can be initiated by mechanical events involving repetitive and overuse athletic movements, such as overhead throwing, running, and jumping, or through direct blunt trauma.1 The tensile or compressive forces exerted on the nerve stimulate the vasa nervorum, resulting in disruption of the microvasculature and the deformation of the connective tissue. Irritation potentiates a transient inflammatory response (i.e., macrophage/monocyte activity) that can induce chemosensitive and immunosensitive reactions with prolonged exposure producing a noxious response.2 The edema produced is a consequence of compromised microcirculation at the endoneural level and may lead to hypoxia, local pain, angiogenesis, scarring, and restricted axoplasmic flow.3 Endoneural edema accumulation is compounded by the lack of lymph tissue present at this level of the nerve to facilitate flow of fluids.4 Continued mechanical exposure—in these athletic cases continued participation in the etiologic activity—potentiates the increased nerve mechanosensitivity, propagating inflammatory responses inflicting chemosensitivity to the nerve and the surrounding musculature.5 The trauma may result in signs and symptoms such as dysesthesia, hyperesthesia, hypoesthesia, paresis (hypotonia), and paresthesia.3,4 Clinical presentations include dysfunction, fatigability, loss of coordination, and disability.35 Postural dysfunction—primarily muscular, capsular, and ligamentous tightness—also occurs as a result of excessive fibrosis, neural budding, ...

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