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The objective of this Instructional Course Lecture is to provide the reader with a current, comprehensive review of fundamental clinical issues surrounding the most commonly encountered compressive neuropathies of the upper extremity. Relevant new data on the pathophysiology of neural compression introduce more specific discussions of the currently favored methods for the evaluation and treatment of carpal tunnel syndrome, cubital tunnel syndrome, and radial nerve entrapment in the proximal part of the forearm.Recent experimental studies have demonstrated that a consistent sequence of events takes place when external compression forces are elevated around a peripheral nerve. Mechanical deformation has been found to be greatest in the superficial regions of the nerve and in the zones between compressed and uncompressed segments. External pressures of twenty to thirty millimeters of mercury (2.66 to 4.00 kilopascals) have been shown to impair venular flow in the epineurium and to retard intracellular axonal transport [15,16,17]. Pressures as low as thirty millimeters of mercury (4.00 kilopascals) cause changes in the permeability of intraneural blood vessels, further increasing intraneural interstitial fluid pressure. Patients with carpal tunnel syndrome have been shown to have intracarpal tunnel interstitial pressures at levels that are within this range (thirty millimeters of mercury with the wrist in neutral position, increased to ninety millimeters of mercury (twelve kilopascals) with the wrist in palmar flexion) . Experimentally induced higher pressures (130 to 150 millimeters of mercury (17.32 to 20.00 kilopascals)) cause an acute block of conduction [18,31,33], and higher pressures cause marked changes in intraneural blood flow, vessel permeability, and fiber morphology (epineurial and perineurial thickening and eccentric positioning of nuclei and dispersion of Nissl substance within nerve cell bodies), leading to rapid deterioration of nerve function [8,40,68,79].Clinically, the presentation of acute and chronic nerve-compression lesions appears consistent with the sequence of events that has been identified experimentally. Low-level compression forces of relatively brief duration appear to cause changes in intraneural microcirculation that are intermittent and rapidly reversible on decompression. Higher levels of compression, maintained for longer periods of time, impair axonal transport and cause changes in the structure and function of peripheral nerves and nerve cell bodies, so that a longer period of time after decompression is required before recovery should be anticipated.The most commonly encountered peripheral neuropathy, carpal tunnel syndrome, occurs most frequently during middle or advanced age. (In a study performed at the Mayo Clinic , the mean age of 1215 patients was fifty-four years and 83 per cent of the patients were more than forty years old.) Occurring twice as frequently in women as in men, median-nerve compression [71,96] causes symptoms of paresthesias and numbness in the median-nerve distribution or in the entire hand, which frequently awaken patients from sleep. Motor abnormalities, including weakness and atrophy of the abductor pollicis brevis and opponens pollicis muscles, occur in advanced stages of compression.While a precise cause for symptoms of median-nerve compression may not be identifiable in many patients, a number of associated conditions should be considered during routine evaluation. In a useful classification of the causes of median-nerve compression, Szabo and Madison considered anatomical, physiological, and patterns-of-use factors . Anatomical factors include conditions leading to a decrease in the size of the carpal tunnel (for example, acromegaly and osseous abnormalities of the wrist and distal part of the radius) and those causing an increase in the contents of the carpal canal (for example, benign tumors, abnormal muscle bellies, non-specific synovitis, and hematomas).