Abstract

Clinical differences between respiratory disturbances resulting from spinal cord involvement and breathing defects produced by brain stem lesions have been recognized in poliomyelitis for over 50 years. Despite this long recognition, there have been comparatively few detailed studies of mode of development, frequency, or pathological physiology of respiratory failure in poliomyelitis. The earliest reference to supraspinal lesions causing respiratory difficulties in poliomyelitis appears to have been that of Wickman, 1 who stated in 1905 that respiratory paralysis could result from involvement of either the center for intercostal muscles or the nucleus of pneumogastric nerve. Petren and Ehrenberg, 2 in 1909, more correctly designated the bulbar center for respiration as source of supraspinal respiratory defects in poliomyelitis. Subsequently, a number of authors made direct or passing reference to shallow, irregular breathing with marked variation in rate and depth as characteristic of central respiratory failure.

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