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I N recent years there has been increasing interest in the respiratory complications of cerebral trauma as well as the role of the cerebrospinal fluid (CSF) in respiration. 9 Published reports have concentrated on the respiratory, acid-base, and blood gas alterations seen in more severe forms of cranial trauma where the comparability of the level of injury was questionable, and multiple injuries were frequently involved. The question then arises: What part of the devastating effects of respiratory disturbance after cranial trauma is precipitated by primary neurogenic factors and what part follows as secondary effects of airway obstruction and pulmonary insufficiency? Ducker and associates have helped to elucidate part of this problem in their study of the role of raised intracranial pressure and the Cushing reflex in the genesis of pulmonary edema after head injury. ~,~,21 In an attempt to separate the primary central nervous system derangements from those caused by secondary airway and pulmonary factors, we have begun a study of respiratory function, blood, and CSF pH and gas tensions after experimental cerebral concussion (ECC). This model of head injury represents our baseline of minimal and reversible brain trauma wherein the physiopathology of blunt head injuries may be analyzed, and on which studies of more severe injury may be built. The criteria for concussion and the biomechanical aspects of the trauma were developed for the Rhesus monkey, as previously described by Ommaya, et al. ~,6,17,~8
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Grubb et al. (1970) studied this question.
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