Arch Surg. 1935;31(5):823-832. doi:10.1001/archsurg.1935.01180170148012.
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Within recent years there has been a notable increase in what for lack of a better term have been classed simply as "head injuries." Although the term does not so specifically indicate, "head injury" has come to be synonymous with "brain injury." It has been assumed that cerebral trauma sufficient to cause subjective symptoms or to exhibit objective signs would be attended by the usual phenomena of injury elsewhere, viz., edema, hemorrhage and gross structural damage, and that occurring within a closed container such as the skull it would have as its most constant and formidable phenomenon increased intracranial pressure.1 It is on this assumption that most of the accepted treatment of craniocerebral trauma is based. It is assumed that the most common occurrence following brain trauma is cerebral edema and that this is one of the prominent factors causing death from such injuries.2 In accordance with this


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