Abstract
Neurosurgeons commonly teach their trainees and explain to families that patients with prolonged traumatic coma unaccompanied by mass lesions have suffered “brain damage” as a result of their trauma. Despite this frequently held belief, there is little to document the nature of the “brain damage” that results from the immediate effects of trauma. Consequently, brain swelling, edema, ischemia or other secondary mechanisms are offered in explanation for the clinical symptoms and the outcome from injury. Evidence from our own investigations coupled with that of others supports the concept that primary injury to axons is responsible for many, if not most, cases of traumatic coma that is not due to mass lesions. We have named the condition Diffuse Axonal Injury (DAI). The term DAI, therefore, is descriptive of both the clinical complex of prolonged traumatic coma and the pathologic substrate that underlies that complex. This paper reviews the genesis of the concept of DAI and discusses the implications of DAI as an approach to prolonged traumatic coma.
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© 1986 Plenum Press, New York
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Gennarelli, T.A., Adams, J.H., Graham, D.I. (1986). Diffuse Axonal Injury — A New Conceptual Approach to an Old Problem. In: Baethmann, A., Go, K.G., Unterberg, A. (eds) Mechanisms of Secondary Brain Damage. NATO ASI Series, vol 115. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-5203-7_2
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DOI: https://doi.org/10.1007/978-1-4684-5203-7_2
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