CENTRAL NERVOUS SYSTEM RESUSCITATION - 10/09/11
Résumé |
Brain injury is the leading cause of death among individuals aged 28 to 45 years in the United States and Europe, with an incidence in the United States of 17 to 40 per 100,000 population. 202, 238 The occurrence of traumatic brain injury (TBI) requiring hospitalization is between 2000 and 5000 per 100,000 people, or between 2 and 12.5 million head injuries per year. 129 The estimated cost of these injuries ranges from $1 billion to $25 billion per year. 129, 192 The cost to families and society is particularly high when it is considered that trauma to the central nervous system (CNS) is particularly common in young people.
Traumatic injury to the CNS results in neurologic dysfunction through both direct (immediate mechanical disruption of brain tissue and neural circuitry) and indirect (secondary or delayed) mechanisms. 153 This delayed injury cascade develops over a period of hours to days to weeks following brain trauma. 47, 228 Although the precise mechanisms underlying post-traumatic secondary damage remain unclear, they are believed to result from alterations in neurochemical or cellular mediators initiated by the trauma. These cellular changes may include alterations in neurotransmitter release, neurotransmitter reuptake or clearance systems, changes in presynaptic or postsynaptic receptor binding, the synthesis of “autodestructive” and inflammatory mediators, or the alteration of endogenous neuroprotective or trophic factors. These fundamental changes in the neurochemistry of the CNS may exert deleterious effects on normal cerebral function including profound changes in regional cerebral blood flow (rCBF), alterations in ion homeostasis and brain swelling, and alterations in the local metabolic environment. 226 Pathologic neurochemical activation following brain trauma may also directly kill neurons or glial cells (neurotoxic effects). Experimental identification of these injury mechanisms and elucidation of the timing of the pathologic neurochemical cascade initiated following trauma may provide enhanced opportunities for treatment with neuroprotective strategies designed to modify the synthesis, release, physiologic activity, or expression of pathogenic factors involved in these neurochemical cascades. Recently, new hope has arisen for the treatment of TBI, based on new research findings regarding the development of novel pharmacologic therapies for brain trauma. The experimental armamentarium of potentially neuroprotective pharmaceutical compounds has expanded enormously over the past several years. Many of these candidate compounds hold a great deal of promise, and this article reviews some of the more promising pharmacologic therapies for the resuscitation of the injured brain.
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| Address reprint requests to Tracy K. McIntosh, PhD Department of Neurosurgery University of Pennsylvania 3320 Smith Walk 105 Hayden Hall Philadelphia, PA 19104 This work was supported, in part, by Grants NS08803 and NS26818 from The National Institute of Neurological Disorders and Stroke, GM34690 from the National Institute of General Medical Sciences, and AG12527 from the National Institute of Aging. |
Vol 15 - N° 3
P. 527-550 - août 1997 Retour au numéro
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- NEUROIMAGING
- Joseph Araiza, Beatrix Araiza
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