Pathophysiology of cerebral ischemia and brain trauma: similarities and differences.
Current knowledge regarding the pathophysiology of cerebral ischemia and brain trauma indicates that similar mechanisms contribute to loss of cellular integrity and tissue destruction. Mechanisms of cell damage include excitotoxicity, oxidative stress, free radical production, apoptosis and inflammation. Genetic and gender factors have also been shown to be important mediators of pathomechanisms present in both injury settings. However, the fact that these injuries arise from different types of primary insults leads to diverse cellular vulnerability patterns as well as a spectrum of injury processes. Blunt head trauma produces shear forces that result in primary membrane damage to neuronal cell bodies, white matter structures and vascular beds as well as secondary injury mechanisms. Severe cerebral ischemic insults lead to metabolic stress, ionic perturbations, and a complex cascade of biochemical and molecular events ultimately causing neuronal death. Similarities in the pathogenesis of these cerebral injuries may indicate that therapeutic strategies protective following ischemia may also be beneficial after trauma. This review summarizes and contrasts injury mechanisms after ischemia and trauma and discusses neuroprotective strategies that target both types of injuries.
Bramlett
Helen M
HM
Department of Neurological Surgery and The Miami Project to Cure Paralysis, University of Miami Medical School, FL 33101, USA.
Dietrich
W Dalton
WD
D000818:Animals; D017209:Apoptosis / Q000502:physiology; D001369:Axons / Q000378:metabolism / Q000473:pathology; D001930:Brain Injuries / Q000453:epidemiology / Q000209:etiology / Q000235:genetics / Q000503:physiopathology*; D002545:Brain Ischemia / Q000453:epidemiology / Q000209:etiology / Q000235:genetics / Q000503:physiopathology*; D004730:Endothelium, Vascular / Q000378:metabolism / Q000473:pathology; D006801:Humans; D007249:Inflammation / Q000378:metabolism; D010974:Platelet Aggregation