Cerebral edema.
Cerebral edema continues to plague clinicians caring for patients with acute catastrophic neurologic disease. The defect responsible for the accumulation of water in the brain appears to reflect loss of the strict permeability barrier of the cerebral vasculature. A greater understanding of the physiologic mechanisms at work in the blood-brain barrier have helped target therapies at the vascular interface between the circulating blood and the brain. The mounting evidence which implicates inflammatory events as causally related to the loss of cerebrovascular impermeability supports the clinical strategy of suppression of acute inflammation. Clearly, further advances in the management of cerebral edema will be strongly influenced by the development of specific anti-inflammatory pharmaceuticals.
Hariri
R J
RJ
Division of Neurosurgery, New York Hospital, Cornell Medical Center, New York.
D000210:Acute-Phase Reaction / Q000473:pathology / Q000503:physiopathology / Q000628:therapy; D000818:Animals; D001253:Astrocytes / Q000473:pathology / Q000502:physiology; D001812:Blood-Brain Barrier / Q000502:physiology; D001921:Brain / Q000098:blood supply; D001929:Brain Edema / Q000473:pathology / Q000503:physiopathology* / Q000628:therapy; D002199:Capillary Permeability / Q000502:physiology; D003422:Critical Care; D016207:Cytokines / Q000502:physiology; D004730:Endothelium, Vascular / Q000473:pathology / Q000503:physiopathology; D005110:Extracellular Space / Q000502:physiology; D006801:Humans; D014666:Vasomotor System / Q000473:pathology / Q000503:physiopathology; D014882:Water-Electrolyte Balance / Q000502:physiology
D016207:Cytokines