Brain cellular injury and recovery--horizons for improving medical therapies in stroke and trauma.
An edited summary of an Interdepartmental Conference arranged by the Department of Medicine of the UCLA School of Medicine, Los Angeles. The Director of Conferences is William M. Pardridge, MD, Professor of Medicine. After ischemic and traumatic brain injury, many cells may be rendered dysfunctional but are not irreversibly damaged or disrupted. The brain tissue may become metabolically deranged, and neurons, while still alive, are paralyzed and cannot create an action potential or conduct an electrical impulse. This injured brain tissue is in a precarious state of increased vulnerability. If the milieu of the favorable, they may recover; if it is slightly unfavorable, they may die. There is now evidence that reversibly injured brain tissue will die from an ischemic or hypoxic insult ordinarily tolerated by the normal brain. The major challenge of modern research in stroke and trauma is to define the chemical and metabolic milieu in which the injured brain exists and to define an ideal milieu for healing.
D000328:Adult; D000818:Animals; D001369:Axons / Q000502:physiology; D001924:Brain Concussion / Q000378:metabolism; D001930:Brain Injuries / Q000378:metabolism / Q000503:physiopathology*; D002415:Cats; D002561:Cerebrovascular Disorders / Q000378:metabolism; D005971:Glutamates / Q000009:adverse effects; D018698:Glutamic Acid; D006801:Humans; D008297:Male
D005971:Glutamates; D018698:Glutamic Acid