Oxygen deficiency and brain damage: localization, evolution in time, and mechanisms of damage.
Observations on some patients with CO intoxication have revealed a delayed type of brain injury, with symptoms appearing days after the initial insult. Possible mechanisms are discussed, with reference to recent experimental results on ischemic brain damage. These results have shown that brief periods of ischemia can cause necrosis of selectively vulnerable neurons, sometimes after a delay of 1-3 days. In at least one affected cell type (CAI pyramids in the hippocampus) delayed neuronal death was preceded by cellular hyperactivity. Recent neurochemical research offers tentative explanations. For example, several reactions triggered by increased calcium concentrations are long-lasting enough to cause sustained alteration of cell function and/or delayed neuronal death. These encompass physical interruption of the cytoskeleton by disassembly of microtubuli and degradation of neurofilaments, protein phosphorylation, and proteolytic degradation of dendritic structures. Reactions interrupting the cytoskeleton could cause cell death by impeding axonal transport, while phosphorylation-proteolysis could induce increased synaptic efficacy, with harmful overactivity.
D000138:Acidosis / Q000150:complications; D000818:Animals; D001921:Brain / Q000098:blood supply* / Q000378:metabolism; D001927:Brain Diseases / Q000209:etiology*; D002118:Calcium / Q000378:metabolism; D002470:Cell Survival; D006706:Homeostasis; D007003:Hypoglycemia / Q000150:complications; D000860:Hypoxia / Q000150:complications* / Q000503:physiopathology; D007511:Ischemia / Q000150:complications* / Q000503:physiopathology; D009474:Neurons / Q000502:physiology; D010101:Oxygen Consumption; D013226:Status Epilepticus / Q000150:complications; D013997:Time Factors
D002118:Calcium