Abstract
Hypoxia, decreased oxygen availability, may serve as a model to help elucidate the pathophysiological basis of the metabolic encephalopathies. These disorders, in which brain metabolism is altered secondarily to systemic changes, include hyperammonemia, hypoglycemia, nutritional deficiencies such as thiamine or niacin, some inborn errors of metabolism, and heavy metal intoxication (Plum, 1975). The metabolic encephalopathies share similar clinical symptoms: decreased mentation and a loss of attention, alertness, orientation, cognition, memory, and perception, which eventually progress to stupor, coma, and finally death (Plum and Posner, 1980). The similar clinical presentation, despite diverse etiologies, suggests that a common molecular mechanism may underlie the altered brain function in all of them. Furthermore, an understanding of how low oxygen alters brain metabolism may help unravel the complex changes that accompany ischemia. During ischemia, tissue perfusion is also comprised, which reduces the substrate supply and allows accumulation of possibly toxic metabolic products, as well as causing hypoxia or anoxia (complete lack of oxygen). Whether ischemic-induced tissue damage is just an exaggeration of hypoxia’s effects or if some unknown variable converts hypoxic changes to ischemic deficits is unknown.
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References
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Gibson, G.E. (1985). Hypoxia. In: McCandless, D.W. (eds) Cerebral Energy Metabolism and Metabolic Encephalopathy. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-1209-3_3
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DOI: https://doi.org/10.1007/978-1-4684-1209-3_3
Publisher Name: Springer, Boston, MA
Print ISBN: 978-1-4684-1211-6
Online ISBN: 978-1-4684-1209-3
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