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TitleCerebral Energy Metabolism and Metabolic Encephalopathy [electronic resource] / edited by David W. McCandless
ImprintBoston, MA : Springer US, 1985
Connect tohttp://dx.doi.org/10.1007/978-1-4684-1209-3
Descript 478p. online resource

SUMMARY

In recent years, there has been rapid growth in knowledge pertaining to the nervous system. This has, in some measure, been due to the development and application of a number of techniques such as the 2-deoxyglucose method and microchemical methods for measuring metabolites and regional cerebral blood flow. Data from the application of these techniques are just beginning to be collected, and the next few years promise to bring many new and exciting findings. The study of energy metabolism in brain is particularly interesting due to the fact that although the brain has scant energy reserves (as compared with the liver), it has one of the highest metabolic rates in the body. Recent studies from several laboratories have shown a surprising divergence of reยญ sponses to metabolic insult in different areas of brain. In this regard, the cerยญ ebellum, for example, may have metabolic features which are uniqve from those of any other region. The high-energy phosphate compounds ATP and phosยญ phocreatine, supplied by the oxidative metabolism of glucose, are necessary for normal cerebral functions such as the maintenance of membrane potentials, transmission of impulses, and synthetic processes. Interruption of substrate or "poisoning" of the system by a variety of means lead to a rapid change in cellular energetics, and ultimately cell death. From the clinical standpoint, an interesting feature of metabolic encephalopathy is that in many cases, early diagnosis and treatment may result in a rapid reversal of symptoms


CONTENT

I. Introduction -- 1 Cerebral Energy Metabolism -- II. Metabolic Encephalopathy Associated with Severe Interruption of Substrate -- 2 Hypoglycemia and Cerebral Energy Metabolism -- 3 Hypoxia -- 4 Ischemic Encephalopathy -- III. Metabolic Encephalopathy Resulting Primarily from Intrinsic Factors -- 5 Pyruvate Dehydrogenase Deficiency Disorders -- 6 Carbon Dioxide Narcosis -- 7 Encephalopathy Due to Short- and Medium-Chain Fatty Acids -- 8 Encephalopathy Due to Mercaptans and Phenols -- 9 Ammonia-Induced Encephalopathy -- 10 Bilirubin Encephalopathy -- 11 Uremic and Dialysis Encephalopathies -- 12 Epilepsy: Pathophysiology of Cerebral Dysfunction -- IV. Metabolic Encephalopathy that May Result from Extrinsic Factors -- 13 Niacin-Nicotinamide Deficiency -- 14 Thiamine Deficiency and Cerebral Energy Metabolism -- 15 Thiamine Deficiency: Cerebral Amino Acid Levels and Neurologic Dysfunction -- 16 Alcohol-Induced Encephalopathy -- 17 Heavy Metal Toxicity and Energy Metabolism in the Developing Brain: Lead as the Model -- 18 General Anesthesia -- 19 Neurochemical Effects of Viral Infections in the Central Nervous System


Medicine Neurosciences Neurology Neurobiology Medicine & Public Health Neurology Neurobiology Neurosciences



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