Cerebral Energy Metabolism and Metabolic Encephalopathy

1. Front Matter

   Pages i-xxii

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2. Introduction

   1. Front Matter

      Pages 1-1

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   2. Cerebral Energy Metabolism

      • Richard Hawkins

      Pages 3-23

3. Metabolic Encephalopathy Associated with Severe Interruption of Substrate

   1. Front Matter

      Pages 25-25

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   2. Hypoglycemia and Cerebral Energy Metabolism

      • David W. McCandless, Marc S. Abel

      Pages 27-41

   3. Hypoxia

      • Gary E. Gibson

      Pages 43-78

   4. Ischemic Encephalopathy

      • W. David Lust, Hajime Arai, Yukimasa Yasumoto, Tim S. Whittingham, Bogden Djuricic, Bogomir B. Mrsulja et al.

      Pages 79-117

4. Metabolic Encephalopathy Resulting Primarily from Intrinsic Factors

   1. Front Matter

      Pages 119-119

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   2. Pyruvate Dehydrogenase Deficiency Disorders

      • Roger F. Butterworth

      Pages 121-141

   3. Carbon Dioxide Narcosis

      • Alexander L. Miller

      Pages 143-162

   4. Encephalopathy Due to Short- and Medium-Chain Fatty Acids

      • Leslie Zieve

      Pages 163-177

   5. Encephalopathy Due to Mercaptans and Phenols

      • Leslie Zieve, Gorig Brunner

      Pages 179-201

   6. Ammonia-Induced Encephalopathy

      • Alan H. Lockwood

      Pages 203-227

   7. Bilirubin Encephalopathy

      • Gerard B. Odell, Henry S. Schutta

      Pages 229-261

   8. Uremic and Dialysis Encephalopathies

      • Paul E. Teschan, Allen I. Arieff

      Pages 263-285

   9. Epilepsy

      • Robert C. Collins

      Pages 287-307

5. Metabolic Encephalopathy That May Result from Extrinsic Factors

   1. Front Matter

      Pages 309-309

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   2. Niacin-Nicotinamide Deficiency

      • Frederick C. Kauffman

      Pages 311-334

   3. Thiamine Deficiency and Cerebral Energy Metabolism

      • David W. McCandless

      Pages 335-351

   4. Thiamine Deficiency

      • Jean Holowach Thurston, Richard E. Hauhart, John A. Dirgo, David B. McDougal Jr.

      Pages 353-359

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 re­ sponses to metabolic insult in different areas of brain. In this regard, the cer­ ebellum, for example, may have metabolic features which are uniqve from those of any other region. The high-energy phosphate compounds ATP and phos­ 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.

• Nervous System
• anatomy
• behavior
• cortex
• metabolism
• physiology
• visual evoked potential (VEP)

• Department of Neurobiology and Anatomy, University of Texas Medical School at Houston, Houston, USA

  David W. McCandless

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