The growth of neurochemistry. molecular biology, and biochemical genetics has led to a burgeoning of new information relevant to the pathogenesis of brain dysfunction. This explosion of exciting new information is crying out for collation and meaningful synthesis. In its totality, it defies systematic summa tion, and, of course, no one author can cope. Thus invitations for contributions were given to various experts in areas which are under active investigation, of current neurological interest, and pregnant. Although this project is relatively comprehensive, by dint of size. other topics might have been included; the selection was solely my responsibility. I believe systematic summation a virtual impossibility-indeed, hardly worth the effort. The attempt to assemble all of the sections involved in a large treatise with multiple authors inevitably results in untoward delays due to the difference in the rate at which various authors work. Therefore, the following strategy has been adopted: multiple small volumes and a relatively flexible format, with publication in order of receipt and as soon as enough chapters are assembled to make publication practical and economical. In this way, the time lag between the ideas and their emergence in print is the shortest.
The growth of neurochemistry. molecular biology, and biochemical genetics has led to a burgeoning of new information relevant to the pathogenesis of brain dysfunction. This explosion of exciting new information is crying out for collation and meaningful synthesis. In its totality, it defies systematic summa tion, and, of course, no one author can cope. Thus invitations for contributions were given to various experts in areas which are under active investigation, of current neurological interest, and pregnant. Although this project is relatively comprehensive, by dint of size. other topics might have been included; the selection was solely my responsibility. I believe systematic summation a virtual impossibility-indeed, hardly worth the effort. The attempt to assemble all of the sections involved in a large treatise with multiple authors inevitably results in untoward delays due to the difference in the rate at which various authors work. Therefore, the following strategy has been adopted: multiple small volumes and a relatively flexible format, with publication in order of receipt and as soon as enough chapters are assembled to make publication practical and economical. In this way, the time lag between the ideas and their emergence in print is the shortest.
1 Pathophysiology of Perinatal Hypoxic-Ischemic Brain Damage.- I. Introduction.- II. Human Perinatal Hypoxia-Ischemia.- III. Neuropathology of Perinatal Hypoxia-Ischemia.- IV. Perinatal Central Nervous System Development.- V. Experimental Approaches to Perinatal Hypoxia-Ischemia.- VI. Conclusions.- References.- 2 Pathogenesis of Brain Dysfunction in Inborn Errors of Amino Acid Metabolism.- I. Introduction.- II. Effects of Metabolic Sequelae on the Fluxes and Transport of Amino Acids.- III. Effects of Metabolic Sequelae on Synthesis of Protein in Brain.- IV. Effects of Metabolie Sequelae on Substances Affecting Neurotransmission in Brain.- V. Effects of Metabolie Sequelae on Carbohydrate Metabolism and Energy Utilization.- VI. Effects of Metabolie Sequelae on Synthesis of Lipids and Myelin.- VII. Comments and Conclusions.- References.- 3 Disorders of Organic Acid Metabolism.- I. Introduction.- II. Inborn Errors of Leucine Metabolism.- III. Inborn Errors of Isoleucine and Valine Metabolism.- IV. Inborn Errors of Metabolism of Other Organic Acids.- V. Inborn Errors of Pyruvate Metabolism.- VI. Disorders of Organic Acid Metabolism Induced by Natural Toxin.- References.- 4 Biological Aspects of Affective Psychoses.- I. Introduction.- II. Clinical Features.- III. The Biogenic Amine Hypothesis.- IV. Indoleamines in Affective Disorders.- V. Lithium and Affective Disorders.- VI. Catecholamines and Affective Disorders.- VII. Neuroendocrine Function in Affective Disorders.- VIII. Conclusions.- References.- 5 Wilson’s Disease.- I. Copper Metabolism.- II. Copper Toxicity.- III. An Inherited Abnormality of Copper Metabolism: Wilson’s Disease.- References.- 6 Pathogenesis of Slow Infections of the Central Nervous System.- I. Introduction.- II. Slow Virus Subacute SpongiformEncephalopathies.- III. Slow Viral Encephalomyelitides.- References.- 7 Pathogenesis of Intrauterine Infections of the Brain.- I. Introduction.- II. Factors Required for the Initiation of Intrauterine Brain Infection.- III. Infections Affecting the Fetal or Newborn Central Nervous System.- IV. Possible Effector Mechanisms of Virus-Mediated Damage to the Developing Brain.- V. Fetal Immunological Response.- VI. Interferons.- VII. Discussion.- References.- 8 Ionizing Radiations and the Nervous System.- I. Introduction.- II. Some Radiobiological Considerations.- III. Developing Organisms.- IV. The Adult.- References.- 9 Brain Dysfunction in Congenital Malformations of the Nervous System.- I. Introduction.- II. Dysraphic States.- III. Cerebral Ageneses and Hypoplasias.- IV. Dysgenesis of the Cerebral Structures.- V. Developmental Cyst Formation.- VI. Congenital Hydrocephalus and Hydranencephaly.- VII. Synopsis.- References.- 10 Pathogenesis of Brain Dysfunction in Deficiency of Thiamine, Riboflavin, Pantothenic Acid, or Vitamin B6.- I. Introduction.- II. Thiamine Deficiency.- III. Riboflavin Deficiency.- IV. Pantothenic Acid Deficiency.- V. Vitamin B6 Deficiency.- References.
Springer Book Archives
 |
Ask a Question About this Product More... |
|
