1. Gross and Microscopic Development of the Central Nervous System --; Timing of Origin of Neuronal Groups --; Mass Growth of the Brain --; Cerebral Cortex --; White Matter --; Periventricular Matrix Tissue --; Myelin Formation, Fine Structure --; Regional Timing of Myelination --; Myelination Gliosis --; Basal Ganglia --; Ventricular System --; Brain Stem Nuclei --; Cerebellum --; Spinal Cord --; Basic Reactions --; References --; First Part. Acquired Lesions in Newborns and Infants --; 2. Hemorrhages Characteristic of Asphyctic Premature Infants --; 3. Cerebral Lesions from Physical Trauma --; 4. Periventricular Infarcts --; 5. Diffuse Fatty Change of White Matter --; 6. Perinatal Lesions of Cerebral and Cerebellar Cortex --; 7. Lesions of Basal Ganglia, Brain Stem, and Cord --; 8. Kernicterus (Bilirubin Encephalopathy) --; 9. Various Topographic Patterns of Postnatal Neuron Loss --; 10. Progressive Sclerosing Cortical Atrophy: Spongy Glio-Neuronal Dystrophy --; 11. Porencephaly, Hydranencephaly, Multilocular Cystic Encephalopathy --; 12. Arterial Occlusive Disease in Infancy --; 13. Thrombosis of Intracranial Sinus and Veins --; 14. Cerebral Lesions in Congenital Cardiac Disease --; 15. Cranio-Cerebral Trauma in Infancy --; 16. Fetal Infections --; 17. Leptomeningitis in Newborns and Infants --; 18. Meningoencephalitic Processes in the Perinatal Period --; 19. Subdural Hematomas, Hygromas and Effusions --; 20. Meningeal Cysts --; 21. Hydrocephalus-Basic Concepts and General Pathology --; 22. Hydrocephalus-Special Pathology --; Second Part. Malformations --; 23. Anencephaly, Rachischisis and Encephaloceles --; 24. Spina Bifida and Related Spinal Lesions --; 25. The Arnold-Chiari Malformation (Cleland-Chiari Malformation) --; 26. Ventral Dysraphic and Various Sacral Lesions --; 27. Disturbances in the Bulk Growth of Nervous Tissue --; 28. Dysplasias of Cerebral Hemispheric Organization --; 29. Dysplasias of Cerebral Cortex --; 30. Dysplasia of Cerebellar Hemispheric Organization --; 31. Dysplasias of Cerebellar Cortex --; 32. Dysplasias of Brain Stem and Spinal Cord --; 33. Dysplasias in Chromosome Disorders --; 34. Dysplasias of Cerebral Vasculature --; Third Part. Metabolic Diseases --; 35. Diseases of Carbohydrate Metabolism --; 36. Sphingolipidoses --; 37. Ceroid Lipofuscinosis; Miscellaneous Lipidoses --; 38. Metachromatic Leukodystrophy (Sulfatase A Deficiency) and Multiple Sulfatase Deficiency --; 39. Globoid Cell Leukodystrophy --; 40. Adreno-Leukodystrophy and Its Relations to 'Schilder Disease' --; 41. Pelizaeus-Merzbacher Disease, Cockayne Syndrome and Related Conditions --; 42. Alexander Disease and Related Conditions --; 43. Axon Dystrophies --; 44. Spongy Degeneration of the Central Nervous System and Other Forms of Spongy Myelinopathy --; 45. Diseases of Intermediary Metabolism --; 46. Involvement of the CNS in Certain Hematologic Diseases of Infancy and Childhood.
یادداشتهای مربوط به خلاصه یا چکیده
متن يادداشت
The present text was envisioned as a supplement to eXlstmg texts on human neuropathology, covering only those aspects of pediatric neuropathol ogy which pertain to and are peculiar of the immature nervous system. No coverage-or only brief comment-is given to diseases commonly found in adults which may, on occasion, occur in childhood or infancy as well. The subject matter is divided into three main categories: 1. The "acquired" lesions dating to the fetal, perinatal or early postnatal periods, 2. the malformations, and 3. the heritable metabolic defects. The first 6 chapters (2-7) are reserved to the lesions most intimately linked to the circumstances of birth. There is some inherent ambiguity in distinguishing between "acquired" lesions and malformations, as, indeed, no sharp distinction can be made between one and the other. Many malformations result from diseases acquired during fetal life and their peculiarity resides in the fact that the organ becomes affected before its development terminates and in such a way that its subsequent development becomes deranged or partly abrogated. A variety of causes acting at the same developmental period or over a common pathogenetic mechanism may produce the same type of derangement, including chemical, physical, infectious or genetic factors, as pointed out repeatedly in the text. Consequently, the definition of a malformation, as differing from an "acquired" residual lesion was made dependant on evidence for the derangement of developmental pro cesses subsequent to the acquisition of the disease.
موضوع (اسم عام یاعبارت اسمی عام)
موضوع مستند نشده
Medicine.
رده بندی کنگره
شماره رده
RJ486
نشانه اثر
.
B974
1975
نام شخص به منزله سر شناسه - (مسئولیت معنوی درجه اول )