Book contents
- Perinatal Neuropathology
- Perinatal Neuropathology
- Copyright page
- Contents
- Preface
- Acknowledgments
- Abbreviations
- Section I Techniques and Practical Considerations
- Section 2 Human Nervous System Development
- Section 3 Stillbirth
- Section 4 Disruptions / Hypoxic-Ischemic Injury
- Cellular Responses
- Gray Matter
- Chapter 32 Supratentorial Gray Matter Damage and Disruptions
- Chapter 33 Brainstem and Spinal Cord Disruptions
- White Matter
- Germinal Matrix
- Cerebellum
- Section 5 Malformations
- Section 6 Perinatal Neurooncology
- Section 7 Spinal and Neuromuscular Disorders
- Section 8 Eye Disorders
- Section 9 Infections: In Utero Infections
- Section 10 Metabolic / Toxic Disorders: Storage Diseases
- Section 11 Forensic Neuropathology
- Appendix 1 Technical Considerations in Perinatal CNS
- Index
- References
Chapter 33 - Brainstem and Spinal Cord Disruptions
from Gray Matter
Published online by Cambridge University Press: 07 August 2021
- Perinatal Neuropathology
- Perinatal Neuropathology
- Copyright page
- Contents
- Preface
- Acknowledgments
- Abbreviations
- Section I Techniques and Practical Considerations
- Section 2 Human Nervous System Development
- Section 3 Stillbirth
- Section 4 Disruptions / Hypoxic-Ischemic Injury
- Cellular Responses
- Gray Matter
- Chapter 32 Supratentorial Gray Matter Damage and Disruptions
- Chapter 33 Brainstem and Spinal Cord Disruptions
- White Matter
- Germinal Matrix
- Cerebellum
- Section 5 Malformations
- Section 6 Perinatal Neurooncology
- Section 7 Spinal and Neuromuscular Disorders
- Section 8 Eye Disorders
- Section 9 Infections: In Utero Infections
- Section 10 Metabolic / Toxic Disorders: Storage Diseases
- Section 11 Forensic Neuropathology
- Appendix 1 Technical Considerations in Perinatal CNS
- Index
- References
Summary
This section will review hypoxic-ischemic damage to the brainstem and spinal cord in the perinatal setting. Such damage may occur in utero, intrapartum, or postnatally, and may be seen in isolation or accompanied by injury to other neuroanatomic locations (i.e., global hypoxic-ischemic damage, clinically corresponding to hypoxic-ischemic encephalopathy [HIE; Chapters 32–33]; or a more modest degree of injury as seen in preterm infants with white matter damage, termed encephalopathy of prematurity [Chapters 34]). Acquired lesions of the brainstem may have features overlapping with specific maldevelopmental syndromes such as Moebius syndrome and Carey-Fineman-Ziter syndrome, recently recognized to occur sporadically or with familial incidence and to have underlying genetic bases (discussed later) [1, 2].
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- Information
- Perinatal Neuropathology , pp. 178 - 182Publisher: Cambridge University PressPrint publication year: 2021