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
- 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
- Storage Diseases
- Kernicterus
- Chapter 61 Clinicopathological Features of Kernicterus
- Mitochondrial Diseases
- Maternal Toxin Exposure
- Section 11 Forensic Neuropathology
- Appendix 1 Technical Considerations in Perinatal CNS
- Index
- References
Chapter 61 - Clinicopathological Features of Kernicterus
from Kernicterus
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
- 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
- Storage Diseases
- Kernicterus
- Chapter 61 Clinicopathological Features of Kernicterus
- Mitochondrial Diseases
- Maternal Toxin Exposure
- Section 11 Forensic Neuropathology
- Appendix 1 Technical Considerations in Perinatal CNS
- Index
- References
Summary
The term kernicterus (lat. yellow nuclei) was first used by the pathologist Christian Schmorl (1903) to describe the yellow staining observed in nuclei of post mortem brains of infants diagnosed with severe neonatal jaundice prior to their death [1]. Kernicterus is caused by hyperbilirubinemia (increased plasma concentration of bilirubin) and is sometimes also referred to as bilirubin encephalopathy. Severe neonatal hyperbilirubinemia is defined as a plasma bilirubin >30 mg/dL (513 μmol/L), and is associated with an increased risk for bilirubin-induced neurologic dysfunction (BIND). The disorder can clinically present in an acute, chronic, or subtle form affecting neonates and infants who are especially vulnerable to the neurotoxic effects of high bilirubin plasma concentrations (Table 61.1). BIND occurs when bilirubin crosses the blood-brain barrier, binds to brain tissue, and causes neurotoxicity. Neonatal brain injury is primarily caused by the pathologic bilirubin accumulation in the grey matter – most commonly basal ganglia, hippocampus, geniculate nuclei, and cranial nerves nuclei.
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- Information
- Perinatal Neuropathology , pp. 385 - 390Publisher: Cambridge University PressPrint publication year: 2021