Hypoxic-ischemic encephalopathy in areas of primary myelination: a neuroimaging and PET study

• Published in: Pediatric neurology Vol. 14; no. 2; pp. 108 - 116
• Main Authors: Azzarelli, Biagio, Caldemeyer, Karen S., Phillips, John P., DeMyer, William E.
• Format: Journal Article
• Language: English
• Published: New York, NY Elsevier Inc 01.02.1996; Elsevier
• Subjects: Adolescent; Biological and medical sciences; Brain Ischemia - diagnosis; Brain Ischemia - diagnostic imaging; Child; Child, Preschool; Female; Gestational Age; Humans; Hypoxia, Brain - diagnosis; Hypoxia, Brain - diagnostic imaging; Infant; Infant, Newborn; Magnetic Resonance Imaging; Male; Medical sciences; Myelin Sheath - physiology; Neurology; Tomography, Emission-Computed; Tomography, X-Ray Computed; Vascular diseases and vascular malformations of the nervous system; Radionuclide study; Human; Nervous system diseases; Oxygen; Cardiovascular disease; Exploration; Nuclear magnetic resonance imaging; Cerebral disorder; Vascular disease; Pathology; Myelination; Newborn; Ischemia; Central nervous system disease; Primary; Hypoxia; Cerebrovascular disease; Brain (vertebrata); Positron; Emission tomography
• ISSN: 0887-8994; 1873-5150
• DOI: 10.1016/0887-8994(96)00010-0

The stage of regional structural and biochemical development of the central nervous system appears as a critical factor determining the distribution of hypoxic-ischemic lesions during the perinatal period. We describe the brain lesions in 12 patients who suffered hypoxia-ischemia during the perinatal period. The gestational age ranged from 35 to 42 weeks and the age at death from 2 to 16 weeks. There is one patient alive at age 18 years and a second patient at age 1 year. The cerebral cortical damage is mainly restricted to areas of primary myelination and adjacent subcortical white matter. In addition, there is thalamic, basal ganglia, brainstem, and spinal cord damage. It is postulated that selective damage occurs in those areas which at the moment of the hypoxic-ischemic insult had achieved higher rates of oxygen-glucose utilization. This hypothesis is supported by studies utilizing positron emission tomography which indicates that glucose utilization in the normal human neonatal brain follows a phylogenetic order. Regions that achieved higher levels of glucose consumption are those that suffered the brunt of the damage in our term neonates.