1043-3155 Pediatr Neurol Briefs pedneurbriefs Pediatr Neurol Briefs Pediatric Neurology Briefs Pediatr Neurol Briefs 2166-6482 1043-3155 2166-3155 Pediatric Neurology Briefs Publishers Chicago, IL, USA PNB-12-41 10.15844/pedneurbriefs-12-6-1 Neonatal Disorders Neurology Pediatrics Nervous System Diseases Child Development Brain Diseases Neurosurgery Child Infant Acute Intrauterine Asphyxial Encephalopathy http://orcid.org/0000-0002-0173-7931 Millichap J. Gordon MD 1 2 * Division of Neurology, Children's Memorial Hospital, Chicago, IL Departments of Pediatrics and Neurology, Northwestern University Feinberg School of Medicine, Chicago, IL Correspondence: Dr. J. Gordon Millichap, E-mail: jgmillichap@northwestern.edu 06 1998 01 05 2016 12 6 41 42 Copyright: © 1998 The Author(s) 1998 This work is licensed under the Creative Commons Attribution 4.0 International License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The syndrome of acute near-total intrauterine asphyxia in the term infant

A clinical-imaging syndrome of acute near-total intrauterine asphyxia is described in 11 term infants followed at Evanston Hospital, and Northwestern University Medical School, Chicago, IL.

 Clinical-Imaging Syndrome Neonatal Encephalopathy Basal Ganglia

A clinical-imaging syndrome of acute near-total intrauterine asphyxia is described in 11 term infants followed at Evanston Hospital, and Northwestern University Medical School, Chicago, IL. Neonatal encephalopathy with signs of brainstem dysfunction were severe in 4 patients and moderate in 7. Development of cognitive function and head size were unaffected in the less severe cases. Brain imaging showed lesions in the thalamus, basal ganglia, and brainstem, with sparing of the cerebral cortex and white matter. Systemic organs showed only subtle signs of injury. The pattern of distribution of injuries correlated with the metabolic rates of the organs involved. The brain and especially subcortical nuclei, tissues with higher metabolic rates, sustained greater damage than nonbrain organs having lower metabolic needs. This acute syndrome is in contrast to a more chronic, less severe intrauterine asphyxia in which the cerebral hemispheres and other organs are more vulverable. [1]

COMMENT. Correlation of brainstem nuclear pathology with rates of tissue metabolism and blood flow has been demonstrated in monkey fetuses exposed to total asphyxia for varying time periods. Those exposed for 18 min showed a more widespread brain injury than fetuses exposed for 15 min. Structures with the highest blood flow rates are most vulnerable. Depression of brain metabolism by barbiturates or hypothermia extends the duration of brain tolerance to effects of asphyxia. Selective brainstem damage occurs after acute total asphyxia whereas the cerebral cortex and subcortical white matter are predominantly affected by prolonged partial asphyxia (Gluck L. (ed) Intrauterine Asphyxia and the Developing Brain. Chicago, Year Book Publ, 1977;p45).

The above NW University clinical study, correlating neurological signs with brain imaging abnormalities, supports previous laboratory findings, and demonstrates the brain stem dysfunction typical of an acute, in contrast to more prolonged, intrauterine asphyxia in the term infant. According to Volpe JJ (Neurology of the Newborn, 2nd ed, Philadelphia, Saunders, 1987), the localization of hypoxic-ischemic encephalopathy in the infant is generally more diffuse than in asphyxiated animals, and selective brainstem injury is rare and frequently fatal. (See Progress in Pediatric Neurology I. PNB Publishers, 1991;p334).

Pasternak JF Gorey MT The syndrome of acute near-total intrauterine asphyxia in the term infant Pediatr Neurol 1998 May 18 5 391 8 9650677 10.1016/S0887-8994(98)00002-2