A common pattern of hypoxic-ischemic cerebral injury in the term newborn involves predominantly cerebral cortex and subcortical white matter. We describe 20 term newborns with moderate or severe acute hypoxic-ischemic encephalopathy who exhibit a different pattern of abnormalities on computed tomography, with evidence of decreased tissue attenuation predominantly in thalami and basal ganglia and relative preservation of cerebral cortex and white matter. Profound, acute hypoxic-ischemic insult (eg, umbilical cord prolapse, uterine rupture, or massive placental abruption) was documented in 16 of 20 infants (80%). Characteristic clinical features during the newborn period included irritability, tonic posturing of limbs, and persistent lower cranial nerve dysfunction, often with prominent tongue fasciculations. This pattern of central injury appears to be highly predictive of poor outcome; 7 newborns (35%) died, and all survivors who had follow-up to 18 months of age (11) had major neurological sequelae (eg, spastic quadriplegia, choreoathetosis, and persistent feeding problems). This pattern of hypoxic-ischemic cerebral injury corresponds closely to experimental animal models of "acute total" perinatal asphyxia.

No abstract

White matter injury (WMI) is the characteristic pattern of brain injury detected on magnetic resonance imaging in the premature newborn. Focal noncystic WMI is increasingly recognized in populations of term newborns. The aim of this study was to describe the occurrence of focal noncystic WMI in a cohort of 48 term newborns with encephalopathy studied with magnetic resonance imaging at 72 Ϯ 12 h of life, and to identify clinical risk factors for this pattern of injury. Eleven newborns (23%; 95% CI 11-35) were found to have WMI (four minimal, three moderate, and four severe). In 10 of the 11 newborns, the WMI was associated with restricted diffusion on apparent diffusion coefficient maps. An increasing severity of WMI was associated with lower gestational age at birth (p ϭ 0.05), but not lower birth weight. Newborns with WMI had milder encephalopathy and fewer clinical seizures relative to other newborns in the cohort. Other brain injuries were seen in three of the 11 newborns: basal nuclei predominant pattern of injury in one and cortical strokes in two. These findings suggest that WMI in the term newborn is acquired near birth and that the state of brain maturation is an important determinant of this pattern of brain injury. injury (WMI) with characteristic topography that is well-recognized by cranial ultrasound in premature newborns (1,2). The increasing use of early-life magnetic resonance imaging (MRI) has revealed a spectrum of WMI that includes focal noncystic WMI (1,3,4). WMI is increasingly recognized as the most prevalent pattern of brain injury in the premature newborn (3,5,6). The severity of WMI in premature newborns is a predictor of adverse neurodevelopmental outcome (3,7). Recent studies suggest that the vulnerability of the premature newborn to WMI relates to the vulnerability of specific developmentally regulated cell populations prevalent in the white matter in the early-mid third trimester of gestation: e.g. late oligodendrocyte progenitor cells and subplate neurons (8 -11).However, WMI does not occur exclusively in premature newborns, and is increasingly recognized in some populations of term newborns. Term newborns with congenital heart disease (CHD) seem to be at particularly high risk of WMI, perhaps due to impairments in in utero brain development (12-15). Recent in vivo data suggest that newborns with CHD have delayed brain development before cardiac surgery, possibly as a result of impaired cerebral oxygen delivery in utero (15). WMI is also recognized in the setting of term neonatal encephalopathy (NE). In a series of postmortem examinations of term newborns with NE, three of 21 newborns (14%) had small foci of established gliosis in the periventricular white matter, in addition to evidence of acute hypoxic-ischemic lesions (16). In newborns with basal ganglia injury in the context of NE, white matter damage is seen on MRI in nearly one half of the cases (17,18). However, the timing of injury and risk factors for WMI in term newborns with NE remain largely unknown.The aim of ...

No abstract