Patterns of brain injury in term neonatal encephalopathy
Received 6 July 2004; received in revised form 27 October 2004; accepted 9 December 2004.
Objectives
To determine whether the pattern of brain injury in term neonatal encephalopathy is associated with distinct prenatal and perinatal factors and to determine whether the pattern of injury is associated with 30-month neurodevelopmental outcome.
Study design
A total of 173 term newborns with neonatal encephalopathy from 2 centers underwent magnetic resonance imaging (MRI) at a median of 6 days of age (range, 1-24 days). Patterns of injury on MRI were defined on the basis of the predominant site of injury: watershed predominant, basal ganglia/thalamus predominant, and normal.
Results
The watershed pattern of injury was seen in 78 newborns (45%), the basal ganglia/thalamus pattern was seen in 44 newborns (25%), and normal MRI studies were seen in 51 newborns (30%). Antenatal conditions such as maternal substance use, gestational diabetes, premature rupture of membranes, pre-eclampsia, and intra-uterine growth restriction did not differ across patterns. The basal ganglia/thalamus pattern was associated with more severe neonatal signs, including more intensive resuscitation at birth (P=.001), more severe encephalopathy (P=.0001), and more severe seizures (P=.0001). The basal ganglia/thalamus pattern was associated with the most impaired motor and cognitive outcome at 30 months.
Conclusion
The patterns of brain injury in term neonatal encephalopathy are associated with different clinical presentations and neurodevelopmental outcomes. Measured prenatal risk factors did not predict the pattern of brain injury.
From the Departments of Neurology, Pediatrics, Radiology, and Biostatistics, University of California at San Francisco, San Francisco, California; and the Departments of Pediatrics and Radiology, Loma Linda University Children's Hospital, Loma Linda, California
Reprint requests: Dr Donna M. Ferriero, Professor of Neurology and Pediatrics, University of California at San Francisco, 521 Parnassus Ave, Room C-215, San Francisco, CA 94143-0663.
Supported by the National Center for Research Resources (5 M01 RR-01271), US Public Health Service, and by the National Institutes of Health (NS35902). Dr Miller is supported by the Canadian Institutes of Health Research. Mr Ramaswamy was supported by the American Pediatric Society - Society for Pediatric Research summer research program (NIH grant HD007446).
ABSTRACT