Abstract

Infants born prematurely are at risk for a perinatal encephalopathy characterized by white and gray matter injuries that affect subsequent cortical development and neural connectivity and potentially increase risk for later psychiatric disorder. To determine the relation of perinatal brain injury, as detected by neonatal head ultrasound, to psychiatric disorders in adolescents who were born prematurely. Prospective cohort. Community. Adolescent survivors of a population-based low-birth-weight (<2000 g; 96% preterm; born 1984-1987) cohort (n=1105) screened as neonates with serial head ultrasounds. Neonatal head ultrasound abnormalities were categorized as either (1) germinal matrix and/or intraventricular hemorrhage or (2) parenchymal lesions and/or ventricular enlargement. Of 862 eligible survivors, 628 (72.9%) were assessed at age 16 years. The sample consisted of 458 nondisabled survivors assessed in person. Main Outcome Measure Adolescent current and lifetime psychiatric disorders assessed with parent report on the Diagnostic Interview Schedule for Children-IV. Compared with no abnormality, germinal matrix/intraventricular hemorrhage increased risk for current major depressive disorder (odds ratio, 2.7; 95% confidence interval, 1.0-6.8) and obsessive-compulsive disorder (9.5; 3.0-30.1). Parenchymal lesions/ventricular enlargement increased risk for current attention-deficit/hyperactivity disorder-inattentive type (odds ratio, 7.6; 95% confidence interval, 2.0-26.5), tic disorders (8.4; 2.4-29.6), and obsessive-compulsive disorder (7.6; 1.39-42.0). Parenchymal lesions/ventricular enlargement were not related to lifetime attention-deficit/hyperactivity disorder-inattentive type, but all other relations were similar for lifetime disorders. Control for other early risk factors did not alter these relations. Most of these relations persisted with control for concurrent cognitive or motor problems. In preterm infants, 2 distinct types of perinatal brain injury detectable with neonatal head ultrasound selectively increase risk in adolescence for psychiatric disorders in which dysfunction of subcortical-cortical circuits has been implicated.

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