Automatically quantified diffuse excessive high signal intensity on MRI predicts cognitive development in preterm infants.

BACKGROUND: Cognitive and language impairments constitute the majority of disabilities observed in preterm infants. It remains unclear if diffuse excessive high signal intensity on magnetic resonance imaging at term represents delayed white matter maturation or pathology. METHODS: We hypothesized that diffusion tensor imaging-based objectively quantified diffuse excessive high signal intensity measures at term will be strong predictors of cognitive and language development at 2 years in a cohort of 41 extremely low birth weight (≤1000 g) infants. Using an automated probabilistic atlas, mean diffusivity maps were used to objectively segment and quantify diffuse excessive high signal intensity volume and mean, axial, and radial diffusivity measures. Standardized neurodevelopment was assessed at 2 years of age using the Bayley Scales of Infant Development, third edition. RESULTS: Thirty-six of the 41 infants (88%) had complete developmental data at follow-up. Objectively quantified diffuse excessive high signal intensity volume correlated significantly with cognitive and language scores at 2 years (P < 0.001 for both). The sum values of the three diffusivity measures in detected diffuse excessive high signal intensity regions also correlated significantly with the Bayley scores (r(2) 34.7%; P < 0.001 for each). Infants in the highest quartile for diffuse excessive high signal intensity volumes had scores between 19 and 24 points lower than infants in the lowest quartile (P < 0.01). When diagnosed subjectively by neuroradiologists however, Bayley scores were not significantly lower in infants with extensive diffuse excessive high signal intensity. CONCLUSIONS: These findings lend further evidence that diffuse excessive high signal intensity is pathologic and that objectively quantified diffusion-based diffuse excessive high signal intensity volume at term is associated with cognitive and language impairments. Our approach could be used for risk stratification and early intervention for such high-risk extremely preterm infants.

Postnatal dexamethasone therapy and cerebral tissue volumes in extremely low birth weight infants.

OBJECTIVE: Our goal was to relate postnatal dexamethasone therapy in extremely low birth weight infants (birth weight of < or = 1000 g) to their total and regional brain volumes, as measured by volumetric MRI performed at term-equivalent age. METHODS: Among 53 extremely low birth weight infants discharged between June 1 and December 31, 2003, 41 had high-quality MRI studies; 30 of those infants had not received postnatal steroid treatment and 11 had received dexamethasone, all after postnatal age of 28 days, for a mean duration of 6.8 days and a mean cumulative dose of 2.8 mg/kg. Anatomic brain MRI scans obtained at 39.5 weeks (mean) postmenstrual age were segmented by using semiautomated and manual, pretested, scoring algorithms to generate three-dimensional cerebral component volumes. Volumes were adjusted according to postmenstrual age at MRI. RESULTS: After controlling for postmenstrual age at MRI, we observed a 10.2% smaller total cerebral tissue volume in the dexamethasone-treated group, compared with the untreated group. Cortical tissue volume was 8.7% smaller in the treated infants, compared with untreated infants. Regional volume analysis revealed a 20.6% smaller cerebellum and a 19.9% reduction in subcortical gray matter in the dexamethasone-treated infants, compared with untreated infants. In a series of regression analyses, the reductions in total cerebral tissue, subcortical gray matter, and cerebellar volumes associated with dexamethasone administration remained significant after controlling not only for postmenstrual age but also for bronchopulmonary dysplasia and birth weight. CONCLUSIONS: We identified smaller total and regional cerebral tissue volumes in extremely low birth weight infants treated with relatively conservative regimens of dexamethasone. These volume deficits may be the structural antecedents of neuromotor and cognitive abnormalities reported after postnatal dexamethasone treatment.