Abstract
The neuroanatomic substrate of cognitive deficits in long-term survivors of prematurity with PVL is poorly understood. The thalamus is critically involved in cognition via extensive interconnections with the cerebral cortex. We hypothesized that the thalamus is atrophic (reduced in volume) in childhood survivors of prematurity with neuroimaging evidence of PVL and that the atrophy is associated with selective microstructural abnormalities within its subdivisions. We performed quantitative volumetric and DTI measurements of the thalamus in 17 children with neuroimaging evidence of PVL (mean postconceptional age, 5.6 ± 4.0 years) who were born prematurely and compared these with 74 term control children (5.7 ± 3.4 years). The major findings were the following: 1) a significant reduction in the overall volume of the thalamus in patients with PVL compared with controls (P < .0001), which also correlated with the severity of PVL (P = .001); 2) significantly decreased FA (P = .003) and increased λ(⊥) (P = .02) in the thalamus overall and increased axial, radial, and mean diffusivities in the pulvinar (P < .03), suggesting injury to afferent and efferent myelinated axons; and 3) a positive correlation of pulvinar abnormalities with those of the parieto-occipital white matter in periventricular leukomalacia, suggesting that the pulvinar abnormalities reflect secondary effects of damaged interconnections between the pulvinar and parieto-occipital cortices in the cognitive visual network. There are volumetric and microstructural abnormalities of the thalamus in preterm children with PVL, very likely reflecting neuronal loss and myelinated axonal injury. The selective microstructural damage in the pulvinar very likely contributes to abnormal cognitive visual processing known to occur in such survivors.
Highlights
MethodsWe performed quantitative volumetric and DTI measurements of the thalamus in 17 children with neuroimaging evidence of PVL (mean postconceptional age, 5.6 Ϯ 4.0 years) who were born prematurely and compared these with 74 term control children (5.7 Ϯ 3.4 years)
AND PURPOSE: The neuroanatomic substrate of cognitive deficits in long-term survivors of prematurity with PVL is poorly understood
The major findings were the following: 1) a significant reduction in the overall volume of the thalamus in patients with PVL compared with controls (P Ͻ .0001), which correlated with the severity of PVL (P ϭ .001); 2) significantly decreased FA (P ϭ .003) and increased Ќ (P ϭ .02) in the thalamus overall and increased axial, radial, and mean diffusivities in the pulvinar (P Ͻ .03), suggesting injury to afferent and efferent myelinated axons; and 3) a positive correlation of pulvinar abnormalities with those of the parieto-occipital white matter in periventricular leukomalacia, suggesting that the pulvinar abnormalities reflect secondary effects of damaged interconnections between the pulvinar and parieto-occipital cortices in the cognitive visual network
Summary
We performed quantitative volumetric and DTI measurements of the thalamus in 17 children with neuroimaging evidence of PVL (mean postconceptional age, 5.6 Ϯ 4.0 years) who were born prematurely and compared these with 74 term control children (5.7 Ϯ 3.4 years). Subjects The inclusion criteria for the preterm survivors with PVL were the following: 1) prematurity (Ͻ37 gestational weeks at birth), and 2) evidence of the sequelae of PVL on conventional MR imaging performed during childhood. These sequelae were defined as periventricular white matter volume loss and signal-intensity hyperintensities on FLAIR.[23] PVL was classified as mild, moderate, or severe on the basis of the degree of posterior lateral ventriculomegaly and the size and number of associated periventricular hyperintensities on T2/ FLAIR in the periatrial regions. The institutional review board at our medical center approved the study protocol
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