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AJNR - American Journal of Neuroradiology

Published ahead of print on January 8, 2009
doi: 10.3174/ajnr.A1399

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American Journal of Neuroradiology 30:623-628, March 2009
© 2009 American Society of Neuroradiology

PEDIATRICS

Abnormal White Matter Signal on MR Imaging Is Related to Abnormal Tissue Microstructure

J.L.Y. Cheong^a,b,c, D.K. Thompson^d, H.X. Wang^d, R.W. Hunt^a,b,e, P.J. Anderson^a,f, T.E. Inder^a,b,e,g and L.W. Doyle^a,b,c

^a Victorian Infant Brain Studies, Murdoch Children's Research Institute, Parkville, Australia
^b Royal Women's Hospital Melbourne, Parkville, Australia
^c Department of Obstetrics and Gynecology, Parkville, Australia
^d University of Melbourne, Howard Florey Institute, Parkville, Australia
^e Royal Children's Hospital, Melbourne, Australia
^f Department of Psychology, University of Melbourne, Melbourne, Australia
^g St. Louis Children's Hospital, Washington University, St Louis, Mo

Please address correspondence to J.L.Y. Cheong, Level 7, Newborn Research, Royal Women's Hospital, 20 Flemington Rd, Parkville, Vic 3052, Australia; e-mail: jeanie.cheong{at}thewomens.org.au

BACKGROUND AND PURPOSE: White matter signal-intensity abnormalities (WMSA) on MR imaging are related to adverse neurodevelopmental outcome in extremely preterm infants. Diffusion tensor imaging (DTI) may detect alterations in cerebral white matter microstructure and thus may help confirm the pathologic basis of WMSA. This study aimed to relate regional DTI measures with severity of WMSA in very preterm infants.

MATERIALS AND METHODS: One hundred eleven preterm infants (birth weight, <1250 g and/or gestational age, <30 weeks) were scanned at term-equivalent age (1.5T). WMSA were classified as normal, focal, or extensive. Apparent diffusion coefficient (ADC), fractional anisotropy (FA), axial (1), and radial ([2 + 3]/2) diffusivity were calculated in 12 regions of interest placed in the bilateral posterior limbs of the internal capsule, frontal (superior and inferior), sensorimotor, and occipital (superior and inferior) white matter regions. Data were compared by using 1-way analysis of variance, with a Bonferroni correction for multiple comparisons.

RESULTS: Thirty-nine infants had normal, 59 infants had focal, and 13 infants had extensive WMSA. Compared with infants with normal or focal WMSA, infants with extensive WMSA had significantly lower FA in the internal capsule (P < .001), right inferior frontal regions (P < .05), and right superior occipital regions (P = .01); and higher radial diffusivity in the right internal capsule (P = .005), bilateral sensorimotor (P < .05), and right superior occipital regions (P < .05). Compared with infants with normal WMSA, infants with extensive WMSA had significantly higher ADC in bilateral sensorimotor regions (P < .01) and right superior occipital regions (P = .01), and lower axial diffusivity in the bilateral sensorimotor regions (P < .05).

CONCLUSIONS: There are significant region-specific changes in ADC, FA, radial diffusivity, and axial diffusivity in preterm infants with extensive WMSA. Altered radial diffusivity was most prominent. This implies that disrupted premyelinating oligodendroglia is the major correlate with extensive WMSA rather than axonal pathology.