Ps. Huppi et al., Microstructural brain development after perinatal cerebral white matter injury assessed by diffusion tensor magnetic resonance imaging, PEDIATRICS, 107(3), 2001, pp. 455-460
Objective. Brain injury in premature infants is characterized predominantly
by perinatally acquired lesions in the cerebral white matter (WM). The imp
act of such injury on the subsequent development of cerebral WM is not clea
r. This study uses diffusion tensor magnetic resonance imaging (MRI) to eva
luate the effects of cerebral WM injury on subsequent microstructural brain
development in different WM areas of the brain.
Methods. Twenty premature infants (gestational age: 29.1 +/- 1.9 weeks) wer
e studied by conventional MRI within the first 3 weeks of life and again at
term, with the addition at the latter time of diffusion tensor MRI. Ten of
the preterm infants had cerebral WM injury identified by the early MRI and
were matched with 10 premature infants of similar gestational age and neon
atal course but with normal neonatal MRI scans. Diffusion tensor MRI at ter
m was acquired in coronal and axial planes and used to determine the appare
nt diffusion coefficient, a measure of overall restriction to water diffusi
on, and the relative anisotropy (RA), a measure of preferred directionality
of diffusion, in central WM, anterior frontal WM, occipital WM, temporal W
M, and the posterior limb of the internal capsule. Diffusion vector maps we
re generated from the diffusion tensor analysis to define the microstructur
al architecture of the cerebral WM regions.
Results. At term, the diffusion tensor MRI revealed no difference in appare
nt diffusion coefficient among preterm infants with or without perinatal WM
lesions. By contrast, RA, the measure of preferred directionality of diffu
sion and thereby dependent on development of axonal fibers and oligodendrog
lia, was 25% lower in central WM, the principal site of the original WM inj
ury. However, RA was unaffected in relatively uninjured WM areas, such as t
emporal, anterior frontal, and occipital regions. Notably, RA values in the
internal capsule, which contains fibers that descend from the injured cere
bral WM, were 20% lower in the infants with WM injury versus those without.
Diffusion vector maps showed striking alterations in the size, orientation
, and organization of fiber tracts in central WM and in those descending to
the internal capsule.
Conclusions. Perinatal cerebral WM injury seems to have major deleterious e
ffects on subsequent development of fiber tracts both in the cerebral WM an
d more distally. The ultimate impact of brain injury in the newborn should
be considered as a function not only of tissue destruction, but also of imp
aired subsequent brain development.