Relationship between MR Imaging and Histopathologic Findings of the Brain in Extremely Sick Preterm Infants
Ursula Felderhoff-Muesera,
Mary A. Rutherforda,
Waney V. Squiera,
Philip Coxa,
Elia F. Maaloufa,
Serena J. Counsella,
Graeme M. Byddera and
A. David Edwards,a
a From the Department of Pediatrics (U.F-M., M.A.R., E.F.M., A.D.E.), The Robert Steiner Magnetic Resonance Unit (M.A.R., S.J.C., G.M.B.), and the Department of Histopathology (P.C.), Imperial College School of Medicine, Hammersmith Hospital, London; and the Department of Neuropathology, Radcliffe/Infirmary, Oxford (W.V.S.).
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FIG 1. Preterm infant of 26 weeks' (+3 days) gestation (case 6) at age 3 weeks.
A, T2-weighted (3500/208) FSE MR sequence shows the anterior cap within the periventricular white matter as high signal intensity (arrow) with a medial low signal component. There are abnormal low signal intensities within the globus pallidus and thalamus.
B, T2-weighted (3500/32/950) IR FSE sequence shows the anterior cap within the periventricular white matter as an area of low signal intensity (arrow) with a high-signal medial component. There are abnormal high signal intensities within the globus pallidus, putamen, and thalamus. The posterior limb of the internal capsule is seen as very low signal intensity.
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FIG 2. T2-weighted (3500/208) FSE sequence in preterm infant (not in study) of 26 weeks' gestation at age 5 weeks shows normal appearance of the corpus callosum (arrowhead) in the posterior periventricular white matter (arrow). FIG 3. T2-weighted (3500/208) FSE sequence in preterm infant of 24 weeks' (+4 days) gestation (case 7) at age 2 days shows the intermediate layer of white matter as low signal intensity (arrow). There are bilateral low signal intensity germinal layer hemorrhages
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FIG 4. Preterm infant of 23 weeks' (+6 days) gestation (case 3) at age 3 weeks.
A, T2-weighted (3500/208) FSE sequence shows a large intraventricular hemorrhage with fan-shaped parenchymal involvement. The perihemorrhagic white matter is of very high signal intensity (arrow).
B, Histologic section shows intraventricular hemorrhage. A zone of venous infarction radiates out into the white matter from the site of bleeding (arrow in center of infarct). Relatively normal white matter is seen to the left of the picture (arrowhead). The infarcted area is very pale owing to tissue loss (hematoxylin-eosin, original magnification x22.5).
C, Higher-magnification histologic section of the venous infarction shows very congested capillaries. The adjacent tissue contains many large macrophages with ingested red cells (arrows). There are few free red cells. The tissue shows early cystic breakdown (hematoxylin-eosin, original magnification x360).
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FIG 5. Postmortem T2-weighted (3500/208) FSE sequence in preterm infant of 2 weeks' (+5 days) gestation (case 4) shows bilateral abnormal signal intensity within the posterior periventricular white matter and a low signal intensity hemorrhagic component on the right
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FIG 6. Preterm infant of 28 weeks' gestation (case 2) at age 4 weeks.
A, T1-weighted (600/20) SE sequence shows abnormal high signal intensity within the posterior putamen (arrowhead), globus pallidus (long arrow) on the right, and lateral thalamus (short arrow). The posterior limb of the internal capsule is of uniform low signal intensity. There is an artifact of uncertain origin over the right insula cortex.
B, High-power histologic section of damaged deep gray matter shows that the posterior limb of the internal capsule is edematous (arrowhead). The adjacent globus pallidus is darkly stained owing to capillary proliferation and mineralization of dead neurons (short arrow). The posterior part of the putamen is pale as a result of extensive tissue loss (long arrow) (hematoxylin-eosin, original magnification x 22.5).
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