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Neuropathology Associated With Diffuse Excessive High Signal Intensity Abnormalities on Magnetic Resonance Imaging in Very Preterm Infants
Abstract Background Diffuse excessive high signal intensity abnormality is the most common finding on term-equivalent age magnetic resonance imaging in extremely preterm infants. Yet its clinical significance remains a matter of debate, in part because of a lack of prior imaging–pathology correlatio...
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Published in: | Pediatric neurology 2016-12, Vol.65, p.78-85 |
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Main Authors: | , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Abstract Background Diffuse excessive high signal intensity abnormality is the most common finding on term-equivalent age magnetic resonance imaging in extremely preterm infants. Yet its clinical significance remains a matter of debate, in part because of a lack of prior imaging–pathology correlational studies. Case Presentations We present two 24-week-gestation infants with complicated clinical courses who died at 33 and 46 weeks postmenstrual age with magnetic resonance imaging evidence of diffuse excessive high signal intensity. Two patients with periventricular leukomalacia and two without injury were examined for comparison. Immunohistochemistry characterized the presence of reactive astrocytes, microglia, myelin, and axons. Infants with periventricular leukomalacia demonstrated the typical microscopic necrosis with spheroids, gliosis/microgliosis with reduction in stainable myelin and axons. Infants with diffuse excessive high signal intensity showed vacuolated regions with increased reactive astrocytes and microglia and fewer oligodendroglial cell bodies/processes and dramatic reduction in axon number. Conclusion These two individuals with diffuse excessive high signal intensity exhibited pathologic characteristics that were overlapping but distinct from those of periventricular leukomalacia. |
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ISSN: | 0887-8994 1873-5150 |
DOI: | 10.1016/j.pediatrneurol.2016.07.006 |