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Neuropathology Associated With Diffuse Excessive High Signal Intensity Abnormalities on Magnetic Resonance Imaging in
Nehal A Parikh1, Christopher R Pierson2, Jerome A Rusin3
1Cincinnati Children's Hospital, The Perinatal Institute, Cincinnati, Ohio; Department of Pediatrics, Ohio State University College of Medicine, Columbus, Ohio.
Insights
Diffuse excessive high signal intensity on MRI in extremely preterm infants may indicate distinct pathology. This finding shows unique microscopic features different from periventricular leukomalacia.
Area of Science:
- Neonatal neurology
- Neuroimaging
- Developmental neuroscience
Background:
- Diffuse excessive high signal intensity (DEHSI) is common on MRI in extremely preterm infants.
- Its clinical significance is debated due to limited imaging-pathology correlation studies.
Observation:
- Two preterm infants (24-week gestation) with DEHSI showed distinct pathology at autopsy.
- Compared to periventricular leukomalacia (PVL) and controls, DEHSI brains had vacuolated regions, increased reactive astrocytes/microglia, and reduced axons/oligodendroglia.
Findings:
- DEHSI brains exhibited unique pathological characteristics, overlapping but distinct from PVL.
- Microscopic analysis revealed reactive gliosis, myelin and axon loss in DEHSI, differing from PVL necrosis.
Implications:
- This study provides crucial imaging-pathology correlation for DEHSI in extremely preterm infants.
- Understanding DEHSI pathology can improve neurodevelopmental outcome prediction and inform therapeutic strategies.
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.
Patient 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.
