Cerebellar Vermian Atrophy after Neonatal Hypoxic-Ischemic Encephalopathy
Michael A. Sargenta,
Kenneth J. Poskitta,
Elke H. Rolandc,
Alan Hillc and
Glenda Hendsonb
a Department of Radiology, British Columbia’s Children’s Hospital, Vancouver, British Columbia, Canada
b Department of Pathology, British Columbia’s Children’s Hospital, Vancouver, British Columbia, Canada
c Division of Neurology, British Columbia’s Children’s Hospital, Vancouver, British Columbia, Canada
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FIG 1. Schematic diagram shows frequency of vermian atrophy in children after neonatal hypoxic-ischemic encephalopathy with thalamic edema.
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FIG 2. Axial view CT scan obtained through the posterior fossa in a 10-month-old female infant (patient 3), who was born before arrival at the hospital, shows focal hypoattenuation in the superior vermis (arrow). The thalami were small but with normal attenuation (not shown). This patient had thalamic edema with normal cortex shown by neonatal CT.
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FIG 3. Axial view T2-weighted fast spin-echo (3555/112) image obtained through the posterior fossa in a 5-month-old male infant (patient 2), who was born after uterine rupture, shows hyperintensity in the cerebellar vermis immediately behind the fourth ventricle (arrow). Neonatal CT performed on day 3 showed abnormal thalami with normal cortex, whereas MR imaging performed on day 17 showed signal intensity abnormalities in the thalami, hippocampus, and rolandic cortex.
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FIG 4. Coronal view T2-weighted fast spin-echo (6480/96) MR image of a 20-month-old boy (patient 5) shows hyperintensity with volume loss in the superior cerebellar vermis (arrow). This child had thalamic edema with normal cortex shown by neonatal CT. Other images in this follow-up study showed symmetrical hyperintensity of the ventrolateral thalami, posterior lentiform nuclei, and periventricular white matter extending to the rolandic cortex but with normal cortical gray matter.
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FIG 5. Midsagittal view T1-weighted (600/10) MR image of the same patient shown in Figure 2 shows volume loss centrally in the cerebellar vermis. Other findings included abnormal lentiform nuclei, signal intensity changes in the thalami, and white matter with mild atrophy of the rolandic cortex. In the midsagittal view, the corpus callosum appears thin.
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FIG 6. Cerebellar vermis of an asphyxiated twin born after cord prolapse. CT performed on day 3 showed thalamic edema without cortical involvement. The neonate died at 16 days old. Photomicrograph of the cerebellum shows loss of Purkinje cells and proliferation of Bergmann glia (arrowhead) (hematoxylin and eosin stain; original magnification, x100).
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