Hypoglossal hypoplasia and hyperplasia of the area postrema following perinatal hypoxic brain damage
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Updated: Jun 17, 2026

Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats
Published on: November 20, 2015
Sachiko Kanda1, Makiko Saito, Masaharu Hayashi
1Department of Pediatrics, Tokyo Metropolitan Fuchu Medical Center for the Disabled, Tokyo, Japan. ktakesachik-tky@umin.ac.jp
Abstract:
We report here an autopsy case of perinatal hypoxic brain damage showing hypoglossal hypoplasia and hyperplasia of the area postrema (AP) in the medulla oblongata. A 16-year-old girl who suffered from severe psychomotor developmental delay, epilepsy and tongue fasciculation, was shown by pathology to have a medullary change, as well as tongue atrophy and severe sclerotic changes in the cerebrum and cerebellum. Moderate to severe neuronal loss and gliosis were found in the brainstem. But neurons were preserved in the trigeminal nuclei, abducens nucleus and dorsal vagal nucleus. We performed a preliminary immunohistochemical analysis of sections of the medulla oblongata in our case, normal controls and disease controls with perinatal hypoxic ischemic encephalopathy (HIE). The normal and disease controls showed neither hypoglossal hypoplasia nor AP hyperplasia. The combination of hypoglossal hypoplasia and AP hyperplasia is unique and intriguing, and further analysis of the AP is required to understand developmental brain disorders.
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