BACKGROUND AND PURPOSE: Research into memory deficits associated with hypoxic-ischemic encephalopathy has typically focused on the hippocampus, but there is emerging evidence that the medial diencephalon may also be compromised. We hypothesized that mammillary body damage occurs in perinatal asphyxia, potentially resulting in mammillary body atrophy and subsequent memory impairment. MATERIALS AND METHODS: We retrospectively reviewed brain MRIs of 235 clinically confirmed full-term patients with hypoxic-ischemic encephalopathy acquired at a single center during 2004?2017. MRIs were performed within 10 days of birth (median, 6; interquartile range, 2). Two radiologists independently assessed the mammillary bodies for abnormal signal on T2-weighted and DWI sequences. Follow-up MRIs were available for 9 patients; these were examined for evidence of mammillary body and hippocampal atrophy. RESULTS: In 31 neonates (13.2%), abnormal high mammillary body signal was seen on T2-weighted sequences, 4 with mild, 25 with moderate, and 2 with severe hypoxic-ischemic encephalopathy. In addition, restricted diffusion was seen in 6 neonates who had MR imaging between days 5 and 7. For these 31 neonates, the most common MR imaging pattern (41.9%) was abnormal signal restricted to the mammillary bodies with the rest of the brain appearing normal. Follow-up MRIs were available for 9 patients: 8 acquired between 3 and 19 months and 1 acquired at 7.5 years. There was mammillary body atrophy in 8 of the 9 follow-up MRIs. CONCLUSIONS: Approximately 13% of full-term infants with hypoxic-ischemic encephalopathy showed abnormal high mammillary body signal on T2-weighted images during the acute phase, which progressed to mammillary body atrophy in all but 1 of the infants who had follow-up MR imaging. This mammillary body involvement does not appear to be related to the severity of encephalopathy, MR imaging patterns of hypoxic-ischemic encephalopathy, or pathology elsewhere in the brain.
机构:
George Washington Univ, Dept Newborn Serv, Washington, DC 20037 USA
Childrens Natl Med Ctr, Washington, DC 20037 USAGeorge Washington Univ, Dept Newborn Serv, Washington, DC 20037 USA
Aly, Hany
Hassanein, Sahar
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Ain Shams Univ, Dept Pediat, Fac Med, Cairo, EgyptGeorge Washington Univ, Dept Newborn Serv, Washington, DC 20037 USA
Hassanein, Sahar
Nada, Ayman
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Ain Shams Univ, Inst Post Grad Childhood Studies, Cairo, EgyptGeorge Washington Univ, Dept Newborn Serv, Washington, DC 20037 USA
Nada, Ayman
Mohamed, Maha H.
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Ain Shams Univ, Dept Pediat, Fac Med, Cairo, EgyptGeorge Washington Univ, Dept Newborn Serv, Washington, DC 20037 USA
Mohamed, Maha H.
Atef, Shereen H.
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Ain Shams Univ, Dept Clin Pathol, Fac Med, Cairo, EgyptGeorge Washington Univ, Dept Newborn Serv, Washington, DC 20037 USA
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Univ Catania, Dept Drug Sci, Catania, ItalyMaastricht Univ, Sch Mental Hlth & Neurosci MHeNS, Dept Neurophysiol, Div Neurosci, NL-6202 AZ Maastricht, Netherlands
Li Volti, G.
Martinez-Martinez, P.
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Maastricht Univ, Sch Mental Hlth & Neurosci MHeNS, Dept Neurophysiol, Div Neurosci, NL-6202 AZ Maastricht, NetherlandsMaastricht Univ, Sch Mental Hlth & Neurosci MHeNS, Dept Neurophysiol, Div Neurosci, NL-6202 AZ Maastricht, Netherlands
Martinez-Martinez, P.
Kramer, B. W.
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Maastricht Univ, Sch Mental Hlth & Neurosci MHeNS, Dept Neurophysiol, Div Neurosci, NL-6202 AZ Maastricht, Netherlands
Maastricht Univ, Med Ctr, Dept Pediat, Div Neonatol, NL-6202 AZ Maastricht, Netherlands
Maastricht Univ, Sch Oncol & Dev Biol Maastricht GROW, NL-6202 AZ Maastricht, NetherlandsMaastricht Univ, Sch Mental Hlth & Neurosci MHeNS, Dept Neurophysiol, Div Neurosci, NL-6202 AZ Maastricht, Netherlands
Kramer, B. W.
Gavilanes, A. W. D.
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Maastricht Univ, Sch Mental Hlth & Neurosci MHeNS, Dept Neurophysiol, Div Neurosci, NL-6202 AZ Maastricht, Netherlands
Maastricht Univ, Med Ctr, Dept Pediat, Div Neonatol, NL-6202 AZ Maastricht, NetherlandsMaastricht Univ, Sch Mental Hlth & Neurosci MHeNS, Dept Neurophysiol, Div Neurosci, NL-6202 AZ Maastricht, Netherlands