Signal Change in the Mammillary Bodies after Perinatal Asphyxia.

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.