A male weighing 2790g was born at 35 weeks’ gestation. As a consequence of placental abruption, the infant was delivered by emergency Caesarean section in Okazaki City Hospital, Japan. His Apgar score was 5 at 5 minutes, and he was obtunded and hypotonic on admission. Artificial ventilation was performed for 6 days. His neurological findings normalized within a few hours of admission. Therapeutic hypothermia was performed for 72 hours following the standardized Japanese method.1 Electroencephalograms at 1, 7, and 15 days of life and serial cranial ultrasonography were normal. Brain magnetic resonance imaging (MRI) was performed using a 1.5T imager (GE Healthcare, Buckinghamshire, UK). Diffusion-weighted and T1-weighted images at 8 days of life showed scattered high-intensity lesions in the bilateral parietal white matter (Fig. 1a). Abnormal high signal intensity in the splenium of the corpus callosum was also seen, but no other abnormality was present. The apparent diffusion coefficient map showed reduced diffusivity in these lesions. All pulse sequences appeared normal at 16 days (Fig. 1b). At 18 months of age, T2-weighted imaging showed several small high-intensity lesions in the bilateral parietal white matter (Fig. 1c). The individual’s psychomotor development was normal at this time. His developmental quotient was normal, at 109 on the Kyoto Scale of Psychological Development, which is a standardized developmental test for infants in Japan (mean 100 [SD 10]). (a) Diffusion-weighted image (repetition time [TR]/echo time [TE]=5200/86ms) at 8 days of life. Several small high-intensity lesions are visible in the bilateral parietal white matter (arrows). (b) Diffusion-weighted image (TR/TE=5600/85ms) at 16 days of life. No abnormal intensity is seen. (c) T2-weighted image (TR/TE=4016/85ms) at 18 months of age. Several small high-intensity lesions are visible in the bilateral parietal white matter (arrows). Punctate white matter lesions were recently demonstrated as small, abnormal intensities in the white matter on MRI in term- or late preterm-born infants with hypoxic–ischaemic encephalopathy.2,3 To our knowledge, however, changes in these lesions over time have not been documented. In the individual described here, the punctate white matter lesions showed pseudonormalization and later gliosis on MRI at 18 months of age.