[Clinical evaluation by MRI on the newborn infants with hypoglycemic brain damage]

Severe and persistent hypoglycemia often leads to brain damage in neonatal period although precise definition of hypoglycemia remains controversial. Little is known whether hypoglycemic brain damage happens to the neonates with hypoglycemic symptoms in early neonatal period and no criteria to diagnose the hypoglycemic brain damage are available. The present study aimed to characterize the clinical symptoms and brain damage by MRI diffusion-weighed imaging in the newborn infants with severe hypoglycemia in order to demonstrate the early findings of their brain damage.

The 6 newborn infants with severe hypoglycemia (whole blood glucose ranging from 0.48 to 1.7 mmol/L) were enrolled in this study, 3 of them were premature infants, 2 were small-for-gestational age infants and 1 was an infant born to a diabetic mother. These infants had a gestational age from 35 to 40 weeks and birth weight from 1545 g to 3900 g. They had no history of perinatal asphyxia, findings indicating sepsis, intracranial infection, inborn error of metabolism or endocrine disorders. They received MRI scans from 24 hours to 48 hours after admission with the sequences of T1WI, T2WI and DWI. The parameters for T1WI of FFE CLEAR were TR/TE 126 ms/2.3 ms, Flip 80; for T2WI of TSE SENSE TR/TE 1856 - 3238 ms/80 - 100 ms, TSE Factor 15. The parameters for DWI were TR/TE 2463 ms/48 ms, EPI factor 45 and b value of 1000, respectively. Two radiologists who knew nothing of the patients' history judged the scanned results.

The 6 newborn infants with severe hypoglycemia showed apparent symptoms and signs indicating dysfunction of central nervous system. Repeated seizures, lethargy and apnea were the most common manifestations. Moreover, seizures recurred in 4 newborns when their blood glucoses remained in normal rage. The main types of seizure were focal and multifocal myoclonus. Intermittent widespread low voltage was seen in 2 cases by 24 hour-EEG. The first time of hypoglycemia was detected from 6 hours to 53 hours after birth in 5 cases, but 12 days in one case, the minimum mean value of blood glucose was 1.05 +/- 0.44 (0.48 - 1.70) mmol/L and repeated hypoglycemia persisted for 47.3 +/- 38.8 (4 - 96) hours. The first MRI scan was accomplished from 2 days to 5 days of life, except for one at 15 days of age. The occipital cortex and white matter were involved most frequently in all cases, but parietal region was involved in 3 cases. Occipital and/or parietal regions showed hyperintensive signals indicating "water restriction (cytotoxic edema)" on DWI for 6 cases at first scan; meanwhile hypointensity on T1WI and hyperintensity on T2WI were seen in 4 cases and one case respectively, the involved area became swollen that the occipital or parietal cortex indistinguishable from subcortical white matter. Three cases received the second scan at about two weeks of age. Hypointensity on T1WI and hyperintensity on T2WI were demonstrated in all, but hypointensity on DWI in one case only and normal signals on DWI in the others. One case was followed-up at 3 month of age, he developed normally, but delayed myelination was found on posterior limb of internal capsule and optic radiation without occipital and parietal cerebral atrophy.

Cerebral occipital and parietal regions are the most vulnerable in severe hypoglycemic condition, changes of which could appear earlier on DWI than on T1WI and T2WI. But the relationship between the early findings on MRI DWI and prognosis remains to be studied further.