• Hesham Montassir, Yoshihiro Maegaki, Kaeko Ogura, Youichi Kurozawa, Ikuo Nagata, Susumu Kanzaki, and Kousaku Ohno.
• Division of Child Neurology, Institute of Neurological Sciences, Faculty of Medicine, Tottori University, Yonago, Japan. hishammontassir@gmail.com
• Brain Dev. 2009 Oct 1; 31 (9): 649-56.

AbstractAlthough associated factors are important for the occurrence of neural damage in neonatal hypoglycemia, they are not fully understood. Sixty patients with neonatal hypoglycemia were studied through a review of their medical records in Tottori University Hospital. The patients were classified into two main groups: Group I were patients who had mental retardation, developmental delay, cerebral palsy or epilepsy while Group II were those who were normal in their follow-up. Group I consisted of 12 patients while Group II consisted of 48 patients. The median gestational age was 38 weeks in Group I and 36.7 weeks in Group II. The frequencies of small for gestational age were similar in both groups. Blood glucose levels less than 15 mg/dl were more frequent in Group 1 (50.0%) than in Group 2 (14.6%) (P=0.015). Duration of hypoglycemia was longer in Group I (median, 14 h) than in Group II (median, 1.75 h) (p<0.001). The following factors were more frequent in Group I than in Group II: toxemia (33.3% and 8.3%, p=0.043), fetal distress (58.3% and 14.5%, p=0.004), an Apgar score of less than 5 at 1 min (33.3% and 6.4%, p=0.025), neonatal seizure (53.8% and 4.3%, p<0.001) and pathological jaundice (41.7% and 6.4%, p=0.006). Cranial CT or MRI revealed cerebral lesions in 8 of the 9 Group I patients in follow-up examinations. This study indicates that severe and prolonged neonatal hypoglycemia can cause cerebral lesions and other perinatal risk factors, such as hypoxia, neonatal seizure and pathological jaundice, would exacerbate hypoglycemic brain injuries.

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