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It is suggested that parasagittal cerebral injury in the asphyxiated full term infant may be common. However, parasagittal cerebral injury is rarely diagnosed in the neonatal period. It is said that cranial ultrasonography and CT scan are not useful to identify this lesion. Recently, it is considered that some of the intellectual deficits and behavioral problems in children at school age may have their origin in perinatal parasagittal cerebral injury. We described a patient with parasagittal cerebral injury demonstrated by CT scan. Infants with neurological abnormalities which include weakness or abnormal muscular tone of proximal upper limbs suggest parasagittal cerebral injury. CT scan obtained between 1 and 3 weeks of life is considered to be useful for the diagnosis. Early diagnosis and follow-up of parasagittal cerebral injury may lead to the understanding of frequency, prognosis and pathogenesis and to its prevention.

An instance of the rare occurrence of neonatal hepatitis and extrahepatic biliary atresia in the same sibship is reported. The older brother with neonatal hepatitis developed jaundice at the age of 4 days and had clay-colored stools from early infancy. Cholangiography by exploratory laparotomy at the age of 3 months showed a normal bile duct pattern. After laparotomy, jaundice rapidly disappeared, and stools became yellow. His liver function has been normal since age 6 months to the present (6 years old). The younger brother developed jaundice and clay-colored stools at the age of 1 month. The diagnosis of extrahepatic biliary atresia was made at laparotomy at the age of 4 1/2 months. Hepatojejunostomy was performed with successful bile drainage, although he had frequent attacks of ascending cholangitis since operation. These cases support a recent hypothesis that neonatal hepatitis and extrahepatic biliary atresia may be produced by the same disease process.

A case of fatal familial intrahepatic cholestasis (Byler disease) developed a neuromuscular syndrome similar to that in experimental vitamin E deficiency and abetalipoproteinemia, and died of hepatic and cardiac failure. Serum vitamin E level was extremely low. Autopsy revealed intrahepatic cholestatic cirrhosis without obliterative lesions in the bile duct system and marked splenomegaly with splenoma-like nodules. The other pathological lesions were considered to be due to chronic vitamin E deficiency as follows:1. Mitochondrial changes especially of the hepatocyte and cardiac muscle. 2. Cardiomyopathy. 3. Myopathy. 4. Vasculopathy. 5. Systemic lipofuscinosis. 6. Lesions of the reproductive and endocrine organs. 7. Kyphoscoliosis and pes cavus. 8. Systemic neuroaxonal dystrophy with peripheral neuropathy.