Objective-Previousreports about changes in cerebral blood flow (CBF) in transient global amnesia disclosed decreased flow in some parts of the brain. However, CBF analyses in most reports were qualitative but not quantitative. The purpose of this study was to determine changes in CBF in transient global amnesia. Methods-The CBF was measured and the vasoreactive response to acetazolamide was evaluated in six patients with transient global amnesia using technetium-99m hexamethylpropylene amine oxime singlephoton emission computed tomography (SPECT). The CBF was measured during an attack in two patients and soon after an attack in the other four. About one month later, CBF was re-evaluated in each patient. Results-Two patients examined during an attack and one patient examined five hours after an attack had increased blood flow in the occipital cortex and cerebellum. Three patients examined at six to 10 hours after an attack had decreased blood flow in the thalamus, cerebellum, or putamen. These abnormalities of blood flow almost disappeared in all patients one month after onset. The vasodilatory response to acetazolamide, which was evaluated initially using SPECT, was poor in areas of increased blood flow. By the second evaluation of CBF with acetazolamide, the vasodilatory response had returned to normal. Conclusions-In a patient with transient global amnesia, CBF increased in the vertebrobasilar territory during the attack and decreased afterwards. The vasodilatory response to acetazolamide may be impaired in the parts of the brain with increased blood flow. It is suggested that transient global amnesia is distinct from migraine but may share the same underlying mechanism.

The authors administered recombinant human granulocyte colony-stimulating factor (rhG-CSF) to 16 patients with advanced non-Hodgkin's lymphoma treated with combination chemotherapy. Groups of three to five patients were treated with 50, 100, 200, and 400 micrograms/m2 per day of rhG-CSF by intravenous infusion for 14 days, beginning 3 days after chemotherapy. There was a strong linear relationship between the dose and the area under the curve over this dose range. The rhG-CSF was rapidly cleared from serum, with a mean half-life of 5.97 hours for the second phase (t1/2). In patients treated with a dose of more than 100 micrograms/m2 per day, the duration of neutropenia (P less than 0.01) and the duration of fever (P less than 0.05) were significantly decreased. The rhG-CSF was well tolerated and the only clinical observation that appeared relating to rhG-CSF administration was slight bone pain. This study strongly suggests that an optimum dose of rhG-CSF in patients after chemotherapy is 100 to 200 micrograms/m2. Our study shows that rhG-CSF is a clinically useful drug for patients treated with myelosuppressive chemotherapy.

The effects of insulin on vasoconstrictor response were studied in diabetics without autonomic neuropathy. Vasoconstrictor response to phenylephrine was measured before and after insulin injection in 10 diabetics. Mean blood pressure, forearm blood flow, and forearm vascular resistance remained unchanged after insulin administration. But the increase in forearm vascular resistance to phenylephrine decreased significantly and heart rate increased significantly after insulin injection. In 9 diabetics, vasoconstrictor response to tilting was measured before and after insulin injection. Mean blood pressure, cardiac index, and the total peripheral resistance index remained unchanged after insulin administration. However, the increase in the total peripheral resistance index to tilting decreased significantly and heart rate increased significantly after insulin injection. Furthermore, a significant fall in mean blood pressure following tilting was observed only after insulin administration. Although blood glucose levels decreased significantly, no hypoglycemic symptoms occurred. The present study suggests that insulin inhibits vasoconstrictor responses to both alpha agonist and tilting in diabetics.

The association of primary biliary cirrhosis (PBC) and bronchial asthma was observed in three patients. All of these patients were female (53, 54, and 41 years old, respectively), and were positive for antimitochondrial antibodies. The patients fulfilled the diagnostic criteria of both PBC and bronchial asthma. Bronchial asthma preceded PBC in two patients, and the reverse order was seen in the other. Patient the clinical symptoms were mainly due to the bronchial asthma. Two patients had asymptomatic PBC and the third patient complained of pruritus. The liver histology showed mild to moderate eosinophilic infiltration in addition to the ductal and hepatic parenchymal changes characteristic of PBC. A survey of 266 cases of PBC referred to us disclosed that, in 6 of these, the PBC was associated with bronchial asthma, while no association with bronchial asthma was the material of found in 166 patients with viral hepatitis in our liver biopsy files. The 3 present cases we experienced suggest that bronchial asthma may be included in the list of extrahepatic diseases associated with PBC. The significance of this association is unclear and may merit further study. Steroid therapy, which is known to cause adverse effects in PBC, was employed for bronchial asthma in these 3 patients. Another therapeutic approach will have to be considered in patients with bronchial asthma associated with PBC.

An autopsy case of hepatocellular carcinoma presenting extrahepatic obstructive jaundice was reported. The patient was a 68‐year‐old man with 5‐year history of chronic liver disease and markedly jaundiced, and died of gastrointestinal hemorrhage. Autopsy revealed hepatocellular carcinoma associated with liver cirrhosis and metastatic polypoid growth in the common bile duct and cystic duct which completely obstructed the duct lumen. Obstructive jaundice secondary to complete obstruction of the common bile duct was a rare complication of hepatocellular carcinoma. The other 85 cases of hepatocellular carcinoma presenting extrahepatic biliary obstruction are reviewed.