Protocols for prevention of cerebral ischemic attacks caused by hyperventilation resulting from crying, as observed in perioperative pediatric moyamoya patients, were evaluated. The first protocol involved the use of sedation when staff were setting up the intravenous lines, performing neuroimaging studies, and controlling postoperative pain. The second involved the use of wound-handling techniques designed to ease postoperative wound care; these included steristrip closure, use of paraffin gauze and not using adhesive tapes. We compared 14 and 11 surgical cases handled before and after the protocols were introduced, respectively. The number of patients with perioperative cerebral infarction decreased from 2 to 0. Appropriate sedation reduced the incidence of transient ischemic attacks from 28.6% to 3.7%. The average postoperative hospital stay was similarly reduced, from 21.3 days to 16.1 days, as a consequence of the reduced incidence of complications. It is concluded that the perioperative risks can be minimized when invasive procedures are managed according to our protocols.

The purpose of this study was to investigate the relationship between cerebral blood flow (CBF) and nitric oxide (NO) synthesis using a rat model of transient forebrain ischemia of varying severity. Forebrain ischemia was induced for 30 min by occlusion of the bilateral common carotid arteries without hemorrhagic hypotension. The production of NO end-products (nitrite and nitrate) was measured by in vivo microdialysis, and CBF by the hydrogen clearance technique. Ischemia induced NO synthesis, although the increase in the quantity of NO end-products was not remarkable during the ischemic period but became prominent after reperfusion. Such increases were abolished by Nomega-nitro-L-arginine methyl ester (L-NAME), although 7-nitroindazole (7-NI) appeared to have only slight effects. The production of NO end-products during ischemia increased when the CBF during ischemia was less than 60 mL/100 g/min. In animals in which the CBF during ischemia was higher than 22.7 mL/100 g/min, the production of NO end-products increased gradually after the induction of ischemia and reached a peak during the reperfusion period, whereas in other animals in which the CBF during ischemia fell below 22.7 mL/100 g/min, the NO end-products decreased during ischemia and increased transiently after reperfusion. These results suggest that the increase in NO end-products is NO synthase (NOS)-dependent and that most of the increase is derived from endothelial NOS. It is also suggested that NO synthesis during ischemia is closely related to CBF, and that severe CBF reduction may inhibit NO synthesis.

A malignant lymphoma developed in the central nervous system (CNS) of a 7-year-old boy 5 years after he had received chemotherapy and cranial irradiation for acute lymphoblastic leukemia (ALL). Bone marrow analysis of the original leukemia showed a pre-B cell phenotype, whereas the resected brain tumor showed a T cell phenotype on immunophenotypic analysis. Because of this difference in immunophenotype, and because the patient had received multiple-drug chemotherapy and 1,800 cGy of cranial irradiation for the original ALL, we consider that the malignant lymphoma was a second neoplasm. This is a very rare case in two respects: it was a malignant lymphoma arising in the CNS as a second neoplasm after ALL and a T cell lymphoma occurring in a child.

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