32nd Annual Meeting of the Scandinavian Society for Psychopharmacology Copenhagen,Denmark April 10–12, 1991 Abstracts

32nd Annual Meeting of the Scandinavian Society for Psychopharmacology Copenhagen, Denmark April 10–12, 1991 Abstracts     

Management of hypothalamic gliomas in children: an analysis of 33 cases

The cases of 33 children with hypothalamic-chiasmatic gliomas are reviewed. Radiation therapy produced clinical or radiographic improvement in 11 (46%) of 24 patients. Progression was documented in 18 patients (54%). Overall, the median time to tumor progression was 60 months; it was 70 months in patients who received radiation therapy and 30 months in those who did not (P less than 0.05). Chemotherapy, either given initially or at the time of progression, caused the tumor to respond or to stabilize in 10 patients. Partial resection of the tumor led to improvement in 3 of 12 patients, obviating the need for a shunt in 2 of them; there were no deaths and postoperative morbidity was transient and minimal (diabetes insipidus, intraventricular hemorrhage, and left hemiparesis in one patient each). The 5- and 10-year survival probabilities were 93 and 74%, respectively. Patients with neurofibromatosis had a better prognosis.     

The effects of inhibitors of arachidonate metabolism on spontaneous and evoked endplate potentials at normal and crotoxin-treated frog neuromuscular junctions

Aspirin (1 mM), a selective cyclooxygenase inhibitor, decreased endplate potential (e.p.p.) amplitude but did not affect either the biphasic changes in m.e.p.p. frequency or triphasic changes in e.p.p. amplitude induced by crotoxin. Nordihydroguaiaretic acid (30 microM), a dual inhibitor of cyclooxygenase and lipoxygenase pathways, increased e.p.p. amplitude but did not affect the characteristic changes in m.e.p.p. frequency and e.p.p. amplitude in response to crotoxin. The incidence of giant m.e.p.p.s was reduced by aspirin and increased by NDGA. Arachidonate metabolism is not a major factor in the induction of neurotoxicity by crotoxin at the frog neuromuscular junction.