Abstract
Until an ultimate therapy for preventing cerebral vasospasm (VS) following rupture of intracranial aneurysm is established, investigative efforts should also be directed towards protection of the brain from ischemic damage caused by VS. Based on this view, a double-blind clinical trial of the cerebral protective agent, Nizofenone (Y-9179), was carried out.
Under the control of the central registry, only subjects having episode of SAH following rupture of aneurysm within 9 days prior to hospitalization were admitted to the study. Patients allocated to treatment received 10 mg of Nizofenone intravenously three times a day for five days, while those to placebo received the same amount of 5% glucose in the identical manner. As a rule, administration of the drug was started as early as possible prior to development of VS. Outcomes of patients were evaluated one month after the drug administration according to their functional capacities.
The study was terminated when subjects accumulated up to 100 cases. Having excluded ten cases of troubled operation or complications not related to SAH, 42 cases were assigned to Nizofenone and 48 cases to placebo. As to the distribution of the baseline variables, there were no statistically significant differences between two groups. Twenty-five out of 42 cases of Nizofenone (59.5%) and 29 out of 48 cases of placebo (60.4%) developed VS. Remarkable difference was not found between the two groups in the outcome of patients who did not develop VS in the course of illness. In patients who developed VS, however, better outcomes were achieved in the Nizofenone group than the placebo with a statistical significance (Mann-Whitney U-test, p<0.05).
The present results will facilitate clinical use of Nizofenone for alleviating delayed ischemic deficits following SAH, although the incidence of VS itself was not decreased by the use of it.
