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British Aneurysm Nimodipine Trial Effect of oral nimodipine on cerebral infarction and outcome after subarachnoid haemorrhage: British aneurysm nimodipine trial J D Pickard, G D Murray, R Illingworth, M D M Shaw, G M Teasdale, P M Foy, P R D Humphrey, D A Lang, R Nelson, P Richards, J Sinar, S Bailey, A Skene Abstract Conclusions-Oral nimodipine 60 mg four hourly Objective-To determine the efficacy of oral is well tolerated and reduces cerebral infarction and nimodipine in reducing cerebral infarction and improves outcome after subarachnoid haemorrhage. poor outcomes (death and severe disability) after subarachnoid haemorrhage. Wessex Neurological Introduction Centre, Southampton Design-Double blind, placebo controlled, General Hospital, randomised trial with three months of follow up and Despite advances that have reduced considerably Southampton S09 4XY intention to treat analysis. To have an 80% chance the risks of operation to secure a ruptured cerebral J D Pickard, MCHIR, with a significance level of 0-05 of detecting a 50% aneurysm the overall mortality and morbidity during professor ofclinical reduction in an incidence of cerebral infarction of the management of patients with subarachnoid neurological sciences 15% a minimum of 540 patients was required. haemorrhage who have survived and not been R Nelson, FRCS, senior Setting-Four regional neurosurgical units in the devastated by the initial ictus has not fallen dramatic- registrar in neurosurgery ally. This is mainly because such patients rebleed and S Bailey, RGN, Medical United Kingdom. Research Council research Patients-In all 554 patients were recruited have delayed cerebral ischaemia. The management sister between June 1985 and September 1987 out of dilemma remains the need to weigh the risk of a population of 1115 patients admitted with sub- precipitating cerebral ischaemia by operation against Medical Statistics Unit, arachnoid haemorrhage proved by the results of that of rebleeding while awaiting surgery. Department of Surgery, lumbar puncture or computed tomography, or both. Subarachnoid haemorrhage provides the clearest University of Glasgow, The main exclusion criterion was admission to clinical opportunity for pretreating ischaemia, but, Glasgow GIl 6NT the neurosurgical units more than 96 hours after although the calcium antagonist nimodipine has been G D Murray, PHD, senior subarachnoid haemorrhage. There were four reported to reduce the incidence of delayed cerebral lecturer in medical statistics breaks of code and no exclusions after entry. One ischaemia after subarachnoid haemorrhage,'2 Regional Neurosciences patient was withdrawn and in 130 treatment was definitive evidence is lacking. Previous trials were Centre, Charing Cross discontinued early. All patients were followed up for small and relied on selecting a subgroup of patients Hospital, London W6 8RF three months and were included in the analysis, with cerebral ischaemia presumed to be due to cerebral R Illingworth, FRCS, except the patient who had been withdrawn. vasospasm. Ischaemia may be the result of several consultant neurosurgeon Interventions-Placebo or nimodipine 60 mg was factors35 and cannot be attributed simply to an P Richards, FRCS, consultant given orally every four hours for 21 days to 276 and exaggerated contraction of cerebral arteries (vaso- neurosurgeon 278 patients, respectively. Treatment was started spasm); thus defining such a subgroup is difficult and within 96 hours after subarachnoid haemorrhage. ignores any potential benefit of treatment in other Mersey Regional causes of ischaemia. Department of Medical and End points -Incidence of cerebral infarction and Surgical Neurology, ischaemic neurological deficits and outcome three Nimodipine has various effects on the cerebral Walton Hospital, Liverpool months after entry. circulation, not all of which may be beneficial. L9 1AE Measurements-Demographic and clinical data, Cerebrovascular smooth muscle is more sensitive M D M Shaw, FRCS, including age, sex, history of hypertension and than systemic arterial smooth muscle to changes in consultant neurosurgeon subarachnoid haemorrhage, severity ofhaemorrhage extracellular calcium concentration and to calcium P M Foy, FRCS, consultant according to an adaptation of the Glasgow coma antagonists such as nimodipine.6-8 In addition to being neurosurgeon scale, number and site of aneurysms on angio- a moderate cerebral vasodilator, however, nimodipine P R D Humphrey, MRCP, impairs cerebrovascular reactivity.9-" Nimodipine consultant graphy, and initial findings on computed tomography neurologist were measured at entry. Deterioration, defined as does not reduce the incidence or severity of cerebral Institute of Neurological development of a focal sign or fall of more than one vasospasm detected by angiography in humans or Sciences, Southern point on the Glasgow coma scale for more than six primates,'2-'7 but it reduces the size of cerebral infarcts General Hospital, Glasgow hours, was investigated by using clinical criteria and in rats when given before but not after occlusion of a G514TF by computed tomography, by lumbar puncture, or cerebral artery. 8 G M Teasdale, FRCS, at necropsy when appropriate. All episodes of We therefore conducted a prospective trial to professor ofneurosurgery deterioration and all patients with a three month establish the effect of nimodipine on the incidence of D A Lang, FRCS, registrar in outcome other than a good recovery were assessed both ischaemic events and proved cerebral infarction neurosurgery a review and on outcome after subarachnoid haemorrhage. J Sinar, FRCS, registrar in by committee. neurosurgery Main results-Demographic and clinical data at entry were similar in the two groups. In patients Department of given nimodipine the incidence ofcerebral infarction Patients and methods Mathematics, University of was 22% (61/278) compared with 33% (92/276) in SELECTION OF PATIENTS AND DIAGNOSIS Nottingham, Nottingham those given placebo, a significant reduction of 34% Eligible patients were admitted to one offour centres NG7 IRD (95% confidence interval 13 to 50%). Poor outcomes (in London, Southampton, Liverpool, and Glasgow) A Skene, PHD, senior lecturer were also significantly reduced by 40% (95% within 96 hours after the onset of symptoms and signs in medical statistics confidence interval 20 to 55%) with nimodipine (20% of subarachnoid haemorrhage. This time limit was in Correspondence to: (55/278) patients given nimodipine v 33% (91/278) specified because our hypothesis was that nimodipine Professor Pickard. in those given placebo). Adverse reactions were should be given soon after the bleed to have a reported in 14 patients given nimodipine and 10 given prophylactic effect upon subsequent ischaemia. The Br.rlcj7 19'9;298:636-42 placebo. diagnosis was confirmed by lumbar puncture or 636 BMJ VOLUME 298 11 MARCH 1989 computed tomography, or both-angiography was not was deemed to be non-compliant. The protocol required before admission to the trial. The reasons allowed for separate analysis of this group, but this was for exclusion were pregnancy; major renal, hepatic, or found not to be necessary. Plasma samples were taken pulmonary disease; pre-existing cardiac decompensa- from 35 patients (eight taking placebo, 27 nimodipine) tion or a recent (within six months) myocardial and nimodipine concentrations measured-there was infarction; age below 18 years; a subarachnoid no evidence of patients given placebo receiving active haemorrhage that produced a coma in the week treatment, or vice versa. preceding the most recent subarachnoid haemorrhage; and the patient or relative being unwilling to give CLINICAL MONITORING consent. Eligibility for the trial was checked in The severity of subarachnoid haemorrhage was specially designed record forms with a check list of graded according to an adaptation of the Glasgow coma entry and exclusion criteria. A separate record was scale,' which is similar to the scale recently adopted by kept of patients who did not fulfil the entry criteria. the World Federation of Neurosurgical Societies.24 Patients' eligibility was rechecked during outcome Patients whose clinical grade was I had a score on the review meetings of all the centres. There were no Glasgow coma scale of 15 and were neurologically exclusions. Written informed consent was obtained intact, apart from having cranial nerve palsy. Those in from the patient, care having been taken to avoid grade II had a score of 15 and were neurologically undue stress, or from a relative. The ethical committee intact, apart from having cranial nerve palsy, with neck of each centre approved the study and the Department stiffness or headache, or both. Those in grade III had a of Health and Social Security supplied a clinical trial score of 13-14 and were with or without neurological exemption for the drug before the start of the study. deficit and those in grade IV a score of 8-12 with or without neurological deficit. Finally, those in grade V DESIGN OF STUDY had a score of 3-7 and were in a coma with or without Our aim was to establish with a prospective, abnormal posturing. multicentre, randomised, double blind, placebo Computed tomography was performed within controlled trial whether oral nimodipine (60 mg every 24 hours after admission to the trial and repeated four hours) reduced the incidence of episodes of whenever necessary if the patient's clinical condition cerebral ischaemia and cerebral infarction arising anew deteriorated at all. Angiography, operation, and other after spontaneous intracranial
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