Background　and　objectives:　Cerebral　vasospasm　is　an　important　cause　of　poor　outcomes　in　subarachnoid　haemorrhage　patients.　This　study　was　designed　to　assess　the　effectiveness　and　safety　of　nimodipine　in　the　prevention　of　cerebral　vasospasm　in　aneurysmal　subarachnoid　haemorrhage　patients.　Methods:　We　searched　Pubmed,　OVID,　Embase,　the　Cochrane　library,　the　stroke　clinical　trial　registry,　and　the　National　Science　and　Technology　Library　database　and　collected　prospective,　randomised,　controlled　clinical　trials　of　the　prophylactic　use　of　nimodipine　for　aneurismal　subarachnoid　haemorrhage　patients.　A　meta-analysis　was　performed　on　the　studies　that　met　the　criteria　for　inclusion.　Results:　Eight　studies　met　the　inclusion　criteria,　and　1514　patients　finished　trial　observation　for　the　different　indicators.　Compared　with　the　placebo　group,　fully　recovered　(all　cases)　patients　increased　64%　in　the　nimodipine　group　(P　=　0.0002,　OR　=　1.64,　95%　CI　1.26-2.13,　NNT=-1.048),　fully　recovered　or　moderately　disabled　(all　cases)　patients　increased　79%　(P　=　0.0007,　OR　=　1.79,　95%　CI　1.28-2.51,　NNT　=　-5.889),　patient　death　(in　cerebral　vasospasm　cases)　decreased　74%　(P　=　0.008,　OR　=　0.26,　95%　CI　0.09-0.71,　NNT　=　2.298),　the　incidence　of　symptomatic　cerebral　vasospasm　decreased　46%　(P　＜　0.00001,　OR　=　0.54,　95%　CI　0.42-0.69,　NNT　=　1.952),　the　incidence　of　delayed　neurological　function　deficits　(all　cases)　decreased　38%　(P　＜　0.0001,　OR　=　0.62,　95%　CI　0.50-0.78,　NNT　=　1.078),　the　occurrence　of　cerebral　infarction　(on　CT　scan)　decreased　58%　(P　=　0.001,　OR　=　0.58,　95%　CI　0.42-0.81,　NNT　=　3.314),　the　occurrence　of　cerebral　infarction　(in　cerebral　vasospasm　cases)　decreased　65%　(P　=　0.003,　OR　=　0.35,　95%　CI　0.17-0.69,　NNT　=　3.688),　the　occurrence　of　cerebral　infarction　(all　cases)　decreased　48%　(P　＜　0.00001,　OR　=　0.52,　95%　CI　0.41-0.66,　NNT　=　1.196),　and　the　difference　in　recurrent　haemorrhage　and　adverse　reactions　between　the　nimodipine　and　placebo　groups　was　not　statistically　significant　(nimodipine　group　versus　placebo　group,　recurrent　haemorrhage　P　=　0.15,　OR　=　0.75,　95%　CI　0.50-1.11;　adverse　reaction　P　=　0.59,　OR　=　1.13,　95%　CI　0.71-1.81).　Conclusion:　Compared　with　placebo,　nimodipine　can　significantly　improve　clinical　outcomes,　as　assessed　by　self-formulated　standards　and　Glasgow　outcome　scores,　and　it　can　significantly　reduce　the　occurrence　of　symptomatic　cerebral　vasospasm　and　delayed　neurological　function　deficits　(all　cases),　as　well　as　cerebral　infarction,　although　the　incidence　rate　of　recurrent　haemorrhage　and　adverse　reactions　is　not　significantly　reduced　by　nimodipine.