***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: In this study with r and omized controls , we administered fludrocortisone acetate to 46 of 91 patients with subarachnoid hemorrhage in an attempt to prevent excessive natriuresis and plasma volume depletion . Fludrocortisone significantly reduced the frequency of a negative sodium balance during the first 6 days ( from 63 % to 38 % , p = 0.041 ) . A negative sodium balance was significantly correlated with decreased plasma volume during both the first 6 days ( p = 0.014 ) and during the entire 12-day study period ( p = 0.004 ) . Although fludrocortisone treatment tended to diminish the decrease in plasma volume , the difference was not significant ( p = 0.188 ) . More patients in the control group developed cerebral ischemia ( 31 % vs. 22 % ) and , consequently , more control patients were treated with plasma volume exp and ers ( 24 % vs. 15 % ) , which may have masked the effects of fludrocortisone on plasma volume .  Fludrocortisone therefore reduces natriuresis and remains of possible therapeutic benefit in the prevention of delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage We enrolled 75 consecutive patients admitted with subarachnoid hemorrhages in a r and omized , double-blind , placebo-controlled trial to determine the effect of early intervention with nimodipine on outcome and cerebral blood flow . The cardioprotective effect of nimodipine was assessed by measuring the electrocardiographic changes over the first 3 days of drug treatment . There was a mild lowering of the mean cerebral blood flow in the nimodipine-treated group over the 21-day period . Analysis of the continuous electrocardiographic traces showed no difference between the nimodipine and placebo groups in the frequency or type of abnormality detected . At 3 months , 4 of the 38 patients receiving nimodipine had died , compared with 10 of the 37 placebo-receiving patients . Of the 50 eligible patients who had a proven cerebral aneurysm , 1 patient ( 4 % ) on nimodipine  died compared with 6 ( 24 % ) receiving placebo ( 0.01 less than P less than 0.05 , chi 2 test ; approximate 95 % confidence interval for mortality difference , 0.4 % to 39.6 % ) . We conclude that nimodipine does not increase the cerebral blood flow or protect the heart after a subarachnoid hemorrhage . There were no side effects from nimodipine . The trend toward improved outcome should be verified in a larger series of patients BACKGROUND AND PURPOSE Cerebral blood flow ( CBF ) is reduced after subarachnoid hemorrhage ( SAH ) , and symptomatic vasospasm is a major cause of morbidity and mortality . Volume expansion has been reported to increase CBF after SAH , but CBF values in hypervolemic ( HV ) and normovolemic ( NV ) subjects have never been directly compared . METHODS On the day after aneurysm clipping , we r and omly assigned 82 patients to receive HV or NV fluid management until SAH day 14 . In addition to 80 mL/h of isotonic crystalloid , 250 mL of 5 % albumin solution was given every 2 hours to maintain normal ( NV group , n=41 ) or elevated ( HV group , n=41 ) cardiac filling pressures . CBF ( (133)xenon clearance ) was measured before r and omization and approximately every 3 days thereafter ( mean , 4.5 studies per patient ) . RESULTS HV patients received significantly more fluid and had higher pulmonary artery diastolic and central venous pressures than NV patients , but there was no effect on net fluid balance or on blood volume measured on the third postoperative day . There was no difference in mean global CBF during the treatment period between HV and NV patients ( P=0.55 , r and om-effects model ) . Symptomatic vasospasm occurred in 20 % of patients in each group and was associated with reduced minimum regional CBF values ( P=0.04 ) . However , there was also no difference in minimum regional CBF between the 2 treatment groups . CONCLUSIONS HV therapy result ed in increased cardiac filling pressures and fluid intake but did not increase CBF or blood volume compared with NV therapy . Although careful fluid management to avoid hypovolemia may reduce the risk of delayed cerebral ischemia after SAH , prophylactic HV therapy is unlikely to confer an additional benefit Background and Purpose — Cerebral vasospasm remains a major source of morbidity after aneurysmal subarachnoid hemorrhage ( SAH ) . We demonstrate that simvastatin reduces serum markers of brain injury and attenuates vasospasm after SAH . Methods — Patients with angiographically documented aneurysmal SAH were r and omized within 48 hours of symptom onset to receive either  simvastatin ( 80 mg daily ; n=19 ) or placebo  ( n=20 ) for 14 days . Plasma alanine aminotransferase , aspartate aminotransferase , and creatine phosphokinase were recorded weekly to evaluate laboratory evidence of hepatitis or myositis . Serum markers of brain injury were recorded daily . The primary end point of vasospasm was defined as clinical impression ( delayed ischemic deficit not associated with rebleed , infection , or hydrocephalus ) in the presence of ≥1 confirmatory radiographic test ( angiography or transcranial Doppler demonstrating mean VMCA > 160 m/sec ) . Results — There were no significant differences in laboratory-defined transaminitis or myositis between groups . No patients developed clinical symptoms of myopathy or hepatitis . Plasma von Willebr and factor and S100&bgr ; were decreased 3 to 10 days after SAH ( P<0.05 ) in patients receiving simvastatin versus placebo . Highest mean middle cerebral artery transcranial Doppler velocities were significantly lower in the simvastatin-treated group ( 103±41 versus 149±47 ; P<0.01 ) . In addition , vasospasm was significantly reduced ( P<0.05 ) in the simvastatin-treated group ( 5 of 19 ) compared with those who received placebo ( 12 of 20 ) . Conclusion — The use of simvastatin as prophylaxis against delayed cerebral ischemia after aneurysmal SAH is a safe and well-tolerated intervention . Its use attenuates serum markers associated with brain injury and decreases the incidence of radiographic vasospasm and delayed ischemic deficit Summary A prospect i ve r and omized double blind study was conducted in 70 patients suffering from subarachnoid haemorrhage , due to aneurysm rupture , to determine if the use of nimodipine reduces the severity of ischaemic deficits secondary to vasospasm . At the end of the study , two patients had severe deficit or died in the treated group , while 10 had a bad outcome in the placebo group . Angiographic vasospasm was not significantly different in its frequency or its severity between the two groups . However , the association of extensive and diffuse vasospasm was less frequent in the nimodipine group . This study confims the effectiveness of Nimodipine in reducing the occurrence of neurological deficit due to vasospasm , even if this action is not observed in all cases Background and Purpose — Methods of performing and reporting r and omized clinical trials ( RCTs ) are available , but weaknesses still occur . For observational studies , methodology is less well described , and weaknesses are even more likely . In recent guidelines for patients with subarachnoid hemorrhage ( SAH ) , 25 % of treatment recommendations are based on clinical trials . To interpret the results of research on the therapeutic effect of treatment modalities , definition of outcome measures is essential . We assessed quality of study design and outcome measures and presence and precision of definitions concerning major complications of SAH in studies evaluating treatment strategies in patients with aneurysmal SAH . Methods — We retrieved and review ed all articles on treatment strategies in patients with SAH that fulfilled a prespecified set of criteria and were published during 1990–1999 in 10 general , neurosurgical , or neurological journals . We categorized articles into RCTs , observational studies with a control group , and observational studies without a control group . We assessed study design by means of a prespecified set of method ological criteria . For outcome measures we assessed whether a prespecified outcome measurement was defined and whether any h and icap scale was used . For complications after SAH we assessed whether the definition included a description of the clinical features and a technical investigation with criteria for abnormal results . Results — We identified 18 RCTs , 24 observational studies with a control group , and 41 uncontrolled observational studies . Two RCTs , no observational studies with a control group , and 15 observational studies without a control group met all criteria for study design . A primary outcome measure was specified in 67 of the 83 studies and was defined in 59 . Any measure of h and icap or information on degree of dependence was given in 65 of 83 studies . A complete definition of delayed cerebral ischemia was given in 13 of 66 studies , of rebleeding in 2 of 26 studies , and of hydrocephalus in 2 of 14 studies . Conclusions — Most studies on treatment strategies in SAH suffer from method ological weaknesses . This implies that current management of patients with SAH is based on weak evidence BACKGROUND Cerebral vasospasm , including its ischemic sequelae , remains a leading cause of death and disability following subarachnoid hemorrhage ( SAH ) . This study was design ed to evaluate whether the low-molecular-weight heparin ( LMWH ) enoxaparin reduces the occurrence of cerebral vasospasm and ischemia following spontaneous SAH . METHODS A prospect i ve , double-blind , r and omized study was conducted in 120 consecutive patients with SAH ( Hunt Hess Scale ( HHS ) I-III ) . Patients received one subcutaneous injection per day of either 20 mg enoxaparin or placebo for 3 weeks following SAH . Efficacy endpoints were the occurrence of cerebral vasospasm , delayed ischemic deficit ( DID ) , cerebral infa rct ion , and overall outcome at 1 year following SAH . RESULTS At 1-year follow-up , enoxaparin significantly reduced DID and cerebral infa rct ion . Delayed ischemic deficit occurred in 8.8 % of the enoxaparin group versus 66.7 % of the placebo group ( P<0.001 ) , while 3.5 % of vasospasm-related cerebral infa rct ions occurred in enoxaparin-treated patients and 28.3 % in placebo-treated patients ( P<0.001 ) . Severe shunt-dependent hydrocephalus was significantly lower in the enoxaparin group ( 1.8 % versus 16.7 % ; P=0.019 ) . Compared with the placebo group , the enoxaparin group had fewer intracranial bleeding events and better overall outcomes at 1-year follow-up . Although there was potential bias as a result of patients in the placebo group being more severely affected ( in terms of HHS ) , treatment with enoxaparin for 3 weeks improved long-term outcome following SAH . CONCLUSIONS Enoxaparin is safe and effective in reducing cerebral vasospasm and ischemia following SAH ( Hunt Hess grade s I-III ) , result ing in a better long-term outcome for the patient Antifibrinolytic agents have been cl aim ed to reduce the rebleed rate in patients with subarachnoid haemorrhage from intracranial aneurysms . However , these agents may in themselves increase the incidence of delayed cerebral ischaemia in these patients . We have used aspirin in an attempt to reduce the incidence of this complication . In a prospect i ve , double-blind trial of aspirin against placebo , 53 patients with subarachnoid haemorrhage were all treated with the antifibrinolytic agent tranexamic acid . Twenty-seven patients received aspirin and 26 patients received placebo .  The morbidity and mortality was similar in each group . A further breakdown into patients who had their aneurysms clipped at craniotomy ( 21 patients ) similarly failed to show a more favourable outcome in either group . It is concluded that aspirin does not affect the outcome in patients with subarachnoid haemorrhage treated with tranexamic acid A water-soluble , novel synthetic compound , AVS ( (+/-)-N , N'-propylenedinicotinamide ; nicaraven ) has no demonstrable vasoactive properties but scavenges hydroxyl radicals in aqueous environmental conditions at neutral pH. Based on the results of preceding experimental and clinical studies showing marked ameliorative effects of AVS on cerebral vasospasm and ischemic brain damage , a multicenter , placebo-controlled double-blind clinical trial was undertaken to verify its beneficial effects on delayed ischemic neurological deficits ( DINDs ) due to vasospasm and on the overall outcome of patients with subarachnoid hemorrhage ( SAH ) . A total of 162 patients with SAH who had Glasgow Coma Scale scores between 7 and 15 on admission were enrolled in the trial . Drug administration ( 4 g AVS or 4 g glucose as placebo ; infused intravenously for 6 - 8 hours once a day ) was begun within 5 days post-SAH and continued for 10 to 14 days . Intent-to-treat analysis of these patients revealed that the overall incidence of DINDs , which was defined as an exacerbation of imp 
    Output:
    
The only proven therapy for vasospasm is nimodipine .
The following conclusions were made : nimodipine is indicated after SAH and tirilazad is not effective .