***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: Fifty-four patients with acute cerebral infa rct ion were included in a double-blind study to evaluate Decadron ® as therapy . When comparison of patients with similar levels of consciousness was made , there was no significant difference between those patients receiving Decadron ® and those receiving placebo therapy . Three patients developed gastrointestinal tract bleeding in the placebo group , but there were none in the Decadron ® -treated group . There was no good correlation between the clinical state of the patient and the CSF pressure , either on admission or during the 14-day course of the study Dexamethasone and a placebo were compared as treatment for 40 patients with intracerebral hemorrhage .  Of 19 patients receiving dexamethasone , 17 ( 89.5 % ) died during their hospital admission . Of 21 patients receiving a placebo , 16 ( 76.2 % ) died . The mortality rate was 100 % in 15 patients in the dexamethasone-treated group who were in coma or deep stupor on admission , and the mortality rate was 92 % in 12 patients with similar levels of consciousness who received a placebo . Several parameters of the neurological examination showed an improved quality of survival in the Decadron ® -treated group , but this was found only at certain days in the study . No overall statistically significant difference was found between the two therapies 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 Using logistic regression , we analyzed the predictive value of a number of entry variables with respect to the outcome variables delayed cerebral ischemia , rebleeding , and poor outcome ( death or severe disability ) in patients with aneurysmal subarachnoid hemorrhage . The entry variables were clinical condition on admission ( grade s on the Glasgow Coma Scale , Hunt and Hess system ) , the amount of subarachnoid and intraventricular blood and the presence of hydrocephalus on the admission computed tomogram , and antifibrinolytic treatment with tranexamic acid . We used data from a prospect ively studied population of 176 patients admitted within 72 hours after subarachnoid hemorrhage . The risk of delayed cerebral ischemia was best predicted by the amount of subarachnoid blood , intraventricular blood , and antifibrinolytic treatment  irrespective of clinical condition and hydrocephalus . The site of delayed cerebral ischemia was not related to the location of the subarachnoid hemorrhage . Antifibrinolytic treatment was the only entry variable ( negatively ) predicting the risk of rebleeding . Death or severe disability after 3 months was best predicted by the amount of subarachnoid blood and the initial clinical condition reflected by the grade on the Glasgow Coma Scale OBJECT To reduce the risk of ischemic complications in patients with subarachnoid hemorrhage ( SAH ) , hypervolemic therapy is generally advocated . However , such conventional treatment can not always ensure the maintenance of an effective intravascular volume expansion , because excessive natriuresis and osmotic diuresis occur after SAH . In this prospect i ve study the authors examined the effects of inhibition of natriuresis with fludrocortisone acetate on intravascular volume expansion during hypervolemic therapy . METHODS Thirty patients with SAH were r and omized and divided into two groups : controls ( Group 1 , 15 patients ) and  patients treated with 0.3 mg/day of fludrocortisone  ( Group 2 , 15 patients ) . In all patients sodium and fluid intake levels were in excess of maintenance requirements in an attempt to maintain a positive water balance and a central venous pressure ( CVP ) of 8 to 12 cm H2O . The mean sodium and water intake levels for 14 days after SAH were significantly reduced by fludrocortisone in Group 2 ( 487+/-34.52 mEq/day and 5159.2+/-249.29 ml/day , respectively ; p<0.01 ) compared with Group 1 ( 634.2+/-42.86 mEq/day and 6611.7+/-365.67 ml/day ) . Fludrocortisone significantly reduced the urinary sodium excretion ( p<0.01 ) and urine volume ( p<0.01 ) in parallel , and effectively prevented a negative shift in the sodium as well as water balance ( p<0.01 ) . The serum sodium level tended to decrease in Group 1 , reaching 135 mEq/L on average , but not in Group 2 ( p<0.01 ) . Hyponatremia in Group 1 was always observed at the optimal range of CVP values . A decrease in serum potassium level within the range of 2.8 to 3.5 mEq/L was transiently noted in 11 patients ( 73.3 % ) of Group 2 , but was easily corrected . Possible side effects of fludrocortisone , such as pulmonary edema , were not encountered . CONCLUSIONS Intravascular volume expansion in the presence of excessive natriuresis requires a large sodium and water intake and is often associated with hyponatremia . Inhibition of natriuresis with fludrocortisone can effectively reduce the sodium and water intake required for hypervolemia and prevent hyponatremia at the same time Fifty-three patients with acute cerebral infa rct ion were treated in a double-blind study with either dexamethasone or placebo within 24 hours of the onset of stroke . Forty-one of these survived for longer than 28 days , and the patients treated with the steroid fared slightly worse than those treated with placebo at the end of this time . Two of the five patients who died in the placebo group died of cerebral edema , compared with three out of seven patients who died in the steroid group . Infectious complications , gastrointestinal hemorrhage , and occasional serious exacerbations of diabetes occurred more commonly in the steroid group Glucocorticoid in high dose has known to reduce vascular sensitivity to various vasoconstrictive stimuli . It inhibits phospholipase to reduce production of prostagl and ins . It stabilizes the cell membrane and prevents cerebral edema . All these pharmacological effects indicate possible usefulness of this drug for the treatment of cerebral ischemia due to vasospasm . Based on these theoretical background s a multi-center controlled double blind clinical study was carried out . The patient who showed manifestations of delayed cerebral ischemia due to vasospasm were selected for this study . As soon as the clinical manifestation appeared , the patient was given either 3 grams of hydrocortisone intravenously in a 60 ml solution or the placebo . The administration was repeated 6 times with interval of 12 hours . The patients were allowed to be treated according to the independent protocol of each institute except for the maximum daily use of glucocorticoid . The effect of the therapy was evaluated at 4th , 7th day and 1 month after the initiation . The study involved 52 institutes and a total of 140 patients , seventy-one patients who received hydrocortisone ( group A ) and 69 patients who received placebo ( group P ) was analysed . There were no significant differences in background data between both groups . In patients with grade I , II or III on admission , the favorable effects of hydrocortisone were demonstrated on changes in neurological findings . In group A , there were significantly more cases of improvement at 4th day for orientation about place and person . At 1 month or on discharge group A showed significant improvement almost in every aspect of neurological findings including mental , speech and motor functions . ( ABSTRACT TRUNCATED AT 250 WORDS To evaluate the efficacy of dexamethasone for treatment of primary supratentorial intracerebral hemorrhage , we studied 93 patients 40 to 80 years old , using a double-blind r and omized block design . After the subjects were stratified according to their level of consciousness ( Glasgow Coma Scale ) , those with objective ly documented primary supratentorial intracerebral hemorrhage were r and omly assigned to either dexamethasone or placebo . For ethical reasons , three interim analyses were planned , to permit early termination of the trial if one study group did better than the other . During the third interim analysis , the death rate at the 21st day was identical in the two groups ( dexamethasone vs. placebo , 21 of 46 vs. 21 of 47 ; chi-square = 0.01 , P = 0.93 ) . In contrast , the rate of complications ( mostly infections and complications of diabetes ) was much higher in the dexamethasone group ( chi-square = 10.89 , P less than 0.001 ) , leading to early termination of the study . In the light of the absence of a demonstrable beneficial effect and the presence of a significant harmful effect , current practice s of using dexamethasone for treatment of primary supratentorial hemorrhage should be reconsidered In a prospect i ve , community-based study of 675 consecutive patients with a first-ever stroke , of whom over 90 % had computed tomography ( CT ) and /or necropsy examinations , 129 deaths occurred within 30 days of the onset of symptoms , a case fatality rate ( CFR ) of 19 % . The 30 day CFR for patients with cerebral infa rct ion was 10 % ( 57 of 545 , for primary intracerebral haemorrhage 52 % ( 34 of 66 ) , for subarachnoid haemorrhage 45 % ( 15 of 33 ) and for those of uncertain pathological type 74 % ( 23 of 31 ) . The CFR for patients who had been functionally dependent pre-stroke was 33 % compared with 17 % for those who had been independent pre-stroke . The age-adjusted relative risk of death for patients who had been functionally dependent pre-stroke was not significantly greater ( 1.8 , 95 % confidence interval 0 to 4.3 ) . There was a significant trend for CFR to increase with age ( Chi square for trend = 4.0 , p less than 0.05 ) . This relationship was found in those patients who had been functionally independent prestroke ( Chi square for trend = 7.9 , p less than 0.005 ) but not in those who had been dependent pre-stroke ( Chi square for trend = 0.5 , NS ) . The pattern of increasing CFR with increasing age amongst those who had been independent prestroke was seen particularly in patients with cerebral infa rct ion ( Chi square for trend = 8.6 , p less than 0.005 ) . The age-adjusted relative risk of death for patients with cerebral infa rct ion who had been functionally dependent pre-stroke was 2.2 ( 95 % confidence interval 1.2 to 4.1 ) . Fifty three percent of all deaths within 30 days of stroke were due to the direct neurological sequelae of the stroke . Patients with primary intracerebral or subarachnoid haemorrhages were significantly more likely to die in this way than those with cerebral infa rct ion ( relative risk 4.1 ; 95 % confidence interval 3.4 - 4.9 ) and 56 % of such deaths occurred within 72 hours of onset . In patients with cerebral infa rct ion , 51 % of deaths were due to complications of immobility ( for example , pneumonia , pulmonary embolism ) and these were more likely to occur after the first week . These findings have implication s for clinical practice and the planning of clinical trials 
    Output:
    
Overall , there is no evidence of a beneficial or adverse effect of corticosteroids in patients with either SAH or PICH .
Confidence intervals are wide and include clinical ly significant effects in both directions