***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: BACKGROUND Induction of hypothermia in patients with brain injury was shown to improve outcomes in small clinical studies , but the results were not definitive . To study this issue , we conducted a multicenter trial comparing the effects of hypothermia with those of normothermia in patients with acute brain injury . METHODS The study subjects were 392 patients 16 to 65 years of age with coma after sustaining closed head injuries who were r and omly assigned to be treated with hypothermia ( body temperature , 33 degrees C ) , which was initiated within 6 hours after injury and maintained for 48 hours by means of surface cooling , or normothermia . All patients otherwise received st and ard treatment . The primary outcome measure was functional status six months after the injury . RESULTS The mean age of the patients and the type and severity of injury in the two treatment groups were similar . The mean ( + /-SD ) time from injury to r and omization was 4.3+/-1.1 hours in the hypothermia group and 4.1+/-1.2 hours in the normothermia group , and the mean time from injury to the achievement of the target temperature of 33 degrees C in the hypothermia group was 8.4+/-3.0 hours . The outcome was poor ( defined as severe disability , a vegetative state , or death ) in 57 percent of the patients in both groups . Mortality was 28 percent in the hypothermia group and 27 percent in the normothermia group ( P=0.79 ) . The patients in the hypothermia group had more hospital days with complications than the patients in the normothermia group . Fewer patients in the hypothermia group had high intracranial pressure than in the normothermia group . CONCLUSIONS Treatment with hypothermia , with the body temperature reaching 33 degrees C within eight hours after injury , is not effective in improving outcomes in patients with severe brain injury OBJECT This study was performed to determine whether mild hypothermia therapy is essential for the treatment of severely head injured patients in whom intracranial pressure ( ICP ) can be maintained below 20 mm Hg by using conventional therapies . METHODS Sixteen consecutive severely head injured patients fulfilled the following criteria : the patient 's ICP was maintained below 20 mm Hg by using fluid restriction , hyperventilation , and high-dose barbiturate therapy ; and the patient had a Glasgow Coma Scale score of 8 or less on admission . After conventional therapies had been applied , the patients were divided r and omly into two groups : the mild hypothermia group ( HT group ; eight patients ) and the normothermia group ( NT group ; eight patients ) . The HT group received mild hypothermia ( intracranial temperature 34 degrees C ) therapy for 48 hours followed by rewarming at 1 degree C per day for 3 days , whereas the NT group received normothermia ( intracranial temperature 37 degrees C ) therapy for 5 days . Specimens of cerebrospinal fluid ( CSF ) taken from an intraventricular catheter every 24 hours were analyzed for the presence of excitatory amino acids ( [ EAAs ] glutamate , aspartate , and glycine ) and cytokines ( tumor necrosis factor-alpha , interleukin [IL]-1beta , IL-6 , IL-8 , and IL-10 ) . The two groups did not differ significantly in patient age , neurological status , or level of ICP . There were no significant differences in daily changes in CSF concentrations of EAAs and cytokines between the two groups . The incidence of pneumonia was slightly higher in the HT group compared with the NT group ( p = 0.059 ) . The incidence of diabetes insipidus associated with hypernatremia was significantly higher in the HT group compared with that in the NT group ( p < 0.01 ) . The two groups did not differ with respect to their clinical outcomes . CONCLUSIONS The authors recommend normothermia therapy for the treatment of severely head injured patients in whom ICP can be maintained at lower than 20 mm Hg by using conventional therapies , because mild hypothermia therapy does not convey any advantage over normothermia therapy in such patients OBJECTIVE To observe the changes of evoked potentials after severe brain injury and the effect of mild hypothermia on acute severe brain injury . METHODS A total of 44 patients with severe closed head injury ( GCS 3 - 8 , admitted within 10 hours from injury ) admitted from May 1998 to March 1999 were selected for this study . All patients were admitted into the intensive care unit and divided into 2 groups , Group A ( GCS 3 - 5 ) and Group B ( GCS 6 - 8 ) . Patients were also r and omly assigned to either normothermia or hypothermia subgroups . Patients in the hypothermia group were cooled to 32 - 34 degrees C. Median nerve short-latency somatosensory evoked potentials ( SLSEP ) and brain stem auditory evoked potentials ( BAEP ) were recorded before cooling and 4 , 24 , 48 , 72 , 96 and 120 hours , respectively after cooling and temperature resuming . SLSEP and BAEP were measured at the same time in the normothermia group ( control group ) . The changes of evoked potentials ( EP ) were analyzed by statistical methods . RESULTS In the Group B , N(20 ) amplitudes in SLSEP and I/V amplitudes in BAEP after mild hypothermia treatment in the hypothermia group differed significantly from those in the control group ( P<0.05 ) . However , in the Group A , no significant difference in all parameters was found . CONCLUSIONS These results demonstrate that mild hypothermia treatment ( 32 - 34 degrees C ) in the Group B has a significant neuroelectrophysiological effect on severe brain injury . Nevertheless , the effect of mild hypothermia in the Group A is not apparent and needs further study ing BACKGROUND Traumatic brain injury initiates several metabolic processes that can exacerbate the injury . There is evidence that hypothermia may limit some of these deleterious metabolic responses . METHODS In a r and omized , controlled trial , we compared the effects of moderate hypothermia and normothermia in 82 patients with severe closed head injuries ( a score of 3 to 7 on the Glasgow Coma Scale ) . The patients assigned to hypothermia were cooled to 33 degrees C a mean of 10 hours after injury , kept at 32 degrees to 33 degrees C for 24 hours , and then rewarmed . A specialist in physical medicine and rehabilitation who was unaware of the treatment assignments evaluated the patients 3 , 6 , and 12 months later with the use of the Glasgow Outcome Scale . RESULTS The demographic characteristics and causes and severity of injury were similar in the hypothermia and normothermia groups . At 12 months , 62 percent of the patients in the hypothermia group and 38 percent of those in the normothermia group had good outcomes ( moderate , mild , or no disabilities ) . The adjusted risk ratio for a bad outcome in the hypothermia group was 0.5 ( 95 percent confidence interval , 0.2 to 1.2 ) . Hypothermia did not improve the outcomes in the patients with coma scores of 3 or 4 on admission . Among the patients with scores of 5 to 7 , hypothermia was associated with significantly improved outcomes at 3 and 6 months ( adjusted risk ratio for a bad outcome , 0.2 ; 95 percent confidence interval , 0.1 to 0.9 at both intervals ) , although not at 12 months ( risk ratio , 0.3 ; 95 percent confidence interval , 0.1 to 1.0 ) . CONCLUSIONS Treatment with moderate hypothermia for 24 hours in patients with severe traumatic brain injury and coma scores of 5 to 7 on admission  hastened neurologic recovery and may have improved the outcome We prospect ively investigated noninvasive selective brain cooling ( SBC ) in patients with severe traumatic brain injury . Sixty-six in- patients were r and omized into three groups . In one group , brain temperature was maintained at 33 - 35 ° C by cooling the head and neck (SBC);in a second group , mild systemic hypothermia ( MSH ; rectal temperature 33 - 35 ° C ) was produced with a cooling blanket ; and a control group was not exposed to hypothermia . Natural re-warming began after 3 days . Mean intracranial pressure 24 , 48 or 72 h after injury was significantly lower in the SBC group than in the control group . Mean serum superoxide dismutase levels on Days 3 and 7 after injury in the SBC and MSH groups were significantly higher than in the control group . The percentage of patients with a good neurological outcome 2 years after injury was 72.7 % , 57.1 % and 34.8 % in the SBC , MSH and control groups , respectively . Complications were managed without severe sequelae . Non-invasive SBC was safe and effective Forty-six patients with severe nonpenetrating brain injury [ Glasgow Coma Scale ( GCS ) 4 - 7 ] were r and omized to st and ard management at 37 degrees C ( n = 22 ) and to  st and ard management with systemic hypothermia to 32 to 33 degrees C ( n = 24 ) . The two groups were balanced in terms of age ( Wilcoxon 's rank sum test , p > 0.95 ) , r and omizing GCS ( chi-square test , p = 0.54 ) , and primary diagnosis . Cooling was begun within 6 h of injury by use of cooling blankets . Metocurine and morphine were given hourly during induction and maintenance of hypothermia . Rewarming was at a rate of 1 degree C per 4 h beginning 48 h after intravascular temperature had reached 33 degrees C. Muscle relaxants and sedation were continued until core temperature reached 35 degrees C. There were no cardiac or coagulopathy-related complications . Seizure incidence was lower in the hypothermia group ( Fisher 's exact text , p = 0.019 ) . Sepsis was seen more commonly in the hypothermia group , but difference was not statistically significant ( chi-square test ) . Mean Glasgow Outcome Scale ( GOS ) score at 3 months after injury showed an absolute increase of 16 % ( i.e. , 36.4 - 52.2 % ) in the number of patients in the Good Recovery/Moderate Disability ( GR/MD ) category as compared with Severe Disability/Vegetative/Dead ( SD/V/D ) ( chi-square test , p > 0.287 ) . Based on evidence of improved neurologic outcome with minimal toxicity , we believe that phase III testing of moderate systemic hypothermia in patients with severe head injury is warranted OBJECT The criteria for the use of mild hypothermia ( 34 degrees C ) in severely head injured patients have not been st and ardized . A prospect i ve r and omized controlled trial was conducted to determine whether mild hypothermia is essential in the treatment of severely head injured patients with low intracranial pressure ( ICP ) . METHODS At 11 medical centers , 91 severely head injured patients with an admission Glasgow Coma Scale score of 8 or less in whom ICP could be maintained below 25 mm Hg by conventional therapies  were divided r and omly into two groups : the  mild hypothermia group ( HT group , 45 patients ) and the normothermia group ( NT group , 46 patients ) . Patients in the HT group were exposed to mild hypothermia ( 34 degrees C ) for 48 hours , followed by rewarming at 1 degrees C per day for 3 days , whereas patients in the NT group were exposed to normothermia ( 37 degrees C ) for 5 days . The two groups were similar with respect to prognostic factors , and there was no difference in clinical outcome at 3 months postinjury . During treatment , there was a significantly greater use of neuromuscular blocking agents in the HT group ( p = 0.011 ) . During the initial 2 weeks postinjury , the incidences of pneumonia , meningitis , leukocytopenia , thrombocytopenia , hypernatremia , hypokalemia , and hyperamylasemia were significantly higher in the HT than in the NT group ( p < 0.05 ) . CONCLUSIONS Mild hypothermia should not be used for the treatment of severely head injured patients with low ICP because this therapy conveys no advantage over normothermia in such patients Objective To examine the levels of thromboxane B2 ( TXB2 ) and 6-keto prostagl and in F1&agr ; ( 6-keto PGF1&agr ; ) production in arterial and internal jugular bulb sera in patients with traumatic brain injury ( TBI ) . TBI is associated with arachidonate release and may be associated with an imbalance of vasoconstricting and vasodilating cyclooxygenase metabolites . Design A prospect i ve , r and omized study . Setting The intensive care unit of a medical university hospital . Interventions Twenty-six ventilated TBI patents ( Glasgow Coma Scale score on admission , ≤8 points ) were divided r and omly into two groups : a hypothermic group ( n = 15 ) , in which the patients were cooled to 32 to 33 ° C after being giving vecuronium , midazolam , and buprenorphine ; and a normothermic group ( n = 11 ) , in which the patients ’ body temperature was controlled at 36 to 37 ° C by surface cooling using the same treatment as the hypothermic group . Body temperature control including normothermia was started 3 to 4 hrs after injury . The duration of hypothermia usually lasted for 3 to 4 days , after which the patients were rewarmed at a rate of approximately 1 ° C per day . Measurements and Main Results Blood sampling for TXB2 and 6-keto PGF1&agr ; was started shortly after admission in both groups . Arter 
    Output:
    
In sum , the present study 's up date d meta- analysis supports previous findings that hypothermic therapy constitutes a beneficial treatment of TBI in specific circumstances .