***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 
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    Input: BACKGROUND The inconsistent effect of hypothermia treatment on severe brain injury in previous trials might be because hypothermia was induced too late after injury . We aim ed to assess whether very early induction of hypothermia improves outcome in patients with severe brain injury . METHODS The National Acute Brain Injury Study : Hypothermia II ( NABIS : H II ) was a r and omised , multicentre clinical trial of patients with severe brain injury who were enrolled within 2·5 h of injury at six sites in the USA and Canada . Patients with non-penetrating brain injury who were 16 - 45 years old and were not responsive to instructions were r and omly assigned ( 1:1 ) by a r and om number generator to hypothermia or normothermia . Patients r and omly assigned to hypothermia were cooled to 35 ° C until their trauma assessment was completed . Patients who had none of a second set of exclusion criteria were either cooled to 33 ° C for 48 h and then gradually rewarmed or treated at normothermia , depending upon their initial treatment assignment . Investigators who assessed the outcome measures were masked to treatment allocation . The primary outcome was the Glasgow outcome scale score at 6 months . Analysis was by modified intention to treat . This trial is registered with Clinical Trials.gov , NCT00178711 . FINDINGS Enrolment occurred from December , 2005 , to June , 2009 , when the trial was terminated for futility . Follow-up was from June , 2006 , to December , 2009 . 232 patients were initially r and omised a mean of 1·6 h ( SD 0·5 ) after injury : 119 to hypothermia and 113 to normothermia . 97 patients ( 52 in the hypothermia group and 45 in the normothermia group ) did not meet any of the second set of exclusion criteria . The mean time to 35 ° C for the 52 patients in the hypothermia group was 2·6 h ( SD 1·2 ) and to 33 ° C was 4·4 h ( 1·5 ) . Outcome was poor ( severe disability , vegetative state , or death ) in 31 of 52 patients in the hypothermia group and 25 of 56 in the normothermia group ( relative risk [ RR ] 1·08 , 95 % CI 0·76 - 1·53 ; p=0·67 ) . 12 patients in the hypothermia group died compared with eight in the normothermia group ( RR 1·30 , 95 % CI 0·58 - 2·52 ; p=0·52 ) . INTERPRETATION This trial did not confirm the utility of hypothermia as a primary neuroprotective strategy in patients with severe traumatic brain injury 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 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 is a major cause of death and severe disability worldwide with 1,000,000 hospital admissions per annum throughout the European Union . Therapeutic hypothermia to reduce intracranial hypertension may improve patient outcome but key issues are length of hypothermia treatment and speed of re-warming . A recent meta- analysis showed improved outcome when hypothermia was continued for between 48 hours and 5 days and patients were re-warmed slowly ( 1 ° C/4 hours ) . Previous experience with cooling also appears to be important if complications , which may outweigh the benefits of hypothermia , are to be avoided . Methods / design This is a pragmatic , multi-centre r and omised controlled trial examining the effects of hypothermia 32 - 35 ° C , titrated to reduce intracranial pressure < 20 mmHg , on morbidity and mortality 6 months after traumatic brain injury . The study aims to recruit 1800 patients over 41 months . Enrolment started in April 2010 . Participants are r and omised to either st and ard care or st and ard care with titrated therapeutic hypothermia . Hypothermia is initiated with 20 - 30 ml/kg of intravenous , refrigerated 0.9 % saline and maintained using each centre 's usual cooling technique . There is a guideline for detection and treatment of shivering in the intervention group . Hypothermia is maintained for at least 48 hours in the treatment group and continued for as long as is necessary to maintain intracranial pressure < 20 mmHg . Intracranial hypertension is defined as an intracranial pressure > 20 mmHg in accordance with the Brain Trauma Foundation Guidelines , 2007 . Discussion The Eurotherm3235Trial is the most important clinical trial in critical care ever conceived by European intensive care medicine , because it was launched and funded by the European Society of Intensive Care Medicine and will be the largest non-commercial r and omised controlled trial due to the substantial number of centres required to deliver the target number of patients . It represents a new and fundamental step for intensive care medicine in Europe . Recruitment will continue until January 2013 and interested clinicians from intensive care units worldwide can still join this important collaboration by contacting the Trial Coordinating Team via the trial website http://www.eurotherm3235trial.eu . Trial registration Current Controlled Trials IS RCT Recent experimental studies have demonstrated that mild hypothermia at about 34 degrees C can be effective in the control of intracranial hypertension . A r and omized controlled study of mild hypothermia was carried out in 33 severely head-injured patients . All patients fulfilled the following criteria : 1 ) persistent intracranial pressure ( ICP ) greater than 20 mm Hg despite fluid restriction , hyperventilation , and high-dose barbiturate therapy ; 2 ) an ICP lower than the mean arterial blood pressure ; and 3 ) a Glasgow Coma Scale score of 8 or less . The patients were divided into two groups : one received  mild hypothermia  ( 16 patients ) and one served as a control group ( 17 patients ) . Mild hypothermia significantly reduced the ICP and increased the cerebral perfusion pressure . Eight patients ( 50 % ) in the hypothermia group and three ( 18 % ) in the control group survived ( p < 0.05 ) , while five ( 31 % ) in the hypothermia group and 12 ( 71 % ) in the control group died of uncontrollable intracranial hypertension ( p < 0.05 ) . In five patients in the hypothermia group , cerebral blood flow was measured by the hydrogen clearance method and arteriojugular venous oxygen difference was evaluated before and during mild hypothermia . Mild hypothermia significantly decreased the cerebral blood flow , arteriojugular venous oxygen difference , and cerebral metabolic rate of oxygen ( p < 0.01 ) . The results of this preliminary investigation suggest that mild hypothermia is a safe and effective method to control traumatic intracranial hypertension and to improve mortality and morbidity rates PURPOSE We investigated the effects of therapeutic mild hypothermia on patients with severe traumatic brain injury after craniotomy ( TBI ) . METHODS Eighty patients with severe TBI after unilateral craniotomy were r and omized into a therapeutic hypothermia group with the brain temperature maintained at 33 degrees C to 35 degrees C for 4 days , and a normothermia control group in the intensive care unit . Vital signs , intracranial pressure , serum superoxide dismutase level , Glasgow Outcome Scale scores , and complications were prospect ively analyzed . RESULTS The mean intracranial pressure values of the therapeutic hypothermia group at 24 , 48 , and 72 hours after injury were much lower than those of the control group ( 23.49 + /- 2.38 , 24.68 + /- 1.71 , and 22.51 + /- 2.44 vs 25.87 + /- 2.18 , 25.90 + /- 1.86 , and 24.57 + /- 3.95 mm Hg ; P = .000 , .000 , and .003 , respectively ) . The mean serum superoxide dismutase levels of the therapeutic hypothermia group at days 3 and 7 were much higher than those of the control group at the same time point ( 533.0 + /- 103.4 and 600.5 + /- 82.9 vs 458.7 + /- 68.1 and 497.0 + /- 57.3 mug/L , respectively ; P = .000 ) . The percentage of favorable neurologic outcome 1 year after injury was 70.0 % and 47.5 % , respectively ( P = .041 ) . Complications , including pulmonary infections ( 57.5 % in the therapeutic hypothermia group vs 32.5 % in the control group ; P = .025 ) were managed without severe sequelae . CONCLUSIONS Therapeutic mild hypothermia provides a promising way in the intensive care unit for patients with severe TBI after craniotomy Studies in adults have demonstrated improved outcomes using moderate hypothermia in the management of acute traumatic brain injury ( 1–6 ) . Moderate hypothermia may reduce secondary brain injury by reducing cerebral ischemia , edema , and tissue injury and by attenuating the production of excitatory amino acids ( 7–10 ) . A rat model utilizing mechanical traumatic brain injury and transient forebrain ischemia demonstrated that the peak time of vulnerability for posttraumatic secondary brain ischemia occurs within the first 24 hrs ( 11 ) . Another model demonstrated that apoptotic cells were detectable for up to 72 hrs after the initial brain injury , reaching a peak at approximately 24 to 48 hrs . In the animals treated with moderate hypothermia ( 32 ° C ) , the numbers of apoptotic cells were reduced , and DNA fragmentation was inhibited ( 12 ) . Studies evaluating the efficacy of moderate hypothermia in the management of acute traumatic brain injury have had variable entry criteria , time to entry , and duration of hypothermia . Shiozaki et al. ( 1 ) utilized hypothermia of 33.5–34.5 ° C for a minimum of 48 hrs after failure of conventional 
    Output:
    
Hypothermia was associated with cerebrovascular disturbances on rewarming and possibly with pneumonia in adult patients .
Given the quality of the data currently available , no benefit of  PTH on mortality or neurological morbidity could be identified .