***TASK*** the task is to summarize an input biomedical literature in six sentences 
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    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
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    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 Animal research suggests that moderate therapeutic hypothermia may improve outcome after a severe head injury , but its efficacy has not been established in humans . The authors r and omly assigned 40 consecutively treated patients with a severe closed head injury ( Glasgow Coma Scale score 3 to 7 ) to either a  hypothermia or a normothermia group .  Using cooling blankets and cold saline gastric lavage , patients in the hypothermia group were cooled to 32 degrees to 33 degrees C ( brain temperature ) within a mean of 10 hours after injury , maintained at that temperature for 24 hours , and rewarmed to 37 degrees to 38 degrees C over 12 hours . Patients in the normothermia group were maintained at 37 degrees to 38 degrees C during this time . Deep-brain temperatures were monitored directly and used for all temperature determinations . Intracranial pressure ( ICP ) , cerebral blood flow ( CBF ) , and cerebral metabolic rate for oxygen ( CMRO2 ) were measured serially for all patients . Hypothermia significantly reduced ICP ( 40 % ) and CBF ( 26 % ) during the cooling period , and neither parameter showed a significant rebound increase after patients were rewarmed . Compared to the normothermia group , the mean CMRO2 in the hypothermia group was lower during cooling and higher 5 days after injury . Three months after injury , 12 of the 20 patients in the hypothermia group had moderate , mild , or no disabilities ; eight of the 20 patients in the normothermia group had improved to the same degree . Both groups had a similar incidence of systemic complications , including cardiac arrhythmias , coagulopathies , and pulmonary complications . It is concluded that therapeutic moderate hypothermia is safe and has sustained favorable effects on acute derangements of cerebral physiology and metabolism caused by severe closed head injury . The trend toward better outcome with hypothermia may indicate that its beneficial physiological and metabolic effects limit secondary 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 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 Summary Treatment resistant intracranial hypertension after severe head injury has a very high mortality with conventional therapy such as hyperventilation and mannitol infusions . In this report , we describe the use of large doses of thiopental as a means of treating such swelling . From a consecutive series of 107 severe head injuries with a Glasgow Coma Score ( GCS ) of 6 or below , we selected all patients below 40 years age with a progressive increase in intracranial pressure ( ICP ) to 40 mm Hg . The first 16 patients ( mean age 20 years , mean GCS 4.3 ) were treated with deep barbiturate coma and hypothermia ( 32–35 degrees Celsius ) until stable lowering of ICP was achieved . The next 15 patients received conventional intensive care and were in other respects very similar to the barbiturate group ( mean age 26 , mean GCS 5.2).After 9–12 months the outcome was classified according to the Glasgow Outcome Scale ( GOS ) . Therapy with barbiturate coma result ed in 6 good/moderate outcomes , 3 severe and 7 dead/vegetative . Conventional treatment result ed in 2 good/moderate outcomes and 13 dead/vegetative . This is a highly significant difference and can not easily be explained by more severe injuries or complications in the conventional group . Superior control of ICP was achieved by large doses of thiopental and the final outcome was better 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 therapy , including barbiturate therapy . Tateishi et al. ( 13 ) induced hypothermia within 24 hrs and continued for a mean duration of 68 hrs ( range , 20–118 hrs ) . Marion et al. ( 2 , 3 ) reported a mean time of 10 hrs from injury to  hypothermia  that was maintained for 24 hrs . Clifton et al. ( 5 , 14 ) induced cooling within 6 hrs of injury and maintained hypothermia for 48 hrs . Although hypothermia has been utilized for 40 yrs in the management of traumatic brain injury in adults ( 15–17 ) , reports of its use in children are few ( 18 ) . Due to the paucity of information in the pediatric population and animal data that suggest that significant secondary brain injury and apoptosis occur 24 to 48 hrs after brain injury ( 11 , 12 ) , we opted for a study design similar to that of Clifton et al. ( 5 , 14 ) . We hypothesized that in children with acute traumatic brain injury , 48 hrs of moderate hypothermia ( 32– 34 ° C , initiated within 6 hrs of injury ) , in conjunction with st and ard conventional management of intracranial hypertension , would result in decreased severity and duration of intracranial hypertension and a favorable cerebral physiology compared with patients treated with normothermia . Furthermore , we hypothesized that this duration of moderate hypothermia would be safe and not associated with serious adverse clinical events , such as bleeding , electrolyte disturbances , pneumonia , or other infections OBJECTIVE The purpose of this r and omized , prospect i ve clinical trial was to determine whether hypotherm 
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REVIEW ERS ' CONCLUSIONS There is no evidence that hypothermia is beneficial in the treatment of head injury .
Hypothermia increases the risk of pneumonia and has other potentially harmful side-effects .
Therefore , it would seem inappropriate to use this intervention outside of controlled trials in subgroups of patients for whom there is good reason to think the treatment would be beneficial