Measurement Of Brain Temperature Research Articles

Sleep-wake behavior and responses to sleep deprivation of mice lacking both interleukin-1β receptor 1 and tumor necrosis factor-α receptor 1

Data indicate that interleukin (IL)-1β and tumor necrosis factor-α (TNFα) are involved in the regulation of non-rapid eye movement sleep (NREMS). Previous studies demonstrate that mice lacking the IL-1β type 1 receptor spend less time in NREMS during the light period, whereas mice lacking the p55 (type 1) receptor for TNFα spend less time in NREMS during the dark period. To further investigate roles for IL-1β and TNFα in sleep regulation we phenotyped sleep and responses to sleep deprivation of mice lacking both the IL-1β receptor 1 and TNFα receptor 1 (IL-1R1/TNFR1 KO). Male adult mice (IL-1R1/TNFR1 KO, n = 14; B6129SF2/J, n = 14) were surgically instrumented with EEG electrodes and with a thermistor to measure brain temperature. After recovery and adaptation to the recording apparatus, 48 h of undisturbed baseline recordings were obtained. Mice were then subjected to 6 h sleep deprivation at light onset by gentle handling. IL-1R1/TNFR1 KO mice spent less time in NREMS during the last 6 h of the dark period and less time in rapid eye movement sleep (REMS) during the light period. There were no differences between strains in the diurnal timing of delta power during NREMS. However, there were strain differences in the relative power spectra of the NREMS EEG during both the light period and the dark period. In addition, during the light period relative power in the theta frequency band of the REMS EEG differed between strains. After sleep deprivation, control mice exhibited prolonged increases in NREMS and REMS, whereas the duration of the NREMS increase was shorter and there was no increase in REMS of IL-1R1/TNFR1 KO mice. Delta power during NREMS increased in both strains after sleep deprivation, but the increase in delta power during NREMS of IL-1R1/TNFR1 KO mice was of greater magnitude and of longer duration than that observed in control mice. These results provide additional evidence that the IL-1β and TNFα cytokine systems play a role in sleep regulation and in the alterations in sleep that follow prolonged wakefulness.

Forced convective head cooling device reduces human cross-sectional brain temperature measured by magnetic resonance: a non-randomized healthy volunteer pilot study

This pilot study in five healthy adult humans forms the pre-clinical assessment of the effect of a forced convective head cooling device on intracranial temperature, measured non-invasively by magnetic resonance spectroscopy (MRS). After a 10 min baseline with no cooling, subjects received 30 min of head cooling followed by 30 min of head and neck cooling via a hood and neck collar delivering 14.5 degrees C air at 42.5 litre s(-1). Over baseline and at the end of both cooling periods, MRS was performed, using chemical shift imaging, to measure brain temperature simultaneously across a single slice of brain at the level of the basal ganglia. Oesophageal temperature was measured continuously using a fluoroptic thermometer. MRS brain temperature was calculated for baseline and the last 10 min of each cooling period. The net brain temperature reduction with head cooling was 0.45 degrees C (SD 0.23 degrees C, P=0.01, 95% CI 0.17-0.74 degrees C) and with head and neck cooling was 0.37 degrees C (SD 0.30 degrees C, P=0.049, 95% CI 0.00-0.74 degrees C). The equivalent net reductions in oesophageal temperature were 0.16 degrees C (SD 0.04 degrees C) and 0.36 degrees C (SD 0.12 degrees C). Baseline-corrected brain temperature gradients from outer through intermediate to core voxels were not significant for either head cooling (P=0.43) or head and neck cooling (P=0.07), indicating that there was not a significant reduction in cooling with progressive depth into the brain. Convective head cooling reduced MRS brain temperature and core brain was cooled.

The Impact of Brain Temperature and Core Temperature on Intracranial Pressure and Cerebral Perfusion Pressure

Hyperthermia has been demonstrated to increase neuronal injury when present during or after an acute brain injury. The assumption that core temperature equals brain temperature exists. If the temperature of an injured brain is higher than core temperature, episodes of neural hyperthermia may go undetected. The objectives of this study were to (1) determine if differences exist between brain temperature and core temperature in subjects with acute neurological injuries in both normothermic and febrile states and (2) investigate the impact of brain and core temperatures on intracranial pressure (ICP) and cerebral perfusion pressure (CPP). The study was conducted through a retrospective chart audit of patients age 18 years or older admitted to a level I trauma center with a diagnosis of brain injury whose condition warranted placement of a pulmonary artery catheter (which measured core temperature) and an intraventricular catheter (which measured brain temperature). Thirty-one charts contained complete data; nine charts provided partial data. Mean brain temperature (100.8 degrees F, SD = 0.69) was found to be significantly higher than mean core temperature (100.2 degrees F, SD = 0.74; p = .00). Brain temperature means were hyperthermic (> or = 100.9 degrees F), while matching core temperatures were normothermic in almost one-third of the subjects. There was no significant difference found between hyperthermic ICP or CPP and normothermic ICP or CPP determined by brain or core temperature. No significant correlation was found between temperature and intracranial dynamics. Future research is needed with prospectively collected data of adequate sample size to continue to investigate the impact of core and brain temperature on the intracranial dynamics of ICP and CPP.

Hyperthermia and voluntary exhaustion: integrating models and future challenges

Over the past decade, research interest has risen on the direct effects of temperature on exercise capacity and tolerance, particular in the heat. Two major paradigms have been proposed for how hyperthermia may contribute to voluntary fatigue during exercise in the heat. One suggests that voluntary exhaustion occurs upon the approach or attainment of a critical internal temperature through impairment in a variety of physiological systems. An alternate perspective proposes that thermal inputs modulate the regulation of self-paced workload to minimize heat storage. This review seeks to summarize recent research leading to the development of these two models for hyperthermia and fatigue and explore possible bridges between them. Key areas for future research and development into voluntary exhaustion in the heat include (i) the development of valid and non-invasive means to measure brain temperature, (ii) understanding variability in perception and physiological responses to heat stress across individuals, (iii) extrapolating laboratory studies to field settings, (iv) understanding the failure in behavioural and physiological thermoregulation that leads to exertional heat illness, and (v) the integration of physiological and psychological parameters limiting voluntary exercise in the heat.

Temperature gradient between brain tissue and arterial blood mirrors the flow‐metabolism relationship in uninjured brain: an experimental study

The purpose of the present experimental study was to determine the feasibility and usefulness of brain temperature measurement (T(br)) and the calculated difference between brain temperature and arterial blood temperature (DeltaT(br-a)) in uninjured brain during variations of cerebral perfusion pressure (CPP) and concomitant changes of the regional cerebral blood flow (rCBF). Nine anaesthetized pigs were subjected to controlled CPP decrease to assess the lower cerebral autoregulation threshold. A parenchymal intracranial pressure (ICP) sensor combined with a microthermistor for temperature measurement, a miniaturized Clark-type electrode measuring brain tissue oxygenation (p(ti)O(2)), a small flexible intraparenchymal thermodilution probe for measuring rCBF and cerebral microdialysis were inserted carefully in the frontal white matter. Analysing the p(ti)O(2) during controlled CPP decrease, we found significant breakpoints of p(ti)O(2) at a CPP of 40 mmHg and 20 mmHg, related to an rCBF of 20 ml/100 g/min and approximately 10 ml/100 g/min. Similarly, the relationship between DeltaT(br-a), and CPP or rCBF revealed a characteristic increase of DeltaT(br-a) in the negative direction up to more than -0.30 degrees C assuming a strong flow dependency. The temperature difference between brain tissue and arterial blood DeltaT(br-a) mainly reflects the cerebral blood flow-brain tissue oxygenation-metabolism relationship as far as the estimation of the individual lower cerebral autoregulation threshold.

Measurement of brain temperature with magnetic resonance spectroscopy in acute ischemic stroke

Pyrexia is associated with poor outcome after stroke, but the temperature changes in the brain after stroke are poorly understood. We used magnetic resonance spectroscopic imaging (water-to-N-acetylaspartate frequency shift) to measure cerebral temperature noninvasively in stroke patients. We performed magnetic resonance diffusion, perfusion (diffusion- and perfusion-weighted imaging), and magnetic resonance spectroscopic imaging, compared temperatures in tissues as defined by the diffusion-weighted imaging appearance (definitely abnormal, possibly abnormal and immediately adjacent normal-appearing brain, and normal brain), and tested associations with lesion and patient characteristics. Among 40 patients, temperature was higher in possibly abnormal (37.63 degrees C) than in definitely abnormal tissue (37.30 degrees C; p < 0.001) or in normal-appearing brain (ipsilateral, 37.16 degrees C; contralateral, 37.22 degrees C; both p < 0.001). Ischemic lesion temperature increased before normal brain temperature. Higher temperatures occurred in lesions that were large, had diffusion/perfusion-weighted imaging mismatch, had reduced cerebral blood flow, and in clinically severe strokes. Only 1 of 25 patients with ischemic lesion temperature greater than 37.5 degrees C was pyrexial. Temperature is elevated in acutely ischemic brain. More work is required to determine whether raised temperature results from ischemic metabolic reactions, impaired heat exchange from reduced cerebral blood flow, or early inflammatory cell activity (or a combination of these), but magnetic resonance spectroscopic imaging could be used in studies of temperature after brain injury and to monitor interventions.

Differences between brain and rectal temperatures during routine critical care of patients with severe traumatic brain injury*

Theoretical models suggest that small differences only exist between brain and body temperature in health. Once the brain is injured, brain temperature is generally regarded to rise above body temperature. However, since reports of the magnitude of the temperature gradient between brain and body vary, it is still not clear whether conventional body temperature monitoring accurately predicts brain temperature at all times. In this prospective, descriptive study, 20 adults with severe primary brain trauma were studied during their stay in the neurointensive care unit. Brain temperature ranged from 33.4 to 39.9 degrees C. Comparisons between paired brain and rectal temperature measurements revealed no evidence of a systematic difference [mean difference -0.04 degrees C (range -0.13 to 0.05 degrees C, 95% CI), p = 0.39]. Contrary to popular belief, brain temperature did not exceed systemic temperature in this relatively homogeneous patient series. The mean values masked inconsistent and unpredictable individual brain-rectal temperature differences (range 1.8 to -2.9 degrees C) and reversal of the brain-body temperature gradient occurred in some patients. Brain temperature could not be predicted from body temperature at all times.

236 Non-Invasive Cerebral Temperature Mapping by Proton Spectroscopic Imaging

Background: Cerebral hypothermia shows promise as a neuroprotective strategy following perinatal hypoxia-ischaemia. A non-invasive technique for the quantification of regional brain temperature is urgently required to assess the cerebral effects of different cooling strategies. We aimed to test the hypothesis that thermometry by proton magnetic resonance spectroscopic imaging (1H-MRSI) is as accurate as invasive monitoring during whole body hypothermia and selective head cooling.Methods: Cerebral magnetic resonance (MR) data was acquired from 6 newborn piglets using a 7 Tesla Bruker Biospec MR system. Mild whole body hypothermia was induced in 3 piglets using a thermally regulated water mattress. For each animal measurements were collected at rectal temperatures (TR) of 38±1°C and 34±1°C. Mild hypothermia was induced in 3 piglets using a water-filled plastic “cooling cap” applied to the animals' scalp. In these animals measurements were obtained at (i) TR 38±1°C; cap temperature (TC) 20°C (ii) TR 34±1°C; TC10±2°C. 1H-MRSI data were acquired from a coronal slice (thickness 4mm; TE 45ms; TR 3000ms, 16x16 voxels each 3.75 x 3.75mm2) and processed using in-house software: for each voxel, separate water and metabolite spectra were obtained from a single non-water suppressed spectrum. The chemical shift difference between the water peak and n-acetylaspartate (NAA) was obtained by a cross-correlation method. This chemical shift difference was converted to absolute temperature using a previously validated calibration curve. A two dimensional cerebral temperature map of the selected slice was obtained in a single measurement. Invasive brain temperature measurements were obtained concurrently using a surgically inserted fibre-optic thermometer, which yielded 4 temperature values at successive 5mm intervals from the probe tip.Results: The graphs demonstrate 4 data points for each subject at each TR.Conclusion: 1H-MRSI is an accurate and robust non-invasive method of cerebral temperature measurement in both total body and selective head cooling models. The determination of regional brain temperature distributions in infants undergoing hypothermia treatment may provide new insights into the local effects of brain cooling and enable its neuroprotective potential to be optimised.

Brain temperature in patients with chronic hydrocephalus after subarachnoid hemorrhage.

The relationships between temperature indices and clinical condition on admission or improvement after ventriculoperitoneal (VP) shunting were evaluated in patients with subarachnoid hemorrhage (SAH). Brain temperatures were measured at intervals of 1 cm from the brain surface to the lateral ventricle at shunt operation. Rectal temperature was also measured. The difference between intraventricular and rectal temperatures was correlated with age (p = 0.0486), Glasgow Coma Scale (p = 0.0129), Hunt and Hess grade (p = 0.0101), and improvement score after VP shunting (p = 0.0104). Measurement of brain temperature may predict the outcome of VP shunting in patients with SAH.

Noninvasive measurement of regional human brain temperature using 1H magnetic resonance spectroscopy at 3T

Noninvasive measurement of regional human brain temperature using 1H magnetic resonance spectroscopy at 3T

17β-estradiol pretreatment reduces ca1sector cell death and the spontaneous hyperthermia that follows forebrain ischemia in the gerbil

Pretreatment with 17β-estradiol attenuates ischemia-induced hippocampal cornu ammonis 1 (CA1) neuronal death. We assessed whether this is mediated through prevention of hyperthermia that normally follows ischemia in gerbils. Male gerbils were given sustained-released 17β-estradiol pellets or sham operation. Later, a guide cannula was implanted for brain temperature measurement and some were implanted with core temperature telemetry probes. Gerbils were subjected to either 5 min bilateral carotid artery occlusion or sham procedures 2 weeks after pellet surgery. Brain temperature was normothermic during surgery in all cases. In experiment 1, only core temperature was measured afterward in untreated and estrogen-treated gerbils. In experiment 2, postischemic core temperature was measured in untreated and two estrogen-treated ischemic groups, one of which had their postischemic temperature increased, via infrared lamp, to mimic the untreated group. Habituation was assessed on days 5 and 6. Hyperthermia, like that which occurs spontaneously, was forced on untreated and estrogen-treated ischemic animals in the third experiment, where brain temperature was measured. CA1 cell counts were assessed after a 7-day survival. A fourth experiment measured brain and core temperature simultaneously in normal gerbils during heating with an infrared lamp. Estrogen did not affect core temperature of non-ischemic gerbils whereas spontaneous postischemic hyperthermia was blocked. Estrogen reduced cell death and provided behavioral protection when gerbils regulated their own core temperature, but not when core hyperthermia was enforced. Conversely, estrogen reduced cell death in gerbils that had their brain temperature elevated. Experiment 4 showed that the brain becomes overheated (by approximately 1 °C) when core temperature is elevated. Accordingly, estrogen likely failed to reduce CA1 injury in experiment 2, when core hyperthermia was enforced, because of overheating the brain. In conclusion, estrogen reduces CA1 cell death by mechanisms other than preventing hyperthermia. Our results also suggest that future studies regulate brain instead of body temperature.

Fluctuations in brain temperature during sexual interaction in male rats: an approach for evaluating neural activity underlying motivated behavior

Since metabolic activity is accompanied by heat release, measurement of brain temperatures offers a method for assessing behavior-associated changes in neural activity. To explore this possibility, we monitored local brain (nucleus accumbens, medial-preoptic hypothalamus, and hippocampus) and body (temporal muscle) temperature in an experienced male rat during sexual behavior with a sexually receptive female. Placement of the female into a neighboring compartment increased the male's temperature and additional increases occurred when rats were allowed to see and partially interact with the female through a Plexiglas barrier with dime-size holes. The temperature increase was robust (1.5–2.0 °C), faster in all brain areas than in muscle, and peaked (38–39 °C) when the barrier was removed and full interaction was allowed. As the male repeatedly mounted and achieved intromission with the female, temperature further increased, peaking at ejaculation (+0.2–0.4 °C). Following ejaculation, the temperature abruptly dropped, until sexual interest and interaction resumed. These biphasic temperature fluctuations were generally similar in each recording location, but all brain sites (particularly, nucleus accumbens and medial–preoptic hypothalamus) showed more profound changes than the muscle. These data generally match single-unit and other physiological findings, suggesting that male sexual behavior is accompanied by sustained and generalized neural activation. This activation is triggered by sexually relevant stimuli (arousal), maintained during repeated mounts and intromissions, and peaked at ejaculation. These findings suggest brain temperature fluctuations not only as a sensitive index of functional neural activation, but as a powerful factor affecting various neural functions and an important part of brain mechanisms underlying motivated behavior.

Brain temperature measurement and regulation in awake and freely moving rodents

Temperature measurement and control are essential in most ischemia experiments. Hypothermia lessens ischemic brain injury whereas hyperthermia exacerbates it. A substantial number of ischemia studies rely solely on rectal temperature measurements during the insult. However, rectal temperature may not accurately reflect brain temperature especially during global ischemia. Furthermore, postischemic temperature changes are often inadequately monitored. Delayed cooling reduces injury, whereas delayed hyperthermia aggravates it. This review summarizes our experiences with core and brain telemetry probes to continually measure temperature in various ischemia models. Furthermore, we discuss methods to simultaneously measure and regulate temperature in the freely moving postischemic rodent, and the need for such control in ischemia research.

Severe brain hypothermia as a factor underlying behavioral immobility during cold-water forced swim

Behavioral immobility during forced swim is usually considered a consequence of inescapable stress, and is used to screen antidepressant drugs. However, immobility in this test may also result from inhibition of neural functions because of brain hypothermia due to body cooling. To explore this possibility, we measured brain temperature dynamics during a 10-min forced swim in cold (25 °C) and warm (37 °C) water and correlated brain temperatures with behavioral changes. Cold water forced swim resulted in significant brain hypothermia (−6–7 °C) and immobility, while no immobility was observed during warm water forced swim, when brain temperature transiently increased (0.5 °C) then decreased below baseline in the post-swim period. These data suggest that immobility, which rapidly develops during forced swim in cold water, may result from dramatic inhibition of neural functions because of severe brain hypothermia.

Naloxone depresses cocaine self-administration and delays its initiation on the following day.

While dopamine mechanisms play a crucial role in cocaine-taking behavior, the contribution of endogenous opioid systems is less clear. We assessed the effects of opioid receptor blockade by naloxone (1 mg/kg, s.c.) on the daily performance and subsequent initiation of cocaine self-administration in trained rats. Naloxone decreased self-administration rate by approximately half, with the effect varying from complete blockade to no change. On the day following naloxone treatment, the latencies from the drug availability cue to the first self-administration were consistently longer than before naloxone treatment. Measurement of brain temperature and behavioral observations suggested a lower than normal level of motivational arousal as a factor for slow initiation of cocaine-taking behavior. After the first drug infusion, however, performance was uniformly normal. These data suggest endogenous opioid systems play a role in cocaine-taking behavior and indicate a residual inhibitory consequence of naloxone treatment on the initiation of this behavior.

Fluctuations in neural activity during cocaine self-administration: clues provided by brain thermorecording

Since metabolic neural activity is accompanied by heat release, measurement of local brain temperature offers a method for assessing alterations in neural activity. This approach, continuous monitoring of local brain (ventral tegmental area, ventral striatum, and hippocampus) and body (temporal muscle) temperature, was used to study intravenous cocaine self-administration in trained rats. The first self-administration of a session was preceded by a strong temperature increase that continued after the drug infusion. After peaking at the time of the second self-administration, temperature plateaued (+0.7 °C) with biphasic fluctuations (±0.10–0.15 °C) around each subsequent self-administration. Temperature gradually increased before and for 30–50 s after the lever-press, but then abruptly decreased to a minimum at 180–240 s, when it began to increase to reach another peak immediately after the next lever-press. Doubling the dose of injected cocaine significantly potentiated the post-cocaine temperature decrease and increased time to the next lever-press. In contrast to drug-reinforced lever-presses, temperatures phasically increased after non-reinforced lever-presses and at the end of a session when the lever was blocked and the rat was hyperactive, trying to reach the inaccessible lever. While temperature changes in each recording location were generally correlative, the initial temperature elevation was stronger in all brain structures than in muscle and ventral striatum was the structure that showed the most pronounced and consistent temperature fluctuations. These data suggest a generalized brain activation associated with cocaine-seeking and cocaine-taking behavior with its phasic fluctuations around individual drug self-injections. While the initial component of brain activation preceding the first lever-press for cocaine is internally determined and closely related to behavioral search, subsequent biphasic fluctuations in neural activity associated with repeated drug intakes appear to be drug-mediated. Cocaine-induced potentiation of monoamine transmission is a possible factor for gradual increases in neural activity that drive cocaine seeking, while a rapid, brain concentration-dependent action on Na + transport (local anesthetic action) is the most probable factor determining an abrupt, transient cessation of neural activation associated with cocaine reward.

Brain temperature measurements during speech in patients with brain tumors: new methods for identification of the speech area in intraoperative brain mappings

In the present study, the usefulness of a functional thermography (fTG) for determining critical speech area was assessed in three patients with brain tumors in language areas. The results of the fTG were also compared with functional MRI (fMRI), subdural electrodes and intraoperative cortical stimulations. Measurements of the regional brain temperature were done using the thermography. The temperature increased after 8–10 s later from the speech and decreased with a few seconds delay after interruption of the task. The areas of increased temperature were coincident with the bridging veins and functional areas identified using fMRI and direct cortical stimulations. The use of fTG increases the sensitivity and specificity for the detection of essential motor language area.

The effect of selective brain cooling on intracerebral temperature during craniotomy.

In this study we investigated the effect of topical application of cool irrigation fluid on brain tissue temperature during craniotomy. Eight patients were given a standard general anaesthetic for craniotomy. Distal oesophageal and nasopharyngeal temperatures were measured continuously and systemic normothermia was maintained. A sterile needle temperature probe was inserted 18 mm into the cerebrum to measure brain temperature. Brain temperatures were recorded for five minutes while the brain was irrigated with 1000 ml of normal saline at a temperature of 30 degrees C. Measurement continued until the brain temperature returned to baseline. The mean maximum decrease in cerebralparenchymal temperaturefollowing irrigation was 1.6 +/- 0.5 degrees C (P<0.01). The average time to return to baseline temperature after cessation of irrigation was 5.3 +/- 1.5 minutes. Cooling the brain has a marked protective effect after brain injury, but systemic hypothermia can produce significant harmful effects. This study demonstrates that the use of cool irrigation fluid during neurosurgery is a simple and effective method of cooling the brain whilst minimizing the use of systemic hypothermia.

Effect of hypothermia on brain tissue oxygenation in patients with severe head injury

There is renewed interest in the use of induced hypothermia as a method of neuroprotection both intraoperatively and in the intensive care management of severe brain injury. In this study we have investigated the effects of hypothermia on brain tissue oxygenation in patients with severe head injury. Thirty patients with severe head injury (Glasgow coma score <8) were monitored with a multimodal sensor inserted into the brain which measures tissue PO2, PCO2, pH and temperature in addition to routine monitoring. Patients were cooled to a minimum of 33 degrees C when clinically indicated. For all 30 patients brain and systemic temperature correlated well (r=0.96). Brain temperature was consistently higher than systemic temperature by 0.41 +/- 0.26 degrees C (confidence limits). Brain tissue PO2 decreased with hypothermia, with a significant reduction below 35 degrees C (P<0.05). These results emphasize the advantage of measuring brain temperature directly, and suggest that decreasing brain temperature below 35 degrees C may impair brain tissue oxygenation.

Differences in brain temperature and cerebral blood flow during selective head versus whole-body cooling.

To compare brain temperature and cerebral blood flow (CBF) during head and body cooling, with and without systemic hypoxemia. Seventeen newborn swine were studied for either measurement of brain temperature alone (n = 9) or measurement of brain temperature and CBF (n = 8). All animals were ventilated and instrumented, and temperature probes were inserted into the rectum, into the brain at depths of 2 and 1 cm from the cortical surface, and on the dural surface. Blood flow was measured with microspheres. The protocol consisted of a control period, an interval of either head or body cooling, and cooling with 15 minutes of superimposed hypoxia. After a 1-hour recovery period, animals were exposed to the same sequence except that the alternate mode of cooling was evaluated. Head cooling with a constant rectal temperature resulted in an increase in the temperature gradient across the brain from the warmer central structures to the cooler periphery (brain 2 cm - dura temperature: 1.3 +/- 1.1 degrees C at control to 7.5 +/- 3.5 degrees C during cooling). Hypoxia superimposed on head cooling decreased the temperature gradient by at least 50%. In contrast, body cooling was associated with an unchanged temperature gradient across the brain (brain 2 cm - dura temperature: 1.5 +/- 1.2 degrees C at control to 1.1 +/- 0.9 degrees C during cooling). Hypoxia superimposed on body cooling did not change brain temperature. Both modes of brain cooling resulted in similar reductions of global CBF ( approximately 40%) and O(2) uptake. Brain hypothermia achieved through head or body cooling results in different brain temperature gradients. Alterations in systemic variables (ie, hypoxemia) alters brain temperature differently in these 2 modes of brain cooling. The mode of brain cooling may affect the efficacy of modest hypothermia as a neuroprotective therapy.