Regional Brain Temperature Research Articles

Neuroprotection provided by hypothermia initiated with high transnasal flow with ambient air in a model of pediatric cardiac arrest.

Clinical trials of hypothermia after pediatric cardiac arrest (CA) have not seen robust improvement in functional outcome, possibly because of the long delay in achieving target temperature. Previous work in infant piglets showed that high nasal airflow, which induces evaporative cooling in the nasal mucosa, reduced regional brain temperature uniformly in half the time needed to reduce body temperature. Here, we evaluated whether initiation of hypothermia with high transnasal airflow provides neuroprotection without adverse effects in the setting of asphyxic CA. Anesthetized piglets underwent sham-operated procedures (n = 7) or asphyxic CA with normothermic recovery (38.5°C; n = 9) or hypothermia initiated by surface cooling at 10 (n = 8) or 120 (n = 7) min or transnasal cooling initiated at 10 (n = 7) or 120 (n = 7) min after resuscitation. Hypothermia was sustained at 34°C with surface cooling until 20 h followed by 6 h of rewarming. At 4 days of recovery, significant neuronal loss occurred in putamen and sensorimotor cortex. Transnasal cooling initiated at 10 min significantly rescued the number of viable neurons in putamen, whereas levels in putamen in other hypothermic groups remained less than sham levels. In sensorimotor cortex, neuronal viability in the four hypothermic groups was not significantly different from the sham group. These results demonstrate that early initiation of high transnasal airflow in a pediatric CA model is effective in protecting vulnerable brain regions. Because of its simplicity, portability, and low cost, transnasal cooling potentially could be deployed in the field or emergency room for early initiation of brain cooling after pediatric CA.NEW & NOTEWORTHY The onset of therapeutic hypothermia after cardiac resuscitation is often delayed, leading to incomplete neuroprotection. In an infant swine model of asphyxic cardiac arrest, initiation of high transnasal airflow to maximize nasal evaporative cooling produced hypothermia sufficient to provide neuroprotection that was not inferior to body surface cooling. Because of its simplicity and portability, this technique may be of use in the field or emergency room for rapid brain cooling in pediatric cardiac arrest victims.

Brain temperature as an indicator of neuroinflammation induced by typhoid vaccine: Assessment using whole-brain magnetic resonance spectroscopy in a randomised crossover study

Prior studies indicate a pathogenic role of neuroinflammation in psychiatric disorders; however, there are no accepted methods that can reliably measure low-level neuroinflammation non-invasively in these individuals. Magnetic resonance spectroscopic imaging (MRSI) is a versatile, non-invasive neuroimaging technique that demonstrates sensitivity to brain inflammation. MRSI in conjunction with echo-planar spectroscopic imaging (EPSI) measures brain metabolites to derive whole-brain and regional brain temperatures, which may increase in neuroinflammation. The validity of MRSI/EPSI for measurement of low level neuroinflammation was tested using a safe experimental model of human brain inflammation – intramuscular administration of typhoid vaccine. Twenty healthy volunteers participated in a double-blind, placebo-controlled crossover study including MRSI/EPSI scans before and 3 h after vaccine/placebo administration. Body temperature and mood, assessed using the Profile of Mood States, were measured every hour up to four hours post-treatment administration. A mixed model analysis of variance was used to test for treatment effects. A significant proportion of brain regions (44/47) increased in temperature post-vaccine compared to post-placebo (p < 0.0001). For temperature change in the brain as a whole, there was no significant treatment effect. Significant associations were seen between mood scores assessed at 4 h and whole brain and regional temperatures post-treatment. Findings indicate that regional brain temperature may be a more sensitive measure of low-level neuroinflammation than whole-brain temperature. Future work where these measurement techniques are applied to populations with psychiatric disorders would be of clinical interest.

Abstract P324: Your Brain May Be "HOTTER" Than You Think, Results From Phase I Check Brain Temperature Study

Background: Hypothermia is a known neuronal protecting agent and used in post cardiac arrest. However, its use for stroke and brain trauma has not made any progress due to the lack of accurate way of measuring brain temperature. Hence, hypothermic degree and duration for it to be therapeutic is unknown. The phase I Check Brain Temperature Study was to define regional brain temperatures in normal individuals via MRI thermometry. The established brain temperature map can be used as the baseline to provide therapeutic hypothermia. Method: Temperatures of 5 regions of interest (ROI) of brain (frontal lobe, thalamus, hypothalamus, occipital lobe and cerebellum) were measured in 10 healthy individuals by using proton resonance frequency MRI spectroscopy single voxel method. The scanning protocol include a whole brain anatomical images, (3DFSPGR : TR/TE=150/3.9ms, FOV=24cm,matrix=256x256, slice thickness =1 mm.) and spectroscopy PRESS (TR/TE=1500/144 ms, 8 nex, 2 x 2 x 2 cm^3) on a GE 3T scanner. Ten right handed men (18&lt;age&lt;80) were recruited and their oral and tympanic temperatures were monitored. Average whole head temperature=average of oral temp+tympanic temp and average brain temp=average of temp of 5 regions of interest. Two tails, paired t-test used to compare temps between subjects and ROIs. Results: Average temperature differences between brain (38.2 °C) and head (36.5 °C) is 1.8 °C (p&lt; 0.0000002). Thalamus has the highest temperature among all ROIs in brain. Brain temperature &gt; oral temperature &gt; tympanic temperature. Conclusion: Brain temperatures may not correlate to body temperatures and there is a regional difference. Our finding will be used as the baseline brain temperature map when hypothermia is applied in patients with hemisphere stroke in the phase II study.

An In Vivo Assessment of Regional Brain Temperature during Whole-Body Cooling for Neonatal Encephalopathy

To assess differences in regional brain temperatures during whole-body hypothermia and test the hypothesis that brain temperature profile is nonhomogenous in infants with hypoxic-ischemic encephalopathy. Infants with hypoxic-ischemic encephalopathy were enrolled prospectively in this observational study. Magnetic resonance (MR) spectra of basal ganglia, thalamus, cortical gray matter, and white matter (WM) were acquired during therapeutic hypothermia. Regional brain tissue temperatures were calculated from the chemical shift difference between water signal and metabolites in the MR spectra after performing calibration measurements. Overall difference in regional temperature was analyzed by mixed-effects model; temperature among different patterns and severity of injury on MR imaging also was analyzed. Correlation between temperature and depth of brain structure was analyzed using repeated-measures correlation. In total, 53 infants were enrolled (31 girls, mean gestational age: 38.6±2weeks; mean birth weight: 3243±613g). MR spectroscopy was acquired at mean age of 2.2±0.6days. A total of 201MR spectra were included in the analysis. The thalamus, the deepest structure (36.4±2.3mm from skull surface), was lowest in temperature (33.2±0.8°C, compared with basal ganglia: 33.5±0.9°C; gray matter: 33.6±0.7°C; WM: 33.8±0.9°C, all P < .001). Temperatures in more superficial gray matter and WM regions (depth: 21.9±2.4 and 21.5±2.2mm) were greater than the rectal temperatures (33.4±0.4°C, P < .03). There was a negative correlation between temperature and depth of brain structure (rrm=-0.36, P < .001). Whole-body hypothermia was effective in cooling deep brain structures, whereas superficial structures were warmer, with temperatures significantly greater than rectal temperatures.

Safety and Reliability of Bedside, Single Burr Hole Technique for Intracranial Multimodality Monitoring in Severe Traumatic Brain Injury.

We aimed to provide a systematic description of our 2-year experience using a standardized bedside, single burr hole approach to intracranial multimodality monitoring (MMM) in patients with severe traumatic brain injury (sTBI), focusing on safety and probe reliability. We performed this observational cohort study at a university-affiliated, Level I trauma center with dedicated 20-bed neuroscience intensive care unit. We included 43 consecutive sTBI patients who required MMM to guide clinical care based on institutional protocol and had a four-lumen bolt placed to measure intracranial pressure, brain tissue oxygen, regional cerebral blood flow, brain temperature, and intracranial electroencephalography. sTBI patients were aged 41.6 ± 17.5years (mean ± SD) and 84% were men. MMM devices were placed at a median of 12.5h (interquartile range [IQR] 9.0-21.4h) after injury and in non-dominant frontal lobe in 72.1% of cases. Monitoring was conducted for a median of 97.1h (IQR 46.9-124.6h) per patient. While minor hemorrhage, pneumocephalus, or small bone chips were common, only one (2.4%) patient experienced significant hemorrhage related to device placement. Radiographically, device malpositioning was noted in 13.9% of patients. Inadvertent device discontinuation occurred for at least one device in 58% of patients and was significantly associated with the frequency of travel for procedures or imaging. Devices remained in place for > 80% of the total monitoring period and generated usable data > 50% of that time. A standardized, bedside single burr hole approach to MMM was safe. Despite some probe-specific recording limitations, MMM provided real-time measurements of intracranial pressure, oxygenation, regional cerebral blood flow, brain temperature, and function.

Comparison of Brain Temperature Distribution in Mathematical and Solid Models of Head Thermal Characteristics

SUMMARYAccurate temperature control of brain tissue during hypothermia treatment is necessary in order to prevent secondary brain damage and to avoid various side effects. Thus, the visualization of the intracerebral temperature distribution in hypothermia treatment was studied at the fundamental level. For this purpose a virtual reality technology was used to create a mathematical model that reflects metabolic heat production and Fourier heat conduction in a brain with the necessary parameters based on various clinical models. In the present study, an experimental system was developed to examine a mathematical simulation of the blood flow in a human head by using a solid brain model constructed using silicon rubber in the shape of a brain based on MRI data, taking into account the metabolic heat given off by three film heaters and including six sensors for the measurement of regional brain temperature. The mathematical simulation describes the internal temperature distribution in a brain with a similar structure to the brain solid model. The results of mathematical simulations and experiments using the brain solid model were quite consistent in the steady state, including control of regional temperature. This allows for the performance of heat conduction experiments under conditions similar to those of a living body, in which the internal temperature is clinically difficult to observe. Thus, the mathematical simulation is confirmed to be useful together with experiments using the solid model for the study of future brain hypothermia treatment.

Brain Temperature in Neonates with Hypoxic-Ischemic Encephalopathy during Therapeutic Hypothermia

To noninvasively determine brain temperature of neonates with hypoxic-ischemic encephalopathy (HIE) during and after therapeutic hypothermia. Using a phantom, we derived a calibration curve to calculate brain temperature based on chemical shift differences in magnetic resonance spectroscopy. We enrolled infants admitted for therapeutic hypothermia and assigned them to a moderate HIE (M-HIE) or severe HIE (S-HIE) group based on Sarnat staging. Rectal (core) temperature and magnetic resonance spectroscopy data used to derive regional brain temperatures (basal ganglia, thalamus, and cortical gray matter) were acquired concomitantly during and after therapeutic hypothermia. We compared brain and rectal temperature in the M-HIE and S-HIE groups during and after therapeutic hypothermia using 2-tailed t-tests. Eighteen patients (14 with M-HIE and 4 with S-HIE) were enrolled. As expected, both brain and rectal temperatures were lower during therapeutic hypothermia than after therapeutic hypothermia. Brain temperature in patients with S-HIE was higher than in those with M-HIE both during (35.1 ± 1.3°C vs 33.7 ± 1.2°C; P < .01) and after therapeutic hypothermia (38.1 ± 1.5°C vs 36.8 ± 1.3°C; P < .01). The brain-rectal temperature gradient was also greater in the S-HIE group both during and after therapeutic hypothermia. For this analysis of a small number of patients, brain temperature and brain-rectal temperature gradient were higher in neonates with S-HIE than in those with M-HIE during and after therapeutic hypothermia. Further studies are needed to determine whether further decreasing brain temperature in neonates with S-HIE is safe and effective in improving outcome.

Dual role of cerebral blood flow in regional brain temperature control in the healthy newborn infant

Small shifts in brain temperature after hypoxia–ischaemia affect cell viability. The main determinants of brain temperature are cerebral metabolism, which contributes to local heat production, and brain perfusion, which removes heat. However, few studies have addressed the effect of cerebral metabolism and perfusion on regional brain temperature in human neonates because of the lack of non-invasive cot-side monitors. This study aimed (i) to determine non-invasive monitoring tools of cerebral metabolism and perfusion by combining near-infrared spectroscopy and echocardiography, and (ii) to investigate the dependence of brain temperature on cerebral metabolism and perfusion in unsedated newborn infants.Thirty-two healthy newborn infants were recruited. They were studied with cerebral near-infrared spectroscopy, echocardiography, and a zero-heat flux tissue thermometer. A surrogate of cerebral blood flow (CBF) was measured using superior vena cava flow adjusted for cerebral volume (rSVC flow). The tissue oxygenation index, fractional oxygen extraction (FOE), and the cerebral metabolic rate of oxygen relative to rSVC flow (CMRO2 index) were also estimated.A greater rSVC flow was positively associated with higher brain temperatures, particularly for superficial structures. The CMRO2 index and rSVC flow were positively coupled. However, brain temperature was independent of FOE and the CMRO2 index. A cooler ambient temperature was associated with a greater temperature gradient between the scalp surface and the body core.Cerebral oxygen metabolism and perfusion were monitored in newborn infants without using tracers. In these healthy newborn infants, cerebral perfusion and ambient temperature were significant independent variables of brain temperature. CBF has primarily been associated with heat removal from the brain. However, our results suggest that CBF is likely to deliver heat specifically to the superficial brain. Further studies are required to assess the effect of cerebral metabolism and perfusion on regional brain temperature in low-cardiac output conditions, fever, and with therapeutic hypothermia.

Ischemic pretreatment delays ischemic brain vasospasm injury in gerbils.

Three experiments were conducted for the present study. First, to elucidate the mechanism and functional significance underlying ischemic vasoconstriction, we investigated the relationship between arteriolar constriction and tissue energy metabolism during bilateral common carotid artery occlusion in gerbils. Second, to identify differences in the postischemic recovery of physiologic parameters between short and prolonged brain ischemia, we measured changes in regional cerebral blood flow, microvessel diameter, brain temperature, and electrophysiologic response. Third, to explore the physiological mechanism of ischemic tolerance, we studied vascular response and intracerebral oxygenation states after acute global ischemia with and without pretreatment by mild ischemic stress. Here, we identify one of the physiologic mechanisms of the ischemic tolerance caused by brief ischemic pretreatment.

Comparison of Brain Temperature Distribution in Mathematical and Solid Models of Head Thermal Characteristics

SUMMARY Accurate temperature control of brain tissue during hypothermia treatment is necessary in order to prevent secondary brain damage and to avoid various side effects. Thus, the visualization of the intracerebral temperature distribution in hypothermia treatment was studied at the fundamental level. For this purpose a virtual reality technology was used to create a mathematical model that reflects metabolic heat production and Fourier heat conduction in a brain with the necessary parameters based on various clinical models. In the present study, an experimental system was developed to examine a mathematical simulation of the blood flow in a human head by using a solid brain model constructed using silicon rubber in the shape of a brain based on MRI data, taking into account the metabolic heat given off by three film heaters and including six sensors for the measurement of regional brain temperature. The mathematical simulation describes the internal temperature distribution in a brain with a similar structure to the brain solid model. The results of mathematical simulations and experiments using the brain solid model were quite consistent in the steady state, including control of regional temperature. This allows for the performance of heat conduction experiments under conditions similar to those of a living body, in which the internal temperature is clinically difficult to observe. Thus, the mathematical simulation is confirmed to be useful together with experiments using the solid model for the study of future brain hypothermia treatment. C⃝ 2015 Wiley Periodicals, Inc. Electr Eng Jpn, 193(2): 58–68, 2015; Published online in Wiley Online Library (wileyonlinelibrary.com). DOI 10.1002/eej.22642

Protective Facemask Impact on Human Thermoregulation: An Overview

The use of protective facemasks (PFMs) negatively impacts respiratory and dermal mechanisms of human thermoregulation through impairment of convection, evaporation, and radiation processes. The relatively minor reported increases in core temperature directly attributable to the wearing of PFMs suggest that associated perceptions of increased body temperature may have a significant psychological component or that regional or global brain temperature changes are involved. Modifications in PFM structure, components, and materials might allow for improved heat dissipation and enhanced compliance with use.

Environmental cooling of the newborn pig brain during whole‐body cooling

Therapeutic hypothermia after perinatal asphyxia decreases brain injury in newborns, whereas hyperthermia worsens the brain injury. We examined how different clinical practices influence regional brain temperatures during hypothermia. Six newborn pigs, which have comparable physiology and brain maturation to human term infants, were maintained at hypothermia (33.5°C) or normothermia with a servo-controlled whole-body cooling device that is in clinical use. Pigs were anesthetized and fully instrumented for cardiovascular and temperature (rectal and regional brain) monitoring. Changes in brain temperatures were measured during four different paradigms to mimic different clinical practices. Inserting an insulating pillow between the head and the heated surface reduced cortex temperature by 1 or 2°C during normothermia (core temperature T(core) 37°C) or hypothermia, T(core) 33.5°C. Reducing ambient temperature from 28°C to 23°C reduced cortex temperature by 3.9 ± 1.9°C. Without a hat and overhead heater at normothermia, cortex and deep brain temperatures were reduced by 1.2 ± 0.8 and 0.7 ± 0.7°C, respectively. Direct overhead heating abolished the normal cortex to deep brain temperature gradient that was maintained if using a head shield. Brain temperature may differ from core temperature during therapeutic hypothermia influenced by different clinical practices.

Regional brain temperature changes caused by an increase in neuronal activity irritated by somatosensory stimulation

Regional brain temperature changes caused by an increase in neuronal activity irritated by somatosensory stimulation

Deep Brain Hyperthermia While Rewarming from Hypothermic Circulatory Arrest

Neurologic injury is a feared and serious long-term complication of cardiopulmonary bypass (CPB) and deep hypothermic circulatory arrest (DHCA). Postoperative hyperthermia was found to enhance postischemic neurologic injury. The use of core temperature as the reference point through CPB assumes parallel changes in brain temperature. We tested the hypothesis that regional and deep brain temperature (DBT) differ during cooling, DHCA, and rewarming. Neonatal piglets (n = 9) were subject to CPB and cooled to rectal temperature (RT) of 18 degrees C, 30 minutes of DHCA were initiated, and subsequently the piglets were rewarmed to RT of 36.5 degrees C and weaned from CPB. Temperature probes were inserted into the DBT targeting the caudate and thalamic nuclei, their position confirmed by pathology. Superficial brain temperature was measured by a temperature probe inserted extradurally. RT, nasopharyngeal (NPT), and tympanic (TT) temperatures were recorded. During cooling the deep brain cooled faster and to lower temperatures compared to RT and TT; NPT reflected DBT accurately. During rewarming DBT was significantly higher than RT and TT. By the end of rewarming the difference between the deep brain and the RT reached statistical significance (30 minutes: 35.1 +/- 0.7 vs. 32.3 +/- 0.7 p < 0.05, respectively, 40 minutes: 37.5 +/- 0.3 vs. 34.7 +/- 0.8 p < 0.05, respectively). Deep brain hyperthermia routinely occurs during the last stages of rewarming following DHCA. DBT is accurately reflected by NPT and is directly correlated with inflow temperature. Therefore, during rewarming inflow temperatures should not exceed 36 degrees C and NPT should be closely monitored.

Increased regional brain temperature by stimulus-induced neuronal activation

Increased regional brain temperature by stimulus-induced neuronal activation

Bench to bedside strategies for optimizing neuroprotection following perinatal hypoxia–ischaemia in high and low resource settings

Background Therapeutic hypothermia gathers impetus in the developed world as a safe and effective therapy for term asphyxial encephalopathy. Although many questions still remain about the optimal application of hypothermic neuroprotection it is difficult to ignore the developing world where the prevalence of asphyxial encephalopathy is much higher. Experimental studies to optimize high tech cooling need to run in parallel with trials to determine the possible benefits of therapeutic hypothermia in low resource settings. Methods We used a validated newborn piglet model of transient HI to determine (i) whether optimal neuroprotection occurs at different temperatures in the cortical and deep grey matter; (ii) the effect of body size on regional brain temperature under normothermia and hypothermia; (iii) the effect of insult severity on the therapeutic window duration; (iv) whether cooling using a water bottle is feasible. In this model hypoxia–ischaemia is induced by reversible occlusion of the common carotid arteries by remotely controlled vascular occluders and simultaneous reduction in the inspired oxygen fraction to 0.12. Intensive care can be administered to the piglet maintaining metabolic and physiological homeostasis throughout the experiment, and cerebral energy metabolism is monitored continuously providing quantitative measures of the HI insult, latent phase and secondary energy failure using phosphorus-31 ( 31P) magnetic resonance spectroscopy (MRS). Results (i) The optimal temperature for cooling was lower in the cortex than deep grey matter. (ii) Cerebral temperatures were body-weight dependent: a smaller body weight led to a lower brain temperature especially with selective head cooling. (iii) Latent-phase duration is inversely related to insult severity. (iv) Low tech, simple cooling methods using a water bottle can induce and maintain moderate hypothermia. Conclusions Small shifts in brain temperature critically influence the survival of neuronal cells and body size critically influences brain-temperature gradients — smaller subjects have a larger surface area to brain volume and hence more heat is lost. The clinical implication is that smaller infants may require higher cap or body temperatures to avoid detrimental effects of over-zealous cooling. Latent-phase brevity may explain less effective neuroprotection following severe HI in some clinical studies. “Tailored” treatments which take into account individual and regional characteristics may increase the effectiveness of therapeutic hypothermia in the developed world. Low tech cooling methods using water bottles may be feasible although adequate staffing and monitoring would be required.

Transient Cooling during Early Reperfusion Attenuates Delayed Edema and Infarct Progression in the Spontaneously Hypertensive Rat. Distribution and Time Course of Regional Brain Temperature Change in a Model of Postischemic Hypothermic Protection

The temperature threshold for protection by brief postischemic cooling was evaluated in a model of transient focal ischemia in the Spontaneously Hypertensive Rat, using an array of epidural probes to monitor regional brain temperatures. Rats were subjected to 90 mins tandem occlusion of the right middle cerebral artery (MCA) and common carotid artery. Systemic cooling to 32 degrees C was initiated 5 mins before recirculation, with simultaneous brain cooling to temperatures ranging from 28 degrees C to 32 degrees C within the MCA territory by means of a temperature-controlled saline drip. Rewarming was initiated at 2 h recirculation and was complete within 30 mins. Tissue damage and edema volume showed clear temperature-dependent reductions when evaluated at 3 days survival, with no protection evident in the group at 32 degrees C but progressive effects on both parameters after deeper cooling. A particularly striking effect was the essentially complete elimination of edema progression between 1 and 3 days. Temperature at distal sites within the MCA territory better predicted reductions in lesion volume, indicating that protection required effective cooling of the penumbral regions destined to be spared. These results show that even brief cooling can be highly protective when initiated at the time of recirculation after focal ischemia, but indicate a substantially lower temperature threshold for hypothermic protection than has been reported for other strains, occlusion methods, and cooling durations.

Mismatch Recovery of Regional Cerebral Blood Flow and Brain Temperature During Reperfusion After Prolonged Brain Ischemia in Gerbils

Recovery of cerebral reperfusion after stroke or cardiac arrest can take a long time. We aimed to identify differences in the postischemic recovery of physiologic parameters between short and prolonged brain ischemia. Eighteen Mongolian gerbils were assigned to one of three groups: 5-minute (G5), 15-minute (G15), or 30-minute (G30) ischemia. With the use of our original microspectroscopy system, global ischemic reperfusion was performed. We measured changes in regional cerebral blood flow (r-CBF), microvessel diameter, and brain temperature (BrT) simultaneously. We also monitored somatosensory evoked potentials (SEPs) to evaluate electrophysiologic response. Both G5 and G15 showed concurrent recovery of r-CBF and BrT with hyperemia and hyperthermia, respectively, 10 to 15 minutes after reperfusion. The increase in BrT was <1 degree C and recovered to baseline within 60 minutes after reperfusion. In G30, recovery of r-CBF was significantly delayed relative to that of BrT. The increase in BrT was >2 degrees C, peaking approximately 15 minutes after reperfusion, and then maintained increases of >1 degree C for 120 minutes. SEPs in G5 and G15 showed concomitant recovery with that of r-CBF, whereas SEP recovery in G30 was delayed relative to that of r-CBF, eventually disappearing. All except one of the G30 gerbils died within 24 hours, but all in G5 and G15 survived. These results suggest that mismatch recovery of r-CBF and BrT after prolonged ischemia initiates metabolic derangement in brain tissue, leading to the electrochemical dysfunction and mortality.

Measurement of regional brain temperature using proton spectroscopic imaging: validation and application to acute ischemic stroke

A magnetic resonance proton spectroscopic imaging (SI) technique was developed to measure regional brain temperatures in human subjects. The technique was validated in a homogeneous phantom and in four healthy volunteers. Simulations and calculations determined the theoretical measurement precision as approximately +/-0.3 degrees C for individual 1-ml voxels. In healthy volunteers, repeated measurements on individual voxels had an S.D. = 1.2 degrees C. In a clinical study, 40 patients with acute ischemic stroke were imaged within 26 h (mean, 10 h) of onset. Temperatures were highest in the region that appeared abnormal (i.e., ischemic) on diffusion-weighted imaging (DWI) compared with a normal-appearing brain. The mean temperature difference between the DWI "lesion" area and the "normal brain" was 0.17 degrees C [P < 10(-3); range, 2.45 degrees C (hotter)-2.17 degrees C (cooler)]. Noninvasive temperature measurement by SI has sufficient precision to be used in studies of pathophysiology in stroke and in other brain disorders and to monitor therapies.

Determination of regional brain temperature using proton magnetic resonance spectroscopy to assess brain–body temperature differences in healthy human subjects

Proton magnetic resonance spectroscopy ((1)H MRS) was used to determine brain temperature in healthy volunteers. Partially water-suppressed (1)H MRS data sets were acquired at 3T from four different gray matter (GM)/white matter (WM) volumes. Brain temperatures were determined from the chemical-shift difference between the CH(3) of N-acetyl aspartate (NAA) at 2.01 ppm and water. Brain temperatures in (1)H MRS voxels of 2 x 2 x 2 cm(3) showed no substantial heterogeneity. The volume-averaged temperature from single-voxel spectroscopy was compared with body temperatures obtained from the oral cavity, tympanum, and temporal artery regions. The mean brain parenchyma temperature was 0.5 degrees C cooler than readings obtained from three extra-brain sites (P < 0.01). (1)H MRS imaging (MRSI) data were acquired from a slice encompassing the single-voxel volumes to assess the ability of spectroscopic imaging to determine regional brain temperature within the imaging slice. Brain temperature away from the center of the brain determined by MRSI differed from that obtained by single-voxel MRS in the same brain region, possibly due to a poor line width (LW) in MRSI. The data are discussed in the light of proposed brain-body temperature gradients and the use of (1)H MRSI to monitor brain temperature in pathologies, such as brain trauma.