Post mortem brain temperature and its influence on quantitative MRI of the brain

Objective MRI temperature sensitivity presents a major issue in in situ post mortem MRI (PMMRI), as the tissue temperatures differ from living persons due to passive cooling of the deceased. This study aims at computing brain temperature effects on the MRI parameters to correct for temperature in PMMRI, laying the foundation for future projects on post mortem validation of in vivo MRI techniques. Materials and methods Brain MRI parameters were assessed in vivo and in situ post mortem using a 3 T MRI scanner. Post mortem brain temperature was measured in situ transethmoidally. The temperature effect was computed by fitting a linear model to the MRI parameters and the corresponding brain temperature. Results Linear positive temperature correlations were observed for T1, T2* and mean diffusivity in all tissue types. A significant negative correlation was observed for T2 in white matter. Fractional anisotropy revealed significant correlations in all gray matter regions except for the thalamus. Discussion The linear models will allow to correct for temperature in post mortem MRI. Comparing in vivo to post mortem conditions, the mean diffusivity, in contrast to T1 and T2, revealed additional effects besides temperature, such as cessation of perfusion and active diffusion.

Brain thermal kinetics at brain-eyelid thermal tunnels overcoming COVID-19 thermometry limitations for automated asymptomatic infection detection in concert with physical and biological principles

For centuries, temperature measurement deficiencies attributable to biological barriers and low thermo-conductivity (k) have precluded accurate surface-based fever assessment. At this stage of the pandemic, infection detection in children (who due to immature immune system may not effectively respond to vaccines) is critical because children can be readily infected and also become a large mutation reservoir. We reveal hitherto-unrecognized worldwide body temperature measurements (T°), in children and adults, over tissue typified by low-k similar to wood that may reach 6.8°C in thermal variability, hampering thereby COVID-19 control. Brain-eyelid thermal tunnels’ (BTT) integration of low-k and high-k regions creating a thermal pathway for undisturbed heat transmission from hypothalamus to high-k skin eliminates current shortcomings and makes the brain indispensable for defeating COVID-19 given that brain thermoregulatory signals are not limited by mutations. Anatomo-histologic, emissive, physiologic, and thermometric bench-to-bedside studies characterized and overcome biophysical limitations of thermometry through high-k eyelid-enabled brain temperature measurements in children and adults. BTT eyelid features fat-free skin (~900 µm) and unique light emission through a blood/fat configuration in the underlying tunnel. Contrarily, forehead features variable and thick dermis (2000–2500 µm) and variable fat layers (1100–2800 µm) resulting in variable low-k as well as temperatures 1.97 °C lower than BTT temperature (BTT°). Highest emission present in only ~3.1% of forehead averaged 1.08±0.49 °C (mean±SD) less than BTT° (p=0.008). Environmental and biological impacts during fanning revealed thermal imaging limitations for COVID-19 screening. Comparison of paired measurements for 100 pediatric patients showed that in the children subgroup above 37°C, BTT° exceeded body core temperature (Core°) in 60/72 patients; the average difference in the 72 patients was 0.62±0.7°C (p<0.001 by unpaired t-test); and in the subgroup beyond 37.5°C, BTT° exceeded Core° in 30/32 patients. Delineating hypothalamic activity in children facilitates early infection detection, which is essential because children’s immunogenicity prevents effective vaccination and causes accelerated viral evolution. Capturing hypothalamic thermal signals from BTT was further supported by brain thermal kinetics via BTT using wearables during anesthesia, sedation, sleep, brain injury, exercise, and asymptomatic infection, which revealed brain/core discordance and enabled automated noninvasive afebrile infection detection for interrupting asymptomatic human-to-human transmission. BTT-based spot-check thermometry can be harmlessly implemented for children worldwide without undue burden and costs; meanwhile, continuous brain-eyelid T° in concert with biological and physical principles affords a new dimension for combating pandemics. The “detection–vaccination” pair solution presented is required to mitigate COVID-19 from spreading indefinitely through mutations and vaccine evasion while opening a viable path for eradicating COVID-19.

Analysis of Mental State of Patients after Drug Addiction and Withdrawal Guided by PETCT Image Based on Optimized Image Fusion Algorithm

Blood oxygen level-dependent functional magnetic resonance imaging (BOLD-fMRI) studies have shown that drug-dependent patients are activated in different addictive brain areas under the stimulation of relevant environmental cues, which in turn leads to craving and relapse. This study uses magnetic resonance spectroscopy to measure brain temperature to explore the brain temperature changes in different addictive brain regions of heroin and methamphetamine addicts in a short-term withdrawal state and to explore whether the quantitative index of brain temperature change can be used as a diagnostic drug Methods. The subjects were scanned by resting-state MRI spectroscopy first and then subjected to MRI spectroscopy scanning under visual stimulation. The subjects were required to watch the heroin/meth-related clue pictures carefully during visual stimulation. The measured chemical shift value of N-acetyl-aspartic acid (NAA) is substituted into the brain temperature calculation formula T = 37 + 100 to obtain the brain temperature before and after visual stimulation. In addition, the anxiety and depression states of heroin and methamphetamine-dependent patients were evaluated. Results. There was no statistically significant change in the brain temperature of the prefrontal cortex before and after visual stimulation in heroin and methamphetamine-dependent subjects; compared with the normal group, there was no change in prefrontal cortex brain temperature before and after visual stimulation in heroin and methamphetamine-dependent subjects. Statistical Significance. The changes of hippocampal temperature before and after visual stimulation in methamphetamine-dependent patients were not statistically significant; compared with the normal group, there was no statistically significant difference in the changes of hippocampal temperature before and after visual stimulation in methamphetamine-dependent patients. Conclusion. This study initially found that the visual cues related to heroin and methamphetamine were not enough to cause significant changes in the brain temperature of the prefrontal cortex.

Association between Lower Body Temperature and Increased Tau Pathology in Cognitively Normal Older Adults

Background Rodent model and in vitro studies suggest body temperature (Tb), and consequently brain temperature, has the potential to bidirectionally interact with tau pathology in Alzheimer’s Disease (AD). Tau phosphorylation is substantially increased by small (< 1°C) reductions in temperature within the human physiological range, and lower brain thermoregulatory areas may be among those first affected by AD pathology. Here, we evaluated whether Tb (as a proxy for brain temperature) is cross-sectionally associated with clinically utilized markers of tau pathology in cognitively normal older adults. Methods Tb was measured with ingestible telemetry continuously over 48 hours, including two nights of nocturnal polysomnography to delineate whether tau pathology is differentially associated with Tb during waking vs sleep. Tau pathology was assessed with plasma and cerebrospinal fluid (CSF) tau phosphorylated at threonine 181 (P-tau), sampled the day following Tb measurement, as well as neurofibrillary tangle (NFT) burden in early Braak stage areas, imaged with MR-PET using the [18F]MK-6240 radiotracer on average one month later. Results Plasma and CSF P-tau levels were highly correlated with one another, and with tau tangle radiotracer uptake. Lower Tb, as quantified by lower mean Tb and a greater proportion of time Tb was under 37.0°C, was associated with increased NFT burden and increased plasma and CSF P-tau levels. NFT burden was associated with lower Tb during waking, but not during sleeping intervals. Conclusions Preliminary results suggest that lower Tb in older adults may be associated with increased soluble and aggregated tau pathology.

Brain Temperature Influences Intracranial Pressure and Cerebral Perfusion Pressure After Traumatic Brain Injury: A CENTER-TBI Study

Background After traumatic brain injury (TBI), fever is frequent. Brain temperature (BT), which is directly linked to body temperature, may influence brain physiology. Increased body and/or BT may cause secondary brain damage, with deleterious effects on intracranial pressure (ICP), cerebral perfusion pressure (CPP), and outcome. Methods Collaborative European NeuroTrauma Effectiveness Research in Traumatic Brain Injury (CENTER-TBI), a prospective multicenter longitudinal study on TBI in Europe and Israel, includes a high resolution cohort of patients with data sampled at a high frequency (from 100 to 500 Hz). In this study, simultaneous BT, ICP, and CPP recordings were investigated. A mixed-effects linear model was used to examine the association between different BT levels and ICP. We additionally focused on changes in ICP and CPP during the episodes of BT changes (Δ BT ≥ 0.5 °C lasting from 15 min to 3 h) up or downward. The significance of ICP and CPP variations was estimated with the paired samples Wilcoxon test (also known as Wilcoxon signed-rank test). Results Twenty-one patients with 2,435 h of simultaneous BT and ICP monitoring were studied. All patients reached a BT of 38 °C and experienced at least one episode of ICP above 20 mm Hg. The linear mixed-effects model revealed an association between BT above 37.5 °C and higher ICP levels that was not confirmed for lower BT. We identified 149 episodes of BT changes. During BT elevations (n = 79) ICP increased, whereas CPP was reduced; opposite ICP and CPP variations occurred during episodes of BT reduction (n = 70). All these changes were of moderate clinical relevance (increase of ICP of 4.5 and CPP decrease of 7.5 mm Hg for BT rise, and ICP reduction of 1.7 and CPP elevation of 3.7 mm Hg during BT defervescence), even if statistically significant (p < 0.0001). It has to be noted, however, that a number of therapeutic interventions against intracranial hypertension was documented during those episodes. Conclusions Patients after TBI usually develop BT > 38 °C soon after the injury. BT may influence brain physiology, as reflected by ICP and CPP. An association between BT exceeding 37.5 °C and a higher ICP was identified but not confirmed for lower BT ranges. The relationship between BT, ICP, and CPP become clearer during rapid temperature changes. During episodes of temperature elevation, BT seems to have a significant impact on ICP and CPP.