Community-engaged pedagogy in an emergency medicine clerkship: Teaching trauma-informed addiction care and harm reduction through a peer-assisted learning case.

Background: The impact of opioid use disorder (OUD) in the United States continues to rise, yet this topic has limited coverage in most medical school curricula. The study partnered with academic and community harm reductionists to design a peer-assisted learning case of opioid withdrawal to teach fourth-year medical students about trauma-informed OUD care and harm reduction services during their emergency medicine clerkship. Methods: Academic and community harm reductionists iteratively codesigned this case in partnership with the research team. Community-engaged pedagogy informed this process to promote social action and power sharing through education. This case was integrated into the existing weekly peer-assisted learning curriculum (i.e., medical students teaching medical students through a structured case) for all fourth-year medical students during their required emergency medicine clinical rotation. Participants completed a postcase evaluation survey. Results: Sixty-four medical students completed the survey between June and November 2022. A total of 98.5% of participants found the educational session quite or extremely relevant to their medical education, and 87.5% believed the case to be quite or extremely effective in achieving the learning objectives. A total of 45.3% initially felt quite or extremely competent in talking with patients about their drug use, whereas 53.2% felt quite or extremely more competent after participating in the case. Finally, 21.9% initially felt quite or extremely competent in proposing a treatment plan for a patient who uses drugs, whereas 62.5% felt quite or extremely more competent after participating in the case. Conclusions: This study supports the feasibility and importance of incorporating the voices of people with lived and living experience into medical school curricular development. This peer-assisted learning case focused on the treatment of OUD in the emergency department was seamlessly integrated into the existing curriculum and well received by medical students. By engaging local experts, it could easily be adapted and expanded to other sites.

The seven day itch: A delayed histamine reaction to stingray injury.

Stingray injuries are common presentations to emergency departments near warm coastal waters. Commonly reported injuries include puncture wounds, lacerations, and envenomations, the latter of which cause severe pain but are usually easily treated with warm water immersion. We report a case of delayed histamine reaction in a patient who sustained a stingray envenomation one week prior which we believe is the first such report in the medical literature but is found on discussion boards for those who have sustained stingray injuries. The literature on such envenomations is reviewed.

Errors of Commission in Cardiac Arrest Care in the Intensive Care Unit.

INTRODUCTION: Cardiopulmonary arrests (CPAs) are common in the intensive care unit (ICU). However, effects of protocol deviations on CPA outcomes in the ICU are relatively unknown. OBJECTIVES: To establish the frequency of errors of commission (EOCs) during CPAs in the ICU and their relationship with CPA outcomes. METHODS: Retrospective analysis of data entered into institutional registry with inclusion criteria of age >18 years and non-traumatic cardiac arrest in the ICU. EOCs consist of administration of drugs or procedures performed during a CPA that are not recommended by ACLS guidelines.Primary outcome: relationship of EOCs with likelihood of return of spontaneous circulation (ROSC). Secondary outcomes: relationship of specific EOCs to ROSC and relationship of EOCs and CPA length on ROSC. RESULTS: Among 120 CPAs studied, there was a cumulative ROSC rate of 66%. Cumulatively, EOCs were associated with a decreased likelihood of ROSC (OR: 0.534, 95% CI: 0.387-0.644). Specifically, administration of sodium bicarbonate (OR: 0.233, 95% CI: 0.084-0.644) and calcium chloride (OR: 0.278, 95% CI: 0.098-0.790) were the EOCs that significantly reduced likelihood of attaining ROSC. Each 5-minute increment in CPA duration and/or increase in number of EOCs corresponded to fewer patients sustaining ROSC. CONCLUSIONS: EOCs during CPAs in the ICU were common. Among all EOCs studied, sodium bicarbonate and calcium chloride seemed to have the greatest association with decreased likelihood of attaining ROSC. Number of EOCs and CPA duration both seemed to have an inversely proportional relationship with the likelihood of attaining and sustaining ROSC. EOCs represent potentially modifiable human factors during a CPA through resources such as life safety nurses.

Apparent diffusion coefficient changes in human brain during sleep - Does it inform on the existence of a glymphatic system?

The role of sleep in brain physiology is poorly understood. Recently rodent studies have shown that the glymphatic system clears waste products from brain more efficiently during sleep compared to wakefulness due to the expansion of the interstitial fluid space facilitating entry of cerebrospinal fluid (CSF) into the brain. Here, we studied water diffusivity in the brain during sleep and awake conditions, hypothesizing that an increase in water diffusivity during sleep would occur concomitantly with an expansion of CSF volume - an effect that we predicted based on preclinical findings would be most prominent in cerebellum. We used MRI to measure slow and fast components of the apparent diffusion coefficient (ADC) of water in the brain in 50 healthy participants, in 30 of whom we compared awake versus sleep conditions and in 20 of whom we compared rested-wakefulness versus wakefulness following one night of sleep-deprivation. Sleep compared to wakefulness was associated with increases in slow-ADC in cerebellum and left temporal pole and with decreases in fast-ADC in thalamus, insula, parahippocampus and striatal regions, and the density of sleep arousals was inversely associated with ADC changes. The CSF volume was also increased during sleep and was associated with sleep-induced changes in ADCs in cerebellum. There were no differences in ADCs with wakefulness following sleep deprivation compared to rested-wakefulness. Although we hypothesized increases in ADC with sleep, our findings uncovered both increases in slow ADC (mostly in cerebellum) as well as decreases in fast ADC, which could reflect the distinct biological significance of fast- and slow-ADC values in relation to sleep. While preliminary, our findings suggest a more complex sleep-related glymphatic function in the human brain compared to rodents. On the other hand, our findings of sleep-induced changes in CSF volume provide preliminary evidence that is consistent with a glymphatic transport process in the human brain.

Neural correlates of visual attention in alcohol use disorder.

Numerous studies have documented cognitive impairments in multiple domains in patients with an alcohol use disorder (AUD), including perceptuomotor, executive, and visuospatial functions. Although the neural underpinnings of cognitive deficits in AUD have been studied extensively, the neural basis of attention deficits in AUD remains relatively unexplored. Here, we investigated neural responses to a visual attention task (VAT) in 19 recently abstinent patients with AUD and 23 healthy control participants (HC) using functional MRI (fMRI). AUD had a mean number of 62 ± 34SD drinks per week and 29 ± 13 years' history of alcohol use. Results show that there were no behavioral differences (accuracy or reaction time) between groups during the VAT. For both groups, the VAT activated brain areas associated with visual attention load (i.e., parietal and prefrontal cortices) and visual processing (i.e., occipital cortex), which is in line with previous reports on the same task in healthy volunteers. Despite similar behavioral performances, AUD participants showed decreased VAT activation in regions of the dorsal and ventral attention networks, including parietal and prefrontal cortices, and in the insula as compared to controls. These findings corroborate differences in attention networks in AUD compared to HC that might underlie attention deficits in AUD, whereas impairments in the insula could reflect a disruption of interoception processing as found in other addictions.

Influence of alcoholism and cholesterol on TSPO binding in brain: PET [11C]PBR28 studies in humans and rodents.

Neuroinflammation appears to contribute to neurotoxicity observed with heavy alcohol consumption. To assess whether chronic alcohol results in neuroinflammation we used PET and [11C]PBR28, a ligand that binds to the 18-kDa translocator protein (TSPO), to compare participants with an alcohol use disorder (AUD: n = 19) with healthy controls (HC: n = 17), and alcohol-dependent (n = 9) with -nondependent rats (n = 10). Because TSPO is implicated in cholesterol's transport for steroidogenesis, we investigated whether plasma cholesterol levels influenced [11C]PBR28 binding. [11C]PBR28 binding did not differ between AUD and HC. However, when separating by TSPO genotype rs6971, we showed that medium-affinity binders AUD participants showed lower [11C]PBR28 binding than HC in regions of interest (whole brain, gray and white matter, hippocampus, and thalamus), but no group differences were observed in high-affinity binders. Cholesterol levels inversely correlated with brain [11C]PBR28 binding in combined groups, due to a correlation in AUD participants. In rodents, we observed no differences in brain [11C]PBR28 uptake between alcohol-dependent and -nondependent rats. These findings, which are consistent with two previous [11C]PBR28 PET studies, may indicate lower activation of microglia in AUD, whereas failure to observe alcohol effects in the rodent model indicate that species differences do not explain the discrepancy with prior rodent autoradiographic studies reporting increases in TSPO binding with chronic alcohol. However, reduced binding in AUD participants could also reflect competition from endogenous TSPO ligands such as cholesterol; and since the rs6971 polymorphism affects the cholesterol-binding domain of TSPO this could explain why differences were observed only in medium-affinity binders.

ß-Amyloid accumulation in the human brain after one night of sleep deprivation.

The effects of acute sleep deprivation on ß-amyloid (Aß) clearance in the human brain have not been documented. Here we used PET and 18F-florbetaben to measure brain Aß burden (ABB) in 20 healthy controls tested after a night of rested sleep (baseline) and after a night of sleep deprivation. We show that one night of sleep deprivation, relative to baseline, resulted in a significant increase in Aß burden in the right hippocampus and thalamus. These increases were associated with mood worsening following sleep deprivation, but were not related to the genetic risk (APOE genotype) for Alzheimer's disease. Additionally, baseline ABB in a range of subcortical regions and the precuneus was inversely associated with reported night sleep hours. APOE genotyping was also linked to subcortical ABB, suggesting that different Alzheimer's disease risk factors might independently affect ABB in nearby brain regions. In summary, our findings show adverse effects of one-night sleep deprivation on brain ABB and expand on prior findings of higher Aß accumulation with chronic less sleep.

Food addiction: A common neurobiological mechanism with drug abuse.

Drugs and food both exert a rewarding effect through the firing of dopamine neurons in the ventral tegmental area, resulting in the release of dopamine into the nucleus accumbens and effects on the mesolimbic pathway. Here, we review the neuroimaging literature to consider the validity of food addiction and the common neurobiological mechanisms that overlap in food and drug addiction. This review paper focuses on findings from Positron Emission Tomography (PET), functional Magnetic Resonance Imaging (fMRI) and structural imaging studies, as well as evidence from neuroimaging studies of bariatric surgery and pharmacological interventions on obese individuals. We examine not only functional and structural changes in the mesolimbic pathways, but also in other frontal areas shown to be involved in drug addiction, including the prefrontal cortex, orbitofrontal cortex and anterior cingulate cortex, as well as changes in neurotransmitter systems beyond dopaminergic systems.

Dynamic brain glucose metabolism identifies anti-correlated cortical-cerebellar networks at rest.

It remains unclear whether resting state functional magnetic resonance imaging (rfMRI) networks are associated with underlying synchrony in energy demand, as measured by dynamic 2-deoxy-2-[18F]fluoroglucose (FDG) positron emission tomography (PET). We measured absolute glucose metabolism, temporal metabolic connectivity (t-MC) and rfMRI patterns in 53 healthy participants at rest. Twenty-two rfMRI networks emerged from group independent component analysis (gICA). In contrast, only two anti-correlated t-MC emerged from FDG-PET time series using gICA or seed-voxel correlations; one included frontal, parietal and temporal cortices, the other included the cerebellum and medial temporal regions. Whereas cerebellum, thalamus, globus pallidus and calcarine cortex arose as the strongest t-MC hubs, the precuneus and visual cortex arose as the strongest rfMRI hubs. The strength of the t-MC linearly increased with the metabolic rate of glucose suggesting that t-MC measures are strongly associated with the energy demand of the brain tissue, and could reflect regional differences in glucose metabolism, counterbalanced metabolic network demand, and/or differential time-varying delivery of FDG. The mismatch between metabolic and functional connectivity patterns computed as a function of time could reflect differences in the temporal characteristics of glucose metabolism as measured with PET-FDG and brain activation as measured with rfMRI.

Neuroimaging the Effectiveness of Substance Use Disorder Treatments.

Neuroimaging techniques to measure the function and biochemistry of the human brain such as positron emission tomography (PET), proton magnetic resonance spectroscopy ((1)H MRS), and functional magnetic resonance imaging (fMRI), are powerful tools for assessing neurobiological mechanisms underlying the response to treatments in substance use disorders. Here, we review the neuroimaging literature on pharmacological and behavioral treatment in substance use disorder. We focus on neural effects of medications that reduce craving (e.g., naltrexone, bupropion hydrochloride, baclofen, methadone, varenicline) and that improve cognitive control (e.g., modafinil, N-acetylcysteine), of behavioral treatments for substance use disorders (e.g., cognitive bias modification training, virtual reality, motivational interventions) and neuromodulatory interventions such as neurofeedback and transcranial magnetic stimulation. A consistent finding for the effectiveness of therapeutic interventions identifies the improvement of executive control networks and the dampening of limbic activation, highlighting their values as targets for therapeutic interventions in substance use disorders.