On Neurocardiology Updates: an Interdisciplinary Field at the Intersection of Neurology and Cardiology.

Ischemic brain injury in hemodialysis patients: which is more dangerous, hypertension or intradialytic hypotension?

Rapid fluid removal during dialysis is associated with cardiovascular morbidity and mortality

The feasibility of using photoacoustic imaging (PAI) to measure electrically-evoked hemodynamic responses in a squirrel monkey brain in vivo was examined. A linear-array photoacoustic computed tomography (PACT) system and a high-resolution photoacoustic microscopy (PAM) system were built for imaging subcortical and cortical brain regions, respectively. The hemodynamic responses at multiple cortices, including premotor, primary motor, and primary somatosensory cortices, were monitored. The variations could be observed in all cortices and their underlying cortical and subcortical brain regions. The results from this study validated the potential of PAI technique for multiscale and multi-resolution functional brain mapping for non-human primates.

Aggressive and antisocial behaviour is associated with impaired emotion regulation and neurobiological alterations that are reflected on the level of autonomic as well as central nervous system functioning. Recent research on central autonomic control – as posited in the neurovisceral integration model – indicates associations between autonomic nervous system (ANS) activity and functional and structural brain correlates. An overlap of the central autonomic network (CAN) with brain regions involved in emotion regulation highlights the relevance of ANS measures in research on emotion regulation and aggression. The main aim of this thesis was to investigate and gain more insight into neurobiological correlates of aggression and emotion regulation in children and adolescents. First, we examined the relationship between resting ANS activity and aggression in more detail than has been done before. We therefore included a comprehensive assessment of ANS activity with two measures of general ANS activity (heart and respiration rate) and two measures capturing parasympathetic nervous system (heart rate variability) and sympathetic nervous system (pre-ejection period) activity separately, while considering relevant covariates such as smoking. A further sub aim was to gain more clarity on the best approach for linking psychopathology and neurobiology. Recent findings on a general psychopathology factor suggest that a dimensional approach captures psychopathology better than a categorical approach. Thus, we chose to compare two analysis approaches: a categorical (chapter 2) – based on DSM-5 – and a dimensional approach (chapter 3). The second aim of the thesis was to investigate functional brain correlates of implicit-controlled emotion regulation in individuals with and without conduct disorder (CD) (chapter 4). The third aim of the thesis was to investigate the relationship between resting heart rate variability and brain structure in female CD patients compared to typically developing adolescents (chapter 5). The findings presented in this dissertation advance the knowledge on the neurobiology of aggression and emotion regulation in children and adolescents. In line with recent evidence, the presented studies suggest that resting ANS activity, especially heart rate, might not be as strongly correlated with antisocial behaviour as previously assumed. In addition, the novel finding of higher respiration rate in female CD suggests that this measure should be further considered in future research – with a particular focus on its potential to impact heart rate variability and emotion regulation. More research on respiration in aggressive individuals could improve current treatment modalities. Further, the result indicating that comorbid internalising disorders in female CD patients are associated with lower heart rate variability warrants additional investigation and consideration of specific treatment needs. This CD group might represent a more severe psychopathological subgroup with more pronounced emotion regulation problems. Our findings of the neural correlates of implicit emotion regulation additionally support the notion of CD being characterised by deficient emotion regulation. Moreover, we reported negative correlations between resting heart rate variability and brain structure in CAN regions, which are implicated in emotion regulation. We highlighted the relevance of smoking for emotion regulation – which has been neglected so far in the context of neurobiological research on aggression and might be an important confounding factor to consider in future studies.

Neurogenic stunned myocardium (NSM) is defined as myocardial injury and dysfunction of a sudden onset, occurring after various types of acute brain injury as a result of an imbalance in the autonomic nervous system. The typical spectrum of clinically observed abnormalities includes acute left ventricular failure, not uncommonly progressing to cardiogenic shock with hypotension that requires inotropic agents, pulmonary oedema and various arrhythmias. Commonly-seen electrocardiographic changes include: prolonged QT interval, ST segment changes, T-wave inversion, a new Q-wave or U-wave. Echocardiography shows both an impaired both systolic and diastolic function of the left ventricle. Biochemical markers of NSM comprise metabolic acidosis and increased cardiac enzymes and markers: creatine kinase (CK), and CK-MB, troponin I and B-type natriuretic peptide. The main cause of NSM is myocardial injury induced by local catecholamine release from nerve endings within the myocardium. Recently, a theory has been proposed to classify NSM as one of the stress-related cardiomyopathies, together with Takotsubo cardiomyopathy, acute left ventricular failure in the critically ill, cardiomyopathy associated with pheochromacytoma and exogenous catecholamine administration. The occurrence of NSM increases the risk of life-threatening complications, death, and worsens neurologic outcome. As far as we know, treatment should generally focus on the underlying neurologic process in order to maximize neurologic recovery. Improvement in neurologic pathology leads to rapid improvement in cardiac function and its full recovery, as NSM is a fully reversible condition if the patient survives. Awareness of the existence of NSM and a deeper knowledge of its etiopathology may reduce diagnostic errors, optimise its treatment.

P4136Neurogenic stunned myoacardium in multiple sclerosis patients

Measures of cardiovascular function suggest autonomic nervous system dysregulation in the male lewis rat after surgical induction of joint injury

ObjectiveThis study aimed to investigate the relationships of heart rate variability (HRV) with the presence, severity, and individual neuroimaging markers of cerebral small vessel disease (CSVD).MethodA total of 4676 participants from the Third China National Stroke Registry (CNSR‐III) study were included in this cross‐sectional analysis. CSVD and its markers, including white matter hyperintensity (WMH), lacunes, enlarged perivascular spaces (EPVS), cerebral microbleeds (CMBs), and brain atrophy (BA), were evaluated. Two common HRV parameters, including the square root of the mean of the sum of the squares of differences between adjacent N–N intervals (RMSSD) and the standard deviation of all N–N intervals (SDNN), were used to evaluate the function of the autonomic nervous system (ANS). Binary or ordinal logistic regression analyses were performed to investigate the association between HRV and CSVD. In addition, two‐sample mendelian randomization (MR) analyses were performed to investigate the causality of HRV with CSVD.ResultsRMSSD was significantly associated with total burden of CSVD (Wardlaw's scale, common odds ratio [cOR] 0.80, 95% confidence interval [CI] 0.67–0.96, p = 0.02; Rothwell's scale, cOR 0.75, 95% CI 0.60–0.93, p = 0.008) and the presence of CSVD (Rothwell, OR 0.75, 95% CI 0.60–0.93, p = 0.008). However, no significant associations between SDNN and the presence or total burden of CSVD were observed. Moreover, RMSSD was related to WMH burden (OR 0.80, 95% CI 0.66–0.96, p = 0.02), modified WMH burden (cOR 0.82, 95% CI 0.69–0.97, p = 0.02), and Deep‐WMH (OR 0.75, 95% CI 0.62–0.91, p = 0.003), while SDNN was related to Deep‐WMH (OR 0.80, 95% CI 0.66–0.96, p = 0.02) and BA (cOR 0.80, 95% CI 0.68–0.95, p = 0.009). Furthermore, adding HRV to the conventional model based on vascualr risk factors enhanced the predictive performance for CSVD, as validated by the integrated discrimination index (p < 0.05). In addition, no causality between HRV and CSVD was observed in two‐sample MR analyses.ConclusionDecreased HRV may be a potential risk factor of CSVD, implying the possible role of the ANS in the pathogenesis of CSVD.

Emotion regulation is a vital life skill, and cognitive reappraisal (CR) is the most effective emotion regulation strategy, which plays a key role in healthy aging. In memory clinic patients, problems with emotion regulation difficulties and cognitive impairment are very common, often accompanied by signs of cerebral small vessel disease (CSVD) on their magnetic resonance imaging (MRI). Is there a correlation among cognitive reappraisal failure, cognitive impairment, and CSVD in these older adults? This study aims to investigate the question. A standardized emotion regulation task was used to measure CR ability. A total of 170 older adults were included in statistical analysis, of which 78 were considered as cognitive reappraisal failure (CR-Failure). All participants completed the emotion regulation task, neuropsychiatric assessments, and MRI scans, with traditional CSVD markers being evaluated. Our analysis indicated that CR ability is negatively correlated with scores on the Hamilton Depression Rating Scale and the Hamilton Anxiety Rating Scale. Additionally, logical memory and executive function are significant factors in CR utilization. A higher burden of CSVD or presence of cognitive impairment is an independent risk factor for cognitive reappraisal failure in memory clinic older adults. Furthermore, cognitive impairment significantly mediates the relationship between greater CSVD burden and CR failure.

The lowering of blood pressure after stroke

Contribution of Cerebrovascular Health to the Diagnosis of Alzheimer Disease

BackgroundHigher intake of vitamin E has been associated with a lower risk of Alzheimer’s disease (AD), however the underlying mechanisms are unclear. One explanation might be that anti‐inflammatory properties of tocopherols prevent microglia activation. In this study we investigated the association of brain tocopherol levels with microglia activation in elderly humans.MethodWe included 113 deceased participants (88.5±6 years, 60% female) from the prospective Memory and Aging Project. Brain levels of α‐ and γ‐tocopherol were measured by HPLC coupled to electrochemical detection. Microglia presence was assessed in three stages of activation, based on morphology; i.e. I – not activated, II – activated, III – most activated. Microglia densities and tocopherol levels were log‐transformed when not normally distributed, standardized and averaged across two cortical and two subcortical brain regions. Linear regression analyses examined associations between tocopherol levels and microglia densities (outcome) in two models; a model adjusted for age, sex, education, APOE ε4 genotype and post mortem time interval (model 1), and a model additionally adjusted for total amyloid load and neurofibrillary tangles severity (model 2).ResultTotal microglia density (stage I‐III) was lower in cortical versus subcortical brain regions (153.2 (111.2‐194.0); 209.2 (175.8‐224.1), p&lt;0.001). Levels of α‐ and γ‐tocopherol and activated microglia (II/III or III only) density did not differ between brain regions. Higher α‐ and γ‐tocopherol levels were associated with lower total and activated microglia densities in cortical (range (B(SE) ‐0.25,‐0.19 (0.09,0.10) p&lt;0.05) but not in subcortical brain regions (range B(SE) ‐0.01, 0.12 (0.09,0.10) p&gt;0.05). When we additionally adjusted for AD neuropathology effect estimates diminished and lost significance except for the association between α‐tocopherol and total microglia density in cortical brain regions (B(SE) ‐0.20 (0.09), p=0.03).ConclusionThese results suggest that the relation between tocopherols and AD might be partly explained by the alleviating effects of tocopherols on microglia activation.

Cerebral small-vessel disease (CSVD) is an umbrella term encompassing chronic, progressive conditions that affect the brain's vasculature. Diverse pathological and neurological factors lead to various clinical and neuroimaging patterns in elderly patients. While depression in the elderly is not uncommon, the connection between CSVD and late-life depression (LLD) remains unclear. CSVD is significant because it is closely linked to chronic hypertension, contributing to microvascular damage and impaired cerebral perfusion. Our objective was to synthesize evidence, evaluate relevant literature to synthesize, and present information relating to the underlying pathophysiology and factors linking CSVD to depression in older adults. Three databases were searched, EMBASE, Ovid MEDLINE, and Web of Science, with the articles selected for inclusion needing to be peer-reviewed, written in English, and published between 1998 and 2022 and have a primary focus on people aged 50 and above who had depression and had a documented history of CSVD. Twenty papers met these criteria and were analyzed, including using statistical correlation.Of the 20 studies, 15 reported a statistically significant correlation between CVSD and LLD, whereas five of the studies found no significant correlation. In the 15 studies that reported a significant relationship between CSVD and LLD, there were a total of 15,158 participants, or an average of approximately 1,011 participants per study. The five studies that did not find a correlation included 2,222 participants, averaging about 444 participants per study. Thus, this review's overall findings are consistent with a significant relationship between CSVD and LLD. White matter hyperintensities (WMHs), one of the findings of CSVD, were found to be a common finding in patients with CSVD and LLD. Increased WMH volume led to an increase in depressive symptoms. However, some studies highlight counterpoints, emphasizing the complexity of the relationship and the influence of non-vascular factors such as neuroinflammation, neurodegeneration, and systemic comorbidities. These findings underscore the importance of early detection of CSVD and interdisciplinary approaches to mitigate the burden of depression and cognitive decline in aging populations. Future research should focus on advanced neuroimaging, genetic profiling, and longitudinal studies to unravel the multifaceted mechanisms linking CSVD and LLD and improve clinical outcomes.

Developing the ability to regulate one's emotions in accordance with contextual demands (i.e., emotion regulation) is a central developmental task of early childhood. These processes are supported by the engagement of the autonomic nervous system (ANS), a physiological hub of a vast network tasked with dynamically integrating real-time experiential inputs with internal motivational and goal states. To date, much of what is known about the ANS and emotion regulation has been based on measures of respiratory sinus arrhythmia, a cardiac indicator of parasympathetic activity. In the present study, we draw from dynamical systems models to introduce two nonlinear indices of cardiac complexity (fractality and sample entropy) as potential indicators of these broader ANS dynamics. Using data from a stratified sample of preschoolers living in high- (i.e., emergency homeless shelter) and low-risk contexts (N = 115), we show that, in conjunction with respiratory sinus arrhythmia, these nonlinear indices may help to clarify important differences in the behavioral manifestations of emotion regulation. In particular, our results suggest that cardiac complexity may be especially useful for discerning active, effortful emotion regulation from less effortful regulation and dysregulation.

The Effects of Shared Reality on Emotional Experience and Regulation Valery Hazanov The current study consisted of a pilot and two experiments that explored the effects of “shared reality”—experiencing commonality with others’ inner states about some aspect of the world—on clinically relevant emotional processes, such as emotional regulation, attachment, well-being, and positive and negative affects. The primary aim was to contribute to our understanding of the implications of social sharing on emotional experience and regulation, using the well-established paradigm of shared reality. Shared reality has been studied thus far in connection to social-cognitive processes such as memory and attribution. The current study is the first application of this paradigm to emotional research. The study showed that shared reality intensifies negative emotional reactions, but not ambiguous ones. In addition, the study showed that shared reality makes people feel less guilty and fearful, but failed to show that it increases secure attachment to others. The study suggests that shared reality operates by making aspects of perceived reality seem more relevant and thus, it is argued, more accesible. Implications of the findings to emotional research and clinical practice, as well as its limitations and possible future directions for research, are discussed. TABLE OF CONTENTS CHAPTER I: INTRODUCTION 1 CHAPTER II: LITERATURE REVIEW 7 Sharing and relational aspects of emotional experience and regulation 7 Shared Reality 14 Related concepts to Shared Reality 21 Summary of relevant research and literature 22 CHAPTER III: SHARED REALITY AND EMOTIONAL EXPERIENCE AND REGULATION: A PILOT STUDY AND TWO SUBSEQUENT STUDIES 23 Pilot Study: Affect Labeling 24 Study 1: Labeling and Shared Reality 30 Summary of the pilot and study 1 and implementations for study 2 40 CHAPTER IV: STUDY 2: SHARED REALITY AND EMOTIONAL EXPERIENCE 45 Method 45 Hypotheses 54 Results of the Second Study 58 CHAPTER V: GENERAL DISCUSSION 66 REFERENCES 80 APPENDICES 88 Appendix A: An Example of an IAPS Image (Lang et. al, 2005) 88 Appendix B: SAM Scale (Lang, 1980) 89 Appendix C: PANAS Scale (Watson & Clark, 1994) 90 Appendix D: MAQ (Carver, 1997) 91 Appendix E: An Example of a Neutral and Ambiguous IAPS Image (Lang et,. al., 2005) 92