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Objective: In healthy volunteers, a positive association has previously been observed between emotional awareness (EA), the ability to identify and describe emotional experiences in oneself and others, and resting heart rate variability (HRV), which is dominated by vagus nerve activity. The current study aimed to investigate the EA-HRV association across multiple assessments in a "real-world" ambulatory context in patients with long QT syndrome (LQTS) who are at genetic risk for sudden cardiac death., Methods: Participants (157 LQTS patients; Mean Age = 35.1, SD Age = 10.4; 115 women) completed the levels of emotional awareness scale (LEAS) on one occasion, which served as our measure of EA. In an ecological momentary assessment study involving 10 assessments per day over 3 days, multiple 5-minute ECG assessments (mean = 24.6, SD = 5.1) were obtained in each patient using a Holter monitor, from which high-frequency HRV (HF-HRV) was computed on each occasion., Results: There was a significant positive association between LEAS scores and HF-HRV controlling for biobehavioral covariates. We also detected a similar inverse relation between EA and mean heart rate., Conclusion: These findings suggest that, in patients with a well-defined genetic risk for ventricular arrhythmia and sudden death, the ability to experience emotions in a complex and differentiated way covaries with greater parasympathetic influences on the heart. These findings are consistent with the overlapping neural substrates of EA and HRV and their common contribution to adaptive emotional responding, consistent with the Neurovisceral Integration Model., (Copyright © 2024 by the American Psychosomatic Society.)

Objective: The influence of unconscious emotional processes on pain remains poorly understood. The present study tested whether cues to forgotten unpleasant images might amplify pain (i.e., in the absence of conscious recall)., Methods: Seventy-two healthy female adults (19 to 34 years) performed an adapted Think/No-think paradigm (T/NT) using 72 combinations of neutral face images (cues) paired with 36 neutral and 36 unpleasant images. After completion of the T/NT task, cues associated with forgotten neutral or unpleasant images were identified. Cues to either neutral or unpleasant images from the NT condition were then presented in randomized order while participants received intermediate-level thermal pain stimulation on the left hand. Ratings of both pain intensity and unpleasantness were acquired after each trial., Results: Mean pain unpleasantness ratings were greater during presentation of cues to forgotten negative versus neutral images (5.52 [SD = 2.06] versus 5.23 [SD = 2.10]; p = .02). This pattern was also present when comparing cues to remembered negative versus neutral images (5.62 [SD = 1.94] versus 5.04 [SD = 1.90]; p < .001). Mean pain intensity ratings were higher for cues to negative versus neutral images when remembered (5.48 [SD = 1.79] versus 5.00 [SD = 1.69]; p < .001), but not when forgotten (5.27 [SD = 1.96] versus 5.16 [SD = 1.93]; p = .30)., Conclusions: Using an adapted T/NT-Pain paradigm, this study demonstrated that cues to nonrecallable (but potentially unconsciously activated) negative emotional memories amplify pain unpleasantness, similar to known effects of conscious negative emotions., (Copyright © 2024 by the American Psychosomatic Society.)

Objectives: Current guidelines emphasize early recognition of pediatric septic shock using clinical examination findings. Elevated serum lactate has been associated with increased mortality in adult patients with septic shock. Our objective was to determine the association between the initial serum lactate obtained in the pediatric emergency department (PED) from patients treated for septic shock and the use of vasoactive medication within 24 hours., Methods: This was a retrospective study from 2008 through 2012 of PED patients at a tertiary care children's hospital. Patients younger than 18 years treated for septic shock were included if they had a serum lactate obtained in the PED., Results: Eight hundred sixty-four PED encounters met inclusion criteria. Median initial PED lactate was 2.1 mmol/L (interquartile range, 1.4-3.2 mmol/L). Overall, 121 patients (14%) received vasoactive medication within 24 hours of the initial PED lactate. A multivariable logistic regression analysis demonstrated associations between initial lactate levels of 3.1 to 5 mmol/L (odds ratio, 1.82; 95% confidence interval, 1.02-3.26) and 5.1 mmol/L or greater (odds ratio, 5.00; 95% confidence interval, 2.56-9.76) and the use of vasoactive medication within 24 hours. Other factors associated with use of vasoactive medication within 24 hours included hypotension, abnormal pulses, and mental status changes., Conclusions: Increased initial lactate is associated with use of vasoactive medication within 24 hours in PED patients with septic shock.

Objective: Two distinct perspectives-typically referred to as the biopsychosocial and biomedical models-currently guide clinical practice. Although the role of psychosocial factors in contributing to physical and mental health outcomes is widely recognized, the biomedical model remains dominant. This is due in part to (a) the largely nonmechanistic focus of biopsychosocial research and (b) the lack of specificity it currently offers in guiding clinicians to focus on social, psychological, and/or biological factors in individual cases. In this article, our objective is to provide an evidence-based and theoretically sophisticated mechanistic model capable of organically integrating biopsychosocial processes., Methods: To construct this model, we provide a narrative review of recent advances in embodied cognition and predictive processing within computational neuroscience, which offer mechanisms for understanding individual differences in social perceptions, visceral responses, health-related behaviors, and their interactions. We also review current evidence for bidirectional influences between social support and health as a detailed illustration of the novel conceptual resources offered by our model., Results: When integrated, these advances highlight multiple mechanistic causal pathways between psychosocial and biological variables., Conclusions: By highlighting these pathways, the resulting model has important implications motivating a more psychologically sophisticated, person-specific approach to future research and clinical application in the biopsychosocial domain. It also highlights the potential for quantitative computational modeling and the design of novel interventions. Finally, it should aid in guiding future research in a manner capable of addressing the current criticisms/limitations of the biopsychosocial model and may therefore represent an important step in bridging the gap between it and the biomedical perspective.

Background: Early adversity predisposes to chronic pain, but a mechanistic explanation is lacking. Survivors of early adversity with chronic pain often seem impaired in their ability to be aware of, understand, and express distressing emotions such as anger and fear in social contexts. In this context, it has been proposed that pain may at times serve as a "psychic regulator" by preventing awareness of more intolerable emotions., Method: This narrative review builds on the premise that physical pain and emotional pain are conscious experiences that can compete for selective attention. We highlight mechanisms whereby the consequences of early adversity may put emotional pain at a competitive disadvantage. A case history, supportive research findings, and an evidence-based neurobiological model are presented., Results: Arising from abuse or neglect in childhood, impairments in the adult capacity to attend to and/or conceptualize the emotional meaning of felt distress may be associated with impaired engagement of the default network and impaired top-down modulation of affective response generation processes. Persistent and poorly conceptualized affective distress may be associated with reduced emotion regulation ability, reduced vagal tone, increased inflammation, and amplified nociceptive signals. Attention to physical pain may be reinforced by the temporary reduction in negative emotions that it causes., Conclusions: These processes jointly promote biased competition favoring attention to physical pain and away from one's own emotions. They may constitute an unintentional analog of the phenomenon of self-injury in patients with borderline personality disorder in whom the intentional infliction of physical pain serves to downregulate intense emotional distress. Attending to, expressing, and understanding previously unacknowledged psychological distress unrelated to pain may facilitate recovery from chronic pain after early adversity. Mechanistic studies that can validate this clinically derived neurobiological hypothesis are urgently needed.

Objective: Changes in heart rate variability (HRV) associated with breathing (respiratory sinus arrhythmia) are known to be parasympathetically (vagally) mediated when the breathing rate is within the typical frequency range (9-24 breaths per minute [bpm]; high-frequency HRV). Slow yogic breathing occurs at rates below this range and increases low-frequency HRV power, which may additionally reflect a significant sympathetic component. Yogic breathing techniques are hypothesized to confer health benefits by increasing cardiac vagal control, but increases in low-frequency HRV power cannot unambiguously distinguish sympathetic from parasympathetic contributions. The aim of this study was to investigate the autonomic origins of changes in low-frequency HRV power due to slow-paced breathing., Methods: Six healthy young adults completed slow-paced breathing with a cadence derived from yogic breathing patterns. The paced breathing took place under conditions of sympathetic blockade, parasympathetic (vagal) blockade, and placebo. HRV spectral power was compared under 11 breathing rates during each session, in counterbalanced order with frequencies spanning the low-frequency range (4-9 bpm)., Results: HRV power across the low-frequency range (4-9 bpm) was nearly eliminated (p = .016) by parasympathetic blockade (mean (SD) spectral power at breathing frequency = 4.1 (2.1)) compared with placebo (69.5 (8.1)). In contrast, spectral power during sympathetic blockade 70.2 (9.1) and placebo (69.5 (8.1)) was statistically indistinguishable (p = .671)., Conclusions: These findings clarify the interpretation of changes in HRV that occur during slow-paced breathing by showing that changes in low-frequency power under these conditions are almost entirely vagally mediated. Slow-paced breathing is an effective tool for cardiac vagal activation.

Early-life adversities (ELA) are associated with subsequent pervasive alterations across a wide range of neurobiological systems and psychosocial factors that contribute to accelerated onset of health problems and diseases. In this article, we provide an integrated perspective on recent developments in research on ELA, based on the articles published in this Special Issue of Psychosomatic Medicine. We focus on the following: 1) the distinction between specific versus general aspects of ELA with regard to the nature of exposure (e.g., physical and sexual abuse, emotional abuse or neglect, relative socioeconomic deprivation), biological and behavioral correlates of ELA, and differences across diseases; 2) the importance of timing in the critical phases of exposure to ELA; and 3) adaptive versus dysfunctional responses to ELA and their consequences for biological and behavioral risk factors for adverse health outcomes. This article concludes with outlining important new targets for research in this area, including the neurobiology of affect as a mechanism linking ELA to adverse health outcomes, and the need for large-scale longitudinal investigations of multisystem processes relevant to ELA in diverse samples, starting prenatally, continuing to late adolescence, and with long-term follow-up assessments that enable evaluation of incident disease outcomes., Competing Interests: The authors have no conflicts of interest to report.

Competing Interests: The authors report no conflicts of interest.

Objectives: Major depression is associated with reduced cardiac vagal control, most commonly indexed by heart rate variability. To examine the dynamics of this abnormality, we examined within-participant covariation over time between brain activity, cardiac vagal control, and depressive symptoms in depressed patients treated with sertraline and in healthy volunteers., Methods: Patients with depression and nondepressed control participants were enrolled in a 12-week protocol. After Week 0 assessment, patients began treatment with sertraline. Neural activity and vagal control were measured for all participants at Weeks 0, 2, 6, and 12 using functional magnetic resonance imaging and synchronized electrocardiographic recordings. At each of the four assessments, a moving window analysis was used to estimate vagal control as assessed by respiratory sinus arrhythmia (RSA) from the electrocardiographic data, which was then regressed onto functional magnetic resonance imaging activity., Results: At baseline, patients showed reduced blood oxygen level-dependent RSA covariation compared with controls within multiple a priori brain regions associated with vagal control, collectively described as the medial visceromotor network (MVN). Sertraline treatment led to a significant increase in brain-RSA covariation for patients compared with controls, despite a lack of improvement in mean RSA., Conclusions: These data suggest a partial normalization of MVN dysfunction in depression during sertraline treatment. Specifically, results indicate a partial recovery of MVN function. However, this recovery was insufficient to cause a significant change in RSA levels. These results may help to explain both improvements with and limitations of sertraline treatment of depression.

Objective: Inhibitor of differentiation-3 (Id3) has been implicated in promoting angiogenesis, a key determinant of high-fat diet (HFD)-induced visceral adiposity. Yet the role of Id3 in HFD-induced angiogenesis and visceral adipose expansion is unknown., Methods and Results: Id3(-/-) mice demonstrated a significant attenuation of HFD-induced visceral fat depot expansion compared to wild type littermate controls. Importantly, unlike other Id proteins, loss of Id3 did not affect adipose depot size in young mice fed chow diet or differentiation of adipocytes in vitro or in vivo. Contrast enhanced ultrasound revealed a significant attenuation of visceral fat microvascular blood volume in HFD-fed mice null for Id3 compared to wild type controls. HFD induced Id3 and VEGFA expression in the visceral stromal vascular fraction and Id3(-/-) mice had significantly lower levels of VEGFA protein in visceral adipose tissue compared to wild type. Furthermore, HFD-induced VEGFA expression in visceral adipose tissue was completely abolished by loss of Id3. Consistent with this effect, Id3 abolished E12-mediated repression of VEGFA promoter activity., Conclusions: Results identify Id3 as an important regulator of HFD-induced visceral adipose VEGFA expression, microvascular blood volume, and depot expansion. Inhibition of Id3 may have potential as a therapeutic strategy to limit visceral adiposity.

Rationale: B cells are abundant in the adventitia of normal and diseased vessels. Yet, the molecular and cellular mechanisms mediating homing of B cells to the vessel wall and B-cell effects on atherosclerosis are poorly understood. Inhibitor of differentiation-3 (Id3) is important for atheroprotection in mice and polymorphism in the human ID3 gene has been implicated as a potential risk marker of atherosclerosis in humans. Yet, the role of Id3 in B-cell regulation of atherosclerosis is unknown., Objective: To determine if Id3 regulates B-cell homing to the aorta and atheroprotection and identify molecular and cellular mechanisms mediating this effect., Methods and Results: Loss of Id3 in Apoe(-/-) mice resulted in early and increased atherosclerosis. Flow cytometry revealed a defect in Id3(-/-) Apoe(-/-) mice in the number of B cells in the aorta but not the spleen, lymph nodes, and circulation. Similarly, B cells transferred from Id3(-/-) Apoe(-/-) mice into B-cell-deficient mice reconstituted spleen, lymph node, and blood similarly to B cells from Id3(+/+) Apoe(-/-) mice, but aortic reconstitution and B-cell-mediated inhibition of diet-induced atherosclerosis was significantly impaired. In addition to retarding initiation of atherosclerosis, B cells homed to regions of existing atherosclerosis, reduced macrophage content in plaque, and attenuated progression of disease. The chemokine receptor CCR6 was identified as an important Id3 target mediating aortic homing and atheroprotection., Conclusions: Together, these results are the first to identify the Id3-CCR6 pathway in B cells and demonstrate its role in aortic B-cell homing and B-cell-mediated protection from early atherosclerosis.

Amiodarone is a class 3 antiarrhythmic agent used for a broad range of arrhythmias including adenosine-resistant supraventricular tachycardia, junctional ectopic tachycardia, and ventricular tachycardia. Compared with adults, there are few data on its use in children with arrhythmias resistant to conventional therapy. National and international guidelines for cardiopulmonary resuscitation and emergency cardiovascular care recommend its use for a variety of arrhythmias based on case reports, cohort studies, and extrapolation from adult data. This article will review the historical development, chemical properties, metabolism, indications and contraindications, and adverse effects of amiodarone in infants and children. After completing this CME activity, the reader should be able to utilize amiodarone in the pediatric population for arrhythmias and identify complications associated with its use.

Phenotypic switching of smooth muscle cells (SMCs) plays a key role in vascular proliferative diseases. We previously showed that Krüppel-like factor 4 (Klf4) suppressed SMC differentiation markers in cultured SMCs. Here, we derive mice deficient for Klf4 by conditional gene ablation and analyze their vascular phenotype following carotid injury. Klf4 expression was rapidly induced in SMCs of control mice after vascular injury but not in Klf4-deficient mice. Injury-induced repression of SMC differentiation markers was transiently delayed in Klf4-deficient mice. Klf4 mutant mice exhibited enhanced neointimal formation in response to vascular injury caused by increased cellular proliferation in the media but not an altered apoptotic rate. Consistent with these findings, cultured SMCs overexpressing Klf4 showed reduced cellular proliferation, in part, through the induction of the cell cycle inhibitor, p21(WAF1/Cip1) via increased binding of Klf4 and p53 to the p21(WAF1/Cip1) promoter/enhancer. In vivo chromatin immunoprecipitation assays also showed increased Klf4 binding to the promoter/enhancer regions of the p21(WAF1/Cip1) gene and SMC differentiation marker genes following vascular injury. Taken together, we have demonstrated that Klf4 plays a critical role in regulating expression of SMC differentiation markers and proliferation of SMCs in vivo in response to vascular injury.

There are two broad themes in psychosomatic medicine research that relate emotions to physical disease outcomes. Theme 1 holds that self-reported negative affect has deleterious effects and self-reported positive affect has salubrious effects on health. Theme 2 holds that interference with the experience or expression of negative affect has adverse health consequences. From the perspective of self-report these two traditions appear contradictory. A key thesis of this paper is that the foundational distinction in cognitive neuroscience between explicit (conscious) and implicit (unconscious) processes, corresponding to Themes 1 and 2, respectively, provides a unifying framework that makes empirical research on unconscious emotional processes more tractable. A psychological model called "levels of emotional awareness" is presented first that places implicit and explicit emotional processes on a cognitive-developmental continuum. This model holds that the ability to become consciously aware of one's own feelings is a cognitive skill that goes through a developmental process similar to that which Piaget described for other cognitive functions. Empirical findings using the Levels of Emotional Awareness Scale are presented. A parallel hierarchical model of the neural substrates of emotional awareness is presented next supported by recent neuroimaging and lesion work. The evidence presented in this review suggests that the neural substrates of implicit and explicit emotional processes are distinct, that the latter have a modulatory effect on the former, and that at the neural level Theme 1 and Theme 2 phenomena share critical similarities. The implications of this psychobiological model for research in psychosomatic medicine are discussed.

Monocyte recruitment and adhesion to vascular endothelium are key early events in atherosclerosis. We examined the role of sphingosine-1-phosphate (S1P) on modulating monocyte/endothelial interactions in the NOD/LtJ (NOD) mouse model of type 1 diabetes. Aortas from nondiabetic and diabetic NOD mice were incubated in the absence or presence of 100 nmol/L S1P. Fluorescently labeled monocytes were incubated with the aortas. Aortas from NOD diabetic mice bound 7-fold more monocytes than nondiabetic littermates (10+/-1 monocytes bound/field for nondiabetic mice vs 74+/-12 monocytes bound/field for diabetic mice, P<0.0001). Incubation of diabetic aortas with 100 nmol/L S1P reduced monocyte adhesion to endothelium by 90%. We found expression of S1P1, S1P2, and S1P3 receptors on NOD aortic endothelial cells. The S1P1 receptor-specific agonist SEW2871 inhibited monocyte adhesion to diabetic aortas. Studies in diabetic S1P3-deficient mice revealed that the S1P3 receptor did not play a pivotal role in this process. S1P reduced endothelial VCAM-1 induction in type 1 diabetic NOD mice, most likely through inhibition of nuclear factor kappaB translocation to the nucleus. Thus, S1P activation of the S1P1 receptor functions in an antiinflammatory manner in type 1 diabetic vascular endothelium to prevent monocyte/endothelial interactions. S1P may play an important role in the prevention of vascular complications of type 1 diabetes.

Changes in the differentiated state of smooth muscle cells (SMCs) play a key role in vascular diseases, yet the mechanisms controlling SMC differentiation are still largely undefined. We addressed the role of basic helix-loop-helix (bHLH) proteins in SMC differentiation by first determining the role of two E-box (CAnnTG) motifs, binding sites for bHLH proteins, in the transcriptional regulation of the SMC differentiation marker gene, smooth muscle alpha-actin (SM alpha-actin), in vivo. Mutation of one or both E-boxes significantly reduced the expression of a -2560- to 2784-bp SM alpha-actin promoter/LacZ reporter gene in vivo in transgenic mice. We then determined the potential role of class I bHLH proteins, E12, E47, HEB, and E2-2, in SM alpha-actin regulation. In cotransfection experiments, E12, HEB, and E2-2 activated the SM alpha-actin promoter. Activation by HEB and E2-2 was synergistic with serum response factor. Additionally, the dominant-negative/inhibitory HLH proteins, Id2, Id3, and Twist, inhibited both the E12 and serum response factor-induced activations of the SM alpha-actin promoter. Finally, we demonstrated that E2A proteins (E12/E47) specifically bound the E-box-containing region of the SM alpha-actin promoter in vivo in the context of intact chromatin in SMCs. Taken together, these results provide the first evidence of E-box-dependent regulation of a SMC differentiation marker gene in vivo in transgenic mice. Moreover, they demonstrate a potential role for class I bHLH factors and their inhibitors, Id and Twist, in SM alpha-actin regulation and suggest that these factors may play an important role in control of SMC differentiation and phenotypic modulation.

Alterations in the differentiated state of vascular smooth muscle cells (SMCs) are known to play a key role in vascular diseases, yet the mechanisms controlling SMC differentiation are still poorly understand. In this review, we discuss our present knowledge of control of SMC differentiation at the transcriptional level, pointing out some common themes, important paradigms, and unresolved issues in SMC-specific gene regulation. We focus primarily on the serum response factor-CArG box-dependent pathway, because it has been shown to play a critical role in regulation of multiple SMC marker genes. However, we also highlight several other important regulatory elements, such as a transforming growth factor beta control element, E-boxes, and MCAT motifs. We present evidence in support of the notion that SMC-specific gene regulation is not controlled by a few SMC-specific transcription factors but rather by complex combinatorial interactions between multiple general and tissue-specific proteins. Finally, we discuss the implications of chromatin remodeling on SMC differentiation.

Objective: Previous research has demonstrated a deficit in the ability to recognize emotions in alexithymic individuals. The repressive coping style is thought to preferentially impair the detection of unpleasant compared with pleasant emotions, and the degree of deficit is typically thought to be less severe than in alexithymia. We compared emotion recognition ability in both individuals with alexithymia and those with the repressive coping style., Methods: Three hundred seventy-nine subjects completed the 20-item Toronto Alexithymia Scale, the Levels of Emotional Awareness Scale, the Marlowe-Crowne Scale (a measure of repressive defensiveness), the Bendig Short Form of the Taylor Manifest Anxiety Scale, and the Perception of Affect Task. The Perception of Affect Task consists of four 35-item emotion recognition subtasks: matching sentences and words, faces and words, sentences and faces, and faces and photographs of scenes. The stimuli in each subtask consist of seven emotions (happiness, sadness, anger, fear, disgust, surprise, and neutral) depicted five times each. Recognition accuracy results were collapsed across subtasks within each emotion category., Results: Highly alexithymic subjects (for all, p<.01) and those with low emotional awareness (for all, p<.001) were consistently less accurate in emotion recognition in all seven categories. Highly defensive subjects (including repressors) were less accurate in the detection of anger, sadness, fear, and happiness (for all, p<.05). Furthermore, scores on the Levels of Emotional Awareness Scale accounted for significantly more variance in performance on the Perception of Affect Task than scores on the Marlowe-Crowne Scale (p<.01)., Conclusions: The results indicate that alexithymia and the repressive coping style are each associated with impairments in the recognition of both pleasant and unpleasant emotions and that the two styles of emotional self-regulation differ more in the magnitude than in the quality of these impairments.

We examined neural activity associated with selectively attending to subjective emotional responses in a study where subjects viewed emotional picture sets. During picture viewing when subjects attended to their subjective emotional responses, highly significant increased neural activity was elicited in rostral anterior cingulate (BA 32) (Z = 6.87, p < 0.001, corrected). By contrast, under the same stimulus conditions when subjects attended to spatial aspects of identical picture sets activation was observed in the parieto-occipital cortex bilaterally (Z = 5.71, p < 0.001, corrected). The findings indicated a specific role for the anterior cingulate cortex in representing subjective emotional responses and are consistent with a suggested role for associated medial prefrontal structures in representing states of mind.

Although clinical observations suggest that alexithymic individuals have a deficit in their ability to recognize emotional stimuli and that this deficit is not simply due to a problem in verbal labeling, these two hypotheses have not been empirically confirmed. Three hundred eighty participants in a community survey without current or past histories of psychiatric disorder completed two independent measures of alexithymia [the Levels of Emotional Awareness Scale (LEAS) and the Toronto Alexithymia Scale (TAS-20)] and the Perception of Affect Task (PAT), a 140-item measure of the ability to match emotion stimuli. The PAT includes four subtasks that require the subject to match verbal or nonverbal emotion stimuli with verbal or nonverbal emotion responses. The subtasks include matching sentences and words (verbal-verbal), faces and words (nonverbal-verbal), sentences and faces (verbal-nonverbal), and faces and photographs of scenes (nonverbal-nonverbal). Across the entire sample, higher (alexithymic) TAS-20 and lower LEAS scores were both correlated with lower accuracy rates on each of the subtasks of the PAT (p < .001), accounting for 10.5% and 18.4% of the variance, respectively. Fifty-one subjects met TAS-20 criteria for alexithymia. Alexithymic individuals scored lower than other subjects on purely nonverbal matching, purely verbal matching, and mixed verbal-nonverbal matching (all p < .001). These results suggest that alexithymia is associated with impaired verbal and nonverbal recognition of emotion stimuli and that the hallmark of alexithymia, a difficulty in putting emotion into words, may be a marker of a more general impairment in the capacity for emotion information processing.

Background and Purpose: The physiological basis for the arrhythmias commonly observed after a stroke is not well understood. Based on evidence that the right and left cerebral hemispheres influence cardiac function in different ways, we sought to determine whether the nature and severity of cardiac arrhythmias in the context of an acute stroke vary in relation to whether the stroke is located in the left or the right hemisphere., Methods: Data were obtained from the medical records of nineteen patients with left hemisphere strokes and nineteen patients with right hemisphere strokes who had also had 24-hour electrocardiographic (Holter) recordings within 2 weeks of admission to a stroke unit. Written Holter monitor reports already on file were used for the data analysis., Results: All four patients with supraventricular tachycardia had right hemisphere strokes (p = 0.05). There was a nonsignificant trend for left hemisphere stroke patients to have more severe ventricular arrhythmias., Conclusions: These data provide partial support for the hypothesis that the two cerebral hemispheres have a differential influence on the nature and severity of arrhythmias following an acute stroke. We speculate that parasympathetic tone was diminished ipsilateral to the affected hemisphere associated with a reciprocal rise in sympathetic tone on that side and recommend that a prospective study be undertaken to test this hypothesis more definitively.

Over a 10-month period, 33 patients with tardive dyskinesia (TD) were evaluated with the Abnormal Involuntary Movement Scale (AIMS) simultaneously and independently by two experienced and two inexperienced raters. The experienced raters generally had higher levels of agreement and their scores were more consistent over time. It is concluded that experience with TD influences AIMS inter-rater reliability and that it is useful to differentiate TD movements into the dimensions of quality, frequency, and amplitude, dimensions not currently used in the AIMS. The usefulness and difficulty of developing more specific guidelines for AIMS ratings are discussed.

A neurophysiologic mechanism for stress-induced cardiac arrhythmias is proposed based on the integration of two bodies of research that have until now developed independently: the role of hemispheric specialization in the mediation of emotional arousal and the role of a lateralized imbalance in sympathetic input to the heart in cardiac arrhythmogenesis. The specific hypothesis is that individuals who manifest more lateralized frontal lobe activity during emotional arousal may concomitantly generate more lateralized sympathetic input to the heart and be at increased risk for fatal cardiac arrhythmias. The theoretical background for the hypothesis is presented, empirical support for the hypothesis is reviewed, and implications for empirical research are discussed.