搜索结果：Autonomic neuroscience : basic & clinical

Non-motor symptoms (NMS) of Parkinson's disease (PD) are well described in both clinical practice and the literature, enabling their management and enhancing our understanding of PD. NMS can dominate the clinical pictures and NMS subtypes have recently been proposed, initially based on clinical observations, and later confirmed in data driven analyses of large datasets and in biomarker-based studies. In this chapter, we provide an update on what is known about three common subtypes of NMS in PD. The pain (Park-pain), sleep dysfunction (Park-sleep), and autonomic dysfunction (Park-autonomic), providing an overview of their individual classification, clinical manifestation, pathophysiology, diagnosis, and potential treatments.

The autonomic nervous system (ANS) is responsible for the precise regulation of tissue functions and organs and, thus, is crucial for optimal stress reactivity, adaptive responses and health in basic and challenged states (survival). The fine-tuning of central ANS activity relies on the internal central autonomic regulation system of the central autonomic network (CAN), while the peripheral activity relies mainly on the two main and interdependent peripheral ANS tracts, the sympathetic nervous system (SNS) and the parasympathetic nervous system (PNS). In disease, autonomic imbalance is associated with decreased dynamic adaptability and increased morbidity and mortality. Acute or prolonged autonomic dysregulation, as observed in stress-related disorders, affects CAN core centers, thereby altering downstream peripheral ANS function. One of the best established and most widely used non-invasive methods for the quantitative assessment of ANS activity is the computerized analysis of heart rate variability (HRV). HRV, which is determined by different methods from those used to determine the fluctuation of instantaneous heart rate (HR), has been used in many studies as a powerful index of autonomic (re)activity and an indicator of cardiac risk and ageing. Psychiatric patients regularly show altered autonomic function with increased HR, reduced HRV and blunted diurnal/circadian changes compared to the healthy state. The aim of this article is to provide basic knowledge on ANS function and (re)activity assessment and, thus, to support a much broader use of HRV as a valid, transdiagnostic and fully translational dynamic biomarker of stress system sensitivity and vulnerability to stress-related disorders in neuroscience research and clinical psychiatric practice. In particular, we review the functional levels of central and peripheral ANS control, the main neurobiophysiologic theoretical models (e.g., polyvagal theory, neurovisceral integration model), the precise autonomic influence on cardiac function and the definition and main aspects of HRV and its different measures (i.e., time, frequency and nonlinear domains). We also provide recommendations for the proper use of electrocardiogram recordings for HRV assessment in clinical and research settings and highlight pathophysiological, clinical and research implications for a better functional understanding of the neural and molecular mechanisms underlying healthy and malfunctioning brain-heart interactions in individual stress reactivity and psychiatric disorders.

Research on the effects of acupuncture on autonomic function has been conducted for several decades, and a few notable studies have emerged in recent years. This study used bibliometric analysis to assess 100 top-cited articles to characterize the current status and research trends over the last three decades. The 100 top-cited publications were identified from the Web of Science Core Collection database. The bibliometrix package in R was used for quantitative and qualitative analyses of the publication patterns and the country/region, institution, and author contributions. VOSviewer was used to construct networks based on co-citation analysis of the journals and the keyword co-occurrence. The 100 top-cited articles were identified with a total of 8,123 citations (range: 37-345). The majority of the articles came from the USA (n = 42), followed by Japan (n = 14) and mainland China (n = 13). Articles from the USA exhibited the largest number of citations (3,582 citations), followed by articles from Japan (1,189 citations), then articles from mainland China (755 citations). Neurosciences/Neurology was the most studied research area (n = 41). The Autonomic Neuroscience: Basic and Clinical published the largest number of papers (n = 14), while Brain Research received the largest number of citations (205 citations). Longhurst JC was the most productive author (10 publications), and Sato A was first among the cited authors (87 citations). The most frequently cited articles that focused on gastrointestinal, cardiovascular, or gynecologic responses to acupuncture regulation of the autonomic nervous system first appeared in the 1990s, peaked in the 2000s, then decreased after 2010. Publication of articles focused on the anti-inflammatory effects of acupuncture associated with autonomic function demonstrated an increasing trend over the last three decades. From the initial studies focusing on the autonomic mechanism of visceral responses to acupuncture, researchers concentrated on exploring the autonomic mechanism of acupuncture in the control of systemic inflammation. Non-invasive electrical methods that activate somato-autonomic reflexes are current translational directions in clinical practice. Additional investigation of the underlying neuroanatomical basis of somato-autonomic reflexes also is needed.

The self is increasingly conceptualized as an embodied, predictive process in contemporary cognitive and affective neuroscience. The brain continually infers the causes of both exteroceptive and interoceptive signals in order to minimize prediction error and maintain allostatic balance. Within this framework, emotion can be understood as an inference about changes in bodily states. Parallel themes have long been articulated in traditional East Asian medicine (TEAM), where emotions are understood to modulate the flow of Qi and clinical practice is aimed at restoring dynamic balance through breath, movement, attention, acupuncture, and related interventions. This study brings these traditions into dialogue, arguing that the phenomenology of bodily patterns and the directional qualities of emotion in TEAM are compatible with predictive-processing accounts of interoception, allostasis, and affect regulation. We summarize key research on autonomic flexibility, emotional "body maps," and interoception; integrate clinical observations from acupuncture practice; offer testable cross-framework hypotheses; and outline implications for mental health and wellbeing. We advocate a pluralistic, pragmatic approach that acknowledges conceptual diversity while using points of convergence to guide research and practice, rather than forcing one framework into the terms of the other. Bridging modern neuroscience with traditional insights can support a more deeply embodied understanding of the self and provide new avenues for investigating the regulation of emotional life.

Obstructive sleep apnoea (OSA) and spondyloarthritis (SpA) are chronic inflammatory disorders associated with substantial cardiometabolic morbidity and impaired quality of life. Increasing evidence suggests that these conditions frequently coexist and may share overlapping pathogenic mechanisms involving intermittent hypoxia, oxidative stress, endothelial dysfunction, autonomic dysregulation, and activation of TNF-α and the IL-17/IL-23 axis. This narrative review summarises current evidence on the epidemiological, mechanistic, and clinical relationship between OSA and SpA, with emphasis on axial spondyloarthritis and psoriatic arthritis. Available studies indicate an increased prevalence of OSA in ankylosing spondylitis and psoriatic arthritis, although evidence remains heterogeneous and limited by small cohorts, cross-sectional designs, and inconsistent use of polysomnography. Structural spinal restriction, obesity, metabolic syndrome, chronic inflammation, and altered sleep architecture may all contribute to OSA susceptibility in SpA populations. Conversely, OSA-related intermittent hypoxia may amplify inflammatory pathways relevant to SpA pathobiology, potentially worsening fatigue, pain, disease activity, and cardiovascular risk. Preliminary evidence also suggests that continuous positive airway pressure and biologic therapies may favourably influence inflammatory and sleep-related outcomes, although disease-specific interventional evidence remains limited. Current evidence suggests a clinically relevant association between OSA and SpA, but the directionality and clinical significance of this interaction remain incompletely understood. Prospective longitudinal and mechanistic studies integrating objective sleep assessment, inflammatory biomarkers, and rheumatologic outcomes are needed to clarify causality and guide multidisciplinary management strategies.

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Adolescents who engage in nonsuicidal self-injury (NSSI) show a high sensitivity to ostracism, and its effects may be amplified by dysregulated stress-system function. However, ecologically grounded experimental studies examining multilevel stress responses in adolescent mental health remain scarce. We used a novel, ecologically valid in-person ostracism paradigm to assess subjective, autonomic, and endocrine responses in adolescents with recent NSSI and to characterize stress trajectories. Fifty adolescents with recent NSSI (mean age = 16.40 years, 76% female) were randomized (1:1) to live social inclusion or exclusion in a face-to-face ball-toss task based on the Cyberball paradigm. Salivary cortisol was sampled at five points from pre-task to 40 min post-task. Heart rate (HR) and heart rate variability (HRV) were recorded at baseline and during the interaction. Subjective stress, tension, and NSSI urges were assessed before and after the task. Perceived exclusion and psychological need threat were also assessed. We found clear ostracism effects on perceived exclusion and basic psychological need threat. Cortisol declined across the paradigm in both conditions (inclusion/exclusion), but the decline was flatter after exclusion, indicating attenuated hypothalamic-pituitary-adrenal axis downregulation. HR decreased modestly over time across conditions, and HRV diverged by condition: it decreased during exclusion and increased during inclusion. There were no condition-related changes in self-reported stress, tension, or NSSI urges. These findings suggest a decoupling between subjective and psychobiological stress systems in adolescents with NSSI in response to ostracism, characterized by rapid parasympathetic withdrawal and a blunted HPA axis downregulation. This pattern may reflect heightened physiological sensitivity to social threat despite limited conscious distress. This study has been registered at the German Clinical Trials Register (ID: DRKS00025905, https://drks.de/search/en/trial/DRKS00025905).

The main unmet need of Parkinson's disease (PD) is the lack of a therapy able to slow progression. The field is shifting from syndromic diagnosis toward biologically anchored definitions and staging, enabling PD identification before motor onset. In this context, imaging biomarkers provide in vivo measures to identify subtypes, enrich cohorts, and track changes in disease-modifying trials. This review focuses on the role of monoaminergic imaging for preclinical intervention. Monoaminergic imaging captures both the core substrate of motor phenoconversion and extranigral mechanisms underlying early non-motor symptoms. Presynaptic dopaminergic imaging remains the most robust marker of conversion risk in prodromal cohorts, while noradrenergic and serotonergic imaging delineate early brainstem and limbic involvement. Peripheral autonomic imaging further extends biomarker coverage, with cardiac sympathetic imaging detecting early extracerebral denervation in prodromal stages. Together, harmonised monoaminergic imaging provides a unifying framework for staging and clinical trial readiness.

Sleep disturbances, gastrointestinal problems, and atypical heart rate are commonly observed in patients with autism spectrum disorder (ASD) and may relate to underlying function of the autonomic nervous system (ANS). The overall objective of the current study was to quantitatively characterize features of ANS function using symptom scales and available electronic health record (EHR) data in a clinically and genetically characterized pediatric cohort. We assessed features of ANS function via chart review of patient records adapted from items drawn from a clinical research questionnaire of autonomic symptoms. This procedure coded for the presence and/or absence of targeted symptoms and was completed in 3 groups of patients, including patients with a clinical neurodevelopmental diagnosis and identified genetic etiology (NPD, n=244), those with an ASD diagnosis with no known genetic cause (ASD, n=159), and age and sex matched controls (MC, n=213). Symptoms were assessed across four main categories: (1) Mood, Behavior, and Emotion; (2) Secretomotor, Sensory Integration; (3) Urinary, Gastrointestinal, and Digestion; and (4) Circulation, Thermoregulation, Circadian function, and Sleep/Wake cycles. Chart review scores indicate an increased rate of autonomic symptoms across all four sections in our NPD group as compared to scores with ASD and/or MC. Additionally, we note several significant relationships between individual differences in autonomic symptoms and quantitative ASD traits. These results highlight EHR review as a potentially useful method for quantifying variance in symptoms adapted from a questionnaire or survey. Further, using this method indicates that autonomic features are more prevalent in children with genetic disorders conferring risk for ASD and other neurodevelopmental diagnoses.

Features of underlying autonomic dysfunction, including sleep disturbances, gastrointestinal problems, and atypical heart rate, have been reported in neurodevelopmental conditions, including autism spectrum disorder (ASD). The current cross-sectional, between-groups study aimed to quantify symptoms of autonomic dysfunction in a neurodevelopmental pediatric cohort characterized by clinical diagnoses as well as genetic etiology. The Pediatric Autonomic Symptom Scales (PASS) questionnaire was used to assess autonomic features across a group of patients with clinical neurodevelopmental diagnoses (NPD; N = 90) and genetic etiologies. Patients were subdivided based on either having a clinical ASD diagnosis (NPD-ASD; n = 37) or other non-ASD neurodevelopmental diagnoses, such as intellectual disability without ASD, speech and language disorders, and/or attention deficit hyperactivity disorder (NPD-OTHER; n = 53). Analyses focused on characterizing differences between the NPD group compared to previously published reference samples, as well as differences between the two NPD subgroups (NPD-ASD and NPD-OTHER). Our results indicate higher PASS scores in our NPD cohort relative to children with and without ASD from a previously published cohort. However, we did not identify significant group differences between our NPD-ASD and NPD-OTHER subgroups. Furthermore, we find a significant relationship between quantitative ASD traits and symptoms of autonomic function. This work demonstrates the utility of capturing quantitative estimates of autonomic trait dimensions that may be significantly linked with psychosocial impairments and other core clinical features of ASD.

The autonomic nervous system (ANS) is essential for maintaining physiological homeostasis. Autonomic nervous system imbalance, characterised by sympathetic hyperactivation and low parasympathetic tone, can occur during the perioperative period. These changes drive systemic stress responses, cardiovascular instability, impaired tissue repair, and immunosuppression, which in turn increase infection risk, neurocognitive decline, and multiorgan dysfunction. Surgical trauma, anaesthesia, pain, hypothermia, and psychological stressors all contribute to this dysregulation, and consequently low parasympathetic tone results in the cholinergic anti-inflammatory pathway being less effective. High sympathetic nervous system activity promotes catecholamine surges and pro-inflammatory cytokine release. Pharmacological interventions, including dexmedetomidine and β-blockers, together with nonpharmacological strategies, such as electroacupuncture and temperature management, are measures that have potential to restore ANS balance. This systematic review covers ANS-mediated organ regulation, pathophysiological consequences of perioperative dysautonomia, and evidence-based therapeutic strategies. By integrating findings from multiple basic and clinical studies, the pivotal roles of ANS modulation in mitigating postoperative complications, including neurocognitive disorders, immunosuppression, and cancer recurrence, are discussed. Maintaining balance of the sympathetic and parasympathetic nervous systems is an important prospect in perioperative medicine that could benefit surgical patients' short- or long-term recovery.

Non-invasive brain stimulation (NIBS) approaches have seen a rise in utilization in both clinical and basic neuroscience in recent years. Here, we concentrate on the two methods that have received the greatest research: transcranial direct current stimulation (tDCS) and repetitive transcranial magnetic stimulation (rTMS). Both approaches have yielded pertinent data regarding the cortical excitability in subjects in good health as well as pertinent advancements in the management of various clinical disorders. NIBS is a helpful method for comprehending the cortical control of the ANS. Previous research has shown that there are notable changes in muscular sympathetic nerve activity when the motor cortex is modulated. Furthermore, in NIBS investigations, the ANS has been employed more frequently as an outcome measure to comprehend the overall impacts of these methods, including their safety profile. Though there is ample proof that brain stimulation has autonomic effects on animals, new research on the connection between NIBS and the ANS has produced contradictory findings. In order to better understand NIBS processes and ANS function, it is crucial to take into account the reciprocal relationship that exists between central modulation and ANS function.

Rett syndrome (RTT) is a rare and severe neurological disorder mainly affecting females, usually linked to methyl-CpG-binding protein 2 (MECP2) gene mutations. Manifestations of RTT typically include loss of purposeful hand skills, gait and motor abnormalities, loss of spoken language, stereotypic hand movements, epilepsy, and autonomic dysfunction. Patients with RTT have a higher incidence of sudden death than the general population. Literature data indicate an uncoupling between measures of breathing and heart rate control that could offer insight into the mechanisms that lead to greater vulnerability to sudden death. Understanding the neural mechanisms of autonomic dysfunction and its correlation with sudden death is essential for patient care. Experimental evidence for increased sympathetic or reduced vagal modulation to the heart has spurred efforts to develop quantitative markers of cardiac autonomic profile. Heart rate variability (HRV) has emerged as a valuable non-invasive test to estimate the modulation of sympathetic and parasympathetic branches of the autonomic nervous system (ANS) to the heart. This review aims to provide an overview of the current knowledge on autonomic dysfunction and, in particular, to assess whether HRV parameters can help unravel patterns of cardiac autonomic dysregulation in patients with RTT. Literature data show reduced global HRV (total spectral power and R-R mean) and a shifted sympatho-vagal balance toward sympathetic predominance and vagal withdrawal in patients with RTT compared to controls. In addition, correlations between HRV and genotype and phenotype features or neurochemical changes were investigated. The data reported in this review suggest an important impairment in sympatho-vagal balance, supporting possible future research scenarios, targeting ANS.

Parkinson's disease (PD) is the second most common, and the fastest growing, neurodegenerative disease worldwide. Non-motor manifestations, particularly autonomic nervous system dysfunction, are common throughout the disease course, in some cases preceding motor symptom onset by years, and are often more disabling and harder to treat than motor symptoms and contribute significantly to disability. An understudied consequence of autonomic and visceral dysfunction in PD is interoception, the neural processing of internal organ system signals. Interoceptive processes form a foundational body-brain interface, mediating basic homeostatic reflexes and complex physiologic and behavioral adaptive responses to internal perturbations. Emerging evidence exists that interoception is impaired in some individuals with PD, potentially explaining why those who have objective evidence of autonomic dysfunction do not always report typical symptoms. Failure to recognize these impairments may lead to missed opportunities for early intervention, particularly in addressing 'silent' autonomic disturbances (e.g., orthostatic hypotension leading to sudden falls, dysphagia leading to aspiration pneumonia). In this narrative review, we synthesize current findings on the neuroanatomical networks underlying interoception, examine clinical manifestations of interoceptive dysfunction across multiple organ systems in PD, and identify key gaps in knowledge. We propose a translational research framework to enhance early detection, symptom management, and intervention strategies for PD. This framework integrates cognitive, mood, and autonomic dysfunctions with clinical factors (disease stage, duration, motor subtype, levodopa status) to understand interoceptive dysfunction within a translational model. This approach highlights novel opportunities for personalized care and improved therapeutic interventions in PD.

To assess the effects of two different body positions on the cardiovascular autonomic profile during a single bout of exercise in patients with postural orthostatic tachycardia syndrome (POTS). Thirteen patients with POTS and thirteen healthy controls (C) participated in the study. ECG, respiration, beat-by-beat arterial pressure and O2 consumption (VO2) were continuously recorded while on a cycle ergometer in supine and upright positions, before and during exercise (6 min, 50 Watts). Spectral analysis of RR intervals and systolic arterial pressure (SAP) variability provided indexes of cardiac sympathovagal interaction (LF/HF ratio), cardiac vagal modulation (HFRR, high-frequency component of RR variability, ~ 0.25 Hz), sympathetic vasomotor control (LFSAP, low-frequency component of SAP variability, 0.1 Hz) and baroreflex sensitivity (BRS, αLF). While supine, patients with POTS showed lower HFRR and αLF, greater heart rate (HR), LF/HF and LFSAP, compared with C, suggesting cardiovascular sympathetic over-activity and reduced BRS. While sitting upright, POTS showed greater HR and reduced HFRR and αLF compared with C. During supine exercise, SAP, HR, LF/HF increased and HFRR and αLF decreased similarly in POTS and C. In POTS, upright sitting exercise was associated with slightly higher V ˙ O 2 , a greater increase in HR whereas LFSAP was lower than in C. Upright exercise was associated with excessive enhancement of HR and a blunted increase of the sympathetic vasomotor control in POTS. Conversely, supine exercise-induced hemodynamic and autonomic changes similar in POTS and C, thus making supine exercise potentially more suitable for physical rehabilitation in POTS.

A central unresolved issue in affective neuroscience is whether human emotions have unique biological signatures in the brain and body. Despite decades of debate, a consensus is lacking on whether emotions are patterned (similar across contexts and characterized by distinct features) or flexible (variable across contexts and lacking distinct features). Studies in other species have revealed the ubiquity of autonomic and motor patterns, and these investigations have elucidated the biology of central pattern generation at the levels of networks, neurons, and synapses. Here, we integrate the knowledge gained from this research and introduce the Dynamic Emotion Fabric Theory (DEFT), a new model of emotions biology. DEFT proposes that, just as fabrics are comprised of both patterns and textures, emotions are accompanied by stereotyped responses that are distinct and recognizable, yet also nuanced and malleable. A neurobiological system that is both automatic-generating patterned reactions essential for survival-and flexible-texturizing each response in context-is equipped to produce the spectrum of human emotions. DEFT provides new insights into the biological basis of emotions and identifies novel areas that warrant further study in humans and other species. This framework has implications for basic affective neuroscience and clinical studies of affective symptoms.

Idiopathic rapid eye movement sleep behavior disorder (iRBD) is a prodromal neurodegenerative disease of misfolded alpha-synuclein (P-SYN) with a high risk of phenoconversion to a clinically apparent synucleinopathy (including Parkinson's disease, multiple system atrophy, or dementia with Lewy bodies) over 15 years. To determine rates of cutaneous P-SYN deposition in iRBD, to quantify changes in PSYN deposition over time, and to determine if P-SYN deposition patterns and amounts predict phenoconversion to a specific type of synucleinopathy. In a prospective, blinded study we will recruit 80 individuals with polysomnography confirmed iRBD or probable RBD using standard diagnostic criteria. Skin biopsies with dual immunohistochemical immunostaining for nerve fibers (protein gene product 9.5) and P-SYN will be completed at 3 sites using standard methodology. Quantitative measures of P-SYN and nerve fiber density will be measured blinded to any clinical data and will be followed longitudinally to determine the final clinical diagnosis. Patients with iRBD are an important population to study due to the high rates of phenoconversion to clinically apparent synucleinopathy. Defining the frequency of P-SYN deposition and the risk of phenoconversion will aid in the development of future clinical trials that seek to alter the natural history of synucleinopathies.

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a chronic, multisystemic disorder characterized by severe, persistent fatigue not alleviated by rest and worsened by minimal exertion, often accompanied by post-exertional malaise (PEM), unrefreshing sleep, cognitive dysfunction, and autonomic disturbances. Despite decades of research, its pathophysiology remains incompletely understood, and skeletal muscle involvement has only recently gained attention. This review aims to provide a historical and pathophysiological synthesis of ME/CFS, emphasizing the pivotal role of skeletal muscle in the onset and persistence of symptoms, and to integrate molecular, cellular, and pathophysiological evidence into a coherent explanatory framework. This is a narrative review of published literature (1990-2025) with critical integration of clinical, biochemical, and experimental data on oxidative stress, mitochondrial dysfunction, Excitation-Contraction (E-C coupling) dysregulation, and muscle secretome alterations in ME/CFS also in relation to post-viral syndromes (e.g., Long COVID). Evidence consistently points to mitochondrial oxidative stress, redox imbalance, impaired Ca2+ handling, and altered signaling pathways in skeletal muscle of patients with ME/CFS. Historical milestones show an evolution from psychogenic interpretations toward recognition of ME/CFS as a biological disorder with neuromuscular and metabolic underpinnings. ME/CFS can be interpreted as a skeletal muscle-metabolic disorder characterized by oxidative distress, mitochondrial dysfunction, and impaired energy regulation, leading to the clinical picture of exercise intolerance and post-exertional malaise. Integrating basic and clinical research through a translational approach provides the foundation for new diagnostic tools, targeted therapies, and biomarkers.

Alzheimer's disease (AD) affects not only memory and cognition but also the body's automatic functions, such as heart rate and blood pressure. These changes reflect the early disruption of the central autonomic network, the system that links the brain and the heart to maintain physiological balance. Electroencephalography (EEG) measures the brain's electrical activity and reveals patterns of cortical slowing and desynchronization, while heart-rate variability (HRV) reflects how flexibly the heart responds to internal and external demands. This narrative review brings together evidence published between 2000 and 2025 on the combined use of EEG and HRV as a single, integrated biomarker for AD. Studies consistently show that EEG-HRV coupling, which reflects how well the brain and heart communicate, provides better accuracy in distinguishing mild cognitive impairment and early AD than either measure alone. The findings reveal a shared loss of co-ordination between neural and autonomic systems, which is a hallmark of neurovisceral decline. The review also identifies key methodological gaps, including inconsistent recording conditions and lack of standardized analytic methods, which currently limit reproducibility. To bridge this gap, a translational roadmap is proposed to outline short-, mid-, and long-term goals for clinical validation, wearable integration, and digital health applications. Together, EEG-HRV coupling represents a scalable, non-invasive, and physiologically grounded tool that could support earlier and personalized monitoring of AD, helping to connect laboratory discovery with real-world clinical care.