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Comprised of the sympathetic nervous system, parasympathetic nervous system, and enteric nervous system, the autonomic nervous system (ANS) provides the neural control of all parts of the body except for skeletal muscles. The ANS has the major responsibility to ensure that the physiological integrity of cells, tissues, and organs throughout the ent...
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... receptors are members of a superfamily of ligand- gated ion channels (ionotropic receptors) that also includes GABA-A, glycine, and some glutamate receptors. Table 6 summarizes some of the properties of N M and N N receptors, including their location, cellular and molecular mechanisms, and membrane and postsynaptic target responses (38,93,156,216) Each nicotinic cholinergic receptor has five subunits that form a central channel through which the passage of Na + and other cations occurs when the receptor is activated. The five subunits come from several types designated as α, β, γ, δ, and ε that are each coded by different genes. ...
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... M 1 − M 3 receptors are found at autonomic synapses. As listed in Table 6, these three receptor subtypes differ in terms of their cellular responses and/or their anatomical location. All three subtypes activate the mitogen-activated protein kinase path- way, but the type of G protein involved in mediating their actions can differ. ...
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... 4 shows some of the locations of these receptor subtypes on smooth muscles, cardiac muscle, and glands on autonomic effector targets. Table 6 summarizes some of the major characteris- tics of these receptors including their location, cellular and molecular mechanisms, and membrane and postsynaptic tar- get responses (38,216,247). A recent review by Tank and Wong (247) goes into more detail regarding the GPCRs and signaling pathways that characterize the various subtypes of adrenoceptors. ...
Similar publications
Chronic heart failure is a common clinical condition characterized by persistent excessive sympathetic nervous system activation. The derangement of the sympathetic activity has relevant implications for disease progression and patient survival. Aiming to positively impact patient outcome, autonomic nervous system modulatory therapies have been dev...
Citations
... The autonomic nervous system is a critical component of the peripheral nervous system that regulates involuntary physiological functions essential for maintaining homeostasis and responding to stress. It controls various involuntary processes, including cardiovascular regulation, respiratory rate, gastrointestinal motility, and glandular secretion [1,2]. ...
Thyroid hormones have a pivotal role in controlling metabolic processes, cardiovascular function, and autonomic nervous system activity. Hypothyroidism, a prevalent endocrine illness marked by inadequate production of thyroid hormone, has been linked to different cardiovascular abnormalities, including alterations in heart rate variability (HRV). The study included 110 patients with hypothyroid disorder. Participants underwent clinical assessments, including thyroid function tests and HRV analysis. HRV, a measure of the variation in time intervals between heartbeats, serves as an indicator of autonomic nervous system activity and cardiovascular health. The HRV values were acquired using continuous 24-h electrocardiogram (ECG) monitoring in individuals with hypothyroidism, as well as after a treatment period of 3 months. All patients exhibited cardiovascular symptoms like palpitations or fatigue but showed no discernible cardiac pathology or other conditions associated with cardiac disease. The findings of our study demonstrate associations between hypothyroidism and alterations in heart rate variability (HRV) parameters. These results illustrate the possible influence of thyroid dysfunction on the regulation of cardiac autonomic function.
... Decreased heart rate variability (HRV) has been observed in patients with an insular infarct, particularly among those with a right side infarct (Tokgözoglu et al., 1999). The autonomic nervous system consists of various interconnected areas in the telencephalon, diencephalon, and brainstem, including the insular cortex and hypothalamus (Wehrwein et al., 2016). The insular cortex appears to play a leading role in autonomic control of cardiac activity. ...
Background
Previous studies have shown that Alzheimer’s disease (AD) can cause myocardial damage. However, whether there is a causal association between AD and non-ischemic cardiomyopathy (NICM) remains unclear. Using a comprehensive two-sample Mendelian randomization (MR) method, we aimed to determine whether AD and family history of AD (FHAD) affect left ventricular (LV) structure and function and lead to NICM, including hypertrophic cardiomyopathy (HCM) and dilated cardiomyopathy (DCM).
Methods
The summary statistics for exposures [AD, paternal history of AD (PH-AD), and maternal history of AD (MH-AD)] and outcomes (NICM, HCM, DCM, and LV traits) were obtained from the large European genome-wide association studies. The causal effects were estimated using inverse variance weighted, MR-Egger, and weighted median methods. Sensitivity analyses were conducted, including Cochran’s Q test, MR-Egger intercept test, MR pleiotropy residual sum and outlier, MR Steiger test, leave-one-out analysis, and the funnel plot.
Results
Genetically predicted AD was associated with a lower risk of NICM [odds ratio (OR) 0.9306, 95% confidence interval (CI) 0.8825–0.9813, p = 0.0078], DCM (OR 0.8666, 95% CI 0.7752–0.9689, p = 0.0119), and LV remodeling index (OR 0.9969, 95% CI 0.9940–0.9998, p = 0.0337). Moreover, genetically predicted PH-AD was associated with a decreased risk of NICM (OR 0.8924, 95% CI 0.8332–0.9557, p = 0.0011). MH-AD was also strongly associated with a decreased risk of NICM (OR 0.8958, 95% CI 0.8449–0.9498, p = 0.0002). Different methods of sensitivity analysis demonstrated the robustness of the results.
Conclusion
Our study revealed that AD and FHAD were associated with a decreased risk of NICM, providing a new genetic perspective on the pathogenesis of NICM.
... ANS signaling, along with the endocrine system and the CNS, facilitates top-down communication, i.e., from the brain to gut [36]. Regular functioning and physiology of the GI tract, such as gut motility, mucus and bicarbonate production release, permeability, mucosal immune barrier, and intestinal fluid maintenance, are controlled by the ANS [37]. Pain and stress can alter the aforementioned conditions and are relayed by the ANS [38]. ...
The microbiota–gut–brain axis (MGBA) has emerged as a key prospect in the bidirectional communication between two major organ systems: the brain and the gut. Homeostasis between the two organ systems allows the body to function without disease, whereas dysbiosis has long-standing evidence of etiopathological conditions. The most common communication paths are the microbial release of metabolites, soluble neurotransmitters, and immune cells. However, each pathway is intertwined with a complex one. With the emergence of in vitro models and the popularity of three-dimensional (3D) cultures and Transwells, engineering has become easier for the scientific understanding of neurodegenerative diseases. This paper briefly retraces the possible communication pathways between the gut microbiome and the brain. It further elaborates on three major diseases: autism spectrum disorder, Parkinson’s disease, and Alzheimer’s disease, which are prevalent in children and the elderly. These diseases also decrease patients’ quality of life. Hence, understanding them more deeply with respect to current advances in in vitro modeling is crucial for understanding the diseases. Remodeling of MGBA in the laboratory uses many molecular technologies and biomaterial advances. Spheroids and organoids provide a more realistic picture of the cell and tissue structure than monolayers. Combining them with the Transwell system offers the advantage of compartmentalizing the two systems (apical and basal) while allowing physical and chemical cues between them. Cutting-edge technologies, such as bioprinting and microfluidic chips, might be the future of in vitro modeling, as they provide dynamicity.
... Physiotherapists working in a direct access setting [24] require skills in a wide range of examination procedure [19,59] in order to rule out autonomic signs or symptoms of serious pathologies mimicking common musculoskeletal disorders [62][63][64], such as congenital craniovertebral anomalies [65,66], cervical vascular pathologies [19,60,61], anatomical instabilities, and autonomic disorders [4] in patients with neck pain or whiplash. Therefore, the relationship between autonomic syndromes and musculoskeletal conditions confirms that ANS must be a foundational knowledge of physiotherapy practice [67]. ...
Background: Harlequin syndrome is a rare autonomic condition consisting of unilateral facial flushing and sweating induced by heat, emotion or physical activity. The affected side presents anhidrosis and midline facial pallor due to denervation of the sympathetic fibers. Case Description: This case describes a patient who reported right-side redness of the face associated with hyperhidrosis during physical activity. She had two previous major motor vehicle accidents. The patient demonstrated difficulties in the visual accommodation of the left eye, but cranial nerve assessment was unremarkable; the patient was then referred to an ophthalmologist, who excluded any autonomic dysfunction as the primary cause of convergence and visual acuity. Outcomes: A left-sided sympathetic dysfunction with Harlequin sign diagnosis was made followed by a progressive compensatory adaptation of the right face. The patient was educated and reassured about the benign nature of her problem. Discussion: Knowledge of the autonomic nervous system is still limited in clinical practice. Although challenging, physiotherapists should develop the knowledge and ability needed to perform appropriate assessment of autonomic dysfunctions. Conclusion: A dispositional reasoning model should be considered in differential diagnosis.
... autonomic nervous system, and to be linked to anxiety-related responses [17]- [19]. These bodily responses are regulated by the autonomic nervous system, a complex network of nerves that controls involuntary functions such as heart rate, blood pressure, and digestion [7]. Research has highlighted the bidirectional signaling between the brain and the autonomic nervous system in regulating anxiety [8]- [11]. ...
Brain-heart interactions (BHI) are critical for generating and processing emotions, including anxiety. Understanding specific neural correlates would be instrumental for greater comprehension and potential therapeutic interventions of anxiety disorders. While prior work has implicated the pontine structure as a central processor in cardiac regulation in anxiety, the distributed nature of anxiety processing across the cortex remains elusive. To address this, we performed a whole-brain-heart analysis using the full frequency directed transfer function to study resting-state spectral differences in BHI between high and low anxiety groups undergoing fMRI scans. Our findings revealed a hemispheric asymmetry in low-frequency interplay (0.05 Hz - 0.15 Hz) characterized by ascending BHI to the left insula and descending BHI from the right insula. Furthermore, we provide evidence supporting the “pacemaker hypothesis”, highlighting the pons’ function in regulating cardiac activity. Higher frequency interplay (0.2 Hz - 0.4Hz) demonstrate a preference for ascending interactions, particularly towards ventral prefrontal cortical activity in high anxiety groups, suggesting the heart’s role in triggering a cognitive response to regulate anxiety. These findings highlight the impact of anxiety on BHI, contributing to a better understanding of its effect on the resting-state fMRI signal, with further implications for potential therapeutic interventions in treating anxiety disorders.
... While postganglionic sympathetic neurons (symNs) release norepinephrine to stimulate the fight-or-flight response and to increase heart beat and vasocontraction, postganglionic parasympathetic neurons (parasymNs) release acetylcholine (ACh) to trigger the opposite response called ''rest-and-digest.'' 1 Autonomic dysfunction has been found in various diseases, such as Parkinson's disease, Alzheimer's dis-ease, hypertension, multiple system atrophy, diabetic autonomic neuropathy, spinal cord injury, COVID-19, and familial dysautonomia (FD). [1][2][3][4] The ''imbalance'' of the ANS, resulting from either the increased sympathetic or decreased parasympathetic tone, or both, contributes to autonomic neuropathy in these diseases. ...
... While postganglionic sympathetic neurons (symNs) release norepinephrine to stimulate the fight-or-flight response and to increase heart beat and vasocontraction, postganglionic parasympathetic neurons (parasymNs) release acetylcholine (ACh) to trigger the opposite response called ''rest-and-digest.'' 1 Autonomic dysfunction has been found in various diseases, such as Parkinson's disease, Alzheimer's dis-ease, hypertension, multiple system atrophy, diabetic autonomic neuropathy, spinal cord injury, COVID-19, and familial dysautonomia (FD). [1][2][3][4] The ''imbalance'' of the ANS, resulting from either the increased sympathetic or decreased parasympathetic tone, or both, contributes to autonomic neuropathy in these diseases. 3,5 In the clinic, ANS function is assessed mostly by indirect methods, for example, skin conductance measurements indicating in/decreased sympathetic/parasympathetic activity. ...
... ParasymNs mainly express cholinergic muscarinic receptors (MusRs). 1 Thus, we assessed the expression of all MusR subtypes in parasymNs and found that the M2 and M4 MusRs to be expressed ( Figure 2D), consistent with findings in human and animal parasymN tissues. 1,43,44 We then treated para-symNs with bethanechol (BeCh) and atropine, clinical MusR agonist and antagonist, respectively. ...
... Number of heart beats per unit of time(Siegel et al., 2018). The sympathetic nervous system increases heart rate, whereas the parasympathetic nervous system suppresses it(Kasahara et al., 2021;Wehrwein et al., 2016). ...
The human electroencephalogram (EEG) is composed of synchronous oscillations within characteristic frequency bands, including 8–13 Hz alpha oscillations that often appear during relaxation. Relaxation is critical for physical and mental health, but the extent to which various EEG components reflect relaxation remains uncertain. This systematic review and meta-analysis investigated associations between EEG components and concurrently measured reference indices of relaxation in healthy adults. A comprehensive database search and screening using preset criteria identified 38 studies involving 1,120 participants published between January 1940 and January 2022 for qualitative synthesis. These studies used various reference relaxation measures such as electrocardiographic indices related to parasympathetic nervous system activity and introspective indices obtained through questionnaires. Risks of bias were evaluated following the risk of bias assessment tool for nonrandomized studies. A meta-analysis of 23 studies using a random-effects model revealed positive correlations between relaxation index and the power of alpha oscillations at central channels (Fisher’s z -transformed correlation coefficient and [95% confidence interval]: 0.23 [0.10–0.36]) and frontal channels (0.16 [0.02–0.31]). The correlation was significantly higher for the central channel compared with other channels. No significant correlations were detected between relaxation indices and other EEG frequencies or channels. The causal relationships between relaxation and alpha power at central and frontal channels warrant further study.
... The ANS plays a crucial role in maintaining biological balance by regulating blood flow and IOP; it is also important in the development or progression of glaucoma [36][37][38][39]. Frequent emotional fluctuations and persistent anxiety reactions can disrupt the equilibrium in the ANS, potentially exacerbating the risk of glaucoma or contributing to its progression [40]. Recognizing and addressing these multifaceted aspects, including the potential neurobiological links, is crucial for providing comprehensive support to individuals hustling through the complexities of living with glaucoma. ...
Glaucoma, a prevalent and debilitating eye disease, has long been associated with vision impairment and blindness. However, recent research has shed light on the often-underestimated psychological dimensions of this condition. Anxiety and depression, two pervasive psychiatric comorbidities, have been increasingly recognized among glaucoma patients. This comprehensive review aims to explore the intricate relationship between psychiatry and ophthalmology, in the context of managing depression and anxiety in glaucoma patients. By meticulously examining peer-reviewed literature, we synthesize current knowledge on the prevalence, risk factors, and underlying mechanisms of anxiety and depression in glaucoma. The evidence reveals that glaucoma patients face an elevated risk of experiencing these mood disorders. Factors such as progressive vision loss, complex medication regimens, and the fear of further visual deterioration contribute to their vulnerability. Moreover, we delve into the bidirectional relationship between glaucoma and mood disorders, shedding light on the complex interplay between ocular and emotional health. Our review investigates the implications of anxiety and depression on glaucoma management, including their potential impact on treatment adherence, disease progression, and overall quality of life. We also explore the neurobiological pathways linking glaucoma and mood disorders, providing a foundation for future research and potential therapeutic interventions. In conclusion, recognizing the psychological burden carried by glaucoma patients is essential for holistic and patient-centered care. This review underscores the pressing need for integrated approaches that bring together ophthalmological and psychiatric expertise to optimize the well-being of individuals facing the challenges of glaucoma. By addressing anxiety and depression in glaucoma care, healthcare providers can enhance the overall quality of life for these patients, ultimately leading to improved outcomes and a brighter future for those affected by this condition. This review offers valuable insight for healthcare practitioners and researchers, providing a concise overview of key topics and research in the field of managing depression and anxiety in glaucoma patients.
... HRV quantifies the variation in time intervals between heartbeats, which indicates the activity of the system (ANS) [75]. It specifically measures the balance between the sympathetic (fight-or-flight) and parasympathetic (rest-and-digest) branches of the ANS [76,77]. When experiencing fatigue, there is usually an increase in sympathetic activity and a decrease in parasympathetic activity, leading to reduced HRV. ...
Cognitive fatigue, a state of reduced mental capacity arising from prolonged cognitive activity, poses significant challenges in various domains, from road safety to workplace productivity. Accurately detecting and mitigating cognitive fatigue is crucial for ensuring optimal performance and minimizing potential risks. This paper presents a comprehensive survey of the current landscape in cognitive fatigue detection. We systematically review various approaches, encompassing physiological, behavioral, and performance-based measures, for robust and objective fatigue detection. The paper further analyzes different challenges, including the lack of standardized ground truth and the need for context-aware fatigue assessment. This survey aims to serve as a valuable resource for researchers and practitioners seeking to understand and address the multifaceted challenge of cognitive fatigue detection.
... The bidirectional communication pathway between the central nervous system and the gut involves the central and enteric nervous systems [7,69], the hypothalamicpituitary-adrenal axis (HPA), and immunological pathways ( Fig. 1) [70]. The autonomous nervous system is a key communication instrument between the brain and the gut, regulating intestinal homeostasis, gut mobility and permeability, bile secretion, fluid maintenance, mucosal neuroimmune response, and immune cell activation [70,71]. ...
It has been convincingly demonstrated in recent years that isolated acute brain injury (ABI) may cause severe dysfunction of peripheral extracranial organs and systems. Of all potential target organs and systems, the lung appears to be the most vulnerable to damage after ABI. The pathophysiology of the bidirectional brain–lung interactions is multifactorial and involves inflammatory cascades, immune suppression, and dysfunction of the autonomic system. Indeed, the systemic effects of inflammatory mediators in patients with ABI create a systemic inflammatory environment (“first hit”) that makes extracranial organs vulnerable to secondary procedures that enhance inflammation, such as mechanical ventilation (MV), surgery, and infections (“second hit”). Moreover, accumulating evidence supports the knowledge that gut microbiota constitutes a critical superorganism and an organ on its own, potentially modifying various physiological functions of the host. Furthermore, experimental and clinical data suggest the existence of a communication network among the brain, gastrointestinal tract, and its microbiome, which appears to regulate immune responses, gastrointestinal function, brain function, behavior, and stress responses, also named the “gut-microbiome–brain axis.” Additionally, recent research evidence has highlighted a crucial interplay between the intestinal microbiota and the lungs, referred to as the “gut-lung axis,” in which alterations during critical illness could result in bacterial translocation, sustained inflammation, lung injury, and pulmonary fibrosis. In the present work, we aimed to further elucidate the pathophysiology of acute lung injury (ALI) in patients with ABI by attempting to develop the “double-hit” theory, proposing the “triple-hit” hypothesis, focused on the influence of the gut–lung axis on the lung. Particularly, we propose, in addition to sympathetic hyperactivity, blast theory, and double-hit theory, that dysbiosis and intestinal dysfunction in the context of ABI alter the gut–lung axis, resulting in the development or further aggravation of existing ALI, which constitutes the “third hit.”
