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1.
Dysautonomia in the pathogenesis of migraine.
Gazerani, P, Cairns, BE
Expert review of neurotherapeutics. 2018;(2):153-165
Abstract
Migraine is a common complex neurological disorder involving multiple brain areas that regulate autonomic, affective, cognitive, and sensory functions. This review explores autonomic nervous system (ANS) dysfunction in migraine headache sufferers. Areas covered: Reference material for this review was obtained through PubMed searches. Migraine attacks can present with up to 4 phases (premonitory, aura, headache, postdrome) each with distinguishable signs and symptoms. Altered ANS tone can be found from the premonitory through the postdrome phases. Features of the migraine attack that are indicative of altered autonomic function, which include nausea, vomiting, diarrhea, polyuria, eyelid edema, conjunctival injection, lacrimation, nasal congestion, and ptosis, are discussed and putative mechanisms explored. In addition, alteration of ANS function by endogenous and exogenous stressors, such as bright lights, hunger, poor sleep quality, menses, and special dietary components is discussed. The influence of currently employed pharmacological treatments on altered autonomic function during the migraine attack is explored. Expert commentary: Migraine-related alterations in ANS function have a complex pattern, but, in general, an imbalance occurs between sympathetic and parasympathetic tone. Through an improved understanding the role of autonomic changes in pathogenesis of migraine, it may be possible to develop even more effective treatments for migraine sufferers.
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2.
Neural control of sweat secretion: a review.
Hu, Y, Converse, C, Lyons, MC, Hsu, WH
The British journal of dermatology. 2018;(6):1246-1256
Abstract
BACKGROUND Humans have 4 million exocrine sweat glands, which can be classified into two types: eccrine and apocrine glands. Sweat secretion, a constitutive feature, is directly involved in thermoregulation and metabolism, and is regulated by both the central nervous system (CNS) and autonomic nervous system (ANS). OBJECTIVES To explore how sweat secretion is controlled by both the CNS and the ANS and the mechanisms behind the neural control of sweat secretion. METHODS We conducted a literature search on PubMed for reports in English from 1 January 1950 to 31 December 2016. RESULTS AND CONCLUSIONS Acetylcholine acts as a potent stimulator for sweat secretion, which is released by sympathetic nerves. β-adrenoceptors are found in adipocytes as well as apocrine glands, and these receptors may mediate lipid secretion from apocrine glands for sweat secretion. The activation of β-adrenoceptors could increase sweat secretion through opening of Ca2+ channels to elevate intracellular Ca2+ concentration. Ca2+ and cyclic adenosine monophosphate play a part in the secretion of lipids and proteins from apocrine glands for sweat secretion. The translocation of aquaporin 5 plays an important role in sweat secretion from eccrine glands. Dysfunction of the ANS, especially the sympathetic nervous system, may cause sweating disorders, such as hypohidrosis and hyperhidrosis.
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3.
Investigating the use of pre-training measures of autonomic regulation for assessing functional overreaching in endurance athletes.
Coates, AM, Hammond, S, Burr, JF
European journal of sport science. 2018;(7):965-974
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Abstract
The use of heart rate variability (HRV) to inform daily training prescription is becoming common in endurance sport. Few studies, however, have investigated the use of pre-training HRV to predict decreased performance or altered exercising autonomic response, typical of functional overreaching (FOR). Further, a new cardiac vagal tone (ProCVT) technology purports to eliminate some of the noise associated with daily HRV, and therefore may be better at predicting same-day performance. The purpose of this investigation was to examine if changes to resting HRV and ProCVT were associated with alterations in performance, maximal heart rate (HRmax), or heart rate recovery (HRrec) in FOR athletes. Twenty-eight recreational cyclists and triathletes were assigned to experimental/control conditions and underwent: 1 week of reduced training, 3 weeks of overload (OL) or regular training (CON), and 1 week of recovery. Testing occurred following the reduced training week (T1), post-3 weeks of training (T2), and following the recovery week (T3). Measures of resting HRV/ProCVT were collected each testing session, followed by maximal incremental exercise tests with HRrec taken 60 s post-exercise. Performance decreased from T1 to T2 in the OL group vs. CON (Δ-9 ± 12 vs. Δ9 ± 11 W, P < .001), as did HRmax (Δ-8 ± 4 vs. Δ-2 ± 4 bpm, P < .001). HRrec increased from T1 to T2 in the OL group vs. CON (Δ10 ± 9 vs. Δ2 ± 5 beats/min, P < .01). HRV and ProCVT did not change in either group. Same-day resting autonomic measures are insufficient in predicting alterations to performance or exercising HR measures following overload training.
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4.
Diagnosis of multiple system atrophy.
Palma, JA, Norcliffe-Kaufmann, L, Kaufmann, H
Autonomic neuroscience : basic & clinical. 2018;:15-25
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Abstract
Multiple system atrophy (MSA) may be difficult to distinguish clinically from other disorders, particularly in the early stages of the disease. An autonomic-only presentation can be indistinguishable from pure autonomic failure. Patients presenting with parkinsonism may be misdiagnosed as having Parkinson disease. Patients presenting with the cerebellar phenotype of MSA can mimic other adult-onset ataxias due to alcohol, chemotherapeutic agents, lead, lithium, and toluene, or vitamin E deficiency, as well as paraneoplastic, autoimmune, or genetic ataxias. A careful medical history and meticulous neurological examination remain the cornerstone for the accurate diagnosis of MSA. Ancillary investigations are helpful to support the diagnosis, rule out potential mimics, and define therapeutic strategies. This review summarizes diagnostic investigations useful in the differential diagnosis of patients with suspected MSA. Currently used techniques include structural and functional brain imaging, cardiac sympathetic imaging, cardiovascular autonomic testing, olfactory testing, sleep study, urological evaluation, and dysphagia and cognitive assessments. Despite advances in the diagnostic tools for MSA in recent years and the availability of consensus criteria for clinical diagnosis, the diagnostic accuracy of MSA remains sub-optimal. As other diagnostic tools emerge, including skin biopsy, retinal biomarkers, blood and cerebrospinal fluid biomarkers, and advanced genetic testing, a more accurate and earlier recognition of MSA should be possible, even in the prodromal stages. This has important implications as misdiagnosis can result in inappropriate treatment, patient and family distress, and erroneous eligibility for clinical trials of disease-modifying drugs.
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Healthy hearts at hectic pace: From daily life stress to abnormal cardiomyocyte function and arrhythmias.
Barbiero, S, Aimo, A, Castiglione, V, Giannoni, A, Vergaro, G, Passino, C, Emdin, M
European journal of preventive cardiology. 2018;(13):1419-1430
Abstract
The hectic pace of contemporary life is a major source of acute and chronic stress, which may have a deleterious impact on body health . In the field of cardiovascular disease, acute emotional stress has been associated with coronary spasm and Takotsubo cardiomyopathy, whereas the manifestations of chronic stress have been overlooked, and most underlying pathophysiology remains to be elucidated. Chronic stress affects the neuronal circuitry composed of cortico-limbic structures and the nuclei regulating autonomic function, eliciting a sympatho-vagal imbalance, characterised by adrenergic activation and vagal withdrawal. Sympathetic terminals are connected to cardiomyocytes in a quasi-synaptic way, producing the so called 'neuro-cardiac junction'. During chronic stress, norepinephrine release is increased, leading to overstimulation of cardiomyocytes via β1-adrenergic receptors, influencing mainly calcium dynamics, and β2-adrenergic receptors, which control housekeeping functions. The circadian rhythm of cardiomyocytes is then impaired, with elongation of the catabolic ('light' phase) over the anabolic ('nocturnal') phase. This leads to a depletion of cell energy storage, and a decreased turnover of cell constituents. Even cell interactions are affected, as coupling between cardiomyocytes decreases while coupling between cardiomyocytes and fibroblasts increases. The ultimate results are changes in the shape and velocity of action potential, fibroblast activation and deposition of extracellular matrix. These alterations may predispose to arrhythmias and may favour the development of a stress-related cardiomyopathy. A better comprehension of this cascade of events may allow us to identify screening protocols and treatment strategies (meditation, yoga, physical activity, psychological assistance, β-blockers) to prevent or relieve ongoing cardiac damage.
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Pathophysiology of essential hypertension: an update.
Saxena, T, Ali, AO, Saxena, M
Expert review of cardiovascular therapy. 2018;(12):879-887
Abstract
Hypertension is caused by increased cardiac output and/or increased peripheral resistance. Areas covered: The various mechanisms affecting cardiac output/peripheral resistance involved in the development of essential hypertension are covered. These include genetics; sympathetic nervous system overactivity; renal mechanisms: excess sodium intake and pressure natriuresis; vascular mechanisms: endothelial cell dysfunction and the nitric oxide pathway; hormonal mechanisms: the renin-angiotensin-aldosterone system (RAAS); obesity, obstructive sleep apnea (OSA); insulin resistance and metabolic syndrome; uric acid; vitamin D; gender differences; racial, ethnic, and environmental factors; increased left ventricular ejection force and hypertension and its association with increased basal sympathetic activity - cortical connections. Expert commentary: Maximum association of hypertension is found with sympathetic overactivity which is directly or indirectly involved in different mechanisms of hypertension including RAAS, OSA, obesity, etc.. It is not overt sympathetic activity but disturbed basal sympathetic tone. Basal sympathetic tone arises from hypothalamus; possibly affected by cortical influences. Therefore, hypertension is not merely a disease of circulatory system alone. Its pathogenesis involves alteration in ANS (autonomic nervous system) and likely in cortical-hypothalamic connections. Assessment of ANS and cortical-hypothalamic connections may be required for better understanding of hypertension.
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Cardiac pacemaker channel (HCN4) inhibition and atrial arrhythmogenesis after releasing cardiac sympathetic activation.
Chobanyan-Jürgens, K, Heusser, K, Duncker, D, Veltmann, C, May, M, Mehling, H, Luft, FC, Schröder, C, Jordan, J, Tank, J
Scientific reports. 2018;(1):7748
Abstract
Clinical trials and studies with ivabradine implicate cardiac pacemaker channels (HCN4) in the pathogenesis of atrial arrhythmias. Because acute changes in cardiac autonomic tone predispose to atrial arrhythmias, we studied humans in whom profound cardiac sympathetic activation was rapidly relieved to test influences of HCN4 inhibition with ivabradine on atrial arrhythmias. We tested 19 healthy participants with ivabradine, metoprolol, or placebo in a double blind, randomized, cross-over fashion on top of selective norepinephrine reuptake inhibition with reboxetine. Subjects underwent combined head up tilt plus lower body negative pressure testing followed by rapid return to the supine position. In the current secondary analysis with predefined endpoints before data unblinding, continuous finger blood pressure and ECG recordings were analyzed by two experienced cardiac electrophysiologists and a physician, blinded for treatment assignment. The total atrial premature activity (referred to as atrial events) at baseline did not differ between treatments. After backwards tilting, atrial events were significantly higher with ivabradine compared with metoprolol or with placebo. Unlike beta-adrenoreceptor blockade, HCN4 inhibition while lowering heart rate does not protect from atrial arrhythmias under conditions of experimental cardiac sympathetic activation. The model in addition to providing insight in the role of HCN4 in human atrial arrhythmogenesis may have utility in gauging potential atrial pro-arrhythmic drug properties.
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Heart rate variability is reduced in underweight and overweight healthy adult women.
Triggiani, AI, Valenzano, A, Ciliberti, MA, Moscatelli, F, Villani, S, Monda, M, Messina, G, Federici, A, Babiloni, C, Cibelli, G
Clinical physiology and functional imaging. 2017;(2):162-167
Abstract
Heart rate variability (HRV) is altered in obese subjects, but whether this is true also in underweight (UW) subjects is still under debate. We investigated the HRV profile in a sample of healthy adult women and its association with adiposity. Five-minute resting state electrocardiographic activity was recorded in 69 subjects grouped according to their body mass index, [23 normal weight (NW), 23 overweight/obese (OW) and 23 UW). Body fat mass (FM) was measured by bio-impedance. Frequency- and time-domain analyses were performed. Compared to NW, UW and OW subjects showed a significant decrease in HRV indices, as revealed by spectral analysis. No differences were observed between UW and OW subjects. A second-order polynomial regression unveiled an inverted U-shaped relationship between FM extent and HRV indices. A decrease of HRV indices was associated with changes in FM extent, proving that in UW and OW subjects, the adaptive flexibility of autonomic cardiac function was reduced. These findings provide important clues to guide future studies addressed to determine how changes in adiposity and autonomic cardiac function may contribute to health risk.
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B-vitamin Supplementation Mitigates Effects of Fine Particles on Cardiac Autonomic Dysfunction and Inflammation: A Pilot Human Intervention Trial.
Zhong, J, Trevisi, L, Urch, B, Lin, X, Speck, M, Coull, BA, Liss, G, Thompson, A, Wu, S, Wilson, A, et al
Scientific reports. 2017;:45322
Abstract
Ambient fine particle (PM2.5) pollution triggers acute cardiovascular events. Individual-level preventions are proposed to complement regulation in reducing the global burden of PM2.5-induced cardiovascular diseases. We determine whether B vitamin supplementation mitigates PM2.5 effects on cardiac autonomic dysfunction and inflammation in a single-blind placebo-controlled crossover pilot trial. Ten healthy adults received two-hour controlled-exposure-experiment to sham under placebo, PM2.5 (250 μg/m3) under placebo, and PM2.5 (250 μg/m3) under B-vitamin supplementation (2.5 mg/d folic acid, 50 mg/d vitamin B6, and 1 mg/d vitamin B12), respectively. At pre-, post-, 24 h-post-exposure, we measured resting heart rate (HR) and heart rate variability (HRV) with electrocardiogram, and white blood cell (WBC) counts with hematology analyzer. Compared to sham, PM2.5 exposure increased HR (3.8 bpm, 95% CI: 0.3, 7.4; P = 0.04), total WBC count (11.5%, 95% CI: 0.3%, 24.0%; P = 0.04), lymphocyte count (12.9%, 95% CI: 4.4%, 22.1%; P = 0.005), and reduced low-frequency power (57.5%, 95% CI: 2.5%, 81.5%; P = 0.04). B-vitamin supplementation attenuated PM2.5 effect on HR by 150% (P = 0.003), low-frequency power by 90% (P = 0.01), total WBC count by 139% (P = 0.006), and lymphocyte count by 106% (P = 0.02). In healthy adults, two-hour PM2.5 exposure substantially increases HR, reduces HRV, and increases WBC. These effects are reduced by B vitamin supplementation.
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Effect of an aerobic exercise intervention on cardiac autonomic regulation: A worksite RCT among cleaners.
Hallman, DM, Holtermann, A, Søgaard, K, Krustrup, P, Kristiansen, J, Korshøj, M
Physiology & behavior. 2017;:90-97
Abstract
OBJECTIVE The aim of this randomized controlled trial (RCT) was to determine whether aerobic exercise during work hours affects cardiac autonomic regulation in cleaners characterized by high levels of occupational physical activity and poor cardiorespiratory fitness. METHOD Eligible cleaners (n=116) were randomized to an aerobic exercise group (n=59) or a reference group (n=57) with lectures. The intervention group received two 30-min sessions per week of supervised aerobic exercise over 4months. Diurnal measurements of heart rate variability (HRV) and physical activity (accelerometry) were obtained at baseline and at 4-month follow-up. Time and frequency domain indices of HRV were derived during work, leisure time and sleep to evaluate cardiac autonomic regulation. Linear mixed models were used to determine the effect of the intervention on HRV indices, with adjustment for age, gender and daily use of antihypertensive and/or heart medication. RESULTS Compared with the reference group, the exercise group increased all HRV indices apart from a reduction in LF/HF ratio from baseline to follow-up both during work (p<0.05) and leisure (p<0.05). In contrast, during sleep, the HRV indices tended to decrease in the exercise group compared with the reference group from baseline to follow-up, being significant for the HF spectral component (p=0.03). CONCLUSION Among cleaners, a worksite aerobic exercise intervention improved cardiac autonomic regulation during work and leisure, but not during sleep. The health effect of this contrasting change in autonomic regulation needs further investigation.