Autonomic Neuroscience-Basic & Clinical最新文献

The autonomic nervous system functions in a fine-tuned manner to dynamically modulate cardiac function during normal physiological state. Autonomic dysregulation in cardiac disease states such as myocardial infarction and heart failure alters this fine balance, which in turn promotes disease progression and arrhythmogenesis. Neuromodulatory interventions that aim to restore this balance at distinct levels of the cardiac neuraxis thus have been shown to be effective in the treatment of arrhythmias. This review first describes the anatomy of the cardiac autonomic nervous system and the pathological changes that occur with neural remodeling in the setting of scar and cardiomyopathy, followed by therapeutic interventions for neuraxial modulation of arrhythmias such as atrial fibrillation and ventricular tachyarrhythmias.

Muscle sympathetic nerve activity (MSNA) is similar between limbs at rest, although a subset of MSNA bursts do demonstrate limb-specific discharge. Whether limb differences in MSNA synchronicity are present during exercise remains controversial. We concurrently measured MSNA from the radial and fibular nerves at rest and during rhythmic handgrip (RHG), static handgrip (SHG), and post-exercise circulatory occlusion (PECO). MSNA burst frequency and incidence were similar between nerve sites during all conditions. Synchronous bursts resulted in larger increases in sympathetic-blood pressure transduction compared to isolated bursts (∆ + 3.6 ± 2.1 vs. +2.3 ± 2.4 mmHg, P = 0.01). The proportion of bursts firing synchronously between nerves at rest was slightly increased during RHG ([rest vs. exercise; mean ± SD] 45.3 ± 7.1 vs. 61.6 ± 7.2 %) and similar during SHG (56.2 ± 7.2 vs. 54 ± 10.6 %). In contrast, burst firing synchronicity increased during PECO (83.8 ± 12.4 %) alongside larger burst amplitudes. Inter-limb differences in resting MSNA are preserved during handgrip exercise, whereas isolated metaboreflex activation results in greater burst synchronization between limbs.

Background and purpose

Autonomic dysfunction has been occasionally described in varicella-zoster virus (VZV) infection, while few systematic reviews are available. We systematically review autonomic dysfunction due to VZV infection.

Methods

This study followed the PRISMA guideline, and three databases were researched and included cross-sectional studies in full-length publications in the English language using appropriate search keywords.

Results

A total of 102 articles were identified initially; finally 45 studies were used for review, comprising pupillomotor dysfunction in 4, sudomotor dysfunction in 2, cardiovascular dysfunction in 2, gastrointestinal dysfunction in 14, and urogenital dysfunction in 23. They can be summarized as (1) VZV infection rarely produces orthostatic hypotension, which involves diffuse sympathetic dysfunction by polyneuropathy. (2) In contrast, VZV infection produces dysfunction of the bladder and the bowel, which involves segmental parasympathetic or sympathetic dysfunction by dorsal root ganglionopathy.

Conclusions

Awareness of VZV-related autonomic dysfunction is important, because such patients may first visit a gastroenterology or urology clinic. Close collaboration among neurologists, dermatologists, gastroenterologists, and urologists is important to start early antiviral agents and maximize bowel and bladder care in such patients.

Techniques grounded on the simultaneous utilization of Tiecks' second order differential equations and spontaneous variability of mean arterial pressure (MAP) and mean cerebral blood flow velocity (MCBFV), recorded from middle cerebral arteries through a transcranial Doppler device, provide a characterization of cerebral autoregulation (CA) via the autoregulation index (ARI). These methods exploit two metrics for comparing the measured MCBFV series with the version predicted by Tiecks' model: normalized mean square prediction error (NMSPE) and normalized correlation ρ. The aim of this study is to assess the two metrics for ARI computation in 13 healthy subjects (age: 27 ± 8 yrs., 5 males) at rest in supine position (REST) and during 60° head-up tilt (HUT) and in 19 patients (age: 64 ± 8 yrs., all males), scheduled for coronary artery bypass grafting, before (PRE) and after (POST) propofol general anesthesia induction. Analyses were carried out over the original MAP and MCBFV pairs and surrogate unmatched couples built individually via time-shifting procedure. We found that: i) NMSPE and ρ metrics exhibited similar performances in passing individual surrogate test; ii) the two metrics could lead to different ARI estimates; iii) CA was not different during HUT or POST compared to baseline and this conclusion held regardless of the technique and metric for ARI estimation. Results suggest a limited impact of the sympathetic control on CA.

Heart is an extensively innervated organ and its function is strictly coordinated by autonomic neural circuits. After pathological events such as myocardial infarction (MI), cardiac nerves undergo a structural and functional remodeling contributing to cardiac dysfunction. Although the efferent component of the cardiac nerves has been well described, sensory innervation of the heart has not been defined in detail. Considering its importance, comprehensive description of vagal afferent innervation on the whole heart would enable a better description of autonomic imbalances manifesting as sympathoexcitation and vagal withdrawal in post-ischemic states. To address this issue, we globally mapped the vagal nodose afferent fibers innervating the whole murine heart with unprecedented resolution. By using the Phox2b-Cre::tdTomato transgenic mouse line, we described the detailed distribution and distinct vagal sensory ending morphologies at both the dorsal and ventral sides of the mouse heart. By neural tracing analysis, we quantitated the distribution and prevalence of vagal afferent nerve fibers with varying diameters across dorsal and ventral surfaces of the heart. Moreover, we demonstrated that vagal afferents formed flower spray and end-net-like endings within the atria and ventricles. As distinct from the atria, vagal afferents formed intramuscular array-like endings within the ventricles. Furthermore, we showed that vagal afferents undergo structural remodeling by forming axonal sprouts around the infarct area in post-MI hearts. These findings improve our understanding of the potential effect of vagal afferent remodeling on autonomic imbalance and generation of cardiac arrhythmias and could prospectively contribute to the development of more effective neuromodulatory therapies.

Background

Neuroplasticity and cardiovascular health behavior are critically important factors for optimal brain health.

Objective

To assess the association between the efficacy of the mechanisms of neuroplasticity and metrics of cardiovascular heath in sedentary aging adults.

Methods

We included thirty sedentary individuals (age = 60.6 ± 3.8 y; 63 % female). All underwent assessments of neuroplasticity, measured by the change in amplitude of motor evoked potentials elicited by single-pulse Transcranial Magnetic Stimulation (TMS) at baseline and following intermittent Theta-Burst (iTBS) at regular intervals. Cardiovascular health measures were derived from the Incremental Shuttle Walking Test and included Heart Rate Recovery (HRR) at 1-min/2-min after test cessation. We also collected plasma levels of brain-derived neurotrophic factor (BDNF), vascular endothelial growth factor (VEGF), and c-reactive protein.

Results

We revealed moderate but significant relationships between TMS-iTBS neuroplasticity, and the predictors of cardiovascular health (|r| = 0.38 to 0.53, p < .05). HRR1 was the best predictor of neuroplasticity (β = 0.019, p = .002). The best fit model (Likelihood ratio = 5.83, p = .016) of the association between neuroplasticity and HRR1 (β = 0.043, p = .002) was selected when controlling for demographics and health status. VEGF and BDNF plasma levels augmented the association between neuroplasticity and HRR1.

Conclusions

Our findings build on existing data demonstrating that TMS may provide insight into neuroplasticity and the role cardiovascular health have on its mechanisms. These implications serve as theoretical framework for future longitudinal and interventional studies aiming to improve cardiovascular and brain health. HRR1 is a potential prognostic measure of cardiovascular health and a surrogate marker of brain health in aging adults.

Introduction

While there is strong evidence for autonomic involvement in cerebrovascular function acutely, long-term role of autonomic nervous system in cerebrovascular function has been controversial. We assessed autoregulation in 10 healthy individuals, nine patients with vasovagal syncope (VVS), and nine with Familial Amyloidotic Polyneuropathy (FAP), in response to head-up tilt test (HUTT).

Methods

Arterial blood pressure heart rate, cardiac output, and bilateral cerebral blood flow velocity (CBFV) at the M1 segment of middle cerebral artery (transcranial Doppler ultrasound) were recorded during supine rest and 70° HUTT. Autoregulation was quantified using a validated nonlinear and nonparametric approach based on projection pursuit regression. Plasma adrenaline and noradrenaline were also measured at rest and during HUTT.

Results

During supine rest and HUTT, plasma noradrenaline content was lower in FAP patients. During HUTT, VVS patients had a hyperadrenergic status; CBFV decreased in all groups, which was greater in FAP patients (p < 0.01). Healthy controls responded to HUTT with a reduction in CBFV responses to increases (p = 0.01) and decreases (p < 0.01) in arterial pressure without any change in the range or effectiveness of autoregulation. VVS patients responded to HUTT with a reduction in falling (p = 0.02), but not rising slope (p = 0.40). Autoregulatory range (p < 0.01) and effectiveness increased (p = 0.09), consistent with the rapid increase in levels of catecholamines. In FAP patients, the level of increase in range of autoregulation was significantly related to the magnitude of increase in plasma noradrenaline in response to HUTT (R² = 0.26, p = 0.05).

Conclusion

Autonomic dysfunction affects the cerebral autoregulatory response orthostatic to challenge.

In the present study, we examined the effects of mild thermal stimulation of the skin on voiding efficiency using urethane-anesthetized rats with reduced voiding efficiency. Spontaneous urination was induced by infusing saline. For each voiding, the voiding efficiency was calculated from the voided volume and the bladder capacity measured. A Peltier thermode was attached to the buttock skin to apply stimulation: cooling between to 25 °C and 35 °C, every 20 s throughout the saline infusion. The voiding efficiency was 29 ± 9 % (mean ± SD) before stimulation and increased significantly by 10–15 % during stimulation. During thermal stimulation, the maximum vesical pressure during micturition was unchanged, but the urethral relaxation duration was significantly prolonged. Applying local anesthesia to the stimulated skin area abolished the changes in voiding efficiency in response to thermal stimulation. These results suggest that the excitation of cutaneous thermoreceptive afferents modulates urethral function during urination, thereby improving voiding efficiency.

We present a framework for the linear parametric analysis of pairwise interactions in bivariate time series in the time and frequency domains, which allows the evaluation of total, causal and instantaneous interactions and connects time- and frequency-domain measures. The framework is applied to physiological time series to investigate the cerebrovascular regulation from the variability of mean cerebral blood flow velocity (CBFV) and mean arterial pressure (MAP), and the cardiovascular regulation from the variability of heart period (HP) and systolic arterial pressure (SAP). We analyze time series acquired at rest and during the early and late phase of head-up tilt in subjects developing orthostatic syncope in response to prolonged postural stress, and in healthy controls. The spectral measures of total, causal and instantaneous coupling between HP and SAP, and between MAP and CBFV, are averaged in the low-frequency band of the spectrum to focus on specific rhythms, and over all frequencies to get time-domain measures. The analysis of cardiovascular interactions indicates that postural stress induces baroreflex involvement, and its prolongation induces baroreflex dysregulation in syncope subjects. The analysis of cerebrovascular interactions indicates that the postural stress enhances the total coupling between MAP and CBFV, and challenges cerebral autoregulation in syncope subjects, while the strong sympathetic activation elicited by prolonged postural stress in healthy controls may determine an increased coupling from CBFV to MAP during late tilt. These results document that the combination of time-domain and spectral measures allows us to obtain an integrated view of cardiovascular and cerebrovascular regulation in healthy and diseased subjects.