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Abstract Background Essential tremor (ET) is a prevalent movement disorder that may be linked to neurodegenerative changes. It is marked by a mix of motor and non-motor symptoms, which include disturbances in the autonomic nervous system. Aim of the study: We aimed to assess autonomic dysfunction in individuals with essential tremor. Thirty patients with essential tremor (Group 1) and 30 age and sex-matched healthy subjects as the control group (Group 2) were recruited. Comprehensive medical and neurological examinations were conducted on all participants, followed by electrophysiological assessments of autonomic function, including heart rate variability (HRV) tests (E/I ratio, Valsalva ratio, 30:15 ratio), adrenergic tests (blood pressure responses to active standing and sustained hand grip), and sympathetic skin response (SSR) tests. Finally, the results of these tests were classified according to the Ewing classification of autonomic failure. Results: The study revealed significant differences between ET patients and the control group. Heart rate variability tests showed a marked difference between the groups. Adrenergic tests, measuring sympathetic innervation, also displayed a significant difference. The sudomotor function test exhibited noteworthy differences in onset latencies and amplitudes in the palm and sole, with ET patients showing prolonged onset latencies and decreased amplitudes. Moreover, the study found a significant correlation between disease severity and autonomic function test results and the Ewing score. Conclusion: The study highlights the presence of autonomic dysfunction in essential tremor patients, with disease severity being associated with the level of autonomic affection, as evidenced by various autonomic function tests and the Ewing score.

According to previous research, people influence each other’s emotional states during social interactions via resonance mechanisms and coordinated autonomic rhythms. However, no previous studies tested if the manipulation of the interoceptive focus (focused attention on the breath for a given time interval) in hyperscanning during synchronized tasks may have an impact on autonomic synchrony. Thus, this study aims to assess the psychophysiological synchrony through autonomic measures recording during dyadic linguistic and motor synchronization tasks performed in two distinct interoceptive conditions: the focus and no focus on the breath condition. 26 participants coupled in 13 dyads were recruited. Individuals’ autonomic measures [electrodermal: skin conductance level and response (SCL, SCR); cardiovascular indices: heart rate (HR) and HR variability (HRV)] was continuously monitored during the experiment and correlational coefficients were computed to analyze dyads physiological synchrony. Inter-subject analysis revealed higher synchrony for HR, HRV, SCL, and SCR values in the focus compared to no focus condition during the motor synchronization task and in general more for motor than linguistic task. Higher synchrony was also found for HR, SCL, and SCR values during focus than no focus condition in linguistic task. Overall, evidence suggests that the manipulation of the interoceptive focus has an impact on the autonomic synchrony during distinct synchronization tasks and for different autonomic measures. Such findings encourage the use of hyperscanning paradigms to assess the effect of breath awareness practices on autonomic synchrony in ecological and real-time conditions involving synchronization.

The precise contributions of afferent feedback to cardiovascular and respiratory responses to exercise are still unclear. Aim of this crossover study was to assess whether and how autonomic cardiovascular and respiratory control differed in response to dynamic (DYN) and isometric contractions (ISO) at a similar, low heart rate (HR) level. Therefore, 22 healthy males (26.7 ± 3.6 yrs) performed two kinds of voluntary exercises at similar HR: ISO and DYN of the right quadriceps femoris muscle. Although HR was eqivalent (82 ± 8 bpm for DYN and ISO, respectively), rating of exertion, blood pressures, and rate pressure product were higher, whereas breathing frequency, minute ventilation, oxygen uptake and carbon dioxide output were significantly lower during ISO. Tidal volume, end-tidal partial pressures of O2 and CO2, respiratory exchange ratio and capillary blood lactate concentration were comparable between both contraction modes. Heart rate variability (HRV) indicators, SDNN, HF-Power and LF-Power, representing both vagal and sympathetic influences, were significantly higher during ISO. Sample entropy, a nonlinear measure of HRV was also significantly affected by contraction mode. It can be concluded that, despite the same net effect on HR, the quality of cardiovascular control during low intensity exercise is significantly different between DYN and ISO. HRV analysis indicated a sympatho-vagal coactivation during ISO. Whether mechanoreceptor feedback alone, a change in central command, or the interaction of both mechanisms is the main contributor of the distinct autonomic responses to the different exercise modes remains to be elucidated.

Several cardiovascular disease (CVD) risk factors (e.g., hypertension, poor glycemic control) can affect and be affected by autonomic nervous system (ANS) activity. Since excess adiposity can influence CVD development through its effect on hypertension and diabetes mellitus, it is important to determine how adiposity and altered ANS activity are related. The present study employed structural equation modeling to investigate the relation between adiposity and ANS activity both directly and indirectly through biological variables typically associated with glycemic impairment and cardiac stress in older adults. Utilizing the Atherosclerosis Risk in Communities (ARIC) dataset, 1,145 non-smoking adults (74±4.8 yrs, 62.8% female) free from known CVD, hypertension, and diabetes and not currently taking beta-blockers were evaluated for fasting blood glucose (FBG), insulin, and HbA1c concentrations, waist circumference (WC), blood pressure (BP), and markers of ANS activity. WC was recorded just above the iliac crest and was used to reflect central adiposity. Resting 2-minute electrocardiograph recordings, pulse wave velocity, and ankle-brachial index data were used to assess the root mean square of successive differences in RR intervals (RMSSD) and the pre-ejection period (PEP), markers of parasympathetic and sympathetic activity, respectively. FBG, insulin, and HbA1c inferred a latent variable termed glycemic impairment (GI), whereas heart rate and diastolic BP inferred a latent variable termed cardiac stress (CS). The structural equation model fit was acceptable [root mean square error of approximation = 0.050 (90% CI = .036, .066), comparative fit index = .970, Tucker Lewis Index = 0.929], with adiposity having both significant direct (β = 0.208, p = 0.018) and indirect (β = -.217, p = .041) effects on PEP through GI. Adiposity displayed no significant direct effect on RMSSD. CS displayed a significant pathway (β = -0.524, p = 0.035) on RMSSD, but the indirect effect of WC on RMSSD through CS did not reach statistical significance (β = -0.094, p = 0.137). These results suggest that adiposity's relation to ANS activity is multifaceted, as increased central adiposity had opposing direct and indirect effects on markers of sympathetic activity in this population of older adults.

BACKGROUND: Spontaneously hypertensive rats develop left ventricular hypertrophy, increased blood pressure and blood pressure variability, which are important determinants of heart damage, like the activation of renin-angiotensin system. AIMS: To investigate the effects of the time-course of hypertension over 1) hemodynamic and autonomic patterns (blood pressure; blood pressure variability; heart rate); 2) left ventricular hypertrophy; and 3) local and systemic Renin-angiotensin system of the spontaneously hypertensive rats. METHODS: Male spontaneously hypertensive rats were randomized into two groups: young (n=13) and adult (n=12). Hemodynamic signals (blood pressure, heart rate), blood pressure variability (BPV) and spectral analysis of the autonomic components of blood pressure were analyzed. LEFT ventricular hypertrophy was measured by the ratio of LV mass to body weight (mg/g), by myocyte diameter (μm) and by relative fibrosis area (RFA, %). ACE and ACE2 activities were measured by fluorometry (UF/min), and plasma renin activity (PRA) was assessed by a radioimmunoassay (ng/mL/h). Cardiac gene expressions of Agt, Ace and Ace2 were quantified by RT-PCR (AU). RESULTS: The time-course of hypertension in spontaneously hypertensive rats increased BPV and reduced the alpha index in adult spontaneously hypertensive rats. Adult rats showed increases in left ventricular hypertrophy and in RFA. Compared to young spontaneously hypertensive rats, adult spontaneously hypertensive rats had lower cardiac ACE and ACE2 activities, and high levels of PRA. No change was observed in gene expression of Renin-angiotensin system components. CONCLUSIONS: The observed autonomic dysfunction and modulation of Renin-angiotensin system activity are contributing factors to end-organ damage in hypertension and could be interacting. Our findings suggest that the management of hypertensive disease must start before blood pressure reaches the highest stable levels and the consequent established end-organ damage is reached.

Background: Chronic fatigue syndrome (CFS) is heterogeneous in nature, yet noclear subclassifications currently exist. There is evidence of dysautonomia in almost90% of patients and CFS is often co-morbid with conditions associated withautonomic nervous system (ANS) dysfunction, such as temporomandibulardisorders (TMD). The present study examined the point prevalence of TMD in asample of people with CFS and explored whether co-morbidity between theconditions is associated with greater ANS dysfunction than CFS alone. Method:Fifty-one patients and 10 controls underwent screening for TMD. Theycompleted a self-report measure of ANS function (COMPASS-31) and objectiveassessment of heart rate variability during rest and standing (derived usingspectral analysis). Frequency densities in the high-frequency (HF) and lowfrequency(LF) band were calculated. Results: Patients with CFS were dividedinto those who screened positive for TMD (n = 16, 31%; CFS + TMD) and thosewho did not (n = 35, 69%; CFS − TMD). Both CFS groups had significantlyhigher self-rated ANS dysfunction than controls. CFS + TMD scored higher thanCFS − TMD on the orthostatic and vasomotor subscales. The CFS + TMD grouphad significantly higher HF and significantly lower LF at rest than the other twogroups. In discriminant function analysis, self-report orthostatic intolerance andHF units correctly classified 75% of participants. Conclusions: Almost one-thirdof CFS patients screened positive for TMD and this was associated with greaterevidence of parasympathetic dysfunction. The presence of TMD shows potentialas an effective screen for patients with CFS showing an autonomic profile andcould help identify subgroups to target for treatment.

In late age the autonomic nervous system (ANS) has diminished ability to maintain physiological homeostasis in the brain in response to challenges such as to systemic blood pressure changes caused by standing. We devised an fMRI experiment aiming to map the cerebral effects of an ANS challenge (Valsalva manoeuvre; VM). We used dual-echo fMRI to measure the effective transverse relaxation rate (R2*, which is inversely proportional to brain tissue oxygenation levels) in 45 elderly subjects (median age: 80 years old, total range: 75-89) during performance of the VM. In addition we collected Fluid Attenuation Inversion Recovery (FLAIR) data from which we quantified white matter hyperintensity (WMH) volumes. We conducted voxelwise analysis of the dynamic changes in R2* during the VM to determine the distribution of oxygenation changes due to the autonomic stressor. In white matter we observed significant decreases in oxygenation levels. These effects were predominantly located in posterior white matter and to a lesser degree in the right anterior brain, both concentrated around the border zones (watersheds) between cerebral perfusion territories. These areas are known to be particularly vulnerable to hypoxia and are prone to formation of white matter hyperintensities. Although we observed overlap between localization of WMH and triggered deoxygenation on the group level we did not find significant association between these independent variables using subject-wise statistics. This could suggest other than recurrent transient hypoxia mechanisms causing/contributing to the formation of WMH.

Over recent years, a considerable increase in the popularity of cryostimulation and whole body cryotherapy (WBC) procedures has occurred both among healthy individuals and in various groups of patients, including those with primary untreated hypertension. The aim of this study was to compare the effects of WBC on the functional parameters of cardiovascular system in normotensive and primarily hypertensive individuals.The study included 26 young male volunteers with normal blood pressure range (NormoBP) and 13 with essential arterial hypertension (HyperBP). Each subject was exposed to cryotherapeutic factor (whole-body cryotherapy/cryostimulation, WBC) at a temperature of approximately -115 degrees C to 125 degrees C for a period of 3 min. The cardiovascular and autonomic parameters were measured noninvasively with Task Force Monitor. Measurements in a supine position and tilt test were performed 'before WBC' and 'after WBC'.Our study revealed that cryogenic temperatures exert strong modulatory effect on the cardiovascular system. Both groups showed adaptive changes of myocardial and vascular parameters in response to rapid cooling of virtually the whole body surface. While the profiles of some of these changes were similar in both the groups, also several considerable intergroup differences were documented. Consequently, the cryostimulation and cryotherapy treatment should be prescribed carefully to individuals who present with cardiovascular failure of any degree. (C) 2014 Elsevier Inc. All rights reserved.

Patients diagnosed with post-traumatic stress disorder (PTSD) are at a significantly elevated risk of developing comorbid inflammatory conditions, but the mechanisms underlying this predilection remain unclear. Our previous work has shown that T-lymphocytes exposed to elevated levels of norepinephrine (NE) displayed a pro-inflammatory signature reminiscent of an autoreactive phenotype. With this, we hypothesized that the increased sympathetic tone observed during psychological trauma may be promoting pro-inflammatory T-lymphocytes, which causes a predisposition to comorbid inflammatory conditions. Here, we examined the consequences of psychological trauma on splenic T-lymphocytes using a mouse model of repeated social defeat stress. Social defeat led to anxiety-like and depression-like behavior as has been previously described. The spleens of socially-defeated mice showed significant elevations of NE, tyrosine hydroxylase (TH), and acetylcholinesterase (ACHE) levels, which appeared to be due in part to increased expression within T-lymphocytes. Additionally, T-lymphocytes from stressed animals showed higher levels of pro-inflammatory cytokines and mitochondrial superoxide. Interestingly, in this model system, close associations exist within splenic T-lymphocytes amid the autonomic, inflammatory, and redox environments, but these only weakly correlate with individual behavioral differences among animals suggesting the psychological and physiological manifestations of trauma may not be tightly coupled. Last, we describe, for the first time, elevations in calprotectin levels within T-lymphocytes and in circulation of psychologically stressed animals. Calprotectin correlated with both behavioral and physiological changes after social defeat, suggesting the potential for a new biological marker and/or therapeutic target for psychological trauma and its inflammatory comorbidities.

Background: Individuals with Down Syndrome (DS) have autonomic dysfunction impacting regulation of heart rate, Blood Pressure (BP), and peripheral vasoconstriction. This may alter central hemodynamics through different wave reflections. We investigated central hemodynamics including wave reflection during rest and a sympathoexcitatory stimulus [Lower Body Negative Pressure (LBNP)] in individuals with DS and controls. Methods: Radial applanation tonometry was performed on participants with and without DS before and during 5-min LBNP stimulus of −20 mmHg. Waveforms were calibrated to mean and diastolic BP. Generalized transfer function was used to estimate aortic pressures [Systolic Blood Pressure (aSBP), Diastolic Blood Pressure (aDBP), mean pressure (aMAP), pulse pressure (aPP)], Augmentation Index (AIx), augmentation index normalized for HR (AIx@75), Augmentation Pressure (AP), Reflection Index (RIx), Time to Reflection (Tr), forward and reflected wave magnitude (Pf and Pb). Results: Fifteen individuals with DS (male n = 12, age 24 ± 4 years, BMI 28 ± 5 kg/m2) and 16 control participants (male n = 12, age 24 ± 4 years, BMI 25 ± 5 kg/m2) participated. Baseline differences showed greater AP, higher AIx and AIx@75, a greater RIx, shorter Tr and larger Pb in individuals with DS (p < 0.05). In response to LBNP, interaction effects were observed for AIx, AIx@75, AP, RIx and Pb, due to reductions in the outcomes in response to LBNP for individuals with DS with no change in the controls. Conclusion: These results show that central hemodynamics and wave reflections are different in individuals with DS at rest and in response to LBNP, probably as a result of anatomical differences and reduced peripheral vasoconstrictive control during LBNP. HIGHLIGHTS •Individuals with DS exhibit greater central hemodynamic load at rest. •Individuals with DS have greater indices of wave reflections at rest. •Individuals with DS maintained blood pressure during LBNP with reduced wave reflection.