Find relevant scholarly articles now

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.

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.