Microneurography as a tool in clinical neurophysiology to investigate peripheral neural traffic in humans

Mano, Tadaaki; Iwase, Satoshi; Toma, Shinobu

doi:10.1016/j.clinph.2006.06.002

Cited by 116 publications

(81 citation statements)

References 235 publications

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“…103 This technique has been used in clinical neurophysiology to evaluate the neural mechanisms of autonomic regulation, motor control, and sensory functions in physiological and pathological conditions. Microneurography has also been used to analyze the muscle sympathetic nerve activity.…”

Section: Microneurographymentioning

confidence: 99%

The Autonomic Nervous System and Heart Failure

Florea

Cohn

2014

Circulation Research

455

366

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Abstract:The pathophysiology of heart failure (HF) is characterized by hemodynamic abnormalities that result in neurohormonal activation and autonomic imbalance with increase in sympathetic activity and withdrawal of vagal activity. Alterations in receptor activation from this autonomic imbalance may have profound effects on cardiac function and structure. Inhibition of the sympathetic drive to the heart through β-receptor blockade has become a standard component of therapy for HF with a dilated left ventricle because of its effectiveness in inhibiting the ventricular structural remodeling process and in prolonging life. Several devices for selective modulation of sympathetic and vagal activity have recently been developed in an attempt to alter the natural history of HF. The optimal counteraction of the excessive sympathetic activity is still unclear. A profound decrease in adrenergic support with excessive blockade of the sympathetic nervous system may result in adverse outcomes in clinical HF. In this review, we analyze the data supporting a contributory role of the autonomic functional alterations on the course of HF, the techniques used to assess autonomic nervous system activity, the evidence for clinical effectiveness of pharmacological and device interventions, and the potential future role of autonomic nervous system modifiers in the management of this syndrome. (Circ Res. 2014;114:1815-1826.) Key Words: autonomic nervous system ■ heart failure ■ norepinephrine ■ receptors, adrenergicThe Autonomic Nervous System and Heart Failure Viorel G. Florea, Jay N. Cohn This Review is in a thematic series on The Autonomic Nervous System and the Cardiovascular System, which includes the following articles: Role of the Autonomic Nervous System in Modulating Cardiac Arrhythmias [Circ Res. 2014;114:1004-1021 The Autonomic Nervous System and Hypertension [Circ Res. 2014;114:1804-1814 The Autonomic Nervous System and Heart Failure Renal Denervation for the Treatment of Cardiovascular High Risk-Hypertension or Beyond? Original received February 10, 2014; revision received April 29, 2014; accepted April 29, 2014. In March 2014, the average time from submission to first decision for all original research papers submitted to Circulation Research was 12.63 days.From the Minneapolis VA Health Care System, Section of Cardiology (V.G.F.) and Rasmussen Center for Cardiovascular Disease Prevention, Department of Medicine (J.N.C.), University of Minnesota Medical School.Correspondence to Jay N. endocardium. Parasympathetic effects are carried by the right and left vagus nerves, originating in the medulla. The vagus nerve further divides into the superior and inferior cardiac nerves, finally merging with the postganglionic sympathetic neurons to form a plexus of nerves at the base of the heart, known as the cardiac plexus. 1The 2 mediators of the SNS, norepinephrine and epinephrine, derive from 2 major sources in the body: the sympathetic nerve endings, which release norepinephrine directly into the synaptic cleft, and the adren...

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Section: Microneurographymentioning

confidence: 99%

The Autonomic Nervous System and Heart Failure

Florea

Cohn

2014

Circulation Research

455

366

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“…To quantify the frequency of MSNA bursts, only bursts with a signal to noise ratio ≥3 were included. 17, 18 Bursts were identified using an automated computer program with preset parameters to exclude observer bias. A preset triangle with a base of 0.8 s, correlated to the known delay between the R-peak on electrocardiogram (ECG) and the postganglionic burst, was used to scan the MSNA signal and identify sympathetic bursts.…”

Section: Measurement Of Sympathetic Activitymentioning

confidence: 99%

Sympathoinhibition by Atorvastatin in Hypertensive Patients

Gomes

Tack

Verheugt

et al. 2010

Circ J

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Background: Experimental animal data suggest that 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) might reduce enhanced sympathetic activity, a hallmark of hypertensive patients. This hypothesis was tested for the first time in patients with primary hypertension. Methods and Results:Using a prospective, randomized, placebo-controlled, double-blind, cross-over design, a proof-of-principle trial was performed in 13 patients with mild to moderate primary hypertension, who were randomly assigned to a regimen of atorvastatin (80 mg/day) for 3 weeks, followed by placebo for 3 weeks or to a regimen of placebo for 3 weeks, followed by atorvastatin (80 mg/day) for 3 weeks. Microneurography was used at the end of each treatment period to measure sympathetic nervous system activity (muscle sympathetic nerve activity: MSNA). Heart rate variability (HRV) and plasma norepinephrine concentrations were also measured. Additionally, effects on blood pressure (BP) and heart rate (HR) were assessed by 24-h ambulatory BP measurement. Atorvastatin reduced postganglionic MSNA (atorvastatin 35.0±2.0 vs placebo: 39.2±1.5 bursts/min, P=0.008) and heart frequency corrected MSNA (atorvastatin: 58.5±2.0 vs placebo: 64.7±3.0 bursts/100 beats, P=0.02). Atorvastatin had no significant effect on plasma norepinephrine levels, HRV, BP or HR. Conclusions:In patients with mild to moderate hypertension, atorvastatin reduces postganglionic MSNA, which supports the hypothesis that HMG-CoA reductase plays a role in sympathetic nervous system activity. (Circ J 2010; 74: 2622 - 2626

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“…On the clinical side, it might be used for diagnostic purposes in patients with sensory disorders e.g. diabetic neuropathy [4,13,25]. On the industrial side, it might support the development of new strategies in clothing design, as this perception has been shown to play a significant role in the onset of thermal discomfort [15].…”

Section: Introductionmentioning

confidence: 99%

The role of decreasing contact temperatures and skin cooling in the perception of skin wetness

Filingeri

Redortier²,

Hodder

et al. 2013

Neuroscience Letters

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Cold sensations are suggested as the primary inducer of the perception of skin wetness.However, limited data are available on the effects of skin cooling. Hence, we investigated the role of peripheral cold afferents in the perception of wetness. Six cold-dry stimuli (producing skin cooling rates in a range of 0.02 to 0.41°C/s) were applied on the forearm of 9 female participants.Skin temperature and conductance, thermal and wetness perception were recorded. Five out of 9 participants perceived wetness as a result of cold-dry stimuli with cooling rates in a range of 0.14 to 0.41°C/s, while 4 did not perceive skin wetness at all. Although skin cooling and cold sensations play a role in evoking the perception of wetness, these are not always of a primary importance and other sensory modalities (i.e. touch and vision), as well as the inter-individual variability in thermal sensitivity, might be equally determinant in characterising this perception.

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Microneurography as a tool in clinical neurophysiology to investigate peripheral neural traffic in humans

Cited by 116 publications

References 235 publications

The Autonomic Nervous System and Heart Failure

The Autonomic Nervous System and Heart Failure

Sympathoinhibition by Atorvastatin in Hypertensive Patients

The role of decreasing contact temperatures and skin cooling in the perception of skin wetness

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