Altered auditory feedback perception following an 8-week mindfulness meditation practice

Publication date: Available online 29 January 2019

Source: International Journal of Psychophysiology

Author(s): Daiki Miyashiro, Akira Toyomura, Tomosumi Haitani, Hiroaki Kumano

Abstract

Our own ongoing motor actions are perceived through sensory feedback pathways, and are integrated with neural processes to modulate further actions. This sensory feedback mechanism is known to contribute to the rehabilitation of impaired motor functions. Recent evidence also suggests that mindfulness meditation improves our awareness to sensation; therefore, enhancement of awareness to sensory feedback through mindfulness meditation training may have potential clinical applications. This study investigated an effect of eight-week practice of mindfulness meditation on speech perception/production processes. Among the thirty participants, half of them engaged in regular meditation practice of 10 min per day for eight weeks, and the other half were not given any instructions for their daily life. The change of speech performance in sentence reading under 200 ms delayed auditory feedback (DAF) condition were assessed compared to without delay condition. Also, event-related potential response to the short sound of /a/, were measured. The result showed that, after the eight-week practice, the meditation group showed significantly improved speech fluency in the DAF condition, when 16-min meditation was introduced before the experiments. Furthermore, significantly increased auditory evoked potentials were observed in the central-parietal region when the participants listened to the delayed auditory feedback sound of their own voice. These findings provide the first glimpses into the possible relationship between mindfulness meditation and auditory feedback. Different instructions for daily activity between the meditation and control groups should be considered in further studies.

Graphical abstract

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Pro‐contractile role of chloride in arterial smooth muscle: Postnatal decline potentially governed by sympathetic nerves

New Findings

What is the topic of this review?

This symposium report discusses previously unrecognized pro‐contractile role of chloride ions in rat arteries at early stages of postnatal development.

What advances does it highlight?

It highlights the postnatal decline in the contribution of chloride ions to regulation of arterial contractile responses and potential trophic role of sympathetic nerves in such developmental alterations.

Abstract

Chloride ions (Cl⁻) are important for smooth muscle contraction in adult vasculature. Arterial smooth muscle undergoes structural and functional remodeling during early postnatal development including changes in K⁺ currents, Ca²⁺‐handling and sensitivity. However, developmental change in the contribution of Cl⁻ to regulation of arterial contraction has not been explored yet. We provide here the first evidence that the role of Cl⁻ for α₁‐adrenergic arterial contraction prominently decreases during early postnatal ontogenesis. The trophic influence of sympathetic nerves is a potential mechanism for postnatal decline of Cl⁻ contribution to the vascular contraction.

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Elbow angle modulates corticospinal excitability to the resting biceps brachii at both spinal and supraspinal levels

New Findings

What is the central question of this study?

Corticospinal excitability to biceps brachii is known to modulate according to upper‐limb posture. Here, cervicomedullary stimulation was used to investigate potential spinal contributions to elbow angle dependent changes in corticospinal excitability at rest.

What is the main finding and its importance?

At more extended elbow angles, biceps responses to cervicomedullary stimulation were decreased, whereas cortically‐evoked responses (normalised to cervicomedullary‐evoked responses) were increased. Results suggest decreased spinal excitability but increased cortical excitability as the elbow is placed in a more extended position, an effect that is unlikely due to cutaneous stretch receptor activation.

Abstract

Corticospinal excitability to biceps brachii is known to modulate according to upper‐limb posture. In Study 1, our aim was to investigate potential spinal contributions to this modulation and the independent effect of elbow angle. Biceps responses to transcranial magnetic stimulation (motor evoked potentials; MEPs) and electrical cervicomedullary stimulation (cervicomedullary motor evoked potentials; CMEPs) were measured at five elbow angles ranging from full extension to 130° of flexion. In Study 2, possible contributions of cutaneous stretch receptors to elbow angle dependent excitability changes were investigated by eliciting MEPs and CMEPs under three conditions of skin stretch about the elbow (stretch to mimic full extension, no stretch, stretch to mimic flexion). Each study had 12 participants. Evoked potentials were acquired at rest with participants seated, the shoulder flexed 90° and forearm supinated. MEPs and CMEPs were normalised to maximal compound muscle action potentials (Mmax). In Study 1, as the elbow was moved to more extended positions, there were no changes in MEPs (p = 0.963), progressive decreases in CMEPs (p < 0.0001; CMEPs at 130° flexion ∼220% of full extension) and increases in MEP/CMEP ratio (p = 0.019; MEP/CMEP at 130° flexion ∼20% of full extension). In Study 2, there were no changes in MEPs (p = 0.830) or CMEPs (p = 0.209) between skin stretch conditions. Therefore, while results suggest a decrease in spinal and an increase in supraspinal excitability at more extended angles, the mechanism for these changes in corticospinal excitability to biceps is not cutaneous stretch receptor feedback.

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Growth failure in focal dermal hypoplasia

Focal dermal hypoplasia (FDH) is a rare genetic disorder caused by mutations in the PORCN gene located on the X chromosome. Short stature was previously noted to be a common finding in FDH, however the etiology of this is unclear. The present study sought to elucidate specific causes for short stature by assessing growth charts, determining bone ages and auxologic measurements, examining laboratory data for the common causes of growth failure, assessing dietary intake, and performing a growth hormone stimulation test. Sixteen patients with FDH between the ages of 3 and 18 years of age consented to the study. While 11 out of 16 patients had short stature based on height less than 2 standard deviations below mid‐parental target height percentile and bone age not suggestive of likely catch‐up growth, only four had a BMI less than the 5th percentile for age. Laboratory studies did not support a gastrointestinal, allergy or autoimmune cause of growth failure. Three patients had results suggestive of possible growth hormone deficiency. Although short stature is a common feature in FDH, our data suggests that severe undernutrition is not common in this group and that there may be underlying treatable causes for this short stature in some patients.

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Repeated anodal trans‐spinal direct current stimulation results in long‐term reduction of spasticity in mice with spinal cord injury

Key points

Spasticity is a disorder of muscle tone that is associated with lesions of the motor system. This condition involves an overactive spinal reflex loop that resists passive lengthening of muscles. Previously, we established that application of anodal trans‐spinal direct current stimulation (tsDCS) for short periods of time to anaesthetized mice sustaining a spinal cord injury leads to an instantaneous reduction of spasticity. However, the long‐term effects of repeated a‐tsDCS and its mechanism of action remained unknown. Here, a‐tsDCS was performed for 7 days and this was found to cause long‐term reduction in spasticity, increase rate‐dependent depression in spinal reflexes, and improve ground and skill locomotion. Pharmacological, molecular, and cellular evidence further suggest that a novel mechanism involving Na‐K‐Cl cotransporter isoform 1 (NKCC1) mediates the observed long‐term effects of repeated a‐tsDCS.

Abstract

Spasticity can cause pain and fatigue, sleep disturbances, it can restrict daily activities such as walking, sitting, and bathing, and it can complicate rehabilitation efforts. Thus, spasticity negatively influences an individual's quality of life and novel therapeutic interventions are needed. We previously demonstrated in anaesthetized mice that a short period of trans‐spinal subthreshold direct current stimulation (tsDCS) reduces spasticity. In the present study, the long‐term effects of repeated tsDCS to attenuate abnormal muscle tone in awake female mice with spinal cord injuries were investigated. A motorized system was used to test velocity‐dependent ankle resistance and associated electromyographical activity. Analysis of ground and skill locomotion was also performed, while electrophysiological, molecular, and cellular studies were conducted to reveal a potential underlying mechanism of action. A four‐week reduction in spasticity was associated with an increase in rate‐dependent depression of spinal reflexes and ground and skill locomotion were improved following 7 d of a‐tsDCS. Secondary molecular, cellular, and pharmacological experiments further demonstrated that the expression of K‐Cl co‐transporter isoform 2 (KCC2) was not changed in animals with spasticity. However, Na‐K‐Cl cotransporter isoform 1 (NKCC1) was significantly up‐regulated in mice that exhibited spasticity. When mice were treated with a‐tsDCS, down regulation of NKCC1 was detected, and this level did not significantly differ from that in the non‐injured control mice. Thus, long lasting reduction of spasticity by a‐tsDCS via down‐regulation NKCC1 may constitute a novel therapy for spasticity following spinal cord injury.

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Vasodilatory function in human skeletal muscle feed arteries with advancing age: the role of adropin

Key points

This study sought to determine the impact of aging on endogenous adropin levels in human skeletal muscle feed arteries (SMFAs) and the role of adropin in age‐related vascular dysfunction. Adropin protein expression falls progressively with advancing age in the human peripheral vasculature and endothelial‐dependent vasodilation, typically attenuated with age, was strongly correlated with SMFA adropin protein levels. Adropin incubation restored age‐related endothelial‐dependent vasodilatory dysfunction and increased p‐eNOS/eNOS ratio in an age‐dependent manner in the SMFAs. The role of NO bioavailability was additionally evidenced by NOS blockade ablating both the positive vascular effects of adropin incubation and the relationship between endothelial function and adropin protein expression. Additional evidence of a mechanistic link between declining adropin and age‐related endothelial dysfunction was documented by a progressively increasing magnitude of effect of adropin‐induced eNOS‐mediated vasodilation with aging. Adropin, appears to be a novel therapeutic target to facilitate the restoration of endothelial function with aging.

Abstract

This study sought to determine the impact of advancing age on endogenous adropin levels in human skeletal muscle feed arteries (SMFAs) and the role of adropin in age‐related vascular dysfunction. Adropin protein expression and vasodilatory capacity was assesed in SMFAs from Young (Y, 27 ± 2 yrs, n = 10), Middle aged (MA, 54 ± 2 yrs, n = 10), and Old (O, 75 ± 2 yrs, n = 16) subjects. Endothelial‐dependent vasodilation, with and without adropin incubation, was assessed in response to flow‐induced shear stress and acetylcholine (ACh). Both SMFA adropin protein expression and endothelial‐dependent vasodilatory function exhibited a progressive, age‐related, reduction (Flow: Y: 65 ± 3; MA: 36 ± 3; O: 15 ± 2%; ACh: Y: 63 ± 2, MA: 34 ± 3 %; O: 23 ± 3 %, P<0.05). There was a strong positive correlation between SMFA adropin protein expression and both flow‐ (r = 0.81, P<0.05) and ACh‐ (r = 0.78, P<0.05). Adropin incubation in the MA and O SMFAs restored the vasodilatory response to flow (MA+Adropin: 59 ± 3; O+Adropin: 47 ± 3 %, P<0.05) and ACh (MA+Adropin: 59 ± 3 %; O+Adropin: 49 ± 2 %, P<0.05). A mechanistic link between adropin and NO biovavailabilty was supported by 1) an increased phosphorylated eNOS/eNOS protein expression with adropin incubation only in the MA and O SMFAs, 2) eNOS blockade ablating both the positive vascular effects of adropin incubation and the relationship between endothelial function and adropin protein expression and, finally, 3) a progressive increase in the magnitude of effect of adropin‐induced eNOS‐mediated vasodilation with advancing age. Adropin could be a novel therapeutic target to facilitate the restoration of endothelial function, through increased NO bioavailability, with advancing age.

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Associations between TMEM196 polymorphisms and NSAID-exacerbated respiratory disease in asthma

Background We previously found differences in the minor allele frequency (MAF) of single-nucleotide polymorphisms (SNPs) in transmembrane protein 196 (TMEM196) between 995 patients with aspirin-tolerant asthma (ATA) and 141 asthmatic patients with NSAID-exacerbated respiratory disease (NERD). In this study, we statistically analyzed the distributions of the genotypes and haplotypes of these SNPs to determine the exact association between TMEM196 genetic variants and the risk for NERD. Materials and methods Lewontin's D′ and r2 values were used to measure linkage disequilibrium between the biallelic loci having MAFs more than 0.05, and haplotypes were inferred using the PHASE algorithm (version 2.0). The genotype distribution was analyzed by logistic regression models using age of onset, smoking status (nonsmoker=0, ex-smoker=1, smoker=2), and BMI as covariates. Regression analysis of the association between SNPs and the risk of NERD was analyzed using SPSS version 12.0 and PLINK version 1.9. Results The MAF of rs9886152 C>T was significantly lower in NERD than in ATA [24.8 vs. 34.0%, odds ratio=0.64 (0.48–0.85), P=2.07×10−3, Pcorr=0.048]. The rate of the rs9886152 C>T minor allele was significantly lower in NERD than in ATA [44.0 vs. 56.4% in the codominant model, P=0.002, Pcorr=0.049, odds ratio=0.64 (0.48–0.85)]. An additional three SNPs (rs9639334 A>G, rs9638765 A>G, and rs2097811 G>A) showed similar associations with the risk of NERD. NERD patients had lower frequencies of the rs9639334 A>G minor allele (51.1 vs. 64.4%, P=0.002, Pcorr=0.043), rs9638765 A>G (49.7 vs. 64.2%, P=0.001, Pcorr=0.017), and rs2097811 G>A (51.1 vs. 64.5%, P=0.002, Pcorr=0.04) compared with ATA patients. Patients homozygous for the minor alleles of the four SNPs showed significantly less of an aspirin-induced decrease in forced expiratory volume in one second compared with those homozygous for the common alleles (P=0.003–0.012). Conclusion The minor alleles of the four SNPs in TMEM196 may exert a protective effect against the development of NERD and may be useful genetic markers to predict the risk of NERD. * Jong-Uk Lee and Hun Soo Chang contributed equally to the writing of this article. Correspondence to Jong-Sook Park, MD, PhD, Department of Internal Medicine, Division of Allergy and Respiratory Medicine, Soonchunhyang University Bucheon Hospital, 1174, Jung Dong, Wonmi Ku, Bucheon, Gyeonggi Do 420-021, Republic of Korea Tel: +82 326 215 105; fax: +82 326 215 023; e-mail: newstart1221@naver.com Received May 1, 2018 Accepted December 4, 2018 Copyright © 2019 Wolters Kluwer Health, Inc. All rights reserved.

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