Motor cortical disinhibition with baroreceptor unloading induced by orthostatic stress

2014 ◽  
Vol 111 (12) ◽  
pp. 2656-2664 ◽  
Author(s):  
Vasiliy E. Buharin ◽  
Andrew J. Butler ◽  
Minoru Shinohara

Unloading of the baroreceptors due to orthostatic stress increases corticospinal excitability. The purpose of this study was to examine the effects of baroreceptor unloading due to orthostatic stress on intracortical excitatory and inhibitory pathways in the motor cortex. With transcranial magnetic stimulation, measures of intracortical excitability for a hand muscle were tested on 2 days in healthy young adults. Lower body negative pressure (LBNP) of 40 mmHg was applied during one of the days and not during the Control day. During application of LBNP heart rate and the low-frequency component of heart rate variability increased, while mean arterial blood pressure was maintained. In the resting state, LBNP decreased short-interval intracortical inhibition (SICI) and had no effect on intracortical facilitation (ICF) or short-interval intracortical facilitation (SICF) compared with the Control day. During isometric contraction, no effects of LBNP were observed on tested measures of intracortical excitability including SICI, SICF, and cortical silent period. It was concluded that baroreceptor unloading due to orthostatic stress results in diminished intracortical inhibition, at least in the resting muscle.

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Florence Morin-Parent ◽  
Camille Champigny ◽  
Angelina Lacroix ◽  
François Corbin ◽  
Jean-François Lepage

AbstractFragile-X syndrome (FXS) is characterized by neurological and psychiatric problems symptomatic of cortical hyperexcitability. Recent animal studies identified deficient γ-aminobutyricacid (GABA) inhibition as a key mechanism for hyperexcitability in FXS, but the GABA system remains largely unexplored in humans with the disorder. The primary objective of this study was to assess GABA-mediated inhibition and its relationship with hyperexcitability in patients with FXS. Transcranial magnetic stimulation (TMS) was used to assess cortical and corticospinal inhibitory and excitatory mechanisms in 18 patients with a molecular diagnosis of FXS and 18 healthy controls. GABA-mediated inhibition was measured with short-interval intracortical inhibition (GABAA), long-interval intracortical inhibition (GABAB), and the corticospinal silent period (GABAA+B). Net intracortical facilitation involving glutamate was assessed with intracortical facilitation, and corticospinal excitability was measured with the resting motor threshold. Results showed that FXS patients had significantly reduced short-interval intracortical inhibition, increased long-interval intracortical inhibition, and increased intracortical facilitation compared to healthy controls. In the FXS group, reduced short-interval intracortical inhibition was associated with heightened intracortical facilitation. Taken together, these results suggest that reduced GABAA inhibition is a plausible mechanism underlying cortical hyperexcitability in patients with FXS. These findings closely match those observed in animal models, supporting the translational validity of these markers for clinical research.


2013 ◽  
Vol 124 (9) ◽  
pp. 1846-1852 ◽  
Author(s):  
Daisuke Sato ◽  
Koya Yamashiro ◽  
Takuya Yoshida ◽  
Hideaki Onishi ◽  
Yoshimitsu Shimoyama ◽  
...  

2020 ◽  
Vol 129 (2) ◽  
pp. 205-217
Author(s):  
Callum G. Brownstein ◽  
Loïc Espeit ◽  
Nicolas Royer ◽  
Thomas Lapole ◽  
Guillaume Y. Millet

This study compared the change in silent period (SP) and short-interval intracortical inhibition (SICI) with conditioning stimulus and single-pulse transcranial magnetic stimulation (TMS) intensities (for SICI and SP, respectively) eliciting maximal and submaximal SICI and SP during fatiguing exercise. The results showed that changes in SICI were only detectable with intensities evoking maximal responses, with no difference between intensities for SP. These findings highlight the importance of maximizing SICI with appropriate intensities before measuring SICI during fatiguing exercise.


2015 ◽  
Vol 309 (12) ◽  
pp. R1474-R1478 ◽  
Author(s):  
Christine M. Clark ◽  
Kevin D. Monahan ◽  
Rachel C. Drew

The ability of the human body to maintain arterial blood pressure (BP) during orthostatic stress is determined by several reflex neural mechanisms. Renal vasoconstriction progressively increases during graded elevations in lower body negative pressure (LBNP). This sympathetically mediated response redistributes blood flow to the systemic circulation to maintain BP. However, how healthy aging affects the renal vasoconstrictor response to LBNP is unknown. Therefore, 10 young (25 ± 1 yr; means ± SE) and 10 older (66 ± 2 yr) subjects underwent graded LBNP (−15 and −30 mmHg) while beat-to-beat renal blood flow velocity (RBFV; Doppler ultrasound), arterial BP (Finometer), and heart rate (HR; electrocardiogram) were recorded. Renal vascular resistance (RVR), an index of renal vasoconstriction, was calculated as mean BP/RBFV. All baseline cardiovascular variables were similar between groups, except diastolic BP was higher in older subjects ( P < 0.05). Increases in RVR during LBNP were greater in the older group compared with the young group (older: −15 mmHg Δ10 ± 3%, −30 mmHg Δ20 ± 5%; young: −15 mmHg Δ2 ± 2%, −30 mmHg Δ6 ± 2%; P < 0.05). RBFV tended to decrease more ( P = 0.10) and mean BP tended to decrease less ( P = 0.09) during LBNP in the older group compared with the young group. Systolic and diastolic BP, pulse pressure, and HR responses to LBNP were similar between groups. These findings suggest that aging augments the renal vasoconstrictor response to orthostatic stress in humans.


2019 ◽  
Vol 30 (5) ◽  
pp. 463-476 ◽  
Author(s):  
Joel Mason ◽  
Ashlyn K. Frazer ◽  
Alan J. Pearce ◽  
Alicia M. Goodwill ◽  
Glyn Howatson ◽  
...  

Abstract Several studies have used transcranial magnetic stimulation to probe the corticospinal-motoneuronal responses to a single session of strength training; however, the findings are inconsistent. This systematic review and meta-analysis examined whether a single bout of strength training affects the excitability and inhibition of intracortical circuits of the primary motor cortex (M1) and the corticospinal-motoneuronal pathway. A systematic review was completed, tracking studies between January 1990 and May 2018. The methodological quality of studies was determined using the Downs and Black quality index. Data were synthesised and interpreted from meta-analysis. Nine studies (n=107) investigating the acute corticospinal-motoneuronal responses to strength training met the inclusion criteria. Meta-analyses detected that after strength training compared to control, corticospinal excitability [standardised mean difference (SMD), 1.26; 95% confidence interval (CI), 0.88, 1.63; p<0.0001] and intracortical facilitation (ICF) (SMD, 1.60; 95% CI, 0.18, 3.02; p=0.003) were increased. The duration of the corticospinal silent period was reduced (SMD, −17.57; 95% CI, −21.12, −14.01; p=0.00001), but strength training had no effect on the excitability of the intracortical inhibitory circuits [short-interval intracortical inhibition (SICI) SMD, 1.01; 95% CI, −1.67, 3.69; p=0.46; long-interval intracortical inhibition (LICI) SMD, 0.50; 95% CI, −1.13, 2.13; p=0.55]. Strength training increased the excitability of corticospinal axons (SMD, 4.47; 95% CI, 3.45, 5.49; p<0.0001). This systematic review and meta-analyses revealed that the acute neural changes to strength training involve subtle changes along the entire neuroaxis from the M1 to the spinal cord. These findings suggest that strength training is a clinically useful tool to modulate intracortical circuits involved in motor control.


2017 ◽  
Vol 29 (1) ◽  
pp. 99-114 ◽  
Author(s):  
Mana Biabani ◽  
Maryam Aminitehrani ◽  
Maryam Zoghi ◽  
Michael Farrell ◽  
Gary Egan ◽  
...  

Abstract Transcranial direct current stimulation (tDCS) is increasingly being used to affect the neurological conditions with deficient intracortical synaptic activities (i.e. Parkinson’s disease and epilepsy). In addition, it is suggested that the lasting effects of tDCS on corticospinal excitability (CSE) have intracortical origin. This systematic review and meta-analysis aimed to examine whether tDCS has any effect on intracortical circuits. Eleven electronic databases were searched for the studies investigating intracortical changes induced by anodal (a) and cathodal (c) tDCS, in healthy individuals, using two paired-pulse transcranial magnetic stimulation (TMS) paradigms: short-interval intracortical inhibition (SICI) and intracortical facilitation (ICF). Additionally, motor-evoked potential (MEP) size alterations, assessed by single-pulse TMS, were extracted from these studies to investigate the probable intracortical origin of tDCS effects on CSE. The methodological quality of included studies was examined using Physiotherapy Evidence Database (PEDro) and Downs and Black’s (D&B) assessment tools. Thirteen research papers, including 24 experiments, were included in this study scoring good and medium quality in PEDro and D&B scales, respectively. Immediately following anodal tDCS (a-tDCS) applications, we found significant decreases in SICI, but increases in ICF and MEP size. However, ICF and MEP size significantly decreased, and SICI increased immediately following cathodal tDCS (c-tDCS). The results of this systematic review and meta-analysis reveal that a-tDCS changes intracortical activities (SICI and ICF) toward facilitation, whereas c-tDCS alters them toward inhibition. It can also be concluded that increases and decreases in CSE after tDCS application are associated with corresponding changes in intracortical activities. The results suggest that tDCS can be clinically useful to modulate intracortical circuits.


2010 ◽  
Vol 103 (1) ◽  
pp. 511-518 ◽  
Author(s):  
R. F. H. Cash ◽  
U. Ziemann ◽  
K. Murray ◽  
G. W. Thickbroom

In human motor cortex transcranial magnetic stimulation (TMS) has been used to identify short-interval intracortical inhibition (SICI) corresponding to γ-aminobutyric acid type A (GABAA) effects and long-interval intracortical inhibition (LICI) and the cortical silent period (SP) corresponding to postsynaptic GABAB effects. Presynaptic GABAB effects, corresponding to disinhibition, can also be identified with TMS and have been shown to be acting during LICI by measuring SICI after a suprathreshold priming stimulus (PS). The duration of disinhibition is not certain and, guided by studies in experimental preparations, we hypothesized that it may be longer-lasting than postsynaptic inhibition, leading to a period of late cortical disinhibition and consequently a net increase in corticospinal excitability. We tested this first by measuring the motor-evoked potential (MEP) to a test stimulus (TS), delivered after a PS at interpulse intervals (IPIs) ≤300 ms that encompassed the period of PS-induced LICI and its aftermath. MEP amplitude was initially decreased, but then increased at IPIs of 190–210 ms, reaching 160 ± 17% of baseline 200 ms after PS ( P < 0.05). SP duration was 181 ± 5 ms. A second experiment established that the onset of the later period of increased excitability correlated with PS intensity ( r2 = 0.99) and with the duration of the SP ( r2 = 0.99). The third and main experiment demonstrated that SICI was significantly reduced in strength at all IPIs ≤220 ms after PS. We conclude that TMS-induced LICI is associated with a period of disinhibition that is at first masked by LICI, but that outlasts LICI and gives rise to a period during which disinhibition predominates and net excitability is raised. Identification of this late period of disinhibition in human motor cortex may provide an opportunity to explore or modulate the behavior of excitatory networks at a time when inhibitory effects are restrained.


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