Posts Tagged Transcranial magnetic stimulation

[ARTICLE] Using Brain Oscillations and Corticospinal Excitability to Understand and Predict Post-Stroke Motor Function – Full Text

What determines motor recovery in stroke is still unknown and finding markers that could predict and improve stroke recovery is a challenge. In this study, we aimed at understanding the neural mechanisms of motor function recovery after stroke using neurophysiological markers by means of cortical excitability (Transcranial Magnetic Stimulation – TMS) and brain oscillations (electroencephalography – EEG). In this cross-sectional study, fifty-five subjects with chronic stroke (62±14 yo, 17 women, 32±42 months post-stroke) were recruited in two sites. We analyzed TMS measures (i.e. motor threshold – MT – of the affected and unaffected sides) and EEG variables (i.e. power spectrum in different frequency bands and different brain regions of the affected and unaffected hemispheres) and their correlation with motor impairment as measured by Fugl-Meyer. Multiple univariate and multivariate linear regression analyses were performed to identify the predictors of good motor function. A significant interaction effect of MT in the affected hemisphere and power in beta bandwidth over the central region for both affected and unaffected hemispheres was found. We identified that motor function positively correlates with beta rhythm over the central region of the unaffected hemisphere, while it negatively correlates with beta rhythm in the affected hemisphere. Our results suggest that cortical activity in the affected and unaffected hemisphere measured by EEG provides new insights on the association between high frequency rhythms and motor impairment, highlighting the role of excess of beta in the affected central cortical region in poor motor function in stroke recovery.

Introduction

Stroke is a leading cause of morbidity, mortality, and disability worldwide (12). Among the sequels of stroke, motor impairment is one of the most relevant, since it conditions the quality of life of patients, it reduces their capability to perform their daily activities and it impairs their autonomy (3). Despite the advancements of the acute stroke therapy, patients require an intensive rehabilitation program that will partially determine the extent of their recovery (4). These rehabilitation programs aim at stimulating cortical plasticity to improve motor performance and functional recovery (5). However, what determines motor improvement is still unknown. Indeed, finding markers that could predict and enhance stroke recovery is still a challenge (6). Different types of biomarkers exist: diagnostic, prognostic, surrogate outcome, and predictive biomarkers (7). The identification of these biomarkers is critical in the management of stroke patients. In the field of stroke research, great attention has been put to biomarkers found in the serum, especially in acute care. However, research on biomarkers of stroke recovery is still limited, especially using neurophysiological tools.

A critical research area in stroke is to understand the neural mechanisms underlying motor recovery. In this context, neurophysiological techniques such as transcranial magnetic stimulation (TMS) and electroencephalography (EEG) are useful tools that could be used to identify potential biomarkers of stroke recovery. However, there is still limited data to draw further conclusions on neural reorganization in human trials using these techniques. A few studies have shown that, in acute and sub-acute stage, stroke patients present increased power in low frequency bands (i.e., delta and theta bandwidths) in both affected and unaffected sides, as well as increased delta/alpha ratio in the affected brain area; these patterns being also correlated to functional outcome (811). Recently, we have identified that, besides TMS-indexed motor threshold (MT), an increased excitability in the unaffected hemisphere, coupled with a decreased excitability in the affected hemisphere, was associated with poor motor function (12), as measured by Fugl-Meyer (FM) [assessing symptoms severity and motor recovery in post-stroke patients with hemiplegia—Fugl-Meyer et al. (13); Gladstone et al. (14)]. However, MT measurement is associated with a poor resolution as it indexes global corticospinal excitability. Therefore, combining this information with direct cortical measures such as cortical oscillations, as measured by EEG, can help us to understand further neural mechanisms of stroke recovery.

To date, there are very few studies looking into EEG and motor recovery. For that reason, we aimed, in the present study, to investigate the relationship between motor impairment, EEG, and TMS variables. To do so, we conducted a prospective multicenter study of patients who had suffered from a stroke, in which we measured functional outcome using FM and performed TMS and EEG recordings. Based on our preliminary work, we expected to identify changes in interhemispheric imbalances on EEG power, especially in frequency bands associated with learning, such as alpha and beta bandwidths. […]

Continue —> Frontiers | Using Brain Oscillations and Corticospinal Excitability to Understand and Predict Post-Stroke Motor Function | Neurology

Figure 1. Topoplots showing the topographic distribution of high-beta bandwidth (25 Hz) for every individual. Red areas represent higher high-beta activity, while blue areas represent lower high-beta activity. Central region (C3 or C4) in red stands for the affected side. For patients with poor motor function, a higher beta activity of the affected central region as compared to the affected side is observed in 16 out of 28 individuals. For patients with good motor function, a similar activity over central regions bilaterally, or higher activity over the unaffected central area can be identified in 21 out of 27 individuals. FM = Fugl-Meyer.

, , , , , , , ,

Leave a comment

[VIDEO] How TMS Works – YouTube

, ,

Leave a comment

[Abstract] Spasticity Management: The Current State of Transcranial Neuromodulation

Abstract

This narrative review aims to provide an objective view of the non-invasive neuromodulation (NINM) protocols available for treating spasticity, including repetitive transcranial magnetic stimulation (rTMS) and transcranial direct current stimulation (tDCS). On the basis of the relevant randomized controlled trials, we infer that NINM is more effective in reducing spasticity when combined with the conventional therapies than used as a stand-alone treatment. However, the magnitude of NINM aftereffects depends significantly on the applied hemisphere and the underlying pathology. Being in line with these arguments, low-frequency rTMS and cathodal-tDCS over the unaffected hemisphere are more effective in reducing spasticity than high-frequency rTMS and anodal-tDCS over the affected hemisphere in chronic post-stroke. However, most of the studies are heterogeneous in the stimulation setup, patient selection, follow-up duration, and the availability of the sham operation. Therefore, the available data on the usefulness of NINM in reducing spasticity need to be confirmed by further larger and multicentric randomized controlled trials to gather evidence on the efficiency of NINM regimens in reducing spasticity in various neurologic conditions.

Source: Spasticity Management: The Current State of Transcranial Neuromodulation

, , , , , , , ,

Leave a comment

[ARTICLE] The impact of large structural brain changes in chronic stroke patients on the electric field caused by transcranial brain stimulation – Full Text

Abstract

Transcranial magnetic stimulation (TMS) and transcranial direct current stimulation (TDCS) are two types of non-invasive transcranial brain stimulation (TBS). They are useful tools for stroke research and may be potential adjunct therapies for functional recovery. However, stroke often causes large cerebral lesions, which are commonly accompanied by a secondary enlargement of the ventricles and atrophy. These structural alterations substantially change the conductivity distribution inside the head, which may have potentially important consequences for both brain stimulation methods. We therefore aimed to characterize the impact of these changes on the spatial distribution of the electric field generated by both TBS methods. In addition to confirming the safety of TBS in the presence of large stroke-related structural changes, our aim was to clarify whether targeted stimulation is still possible. Realistic head models containing large cortical and subcortical stroke lesions in the right parietal cortex were created using MR images of two patients. For TMS, the electric field of a double coil was simulated using the finite-element method. Systematic variations of the coil position relative to the lesion were tested. For TDCS, the finite-element method was used to simulate a standard approach with two electrode pads, and the position of one electrode was systematically varied. For both TMS and TDCS, the lesion caused electric field “hot spots” in the cortex. However, these maxima were not substantially stronger than those seen in a healthy control. The electric field pattern induced by TMS was not substantially changed by the lesions. However, the average field strength generated by TDCS was substantially decreased. This effect occurred for both head models and even when both electrodes were distant to the lesion, caused by increased current shunting through the lesion and enlarged ventricles. Judging from the similar peak field strengths compared to the healthy control, both TBS methods are safe in patients with large brain lesions (in practice, however, additional factors such as potentially lowered thresholds for seizure-induction have to be considered). Focused stimulation by TMS seems to be possible, but standard tDCS protocols appear to be less efficient than they are in healthy subjects, strongly suggesting that tDCS studies in this population might benefit from individualized treatment planning based on realistic field calculations.

1. Introduction

Transcranial brain stimulation (TBS) methods are useful tools to induce and to quantify neural plasticity, and as such are increasingly being used in stroke research and as potential adjunct therapies in stroke rehabilitation. The cerebral lesions caused by stroke result in persisting physical or cognitive impairments in around 50% of all survivors (Di Carlo, 2008Leys et al., 2005 ;  Young and Forster, 2007), meaning that new therapies are urgently needed. Transcranial magnetic stimulation (TMS) and transcranial direct current stimulation (TDCS) are two TBS approaches which are being increasingly utilised in stroke research. Single-pulse TMS combined with electromyography (EMG) or electroencephalography (EEG) can be used to assess cortical excitability, for example to index the functional state of the perilesional tissue. The neuromodulatory effects of repetitive TMS protocols (rTMS) may, in association with neuro-rehabilitative treatments, enhance motor recovery (Liew et al., 2014). Similar results have been demonstrated for TDCS. For example, anodal TDCS of the hand area in the primary motor cortex has been shown to improve motor performance of the affected hand (Allman et al., 2016Hummel et al., 2005 ;  Stagg et al., 2012) and anodal TDCS applied over the left frontal cortex enhanced naming accuracy in patients with aphasia (Baker et al., 2010). However, not all studies report a clear-cut positive impact of TBS on the stroke symptoms. Rather, the observed effects are often weak and not consistent across patients, demonstrating the need for a better understanding of the underlying biophysical and physiological mechanisms.

Compared with healthy subjects, several factors might contribute to a change in the neuroplastic response to TBS protocols in stroke patients, including changes in the neural responsiveness to the applied electric fields, as well as differences in the underlying physiology and metabolism (Blicher et al., 2009Blicher et al., 2015 ;  O’Shea et al., 2014). When the lesions are large, they may also substantially alter the generated electric field pattern, meaning that the assumptions on spatial targeting as derived from biophysical modelling and physiological experiments in healthy subjects might no longer be valid. Stroke lesions are often accompanied by secondary macrostructural changes such as cortical atrophy and enlargement of the ventricles (e.g., Skriver et al., 1990), which may further contribute to changes in the field pattern. In addition, the safety of TBS in patients with large lesions needs to be further clarified, as it is possible that the lesions might cause stimulation “hot spots”. In chronic patients, the stroke cavity becomes filled with corticospinal fluid (CSF), which might cause shunting of current, funnelling the generated currents towards the surrounding brain tissue and potentially causing localized areas of dangerously high field strengths.

Here, using finite-element calculations and individual head models derived from structural MR images, we focused on the impact of a large cortical lesion in chronic stroke on the electric field pattern generated in the brain by TMS and TDCS, respectively. Firstly, we assessed the safety of the stimulation by comparing the achieved field strengths with those estimated for a healthy control. Secondly, we tested how reliably we can accurately target the perilesional tissue, often the desired target for TBS, as reorganisation here is thought to underpin functional recovery (Kwakkel et al., 2004). Finally, we were also interested to see whether any observed changes in the field pattern were specific to a patient with a cortical lesion (which is connected to the CSF layer underneath the skull), or whether similar effects might occur in case of large chronic subcortical lesion. We therefore additionally tested the field distribution in a head model of a patient with a subcortical lesion occurring at a similar position as the cortical lesion.

2. Materials and methods

2.1. Selection of patients

The aim of this study was to characterize the effect of a large chronic cortical stroke lesion on the electric field distribution generated by TBS, and to compare the effects of this lesion to that caused by a large chronic subcortical lesion. MR images of several patients were visually inspected to select two datasets, which had a cortical [P01] and subcortical lesion [P02], respectively, within the same gross anatomical regions.

Patient P01 was a 36 year old female with episodic migraine; she was admitted with left hemiparalysis, fascial palsy and a total NIHSS score of 16 due to a right ICI/MCI occlusion. She was treated with IV thrombolysis and thrombectomy and recanalization was achieved 5 h after symptom onset. One year post-stroke she still suffered from motor impairment (Wolf Motor Function Test [WMFT] score of 30) and was scanned as part of a clinical study investigating the effect of combining Constraint-Induced Movement Therapy and tDCS (Figlewski et al., 2017; Clinical trials NCT01983319, Regional Ethics approval: 1-10-72-268-13). The structural scans showed a cortical lesion in the right parietal lobe (Fig. 1A). The lesion volume, delineated manually with reference to T1- and T2-weighted imaging, was 26,415 mm3.

Fig. 1:Fig. 1.

A) Coronal view of patient P01 with a cortical lesion in the right hemisphere. The top shows the T1-weighted MR image and the bottom the reconstructed head mesh. The view was chosen to include the lesion centre. The lesion is marked by red dashed circles. B) Corresponding view of patient P02 with a large subcortical lesion at a similar location in the right hemisphere. C) Corresponding view of the data set of the healthy control. D) The coil and electrode positions were systematically moved along two directions that were approximately perpendicular to each other. Five positions were manually placed every 2 cm in posterior – anterior direction symmetrically around the centre of the cortical lesion. The same was repeated along the lateral – medial direction. Both lines share the same centre position above the lesion, resulting in 9 positions in total. E) At each position, two coil orientations were tested which resulted in a current flow underneath the coil centre from anterior to posterior (top) and from lateral to medial, respectively (bottom). F) For each position of the yellow “stimulating” electrode, two positions of the blue return electrode were tested. First, the contralateral equivalent of the electrode position above the centre of the cortical lesion was used (top). In addition, a position on the contralateral forehead was tested (bottom).

Patient P02 was a 44 year old female. She woke up with a left hemiparesis and an acute CT scan showed no bleeding. No IV thrombolysis was given due to uncertain timing of symptom onset. An embolic stroke was suspect due to a patent foramen ovale, which was subsequently closed. She was scanned with MRI 9 months post stroke showing a right subcortical infarct, at which time she had a WMFT score of 8. The lesion volume, delineated as for P01, was 56,010 mm3. She was scanned as part of a clinical study investigating the effect of combining tDCS with daily motor training (Allman et al., 2016; Regional Ethics approval: Oxfordshire REC A; 10/H0604/98)….

Continue —> The impact of large structural brain changes in chronic stroke patients on the electric field caused by transcranial brain stimulation

, , , , , ,

Leave a comment

[Abstract] Targeting interhemispheric inhibition with neuromodulation to enhance stroke rehabilitation

Highlights

  • This review focuses on interhemispheric inhibition and its role in the healthy and stroke lesioned brain.
  • Measurement method and movement phase should be considered when comparing studies associating interhemispheric inhibition with functional recovery.
  • Neuromodulation of interhemispheric inhibition to augment stroke recovery requires the targeting of specific neural circuitry. We discuss the effectiveness of current and novel neurostimulation techniques at targeting interhemispheric inhibition and enhancing stroke rehabilitation.

Abstract

Background/Objectives

Interhemispheric inhibition in the brain plays a dynamic role in the production of voluntary unimanual actions. In stroke, the interhemispheric imbalance model predicts the presence of asymmetry in interhemispheric inhibition, with excessive inhibition from the contralesional hemisphere limiting maximal recovery. Stimulation methods to reduce this asymmetry in the brain may be promising as a stroke therapy, however determining how to best measure and modulate interhemispheric inhibition and who is likely to benefit, remain important questions.

Methods

This review addresses current understanding of interhemispheric inhibition in the healthy and stroke lesioned brain. We present a review of studies that have measured interhemispheric inhibition using different paradigms in the clinic, as well as results from recent animal studies investigating stimulation methods to target abnormal inhibition after stroke.

Main findings/Discussion

The degree to which asymmetric interhemispheric inhibition impacts on stroke recovery is controversial, and we consider sources of variation between studies which may contribute to this debate. We suggest that interhemispheric inhibition is not static following stroke in terms of the movement phase in which it is aberrantly engaged. Instead it may be dynamically increased onto perilesional areas during early movement, thus impairing motor initiation. Hence, its effect on stroke recovery may differ between studies depending on the technique and movement phase of eliciting the measurement. Finally, we propose how modulating excitability in the brain through more specific targeting of neural elements underlying interhemispheric inhibition via stimulation type, location and intensity may raise the ceiling of recovery following stroke and enhance functional return.

Source: Targeting interhemispheric inhibition with neuromodulation to enhance stroke rehabilitation – Brain Stimulation: Basic, Translational, and Clinical Research in Neuromodulation

, , , , ,

Leave a comment

[Abstract] TMS measures of motor cortex function after stroke: A meta-analysis

Highlights

    The neurophysiological effects of stroke are localised to the affected motor cortex.There is no clear evidence of imbalanced interhemispheric inhibition after stroke.Facilitating the affected motor cortex may be most beneficial in selected patients.

Abstract

Background

Transcranial magnetic stimulation (TMS) is commonly used to measure the effects of stroke on corticomotor excitability, intracortical function, and interhemispheric interactions. The interhemispheric inhibition model posits that recovery of motor function after stroke is linked to rebalancing of asymmetric interhemispheric inhibition and corticomotor excitability. This model forms the rationale for using neuromodulation techniques to suppress unaffected motor cortex excitability, and facilitate affected motor cortex excitability. However, the evidence base for using neuromodulation techniques to promote post-stroke motor recovery is inconclusive.

Objective

The aim of this meta-analysis was to compare measures of corticomotor excitability, intracortical function, and interhemispheric inhibition, between the affected and unaffected hemispheres of people with stroke, and measures made in healthy adults.

Methods

A literature search was conducted to identify studies that made TMS measures of the motor cortex in adult stroke patients. Two authors independently extracted data, and the quality of included studies was assessed. TMS measures were compared between the affected and unaffected hemispheres of stroke patients, between the affected hemisphere and healthy controls, and between the unaffected hemisphere and healthy controls. Analyses were carried out with data grouped according to the muscle from which responses were recorded, and separately according to time post-stroke (<3 months, and ≥6 months). Meta-analyses were carried out using a random effects model.

Results

There were 844 studies identified, and 112 studies included in the meta-analysis. Results were very similar across muscle groups. Affected hemisphere M1 excitability is lower than unaffected and healthy control M1 excitability after stroke. Affected hemisphere short interval intracortical inhibition (SICI) is lower than unaffected and healthy control SICI early after stroke, and not different in the chronic phase. There were no differences detected between the unaffected hemisphere and healthy controls. There were only seven studies of interhemispheric inhibition that could be included, with no clear effects of hemisphere or time post-stroke.

Conclusions

The neurophysiological effects of stroke are primarily localised to the affected hemisphere, and there is no clear evidence for hyper-excitability of the unaffected hemisphere or imbalanced interhemispheric inhibition. This indicates that facilitating affected M1 excitability directly may be more beneficial than suppressing unaffected M1 excitability for promoting post-stroke recovery.

Source: TMS measures of motor cortex function after stroke: A meta-analysis

, , , , , , ,

Leave a comment

[Abstract] TMS measures of motor cortex function after stroke: A meta-analysis

Highlights

  • The neurophysiological effects of stroke are localised to the affected motor cortex.
  • There is no clear evidence of imbalanced interhemispheric inhibition after stroke.
  • Facilitating the affected motor cortex may be most beneficial in selected patients.

Abstract

Background

Transcranial magnetic stimulation (TMS) is commonly used to measure the effects of stroke on corticomotor excitability, intracortical function, and interhemispheric interactions. The interhemispheric inhibition model posits that recovery of motor function after stroke is linked to rebalancing of asymmetric interhemispheric inhibition and corticomotor excitability. This model forms the rationale for using neuromodulation techniques to suppress unaffected motor cortex excitability, and facilitate affected motor cortex excitability. However, the evidence base for using neuromodulation techniques to promote post-stroke motor recovery is inconclusive.

Objective

The aim of this meta-analysis was to compare measures of corticomotor excitability, intracortical function, and interhemispheric inhibition, between the affected and unaffected hemispheres of people with stroke, and measures made in healthy adults.

Methods

A literature search was conducted to identify studies that made TMS measures of the motor cortex in adult stroke patients. Two authors independently extracted data, and the quality of included studies was assessed. TMS measures were compared between the affected and unaffected hemispheres of stroke patients, between the affected hemisphere and healthy controls, and between the unaffected hemisphere and healthy controls. Analyses were carried out with data grouped according to the muscle from which responses were recorded, and separately according to time post-stroke (<3 months, and ≥ 6 months). Meta-analyses were carried out using a random effects model.

Results

There were 844 studies identified, and 112 studies included in the meta-analysis. Results were very similar across muscle groups. Affected hemisphere M1 excitability is lower than unaffected and healthy control M1 excitability after stroke. Affected hemisphere short interval intracortical inhibition (SICI) is lower than unaffected and healthy control SICI early after stroke, and not different in the chronic phase. There were no differences detected between the unaffected hemisphere and healthy controls. There were only seven studies of interhemispheric inhibition that could be included, with no clear effects of hemisphere or time post-stroke.

Conclusions

The neurophysiological effects of stroke are primarily localised to the affected hemisphere, and there is no clear evidence for hyper-excitability of the unaffected hemisphere or imbalanced interhemispheric inhibition. This indicates that facilitating affected M1 excitability directly may be more beneficial than suppressing unaffected M1 excitability for promoting post-stroke recovery.

Source: TMS measures of motor cortex function after stroke: A meta-analysis – Brain Stimulation: Basic, Translational, and Clinical Research in Neuromodulation

, , , , , , , , ,

Leave a comment

[WEB SITE] Transcranial magnetic stimulation Overview – Mayo Clinic

Overview

Transcranial magnetic stimulation (TMS) is a noninvasive procedure that uses magnetic fields to stimulate nerve cells in the brain to improve symptoms of depression. TMS is typically used when other depression treatments haven’t been effective.

How it works

During a TMS session, an electromagnetic coil is placed against your scalp near your forehead. The electromagnet painlessly delivers a magnetic pulse that stimulates nerve cells in the region of your brain involved in mood control and depression. And it may activate regions of the brain that have decreased activity in people with depression.

Though the biology of why rTMS works isn’t completely understood, the stimulation appears to affect how this part of the brain is working, which in turn seems to ease depression symptoms and improve mood.

Treatment for depression involves delivering repetitive magnetic pulses, so it’s called repetitive TMS or rTMS.

Visit Site —> Transcranial magnetic stimulation Overview – Mayo Clinic

, , , ,

Leave a comment

[Abstract] Bilateral sequential motor cortex stimulation and skilled task performance with non-dominant hand

Highlights

  • Both, contralateral M1 iTBS and ipsilateral M1 cTBS improved non-dominant skilled-task performance.
  • Bilateral sequential M1 TBS (contralateral cTBS followed by ipsilateral iTBS) improved skilled-task performance more than unilateral or sham TBS.
  • Bilateral sequential M1 TBS may be particularly effective in improving motor learning, also in the neurorehabilitation setting.

Abstract

Objective

To check whether bilateral sequential stimulation (BSS) of M1 with theta burst stimulation (TBS), using facilitatory protocol over non-dominant M1 followed by inhibitory one over dominant M1, can improve skilled task performance with non-dominant hand more than either of the unilateral stimulations do. Both, direct motor cortex (M1) facilitatory non-invasive brain stimulation (NIBS) and contralateral M1 inhibitory NIBS were shown to improve motor learning.

Methods

Forty right-handed healthy subjects were divided into 4 matched groups which received either ipsilateral facilitatory (intermittent TBS [iTBS] over non-dominant M1), contralateral inhibitory (continuous TBS [cTBS] over dominant M1), bilateral sequential (contralateral cTBS followed by ipsilateral iTBS), or placebo stimulation. Performance was evaluated by Purdue peg-board test (PPT), before (T0), immediately after (T1), and 30 min after (T2) an intervention.

Results

In all groups and for both hands, the PPT scores increased at T1 and T2 in comparison to T0, showing clear learning effect. However, for the target non-dominant hand only, immediately after BSS (at T1) the PPT scores improved significantly more than after either of unilateral interventions or placebo.

Conclusion

M1 BSS TBS is an effective intervention for improving motor performance.

Significance

M1 BSS TBS seems as a promising tool for motor learning improvement with potential uses in neurorehabilitation.

Source: Bilateral sequential motor cortex stimulation and skilled task performance with non-dominant hand – Clinical Neurophysiology

, , , , , , , , , , ,

Leave a comment

[Abstract] Individual differences in contralateral motor cortex (CMC) plasticity during short-term upper limb immobilisation (ULI) in healthy individuals – A transcranial magnetic stimulation (TMS) study

By decreasing CMC excitability, ULI holds the potential for being explored as a stroke model in healthy individuals for developing rehabilitation strategies ( Furlan et al., 2016 ). Determining the minimum effective restriction time is critical for optimising the immobilisation paradigm and facilitating its application.

Question

How does CMC excitability change over a period of 9 h of ULI?

Methods

Healthy individuals will have their right (dominant) upper limb immobilised for 9 h. CMC excitability will be assessed with TMS immediately before and after 3, 6, and 9 h of immobilisation. The TMS coil will be positioned over the hot spot of the right FDI muscle. Frameless stereotaxy will be used to keep the position of the coil constant across all TMS assessments. Fifteen MEPs will be recorded from the target muscle during each TMS assessment by using a fixed suprathreshold stimulation intensity (sSI). IO curves will also be obtained at each assessment by using 50, 70, 90, 110, and 130% of sSI.

Results

Fig. 1 shows preliminary MEP data from 5 participants. At the group level there was a depressant effect of immobilisation on CMC excitability. CMC excitability decreased to 63 and 54% of the baseline value after 3 and 6 h of immobilisation, respectively. However, after 9 h, excitability levels increased to 84% of the baseline value, suggesting that CMC excitability might follow a U-shaped curve during ULI. At the individual level there was great variability in CMC excitability among participants over the course of immobilisation, particularly in terms of the position of the deflection point of the excitability curve.

Conclusion

Our data is in line with previous studies reporting inter-individual differences in CMC plasticity after ULI ( Rosenkranz et al., 2014 ). Importantly, our study shows how these differences develop during ULI. This information should be given consideration when seeking for the ideal length of the immobilisation protocol.

Source: P311 Individual differences in contralateral motor cortex (CMC) plasticity during short-term upper limb immobilisation (ULI) in healthy individuals – A transcranial magnetic stimulation (TMS) study – Clinical Neurophysiology

, , , , , , , , ,

Leave a comment

%d bloggers like this: