Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Showing posts with label motor cortex excitability. Show all posts
Showing posts with label motor cortex excitability. Show all posts

Saturday, January 28, 2023

Primary motor cortex excitability during recovery after stroke: implications for neuromodulation

Implications is a shitworthy useless word meaning nothing helpful to survivor recovery.  I'd fire you all. Will you actually try to help survivors recover?

Primary motor cortex excitability during recovery after stroke: implications for neuromodulation

 Cathy M. Stinear a,b, 
Matthew A. Petoe a,b, 
Winston D. Byblow b,c,*
a Department of Medicine, University of Auckland, Private Bag 92019, Auckland 1142, New Zealand
b Centre for Brain Research, University of Auckland, Private Bag 92019, Auckland 1142, New Zealand
c Department of Sport & Exercise Science, University of Auckland, Private Bag 92019, Auckland 1142, New Zealand
a r t i c l e i n f o
 Article history:
Received 14 March 2015Received in revised form27 May 2015Accepted 22 June 2015Available online xxx
Keywords:
StrokeSub-acuteUpper limbTranscranial magnetic stimulationMotor cortex

Abstract

Background:
 Non-invasive brain stimulation techniques may be useful adjuvants to promote recoveryafter stroke. They are typically used to facilitate ipsilesional cortical excitability directly, or indirectly bysuppressing contralesional cortical excitability and reducing interhemispheric inhibition from the con-tralesional to ipsilesional hemisphere. However, most of the evidence for this approach comes fromstudies of patients at the chronic stage of recovery.
 
Hypothesis:
 We hypothesized that corticomotor excitability and interhemispheric inhibition wouldinitially be asymmetric, with greater interhemispheric inhibition from contralesional to ipsilesional M1.We also hypothesized that balancing of corticomotor excitability and interhemispheric inhibition wouldbe associated with greater improvements in paretic upper-limb impairment and function.
 
Methods:
 We conducted a retrospective analysis of longitudinal data collected from 46 patients during the
 first six months after stroke. Transcranial magnetic stimulation was used to measure rest motorthreshold, stimulus-response curves, and ipsilateral silent periods from the extensor carpi radialismuscles of both upper limbs. Analyses of variance and linear regression modeling were used to evaluatethe effect of time on corticomotor excitability and interhemispheric inhibition in both hemispheres, andassociations between these effects and improvements in paretic upper-limb impairment and function.
 
Results:
 All participants had subcortical damage and only two had motor cortex involvement. As expected, ipsilesional corticomotor excitability was initially suppressed and increased over time, and this increase was associated with improved upper-limb impairment and function. However, interhemispheric inhibition was symmetrical and stable over time, and there was no evidence for a decrease in contralesional corticomotor excitability.
 
Conclusions:
 Neuromodulation interventions applied during spontaneous recovery may be more beneficial if they facilitate ipsilesional corticomotor excitability directly.

Monday, October 11, 2021

Motor Cortical Network Flexibility is Associated With Biomechanical Walking Impairment in Chronic Stroke

 So you described a problem, but did nothing to solve it. Useless.

Motor Cortical Network Flexibility is Associated With Biomechanical Walking Impairment in Chronic Stroke

First Published September 27, 2021 Research Article 

Background: 

The inability to flexibly modulate motor behavior with changes in task demand or environmental context is a pervasive feature of motor impairment and dysfunctional mobility after stroke.  

Objective: 

The purpose of this study was to test the reactive and modulatory capacity of lower-limb primary motor cortical (M1) networks using electroencephalography (EEG) measures of cortical activity evoked by transcranial magnetic stimulation (TMS) and to evaluate their associations with clinical and biomechanical measures of walking function in chronic stroke.  

Methods: 

TMS assessments of motor cortex excitability were performed during rest and active ipsilateral plantarflexion in chronic stroke and age-matched controls. TMS-evoked motor cortical network interactions were quantified with simultaneous EEG as the post-TMS (0–300 ms) beta (15–30 Hz) coherence between electrodes overlying M1 bilaterally. We compared TMS-evoked coherence between groups during rest and active conditions and tested associations with poststroke motor impairment, paretic propulsive gait deficits, and the presence of paretic leg motor evoked potentials (MEPs).  

Results: 

Stroke (n = 14, 66 ± 9 years, F = 4) showed lower TMS-evoked cortical coherence and activity-dependent modulation compared to controls (n = 9, 68 ± 6 years, F = 3). Blunted reactivity and atypical modulation of TMS-evoked coherence were associated with lower paretic ankle moments for propulsive force generation during walking and absent paretic MEPs.  

Conclusions: 

Impaired flexibility of motor cortical networks to react to TMS and modulate during motor activity is distinctly associated with paretic limb biomechanical walking impairment, and may provide useful insight into the neuromechanistic underpinnings of chronic post-stroke mobility deficits.

 

Wednesday, April 28, 2021

Primary motor cortex excitability during recovery after stroke: implications for neuromodulation

I would need this translated into layperson terms before I could tell my stroke professionals what is needed to be done.

Primary motor cortex excitability during recovery after stroke: implications for neuromodulation

2015, Brain Stimulation

 
Original Research
Primary Motor Cortex Excitability During Recovery AfterStroke: Implications for Neuromodulation
Cathy M. Stinear
a
,
b
, Matthew A. Petoe
a
,
b
, Winston D. Byblow
b
,
c
,
*
a
Department of Medicine, University of Auckland, Private Bag 92019, Auckland 1142, New Zealand
b
Centre for Brain Research, University of Auckland, Private Bag 92019, Auckland 1142, New Zealand
c
Department of Sport & Exercise Science, University of Auckland, Private Bag 92019, Auckland 1142, New Zealand
a r t i c l e i n f o
 Article history:
Received 14 March 2015Received in revised form27 May 2015Accepted 22 June 2015Available online xxx
Keywords:
Stroke Sub-acute Upper limb Transcranial magnetic stimulation Motor cortex

a b s t r a c t

Background:
 Non-invasive brain stimulation techniques may be useful adjuvants to promote recovery after stroke. They are typically used to facilitate ipsilesional cortical excitability directly, or indirectly bysuppressing contralesional cortical excitability and reducing interhemispheric inhibition from the contralesional to ipsilesional hemisphere. However, most of the evidence for this approach comes from studies of patients at the chronic stage of recovery.
Hypothesis:
 We hypothesized that corticomotor excitability and interhemispheric inhibition wouldinitially be asymmetric, with greater interhemispheric inhibition from contralesional to ipsilesional M1.We also hypothesized that balancing of corticomotor excitability and interhemispheric inhibition wouldbe associated with greater improvements in paretic upper-limb impairment and function.
Methods:
 We conducted a retrospective analysis of longitudinal data collected from 46 patients during the
 first six months after stroke. Transcranial magnetic stimulation was used to measure rest motor threshold, stimulus-response curves, and ipsilateral silent periods from the extensor carpi radialis muscles of both upper limbs. Analyses of variance and linear regression modeling were used to evaluate the effect of time on corticomotor excitability and interhemispheric inhibition in both hemispheres, and associations between these effects and improvements in paretic upper-limb impairment and function.
Results:
 All participants had subcortical damage and only two had motor cortex involvement. As expected, ipsilesional corticomotor excitability was initially suppressed and increased over time, and this increase was associated with improved upper-limb impairment and function. However, interhemispheric inhibition was symmetrical and stable over time, and there was no evidence for a decrease in contralesional corticomotor excitability.
Conclusions:
 Neuromodulation interventions applied during spontaneous recovery may be more bene-

cial if they facilitate ipsilesional corticomotor excitability directly.

 2015 Elsevier Inc. All rights reserved.

Friday, July 31, 2020

Mirror Symmetric Bimanual Movement Priming Can Increase Corticomotor Excitability and Enhance Motor Learning

'Can increase' IS NOT GOOD ENOUGH.  Do the fucking research that tells us yes/no whether it works or not. This laziness needs to stop. And in 8 years there was no followup to come up with a protocol or declare it worthless.  And measuring excitability or priming or motor evoked potentials does nothing for survivors, you measure functional movements which survivors actually care about. Think for once what survivors want.

Mirror Symmetric Bimanual Movement Priming Can Increase Corticomotor Excitability and Enhance Motor Learning

2012, PLoS ONE


Mirror Symmetric Bimanual Movement Priming Can Increase Corticomotor Excitability and Enhance MotorLearning
Winston D. Byblow 1,4*,
 Cathy M. Stinear3,4, 
Marie-Claire Smith 1,3, 
Lotte Bjerre 2, 
Brian K. Flaskager 2,
Alana B. McCambridge 1
1 Movement Neuroscience Laboratory, Department of Sport & Exercise Science, The University of Auckland, Auckland, New Zealand,
 2 Center for Sensory-MotorInteraction (SMI), Department of Health Science and Technology, Aalborg University, Aalborg, Denmark,
 3 Neurology Research Group, Department of Medicine, TheUniversity of Auckland, Auckland, New Zealand,
 4 Centre for Brain Research, The University of Auckland, Auckland, New Zealand

Abstract

Repetitive mirror symmetric bilateral upper limb may be a suitable priming technique for upper limb rehabilitation after stroke. Here we demonstrate neurophysiological and behavioural after-effects in healthy participants after priming with 20 minutes of repetitive active-passive bimanual wrist flexion and extension in a mirror symmetric pattern with respect to the body midline (MIR) compared to an control priming condition with alternating flexion-extension (ALT). Transcranial magnetic stimulation (TMS) indicated that corticomotor excitability (CME) of the passive hemisphere remained elevated compared to baseline for at least 30 minutes after MIR but not ALT, evidenced by an increase in the size of motor evoked potentials in ECR and FCR. Short and long-latency intracortical inhibition (SICI, LICI), short afferent inhibition (SAI) and
interhemispheric inhibition (IHI) were also examined using pairs of stimuli. LICI differed between patterns, with less LICI after MIR compared with ALT, and an effect of pattern on IHI, with reduced IHI in passive FCR 15 minutes after MIR compared with ALT and baseline. There was no effect of pattern on SAI or FCR H-reflex. Similarly, SICI remained unchanged after20 minutes of MIR. We then had participants complete a timed manual dexterity motor learning task with the passive handduring, immediately after, and 24 hours after MIR or control priming. The rate of task completion was faster with MIR priming compared to control conditions. Finally, ECR and FCR MEPs were examined within a pre-movement facilitation paradigm of wrist extension before and after MIR. ECR, but not FCR, MEPs were consistently facilitated before and after MIR,demonstrating no degradation of selective muscle activation. In summary, mirror symmetric active-passive bimanual movement increases CME and can enhance motor learning without degradation of muscle selectivity. These findings rationalise the use of mirror symmetric bimanual movement as a priming modality in post-stroke upper limb rehabilitation.
Citation:
 Byblow WD, Stinear CM, Smith M-C, Bjerre L, Flaskager BK, et al. (2012) Mirror Symmetric Bimanual Movement Priming Can Increase Corticomotor Excitability and Enhance Motor Learning. PLoS ONE 7(3): e33882. doi:10.1371/journal.pone.0033882
Editor:
 Alessio Avenanti, University of Bologna, Italy
Received
 June 6, 2011;
 Accepted
 February 23, 2012;
 Published
 March 22, 2012

Monday, September 23, 2019

Primary motor cortex excitability during recovery after stroke: implications for neuromodulation

'May' is not useful at all for what survivors need to recover. Doing a half-assed job doesn't help survivors one bit. 

Primary motor cortex excitability during recovery after stroke: implications for neuromodulation

Cathy M. Stineara,b, Matthew A. Petoea,b, Winston D. Byblowb,c,*a Department of Medicine, University of Auckland, Private Bag 92019, Auckland 1142, New Zealand b Centre for Brain Research, University of Auckland, Private Bag 92019, Auckland 1142, New Zealand c Department of Sport & Exercise Science, University of Auckland, Private Bag 92019, Auckland 1142, New Zealand a r t i c l e i n f o  Article history: Received 14 March 2015 Received in revised form 27 May 2015 Accepted 22 June 2015 Available online xxx Keywords: Stroke Sub-acute Upper limb Transcranial magnetic stimulation Motor cortex

Abstract 

Background:  Non-invasive brain stimulation techniques may be useful adjuvants to promote recovery after stroke. They are typically used to facilitate ipsilesional cortical excitability directly, or indirectly by suppressing contralesional cortical excitability and reducing interhemispheric inhibition from the contralesional to ipsilesional hemisphere. However, most of the evidence for this approach comes fromstudies of patients at the chronic stage of recovery.
Hypothesis:  We hypothesized that corticomotor excitability and interhemispheric inhibition wouldinitially be asymmetric, with greater interhemispheric inhibition from contralesional to ipsilesional M1. We also hypothesized that balancing of corticomotor excitability and interhemispheric inhibition would be associated with greater improvements in paretic upper-limb impairment and function.
Methods:  We conducted a retrospective analysis of longitudinal data collected from 46 patients during the  first six months after stroke. Transcranial magnetic stimulation was used to measure rest motor threshold, stimulus-response curves, and ipsilateral silent periods from the extensor carpi radialis muscles of both upper limbs. Analyses of variance and linear regression modeling were used to evaluate the effect of time on corticomotor excitability and interhemispheric inhibition in both hemispheres, and associations between these effects and improvements in paretic upper-limb impairment and function.
Results:  All participants had subcortical damage and only two had motor cortex involvement. As ex-pected, ipsilesional corticomotor excitability was initially suppressed and increased over time, and this increase was associated with improved upper-limb impairment and function. However, interhemisphericinhibition was symmetrical and stable over time, and there was no evidence for a decrease in contralesional corticomotor excitability.
Conclusions:  Neuromodulation interventions applied during spontaneous recovery may be more beneficial if they facilitate ipsilesional corticomotor excitability directly.

Tuesday, September 3, 2019

Task-oriented Motor Learning in Upper Extremity Rehabilitation Post Stroke

I absolutely hate any research that thinks motor area excitability is useful for survivor rehab rather then EXACT STROKE REHAB PROTOCOLS.  This is useless for survivors. Ignoring spasticity is the height of incompetence since 30% of survivors have it. The idea is to leave no survivor behind. 

Task-oriented Motor Learning in Upper Extremity Rehabilitation Post Stroke 

First Published August 27, 2019 Research Article

Background: 
 Upper extremity deficits are the most popular symptoms following stroke. Task-oriented training has the ability to increase motor area excitability in the brain, which can stimulate the recovery of motor control.
Objective: 
This study was aimed to examine the efficiency of the task-oriented approach on paretic upper extremity following a stroke, and to identify efficient treatment dosage in those populations.
Method: We searched through PubMed, Scopus, Physiotherapy Evidence Database (PEDro), National Rehabilitation Information (REHABDATA), and Web of Science databases. Randomized clinical trials (RCTs) and pseudo-RCTs those investigating upper extremity in patients with stroke published in English language were selected. Different scales and measurement methods to assess range of motion, strength, spasticity, and upper extremity function were considered. The quality assessment of included articles was evaluated utilizing the PEDro scale. Effect sizes were calculated.
Results: 
Six RCTs were included in the present study. The quality assessment for included studies ranged from 6 to 8 with 6.5 as a median. A total of 456 post-stroke patients, 41.66% of which were women, were included in all studies. The included studies demonstrated a meaningful influence of task-oriented training intervention on the hemiplegic upper limb motor functions but not spasticity post-stroke.
Conclusion: 
 Task-oriented training does not produce a superior effect than other conventional physical therapy interventions in treating upper extremity in patients with stroke. There is no evidence supporting the beneficial effect of task-oriented on spasticity. Task-oriented training with the following dosage 30 to 90 minutes/session, 2 to 3 sessions weekly for 6 to 10 weeks may improve(Useless) motor function and strength of paretic upper extremity post-stroke.

Saturday, September 1, 2018

Using priming to promote neuroplasticity and motor learning post-stroke

In your Aim 1 you already have a high functioning survivor selected, high intensity walking is not normally possible. It took me years to get to that point. 
http://dspace.udel.edu/handle/19716/23718

Author: Li, Xin
Citable URI: http://udspace.udel.edu/handle/19716/23718
Advisor: Morton, Susanne M.; Reisman, Darcy S.
Publisher: University of Delaware
Date Issued: 2018
Abstract: The majority of stroke survivors experience persistent motor impairments even with rehabilitation treatments. An underlying mechanism for this is the decreased motor cortical excitability in the lesioned hemisphere after stroke. Priming techniques, such as acute exercise and transcranial direct current stimulation (tDCS), can increase motor cortical excitability and enhance motor learning in healthy individuals. But whether they have the same effects in people with stroke is unclear. Selective serotonin-reuptake inhibitors, a type of antidepressant medication, can change motor cortical excitability in healthy individuals and in acute stroke survivors. Moreover, they can interact with tDCS, changing the effects of tDCS in healthy individuals. Given that up to 30% of stroke survivors take antidepressant medications, this is an important factor to consider when evaluating the effects of tDCS in stroke. The overall purpose of this dissertation was to investigate the neurophysiological effects of exercise priming and tDCS (with chronic antidepressant intake as a factor), and to investigate the effects of tDCS on locomotor learning in people with chronic stroke. ☐ In Aim 1, we showed that exercise priming, in the form of 5 minutes of high-intensity walking, induced increased motor cortical excitability in the lesioned hemisphere, as measured in a resting upper extremity muscle. This finding is significant because it provides evidence on the effectiveness of a clinically feasible exercise priming paradigm to induce broad excitability changes in the brain. ☐ In Aim 2, we showed that stroke survivors taking antidepressant medications had higher motor cortical excitability in the non-lesioned hemisphere compared to those not on antidepressants. We also found that application of anodal tDCS as a primer over the lesioned hemisphere produced differential effects on excitability in the unstimulated, non-lesioned hemisphere, depending on antidepressant-taking status. In antidepressant-takers, motor cortical excitability in the non-lesioned hemisphere increased, while it decreased compared to sham in those not taking antidepressants. These findings draw attention to the fact that stroke survivors may not respond in the same way to tDCS as healthy individuals, and that antidepressants, and potentially other medications and stroke-related factors, must be considered and their effects investigated before providing tDCS as a clinical treatment. ☐ Finally,
in Aim 3, we showed that anodal tDCS over the lesioned hemisphere did not have any effect on split-belt treadmill locomotor learning and retention in chronic stroke survivors. We speculate that split-belt adaptation may not be sensitive to modulation by tDCS. Future studies should investigate whether tDCS affects other types of locomotor learning. ☐ Overall, this work demonstrates the potential of exercise priming for stroke recovery, and highlights the complexity of tDCS usage in people with chronic stroke. Future studies should focus on how individual differences affect priming in stroke.
URI: http://udspace.udel.edu/handle/19716/23718

Tuesday, April 18, 2017

Strength of ~20-Hz Rebound and Motor Recovery After Stroke

No clue what use this is to your recovery. A great stroke association president would get from every researcher and research paper specifics on how the knowledge acquired can be used to help stroke recovery.  Right now stroke survivors have to guess on what the interventions look like. Having to do that is pure stupidity on the part of our stroke medical professionals. 
http://journals.sagepub.com/doi/abs/10.1177/1545968316688795
First Published February 4, 2017


Background. Stroke is a major cause of disability worldwide, and effective rehabilitation is crucial to regain skills for independent living. Recently, novel therapeutic approaches manipulating the excitatory-inhibitory balance of the motor cortex have been introduced to boost recovery after stroke. However, stroke-induced neurophysiological changes of the motor cortex may vary despite of similar clinical symptoms. Therefore, better understanding of excitability changes after stroke is essential when developing and targeting novel therapeutic approaches.  
Objective and Methods. We identified recovery-related alterations in motor cortex excitability after stroke using magnetoencephalography. Dynamics (suppression and rebound) of the ~20-Hz motor cortex rhythm were monitored during passive movement of the index finger in 23 stroke patients with upper limb paresis at acute phase, 1 month, and 1 year after stroke.  
Results. After stroke, the strength of the ~20-Hz rebound to stimulation of both impaired and healthy hand was decreased with respect to the controls in the affected (AH) and unaffected (UH) hemispheres, and increased during recovery. Importantly, the rebound strength was lower than that of the controls in the AH and UH also to healthy-hand stimulation despite of intact afferent input. In the AH, the rebound strength to impaired-hand stimulation correlated with hand motor recovery. Conclusions. Motor cortex excitability is increased bilaterally after stroke and decreases concomitantly with recovery. Motor cortex excitability changes are related to both alterations in local excitatory-inhibitory circuits and changes in afferent input. Fluent sensorimotor integration, which is closely coupled with excitability changes, seems to be a key factor for motor recovery.

Sunday, February 5, 2017

Strength of ~20-Hz Rebound and Motor Recovery After Stroke

No clue what this means. Only 57 references to support it that your doctor should know all about. 

Strength of ~20-Hz Rebound and Motor Recovery After Stroke

http://journals.sagepub.com/doi/abs/10.1177/1545968316688795
First Published February 4, 2017 research-article

Background
 Stroke is a major cause of disability worldwide, and effective rehabilitation is crucial to regain skills for independent living. Recently, novel therapeutic approaches manipulating the excitatory-inhibitory balance of the motor cortex have been introduced to boost recovery after stroke. However, stroke-induced neurophysiological changes of the motor cortex may vary despite of similar clinical symptoms. Therefore, better understanding of excitability changes after stroke is essential when developing and targeting novel therapeutic approaches.  
Objective and Methods
We identified recovery-related alterations in motor cortex excitability after stroke using magnetoencephalography. Dynamics (suppression and rebound) of the ~20-Hz motor cortex rhythm were monitored during passive movement of the index finger in 23 stroke patients with upper limb paresis at acute phase, 1 month, and 1 year after stroke.  
Results
 After stroke, the strength of the ~20-Hz rebound to stimulation of both impaired and healthy hand was decreased with respect to the controls in the affected (AH) and unaffected (UH) hemispheres, and increased during recovery. Importantly, the rebound strength was lower than that of the controls in the AH and UH also to healthy-hand stimulation despite of intact afferent input. In the AH, the rebound strength to impaired-hand stimulation correlated with hand motor recovery. 

Conclusions. Motor cortex excitability is increased bilaterally after stroke and decreases concomitantly with recovery. Motor cortex excitability changes are related to both alterations in local excitatory-inhibitory circuits and changes in afferent input. Fluent sensorimotor integration, which is closely coupled with excitability changes, seems to be a key factor for motor recovery.