Posts Tagged Motor recovery

[Abstract] Supporting Stroke Motor Recovery Through a Mobile Application: A Pilot Study

Abstract

Neuroplasticity and motor learning are promoted with repetitive movement, appropriate challenge, and performance feedback. ARMStrokes, a smartphone application, incorporates these qualities to support motor recovery. Engaging exercises are easily accessible for improved compliance. In a multiple-case, mixed-methods pilot study, the potential of this technology for stroke motor recovery was examined. Exercises calibrated to the participant’s skill level targeted forearm, elbow, and shoulder motions for a 6-wk protocol. Visual, auditory, and vibration feedback promoted self-assessment. Pre- and posttest data from 6 chronic stroke survivors who used the app in different ways (i.e., to measure active or passive motion, to track endurance) demonstrated improvements in accuracy of movements, fatigue, range of motion, and performance of daily activities. Statistically significant changes were not obtained with this pilot study. Further study on the efficacy of this technology is supported.

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Source: Supporting Stroke Motor Recovery Through a Mobile Application: A Pilot Study | American Journal of Occupational Therapy

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[WEB SITE] Spasticity, Motor Recovery, and Neural Plasticity after Stroke – Full Text

Spasticity and weakness (spastic paresis) are the primary motor impairments after stroke and impose significant challenges for treatment and patient care. Spasticity emerges and disappears in the course of complete motor recovery. Spasticity and motor recovery are both related to neural plasticity after stroke. However, the relation between the two remains poorly understood among clinicians and researchers. Recovery of strength and motor function is mainly attributed to cortical plastic reorganization in the early recovery phase, while reticulospinal (RS) hyperexcitability as a result of maladaptive plasticity, is the most plausible mechanism for post-stroke spasticity. It is important to differentiate and understand that motor recovery and spasticity have different underlying mechanisms. Facilitation and modulation of neural plasticity through rehabilitative strategies, such as early interventions with repetitive goal-oriented intensive therapy, appropriate non-invasive brain stimulation, and pharmacological agents, are the key to promote motor recovery. Individualized rehabilitation protocols could be developed to utilize or avoid the maladaptive plasticity, such as RS hyperexcitability, in the course of motor recovery. Aggressive and appropriate spasticity management with botulinum toxin therapy is an example of how to create a transient plastic state of the neuromotor system that allows motor re-learning and recovery in chronic stages.

Introduction

According to the CDC, approximately 800,000 people have a stroke every year in the United States. The continued care of seven million stroke survivors costs the nation approximately $38.6 billion annually. Spasticity and weakness (i.e., spastic paresis) are the primary motor impairments and impose significant challenges for patient care. Weakness is the primary contributor to impairment in chronic stroke (1). Spasticity is present in about 20–40% stroke survivors (2). Spasticity not only has downstream effects on the patient’s quality of life but also lays substantial burdens on the caregivers and society (2).

Clinically, poststroke spasticity is easily recognized as a phenomenon of velocity-dependent increase in tonic stretch reflexes (“muscle tone”) with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex (3). Though underlying mechanisms of spasticity remain poorly understood, it is well accepted that there is hyperexcitability of the stretch reflex in spasticity (47). Accumulated evidence from animal (8) and human studies (918) supports supraspinal origins of stretch reflex hyperexcitability. In particular, reticulospinal (RS) hyperexcitability resulted from loss of balanced inhibitory, and excitatory descending RS projections after stroke is the most plausible mechanism for poststroke spasticity (19). On the other hand, animal studies have strongly supported the possible role of RS pathways in motor recovery (2036), while recent studies with stroke survivors have demonstrated that RS pathways may not always be beneficial (3738). The relation between spasticity and motor recovery and the role of plastic changes after stroke in this relation, particularly RS hyperexcitability, remain poorly understood among clinicians and researchers. Thus, management of spasticity and facilitation of motor recovery remain clinical challenges. This review is organized into the following sessions to understand this relation and its implication in clinical management.

• Poststroke spasticity and motor recovery are mediated by different mechanisms

• Motor recovery are mediated by cortical plastic reorganizations (spontaneous or via intervention)

• Reticulospinal hyperexcitability as a result of maladaptive plastic changes is the most plausible mechanism for spasticity

• Possible roles of RS hyperexcitability in motor recovery

• An example of spasticity reduction for facilitation of motor recovery […]

Continue —> Frontiers | Spasticity, Motor Recovery, and Neural Plasticity after Stroke | Neurology

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[ARTICLE] Spasticity, Motor Recovery, and Neural Plasticity after Stroke – Full Text

Abstract

Spasticity and weakness (spastic paresis) are the primary motor impairments after stroke and impose significant challenges for treatment and patient care. Spasticity emerges and disappears in the course of complete motor recovery. Spasticity and motor recovery are both related to neural plasticity after stroke. However, the relation between the two remains poorly understood among clinicians and researchers.

Recovery of strength and motor function is mainly attributed to cortical plastic reorganization in the early recovery phase, while reticulospinal (RS) hyperexcitability as a result of maladaptive plasticity, is the most plausible mechanism for poststroke spasticity. It is important to differentiate and understand that motor recovery and spasticity have different underlying mechanisms. Facilitation and modulation of neural plasticity through rehabilitative strategies, such as early interventions with repetitive goal-oriented intensive therapy, appropriate non-invasive brain stimulation, and pharmacological agents, are the keys to promote motor recovery.

Individualized rehabilitation protocols could be developed to utilize or avoid the maladaptive plasticity, such as RS hyperexcitability, in the course of motor recovery. Aggressive and appropriate spasticity management with botulinum toxin therapy is an example of how to create a transient plastic state of the neuromotor system that allows motor re-learning and recovery in chronic stages.

Introduction

According to the CDC, approximately 800,000 people have a stroke every year in the United States. The continued care of seven million stroke survivors costs the nation approximately $38.6 billion annually. Spasticity and weakness (i.e., spastic paresis) are the primary motor impairments and impose significant challenges for patient care. Weakness is the primary contributor to impairment in chronic stroke (1). Spasticity is present in about 20–40% stroke survivors (2). Spasticity not only has downstream effects on the patient’s quality of life but also lays substantial burdens on the caregivers and society (2).

Clinically, poststroke spasticity is easily recognized as a phenomenon of velocity-dependent increase in tonic stretch reflexes (“muscle tone”) with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex (3). Though underlying mechanisms of spasticity remain poorly understood, it is well accepted that there is hyperexcitability of the stretch reflex in spasticity (47). Accumulated evidence from animal (8) and human studies (918) supports supraspinal origins of stretch reflex hyperexcitability. In particular, reticulospinal (RS) hyperexcitability resulted from loss of balanced inhibitory, and excitatory descending RS projections after stroke is the most plausible mechanism for poststroke spasticity (19). On the other hand, animal studies have strongly supported the possible role of RS pathways in motor recovery (2036), while recent studies with stroke survivors have demonstrated that RS pathways may not always be beneficial (3738). The relation between spasticity and motor recovery and the role of plastic changes after stroke in this relation, particularly RS hyperexcitability, remain poorly understood among clinicians and researchers. Thus, management of spasticity and facilitation of motor recovery remain clinical challenges. This review is organized into the following sessions to understand this relation and its implication in clinical management.

  • Poststroke spasticity and motor recovery are mediated by different mechanisms
  • Motor recovery are mediated by cortical plastic reorganizations (spontaneous or via intervention)
  • Reticulospinal hyperexcitability as a result of maladaptive plastic changes is the most plausible mechanism for spasticity
  • Possible roles of RS hyperexcitability in motor recovery
  • An example of spasticity reduction for facilitation of motor recovery

Continue —> Spasticity, Motor Recovery, and Neural Plasticity after Stroke

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[ARTICLE] Spasticity, Motor Recovery, and Neural Plasticity after Stroke – Full Text

Spasticity and weakness (spastic paresis) are the primary motor impairments after stroke and impose significant challenges for treatment and patient care. Spasticity emerges and disappears in the course of complete motor recovery. Spasticity and motor recovery are both related to neural plasticity after stroke. However, the relation between the two remains poorly understood among clinicians and researchers. Recovery of strength and motor function is mainly attributed to cortical plastic reorganization in the early recovery phase, while reticulospinal (RS) hyperexcitability as a result of maladaptive plasticity, is the most plausible mechanism for post-stroke spasticity. It is important to differentiate and understand that motor recovery and spasticity have different underlying mechanisms. Facilitation and modulation of neural plasticity through rehabilitative strategies, such as early interventions with repetitive goal-oriented intensive therapy, appropriate non-invasive brain stimulation, and pharmacological agents, are the key to promote motor recovery. Individualized rehabilitation protocols could be developed to utilize or avoid the maladaptive plasticity, such as RS hyperexcitability, in the course of motor recovery. Aggressive and appropriate spasticity management with botulinum toxin therapy is an example of how to create a transient plastic state of the neuromotor system that allows motor re-learning and recovery in chronic stages.

Introduction

According to the CDC, approximately 800,000 people have a stroke every year in the United States. The continued care of seven million stroke survivors costs the nation approximately $38.6 billion annually. Spasticity and weakness (i.e., spastic paresis) are the primary motor impairments and impose significant challenges for patient care. Weakness is the primary contributor to impairment in chronic stroke (1). Spasticity is present in about 20–40% stroke survivors (2). Spasticity not only has downstream effects on the patient’s quality of life but also lays substantial burdens on the caregivers and society (2).

Clinically, poststroke spasticity is easily recognized as a phenomenon of velocity-dependent increase in tonic stretch reflexes (“muscle tone”) with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex (3). Though underlying mechanisms of spasticity remain poorly understood, it is well accepted that there is hyperexcitability of the stretch reflex in spasticity (47). Accumulated evidence from animal (8) and human studies (918) supports supraspinal origins of stretch reflex hyperexcitability. In particular, reticulospinal (RS) hyperexcitability resulted from loss of balanced inhibitory, and excitatory descending RS projections after stroke is the most plausible mechanism for poststroke spasticity (19). On the other hand, animal studies have strongly supported the possible role of RS pathways in motor recovery (2036), while recent studies with stroke survivors have demonstrated that RS pathways may not always be beneficial (37, 38). The relation between spasticity and motor recovery and the role of plastic changes after stroke in this relation, particularly RS hyperexcitability, remain poorly understood among clinicians and researchers. Thus, management of spasticity and facilitation of motor recovery remain clinical challenges. This review is organized into the following sessions to understand this relation and its implication in clinical management.

• Poststroke spasticity and motor recovery are mediated by different mechanisms

• Motor recovery are mediated by cortical plastic reorganizations (spontaneous or via intervention)

• Reticulospinal hyperexcitability as a result of maladaptive plastic changes is the most plausible mechanism for spasticity

• Possible roles of RS hyperexcitability in motor recovery

• An example of spasticity reduction for facilitation of motor recovery

Continue —> Frontiers | Spasticity, Motor Recovery, and Neural Plasticity after Stroke | Stroke

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[ARTICLE] Task-Specific Motor Rehabilitation Therapy After Stroke Improves Performance in a Different Motor Task: Translational Evidence – Full Text

Abstract

While the stroke survivor with a motor deficit strives for recovery of all aspects of daily life movements, neurorehabilitation training is often task specific and does not generalize to movements other than the ones trained. In rodent models of post-stroke recovery, this problem is poorly investigated as the training task is often the same as the one that measures motor function. The present study investigated whether motor training by pellet reaching translates into enhancement of different motor functions in rats after stroke. Adult rats were subjected to 60-min middle cerebral artery occlusion (MCAO). Five days after stroke, animals received either training consisting of 7 days of pellet reaching with the affected forelimb (n = 18) or no training (n = 18). Sensorimotor deficits were assessed using the sticky tape test and a composite neuroscore. Infarct volumes were measured by T2-weighted MRI on day 28. Both groups of rats showed similar lesion volume and forelimb impairment after stroke. Trained animals improved in the sticky tape test after day 7 post-stroke reaching peak performance on day 14. More reaching attempts during rehabilitation were associated with a better performance in the sticky tape removal time. Task-oriented motor training generalizes to other motor functions after experimental stroke. Training intensity correlates with recovery.

Introduction

About 60% of stroke survivors suffer from motor disability 6 months after stroke [1, 2]. By training of motor skills, rehabilitation aims to maximize patients’ functional independence and quality of life. The physiological mechanisms of training interventions are incompletely understood, especially their generalization, i.e., how and how much improvement in the specific task trained generalizes to other movements. These mechanisms need to be explored in animal models to optimize and develop treatments.

In rodents, post-stroke motor rehabilitation by pellet-reaching training improves pellet-reaching success [3]. This is accompanied by reorganization in motor cortex regions controlling the affected limb [4], e.g., an increase in dendritic complexity [5, 6]. The issue of generalization of trained to other tasks has not been addressed in animal models of post-stroke recovery.

The present study investigated whether motor training by pellet reaching translates into improvement in other motor tasks in a rat stroke model. The transient middle cerebral artery occlusion (MCAO) was chosen for stroke induction, because the lesion is not confined to the motor cortex but has a variable spread towards adjacent cortical and subcortical areas, similar to human stroke.

Continue —> Task-Specific Motor Rehabilitation Therapy After Stroke Improves Performance in a Different Motor Task: Translational Evidence | SpringerLink

Fig. 1 Flow of the experiments. a Experimental schedule. b Photos illustrating rats during pellet-reaching training. c Representative MRI-T2 images from the rehabilitation and no rehabilitation group 28 days after MCAO

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[Abstract] Quantitative EEG for Predicting Upper-limb Motor Recovery in Chronic Stroke Robot-assisted Rehabilitation – IEEE Xplore Document

Abstract:

Stroke is a leading cause for adult disability, which in many cases causes motor deficits. Despite the developments in motor rehabilitation techniques, recovery of upper limb functions after stroke is limited and heterogeneous in terms of outcomes, and knowledge of important factors that may affect the outcome of the therapy is necessary to make a reasonable prediction for individual patients.
In this study, we assessed the relationship between quantitative electroencephalographic (QEEG) measures and the motor outcome in chronic stroke patients that underwent a robot-assisted rehabilitation program to evaluate the utility of QEEG indices to predict motor recovery. For this purpose, we acquired resting-state electroencephalographic signals from which the Power Ratio Index (PRI), Delta/Alpha Ratio (DAR), and Brain Symmetry Index (BSI) were calculated. The outcome of the motor rehabilitation was evaluated using upper-limb section of the Fugl-Meyer Assessment.
We found that PRI was significantly correlated with the motor recovery, suggesting that this index may provide useful information to predict the rehabilitation outcome.

Source: Quantitative EEG for Predicting Upper-limb Motor Recovery in Chronic Stroke Robot-assisted Rehabilitation – IEEE Xplore Document

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[ARTICLE] Anatomical Parameters of tDCS to Modulate the Motor System after Stroke: A Review – Full Text

Transcranial direct current stimulation (tDCS) is a noninvasive brain stimulation method to modulate the local field potential in neural tissue and consequently, cortical excitability. As tDCS is relatively portable, affordable, and accessible, the applications of tDCS to probe brain-behavior connections have rapidly increased in the last ten years. One of the most promising applications is the use of tDCS to modulate excitability in the motor cortex after stroke and promote motor recovery. However, the results of clinical studies implementing tDCS to modulate motor excitability have been highly variable, with some studies demonstrating that as many as 50% or more of patients fail to show a response to stimulation. Much effort has therefore been dedicated to understanding the sources of variability affecting tDCS efficacy. Possible suspects include the placement of the electrodes, task parameters during stimulation, dosing (current amplitude, duration of stimulation, frequency of stimulation), individual states (e.g., anxiety, motivation, attention), and more. In this review, we first briefly review potential sources of variability specific to stroke motor recovery following tDCS. We then examine how the anatomical variability in tDCS placement (e.g., neural target(s) and montages employed) may alter the neuromodulatory effects that tDCS exerts on the post-stroke motor system.

Introduction

Stroke is a neurological deficit induced by the interruption of the blood flow to the brain due to either a vessel occlusion or less frequently an intracerebral hemorrhage (1). Both may induce direct damage of brain tissue at the site of the lesion, along with potential for additional damage in the surrounding tissue, and long-range dysfunction through the interruption of structural and functional pathways in the brain. This also leads to a deregulation of cortical excitability (24) and abnormal interhemispheric interactions. Stroke may thus induce many neurological deficits and could result in death. According to the World Stroke Organization, one out of six people will suffer from a stroke, making stroke a leading cause of adult long-term disability worldwide (57). Importantly, one of the main challenges after stroke is the loss of one’s functional motor abilities. Research suggests that only 12% of stroke survivors achieve complete motor recovery by 6 months after the stroke (8). In addition, older individuals are more vulnerable to stroke and thus the incidence of stroke is expected to continue rising over the next few decades (9, 10). Accordingly, there is a need to find new potential therapeutic tools to enhance post-stroke motor recovery. Rebalancing interhemispheric interactions and/or restoring excitability in the ipsilesional hemisphere is thought to be beneficial for post-stroke motor recovery (1117). Thus, techniques aimed at restoring functional brain activity are a promising way to enhance neural recovery after injury. Most of the literature on stroke recovery focuses on the recovery of upper limb motor function. Since the neural mechanisms involved in motor recovery of upper versus lower limbs may differ, in this review, we focus only on upper limb motor recovery after stroke.

Non-invasive brain stimulation (NIBS) techniques show strong therapeutic potential for post-stroke motor rehabilitation due to their ability to modulate cortical excitability (1821). In particular, transcranial direct current stimulation (tDCS) has emerged as a viable neurorehabilitation tool due to its limited side-effects (22, 23) and safety [e.g., no known risk of neural damage or induction of seizures, as can be found in other NIBS methods like repetitive transcranial magnetic stimulation (rTMS) (24, 25)]. In addition, tDCS stimulators are commercially available and relatively affordable, on the order of several hundred dollars, and application of tDCS is considered relatively simple. By delivering a low-intensity direct current (between 0.5 and 2 mA) to the scalp via two saline-soaked electrodes—an anode and a cathode—tDCS can modulate the transmembrane potential of neurons, modifying cortical excitability and inducing changes in neural plasticity (see Figure 1) (2630). In addition, recent work has attempted to enhance the spatial resolution of tDCS stimulation, using a new technique called high-definition tDCS (HD-tDCS) (3134). With this technique, brain regions are more focally targeted using arrays of smaller electrodes arranged on the scalp (Figure 2), using multiple anodes and cathodes (see section on Focal versus Broad Stimulation for a more detailed description). Recently, there has also been increased interest in combining tDCS with imaging methods, such as fMRI or EEG, in order to better understand the local and global effects of tDCS on neural plasticity throughout the brain (35). These methods have all contributed to the growth and interest of tDCS as a viable neuromodulatory method for stroke.

Figure 1. Conventional transcranial direct current stimulation (tDCS) setup. The conventional tDCS setup requires a small tDCS stimulator with a 9-V battery, two saline-soaked sponge electrodes and one rubber band to hold the electrodes in place on the head. While there are many options for convention tDCS, the unit shown here is the Chattanooga Iontophoresis device.

Continue —> Frontiers | Anatomical Parameters of tDCS to Modulate the Motor System after Stroke: A Review | Movement Disorders

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[ARTICLE] Can Neurological Biomarkers of Brain Impairment Be Used to Predict Poststroke Motor Recovery? – Full Text

Background. There is growing interest to establish recovery biomarkers, especially neurological biomarkers, in order to develop new therapies and prediction models for the promotion of stroke rehabilitation and recovery. However, there is no consensus among the neurorehabilitation community about which biomarker(s) have the highest predictive value for motor recovery. Objective. To review the evidence and determine which neurological biomarker(s) meet the high evidence quality criteria for use in predicting motor recovery. Methods. We searched databases for prognostic neuroimaging/neurophysiological studies. Methodological quality of each study was assessed using a previously employed comprehensive 15-item rating system. Furthermore, we used the GRADE approach and ranked the overall evidence quality for each category of neurologic biomarker. Results. Seventy-one articles met our inclusion criteria; 5 categories of neurologic biomarkers were identified: diffusion tensor imaging (DTI), transcranial magnetic stimulation (TMS), functional magnetic resonance imaging (fMRI), conventional structural MRI (sMRI), and a combination of these biomarkers. Most studies were conducted with individuals after ischemic stroke in the acute and/or subacute stage (~70%). Less than one-third of the studies (21/71) were assessed with satisfactory methodological quality (80% or more of total quality score). Conventional structural MRI and the combination biomarker categories ranked “high” in overall evidence quality. Conclusions. There were 3 prevalent methodological limitations: (a) lack of cross-validation, (b) lack of minimal clinically important difference (MCID) for motor outcomes, and (c) small sample size. More high-quality studies are needed to establish which neurological biomarkers are the best predictors of motor recovery after stroke. Finally, the quarter-century old methodological quality tool used here should be updated by inclusion of more contemporary methods and statistical approaches.

There is growing interest in establishing stroke recovery biomarkers. Researchers define stroke recovery biomarkers as surrogate indicators of disease state that can have predictive value for recovery or treatment response.1 Specifically, previous studies have suggested that better understanding of neurological biomarkers, derived from brain imaging and neurophysiological assessments, is likely to move stroke rehabilitation research forward.1,2

Recovery biomarkers acquired during the acute and subacute phases (acute—within 1 week after onset; subacute—between 1 week and 3 months after onset) may be vital to set attainable neurorehabilitation goals and to choose proper therapeutic approaches based on the recovery capacity. Furthermore, motor recovery prediction using neurological biomarkers in the chronic phase (more than 3 months after onset) can be useful to determine whether an individual will benefit from specific therapeutic interventions applied after the normal period of rehabilitation has ended. Hence, use of recovery biomarkers is likely to improve customization of physical interventions for individual stroke survivors regarding their capacity for recovery, and to facilitate development of new neurorehabilitation approaches.

There have been fundamental changes in recovery biomarkers from simple clinical behavioral biomarkers to brain imaging and neurophysiological biomarkers. In particular, a number of recent studies have shown that neurologic biomarkers (ie, neuroimaging and/or neurophysiological measures of brain) are more predictive of motor recovery than clinical behavioral biomarkers.35

Although there is some evidence that neurological biomarkers are more valuable as predictors of motor recovery than clinical behavioral biomarkers, there are significant gaps between the published evidence and clinical usage. First, there is no consensus on which specific neurological biomarkers would be best for prediction models.4,6,7 Viable neurological biomarker of motor recovery have evolved from lesion size and location, prevalent in the early 1990s8 to more contemporary complex brain network analysis variables.9 Despite this evolution, there is a paucity of high-level evidence for determining the most critical neurological biomarkers of motor recovery. A number of literature reviews and systematic reviews of studies published since the 1990s aimed to identify the most appropriate biomarkers of motor recovery or functional independence.8,1012 Among these reviews, only one by Schiemanck and colleagues8 assessed the evidence quality of neurologic biomarkers, while many focused on clinical measures (ie, clinical motor and/or functional measures).11 Their review was limited to only 13 studies that employed structural magnetic resonance imaging (sMRI) measures of lesion volume as neurologic biomarkers. Besides lesion volume derived from structural MRI, there are other viable neurological biomarkers of brain impairment. Therefore, this systematic review includes a broad set of relevant biomarkers for consideration as critical predictors for inclusion in motor recovery prediction models.

Furthermore, there is some evidence to suggest that multivariate prediction models that use neurological biomarkers in addition to clinical outcome measures are more accurate than those that use clinical outcome measures alone.2,13 However there is still no consensus about whether incorporating behavioral and neurological predictors in a multimodal prediction model is superior (ie, more accurate) to a univariate model that includes either behavioral or neurological predictors alone.

Taken together, this systematic review has 2 aims. The first is to conduct a critical and systematic comparison of selected studies to determine which neurological biomarker(s) is likely to have sufficient high-level evidence in order to render the most accurate prediction of motor recovery after stroke. The second aim is to identify whether adding clinical measures along with neurological biomarkers in the model improves the accuracy of the model compared to the models that use neurological biomarkers alone.

Continue —> Can Neurological Biomarkers of Brain Impairment Be Used to Predict Poststroke Motor Recovery? A Systematic Review – Aug 08, 2016

Figure

Figure 1. Evidence search strategy diagram.

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[ARTICLE] Using Biophysical Models to Understand the Effect of tDCS on Neurorehabilitation: Searching for Optimal Covariates to Enhance Poststroke Recovery – Full Text

Stroke is a leading cause of worldwide disability, and up to 75% of survivors suffer from some degree of arm paresis. Recently, rehabilitation of stroke patients has focused on recovering motor skills by taking advantage of use-dependent neuroplasticity, where high-repetition of goal-oriented movement is at times combined with non-invasive brain stimulation, such as transcranial direct current stimulation (tDCS). Merging the two approaches is thought to provide outlasting clinical gains, by enhancing synaptic plasticity and motor relearning in the motor cortex primary area. However, this general approach has shown mixed results across the stroke population. In particular, stroke location has been found to correlate with the likelihood of success, which suggests that different patients might require different protocols. Understanding how motor rehabilitation and stimulation interact with ongoing neural dynamics is crucial to optimize rehabilitation strategies, but it requires theoretical and computational models to consider the multiple levels at which this complex phenomenon operate. In this work, we argue that biophysical models of cortical dynamics are uniquely suited to address this problem. Specifically, biophysical models can predict treatment efficacy by introducing explicit variables and dynamics for damaged connections, changes in neural excitability, neurotransmitters, neuromodulators, plasticity mechanisms and repetitive movement, which together can represent brain state, effect of incoming stimulus and movement-induced activity. In this work, we hypothesize that effects of tDCS depend on ongoing neural activity, and that tDCS effects on plasticity may be also related to enhancing inhibitory processes. We propose a model design for each step of this complex system, and highlight strengths and limitations of the different modeling choices within our approach. Our theoretical framework proposes a change in paradigm, where biophysical models can contribute to the future design of novel protocols, in which combined tDCS and motor rehabilitation strategies are tailored to the ongoing dynamics that they interact with, by considering the known biophysical factors recruited by such protocols and their interaction.

Source: Frontiers | Using Biophysical Models to Understand the Effect of tDCS on Neurorehabilitation: Searching for Optimal Covariates to Enhance Poststroke Recovery | Stroke

Figure 1. Diagram of top-down and bottom-up stroke neurorehabilitation strategies. Sensory–motor training and brain stimulation contribute to rehabilitation protocols that exploit neural plasticity. The bottom-up approach includes sensory–motor training, which can be aided by robots, electrical stimulation of the periphery, and constrains. The top-down approaches include methods to stimulate the brain non-invasively.

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[Abstract] Strength of ~20-Hz Rebound and Motor Recovery After Stroke.

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.

Source: Strength of ~20-Hz Rebound and Motor Recovery After Stroke – Feb 04, 2017

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