Posts Tagged Motor recovery

[Abstract] Gross Motor AbiLity predictS Response to upper extremity rehabilitation in chronic stroke  

Abstract

The majority of rehabilitation research focuses on the comparative effectiveness of different interventions in groups of patients, while much less is currently known regarding individual factors that predict response to rehabilitation. In a recent article, authors presented a prognostic model to identify the sensorimotor characteristics predictive of the extent of motor recovery after Constraint-Induced Movement (CI) therapy amongst individuals with chronic mild-to-moderate motor deficit using the enhanced probabilistic neural network (EPNN). This follow-up paper examines which participant characteristics are robust predictors of rehabilitation response irrespective of the training modality. To accomplish this, EPNN was first applied to predict treatment response amongst individuals who received a virtual-reality gaming intervention (utilizing the same enrollment criteria as the prior study). The combinations of predictors that yield high predictive validity for both therapies, using their respective datasets, were then identified. High predictive classification accuracy was achieved for both the gaming (94.7%) and combined datasets (94.5%). Though CI therapy employed primarily fine-motor training tasks and the gaming intervention emphasized gross-motor practice, larger improvements in gross motor function were observed within both datasets. Poorer gross motor ability at pre-treatment predicted better rehabilitation response in both the gaming and combined datasets. The conclusion of this research is that for individuals with chronic mild-to-moderate upper extremity hemiparesis, residual deficits in gross motor function are highly responsive to motor restorative interventions, irrespective of the modality of training.

Source: Gross Motor AbiLity predictS Response to upper extremity rehabilitation in chronic stroke – ScienceDirect

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[Abstract+References] High-Intensity Chronic Stroke Motor Imagery Neurofeedback Training at Home: Three Case Reports 

Motor imagery (MI) with neurofeedback has been suggested as promising for motor recovery after stroke. Evidence suggests that regular training facilitates compensatory plasticity, but frequent training is difficult to integrate into everyday life. Using a wireless electroencephalogram (EEG) system, we implemented a frequent and efficient neurofeedback training at the patients’ home. Aiming to overcome maladaptive changes in cortical lateralization patterns we presented a visual feedback, representing the degree of contralateral sensorimotor cortical activity and the degree of sensorimotor cortex lateralization. Three stroke patients practiced every other day, over a period of 4 weeks. Training-related changes were evaluated on behavioral, functional, and structural levels. All 3 patients indicated that they enjoyed the training and were highly motivated throughout the entire training regime. EEG activity induced by MI of the affected hand became more lateralized over the course of training in all three patients. The patient with a significant functional change also showed increased white matter integrity as revealed by diffusion tensor imaging, and a substantial clinical improvement of upper limb motor functions. Our study provides evidence that regular, home-based practice of MI neurofeedback has the potential to facilitate cortical reorganization and may also increase associated improvements of upper limb motor function in chronic stroke patients.

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5. Cicinelli P, Marconi B, Zaccagnini M, Pasqualetti P, Filippi MM, Rossini PM. Imagery-induced cortical excitability changes in stroke: a transcranial magnetic stimulation study. Cereb Cortex. 2006;16:247253. Google Scholar CrossRef, Medline
6. Langhorne P, Coupar F, Pollock A. Motor recovery after stroke: a systematic review. Lancet Neurol. 2009;8:741754. Google Scholar CrossRef, Medline
7. Page SJ, Levine P, Leonard AC. Effects of mental practice on affected limb use and function in chronic stroke. Arch Phys Med Rehabil. 2005;86:399402. Google Scholar CrossRef, Medline
8. Crosbie JH, McDonough SM, Gilmore DH, Wiggam MI. The adjunctive role of mental practice in the rehabilitation of the upper limb after hemiplegic stroke: a pilot study. Clin Rehabil. 2004;18:6068. Google Scholar Link
9. Liu KP, Chan CC, Lee TM, Hui-Chan CW. Mental imagery for promoting relearning for people after stroke: a randomized controlled trial. Arch Phys Med Rehabil. 2004;85:14031408. Google Scholar CrossRef, Medline
10. Grosse-Wentrup M, Mattia D, Oweiss K. Using brain-computer interfaces to induce neural plasticity and restore function. J Neural Eng. 2011;8:025004. Google Scholar CrossRef
11. Buch E, Weber C, Cohen LG, . Think to move: a neuromagnetic brain-computer interface (BCI) system for chronic stroke. Stroke. 2008;39:910917. Google Scholar CrossRef, Medline
12. Broetz D, Braun C, Weber C, Soekadar SR, Caria A, Birbaumer N. Combination of brain-computer interface training and goal-directed physical therapy in chronic stroke: a case report. Neurorehabil Neural Repair. 2010;24:674679. Google Scholar Link
13. Caria A, Weber C, Brötz D, . Chronic stroke recovery after combined BCI training and physiotherapy: a case report. Psychophysiology. 2011;48:578582. Google Scholar CrossRef, Medline
14. Ramos-Murguialday A, Broetz D, Rea M, . Brain-machine interface in chronic stroke rehabilitation: a controlled study. Ann Neurol. 2013;74:100108. Google Scholar CrossRef, Medline
15. Shindo K, Kawashima K, Ushiba J, . Effects of neurofeedback training with an electroencephalogram-based brain-computer interface for hand paralysis in patients with chronic stroke: a preliminary case series study. J Rehabil Med. 2011;43:951957. Google Scholar CrossRef, Medline
16. Pichiorri F, Morone G, Petti M, . Brain-computer interface boosts motor imagery practice during stroke recovery. Ann Neurol. 2015;77:851865. Google Scholar CrossRef, Medline
17. Zich C, Debener S, Kranczioch C, Bleichner MG, Gutberlet I, De Vos M. Real-time EEG feedback during simultaneous EEG-fMRI identifies the cortical signature of motor imagery. Neuroimage. 2015;114:438447. Google Scholar CrossRef, Medline
18. Debener S, Minow F, Emkes R, Gandras K, De Vos M. How about taking a low-cost, small, and wireless EEG for a walk? Psychophysiology. 2012;49:16171621. Google Scholar CrossRef, Medline
19. Kranczioch C, Zich C, Schierholz I, Sterr A. Mobile EEG and its potential to promote the theory and application of imagery-based motor rehabilitation. Int J Psychophysiol. 2014;91:1015. Google Scholar CrossRef, Medline
20. De Vos M, Kroesen M, Emkes R, Debener S. P300 speller BCI with a mobile EEG system: comparison to a traditional amplifier. J Neural Eng. 2014;11:036008. Google Scholar CrossRef
21. Debener S, Emkes R, De Vos M, Bleichner M. Unobtrusive ambulatory EEG using a smartphone and flexible printed electrodes around the ear. Sci Rep. 2015;5:16743. Google Scholar CrossRef, Medline
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24. Ward NS, Brown MM, Thompson AJ, Frackowiak RSJ. Neural correlates of motor recovery after stroke: a longitudinal fMRI study. Brain. 2003;126:24762496. Google Scholar CrossRef, Medline
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28. Feydy A, Carlier R, Roby-Brami A, . Longitudinal study of motor recovery after stroke: recruitment and focusing of brain activation. Stroke. 2002;33:16101617. Google Scholar CrossRef, Medline
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33. Zich C, De Vos M, Kranczioch C, Debener S. Wireless EEG with individualized channel layout enables efficient motor imagery training. Clin Neurophysiol. 2015;126:698710. Google Scholar CrossRef, Medline
34. Blankertz B, Losch F, Krauledat M, Dornhege G, Curio G, Müller K-R. The Berlin brain-computer interface: accurate performance from first-session in BCI-naïve subjects. IEEE Trans Biomed Eng. 2008;55:24522462. Google Scholar CrossRef, Medline
35. Blokland Y, Spyrou L, Thijssen D, . Combined EEG-fNIRS decoding of motor attempt and imagery for brain switch control: an offline study in patients with tetraplegia. IEEE Trans Neural Syst Rehabil Eng. 2014;22:222229. Google Scholar CrossRef, Medline
36. Zich C, Debener S, Kranczioch C, Chen L-C, De Vos M. Lateralization patterns for movement execution and imagination investigated with concurrent EEG-fMRI and EEG-fNRIS. In: Müller-Putz GR, Huggins JE, Steyrl D, eds. Proceedings of the Sixth International Brain-Computer Interface Meeting: BCI Past, Present, and Future, Pacific Grove, California, USA. Graz, Austria: Verlag der Technischen Universität Graz; 2016:101. Google Scholar
37. Zich C, Debener S, Thoene A-K, Chen L-C, Kranczioch C. Simultaneous EEG-fNIRS reveals how age and feedback affect motor imagery signatures. Neurobiol Aging. 2017;49:183197. Google Scholar CrossRef, Medline

Source: High-Intensity Chronic Stroke Motor Imagery Neurofeedback Training at Home: Three Case ReportsClinical EEG and Neuroscience – Catharina Zich, Stefan Debener, Clara Schweinitz, Annette Sterr, Joost Meekes, Cornelia Kranczioch, 2017

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[Abstract] Effects of mirror therapy combined with neuromuscular electrical stimulation on motor recovery of lower limbs and walking ability of patients with stroke: a randomized controlled study 

To investigate the effectiveness of mirror therapy combined with neuromuscular electrical stimulation in promoting motor recovery of the lower limbs and walking ability in patients suffering from foot drop after stroke.

Randomized controlled study.

Inpatient rehabilitation center of a teaching hospital.

Sixty-nine patients with foot drop.

Patients were randomly divided into three groups: control, mirror therapy, and mirror therapy + neuromuscular electrical stimulation. All groups received interventions for 0.5 hours/day and five days/week for four weeks.

10-Meter walk test, Brunnstrom stage of motor recovery of the lower limbs, Modified Ashworth Scale score of plantar flexor spasticity, and passive ankle joint dorsiflexion range of motion were assessed before and after the four-week period.

After four weeks of intervention, Brunnstrom stage (P = 0.04), 10-meter walk test (P < 0.05), and passive range of motion (P < 0.05) showed obvious improvements between patients in the mirror therapy and control groups. Patients in the mirror therapy + neuromuscular electrical stimulation group showed better results than those in the mirror therapy group in the 10-meter walk test (P < 0.05). There was no significant difference in spasticity between patients in the two intervention groups. However, compared with patients in the control group, patients in the mirror therapy + neuromuscular electrical stimulation group showed a significant decrease in spasticity (P < 0.001).

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5. Samuelkamaleshkumar S, Reethajanetsureka S, Pauljebaraj P, Mirror therapy enhances motor performance in the paretic upper limb after stroke: a pilot randomized controlled trial. Arch Phys Med Rehabil 2014; 95: 20002005. Google Scholar CrossRef, Medline
6. Sousa Nanji L, Torres Cardoso A, Costa J, Analysis of the Cochrane review: interventions for improving upper limb function after stroke. Cochrane Database Syst Rev 2014; 11: CD010820; Acta Med Port 2015; 28: 551553. Google Scholar
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8. Stein C, Fritsch CG, Robinson C, Effects of electrical stimulation in spastic muscles after stroke: systematic review and meta-analysis of randomized controlled trials. Stroke 2015; 46: 21972205. Google Scholar CrossRef, Medline
9. Knutson JS, Fu MJ, Sheffler LR, Neuromuscular electrical stimulation for motor restoration in hemiplegia. Phys Med Rehabil Clin N Am 2015; 26: 729745. Google Scholar CrossRef, Medline
10. Sabut SK, Sikdar C, Kumar R, Functional electrical stimulation of dorsiflexor muscle: effects on dorsiflexor strength, plantarflexor spasticity, and motor recovery in stroke patients. NeuroRehabilitation 2011; 29: 393400. Google Scholar Medline
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14. Yun GJ, Chun MH, Park JY, The synergic effects of mirror therapy and neuromuscular electrical stimulation for hand function in stroke patients. Ann Rehabil Med 2011; 35: 316321. Google Scholar CrossRef, Medline
15. Lee D, Lee G, Jeong J. Mirror Therapy with Neuromuscular Electrical Stimulation for improving motor function of stroke survivors: a pilot randomized clinical study. Technol Health Care 2016; 24: 503511. Google Scholar CrossRef, Medline
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Source: Effects of mirror therapy combined with neuromuscular electrical stimulation on motor recovery of lower limbs and walking ability of patients with stroke: a randomized controlled studyClinical Rehabilitation – Qun Xu, Feng Guo, Hassan M Abo Salem, Hong Chen, Xiaolin Huang, 2017

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[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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