Archive for category Neuroplasticity

[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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[WEB SITE] Study investigates plasticity of motor representations in patients with brain tumors

Winner of the Brainlab Community Neurosurgery Award, Sandro Krieg, MD, presented his research, Plasticity of Motor Representations in Patients with Brain Lesions: a Navigated TMS Study, during the 2017 American Association of Neurological Surgeons (AANS) Annual Scientific Meeting.

This study investigated the spatial distributions of motor representations in terms of tumor-induced brain plasticity by analyzing navigated transcranial magnetic stimulation (nTMS) motor maps derived from 100 patients with motor eloquently located brain tumors in or adjacent to the precentral gyrus (PrG).

The research evoked 8,774 motor potentials (MEPs) that were elicited in six muscles of the upper and lower extremity by stimulating four gyri in patients with five possible tumor locations. Regarding the MEP frequency of each muscle-gyrus subdivision per patient, the expected frequency was 3.53 (8,774 divided by 100 patients, further divided by six muscles and four gyri). Accordingly, the patient ratio for each subdivision was calculated by defining the per-patient minimum data points as three.

The tumor-location specific patient ratios were higher for frontal tumors in both gyri than for other tumor locations. This suggests that the finger representation reorganization in these frontal gyri, which corresponds to location of dorsal premotor areas, might be due to within-premotor reorganization rather than relocation of motor function from PrG into premotor areas one might expect from the Rolandic tumors. The research indicates that reorganization of the finger motor representations might be limited along the middle-to-dorsal dimension of the dorsal premotor areas (posterior MFG and SFG) and might not cross rostrally from the primary motor cortex (PrG) to the dorsal premotor cortex.

Source: Study investigates plasticity of motor representations in patients with brain tumors

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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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[BLOG POST] How to Make New Brain Cells and Improve Brain Function

Scientists used to believe that the brain stopped making new brain cells past a certain age. But that believe changed in the late 1990’s as a result of several studies which were performed on mice at the Salk Institute.

After conducting maze tests, neuroscientist Fred H. Gage and his colleagues examined brain samples collected from mice. What they found challenged long standing believes held about neurogenesis, or the creation of new neurons.

To their astonishment, they discovered that the mice were creating new neurons. Their brains were regenerating themselves.

All of the mice showed evidence of neurogenesis but the brains of the athletic mice showed even more.

 These mice, the ones that scampered on running wheels, were producing two to three times as many new neurons as the mice that didn’t exercise.

The difference between the mice who performed well on the maze tests and those that floundered was exercise.

That’s great for the mice, but what about humans?

To find out if neurogensis occurred in adult humans, Gage and his colleagues obtained brain tissue from deceased cancer patients who had donated their bodies to research. While still living, these people were injected with the same type of compound used on Gage’s mice to detect new neuron growth. When Gage dyed their brain samples, he saw new neurons. Like in the mice study, they found evidence of neurogenesis – the growth of new brain cells.

From the mice study, it appears that those who exercise produce even more new brain cells than those who don’t. Several studies on humans seem to suggest the same thing.

Studies performed at both the University of Illinois at Urbana- Champaign and Columbia University in New York City have shown that exercise benefits brain function. The test subjects were given aerobic exercises such as walking for at least one hour three times a week. After 6 months they showed significant improvements in memory as measured by a word-recall test. Using fMRI scans they also showed increases in blood flow to the hippocampus (part of the brain associated with memory and learning). Scientists suspect that the blood pumping into that part of the brain was helping to produce fresh neurons.

Dr. Patricia A. Boyle and her colleagues of Rush Alzheimer’s Disease Center in Chicago found that the greater a person’s muscle strength, the lower their likelihood of being diagnosed with Alzheimer’s. The same was true for the loss of mental function that often precedes full-blown Alzheimer’s.

Neuroscientist Gage, by the way, exercises just about every day, as do most colleagues in his field. As Scott Small a neurologist at Columbia explains,

 I constantly get asked at cocktail parties what someone can do to protect their mental functioning. I tell them, ‘Put down that glass and go for a run.

So if you want to grow some new brain cells and improve your brain function, go get some exercise!

Source: How to Make New Brain Cells and Improve Brain Function | Online Brain Games Blog

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[WEB SITE] Traumatic Brain Injury Resource Guide – Neuroplasticity

Neuroplasticity

by Lisa Kreber, Ph.D. CBIS
Senior Neuroscientist, Centre for Neuro Skills

What is Neuroplasticity?
Neuronal Firing
How Neuroplasticity Works
Mechanisms of Plasticity
Synaptogenesis
Stem Cells
Modulation of Neurotransmission
Unmasking
Forms of Neuronal Plasticity
Neuronal Remodeling
Depression and Hippocampal Plasticity
Appreciating Plasticity
Ten Principles of Neuroplasticity
Learning, Injury and Recovery

Source: Traumatic Brain Injury Resource Guide – Neuroplasticity

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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] Body-Machine Interfaces after Spinal Cord Injury: Rehabilitation and Brain Plasticity – Full Text HTML

Abstract

The purpose of this study was to identify rehabilitative effects and changes in white matter microstructure in people with high-level spinal cord injury following bilateral upper-extremity motor skill training. Five subjects with high-level (C5–C6) spinal cord injury (SCI) performed five visuo-spatial motor training tasks over 12 sessions (2–3 sessions per week). Subjects controlled a two-dimensional cursor with bilateral simultaneous movements of the shoulders using a non-invasive inertial measurement unit-based body-machine interface. Subjects’ upper-body ability was evaluated before the start, in the middle and a day after the completion of training. MR imaging data were acquired before the start and within two days of the completion of training. Subjects learned to use upper-body movements that survived the injury to control the body-machine interface and improved their performance with practice. Motor training increased Manual Muscle Test scores and the isometric force of subjects’ shoulders and upper arms. Moreover, motor training increased fractional anisotropy (FA) values in the cingulum of the left hemisphere by 6.02% on average, indicating localized white matter microstructure changes induced by activity-dependent modulation of axon diameter, myelin thickness or axon number. This body-machine interface may serve as a platform to develop a new generation of assistive-rehabilitative devices that promote the use of, and that re-strengthen, the motor and sensory functions that survived the injury.

1. Introduction

Despite progress in the field of assistive technologies for people who suffered an injury to the spinal cord, most of the current devices to control computers and wheelchairs are set in place to require as little physical effort from the user as possible, and little attention has been paid to maintaining and strengthening the neural and muscular resources that survived the injury [1,2,3,4]. Spinal cord injury (SCI) leads to motor impairment, weakness, muscular and cortical atrophy and altered reflexes, and these have been shown to progress further with lack of exercise [5,6,7,8,9,10]. Even in individuals with injuries to the cervical spinal cord, some motor and sensory capacities may remain available in the upper body. Several studies have shown that using their remaining functions and keeping an active body is critical for people with SCI in order to avoid the collateral effects of paralysis and to potentially recover some of the lost mobility [5,6,7,11]. Therefore, it is crucial to develop the next generation of assistive-rehabilitative devices that promote learning through upper-body coordination.
Acquisition, retention and refinement of motor skills all rely on the capability of the nervous system to create new patterns of neural activation for accomplishing new tasks and for recovering lost motor functions [12]. Recent advances in neural imaging have allowed learning studies on juggling [13], balance [14] and body-machine interfaces (BMIs) by our group [15], to demonstrate motor skill learning-induced structural changes of cortical and subcortical areas in both gray matter and white matter by using diffusion tensor imaging (DTI). DTI non-invasively measures the direction and rate of water diffusion within tissue. White matter integrity is commonly measured by fractional anisotropy (FA), a normalized measure of the variance of the diffusion ellipsoid at each voxel [16]. FA values for white matter tissue have been shown to be affected by physiological parameters, such as axon diameter, axon number and myelin thickness [17].
Loss of somatosensory afference leads to functional cortical reorganization [18,19,20]. SCI has been shown to lead to spinal cord atrophy, cortical atrophy of primary and sensory cortex [8], descending motor tracts [9] and cortical reorganization of the sensorimotor system [8,10], and the degree of cortical reorganization is associated with the level of disability. Although the goal of most SCI treatments is to re-establish neural connections in order to restore motor function, it is unclear whether the anatomical and functional changes that follow injury can be reversed.
In this study, we investigated the rehabilitative effects and learning-induced changes in the brain white matter microstructure of people with high-level SCI after they practiced coordinated upper-body movements to control a computer cursor through a novel body-machine interface. Subjects learned to use the remaining ability of their shoulders and upper arms to perform movements that controlled a computer cursor to complete different related tasks. Complementary to [15], the purpose of this study was to identify changes in motor function and white matter by comparing clinical scores and FA values pre- and post-bilateral upper-body motor skill training in people with a high-level spinal cord injury. We started from the assumption that motor learning is likely to be associated with different brain reorganization in unimpaired subjects compared to subjects with tetraplegia, in consideration also of the greater need for the reorganization of motor functions in the latter group.

Continue —> Brain Sciences | Free Full-Text | Body-Machine Interfaces after Spinal Cord Injury: Rehabilitation and Brain Plasticity | HTML

Figure 5. Regions showing lower fractional anisotropy (FA) in spinal cord injury (SCI) subjects compared to controls. (A) Brain regions associated with motor function used to perform tract-based spatial statistics (TBSS) and ROI analyses; (B) TBSS results. Regions showing significantly higher (red-yellow) and lower (blue-light blue) FA values in SCI versus control subjects overlaid over the standard Montreal Neurological Institute (MNI)152 T1-weighted anatomical scan (p < 0.05, uncorrected). The location of each slice in Montreal Neurological Institute space is shown at the lower left section. a-s-pCR, anterior, superior and posterior corona radiata; CG, cingulum; g-bCC, genu and body of corpus callosum; a-pIC, anterior and posterior limbs of internal capsule.

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[WEB SITE] The Rehabilitation Gaming System

slideshow 1RGS is a highly innovative Virtual Reality (VR) tool for the rehabilitation of deficits that occur after brain lesions and has been successfully used for the rehabilitation of the upper extremities after stroke.
The RGS is based on the neurobiological considerations that plasticity of the brain remains  throughout life and therefore can be utilized to achieve functional reorganization of the brain areas affected by stroke. This can be realized by means of activation of secondary motor areas such as the so called mirror neurons system.

RGS deploys a deficit oriented training approach. Specifically, while training with RGS the patient is playing individualized games where movement execution is combined with the observation of correlated actions performed by a virtual body. The system optimizes the user’s training by analyzing the qualitative and quantitative aspects of the user’s performance. This warranties a detailed assessment of the deficits of the patient and their recovery dynamics.

Key articles and Recent publications

also see specs.upf.edu

Source: The Rehabilitation Gaming System | Rehabilitation Gaming System

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[ARTICLE] Neuroplastic Changes Following Brain Ischemia and their Contribution to Stroke Recovery: Novel Approaches in Neurorehabilitation – Full Text

Ischemic damage to the brain triggers substantial reorganization of spared areas and pathways, which is associated with limited, spontaneous restoration of function. A better understanding of this plastic remodeling is crucial to develop more effective strategies for stroke rehabilitation. In this review article, we discuss advances in the comprehension of post-stroke network reorganization in patients and animal models. We first focus on rodent studies that have shed light on the mechanisms underlying neuronal remodeling in the perilesional area and contralesional hemisphere after motor cortex infarcts. Analysis of electrophysiological data has demonstrated brain-wide alterations in functional connectivity in both hemispheres, well beyond the infarcted area. We then illustrate the potential use of non-invasive brain stimulation (NIBS) techniques to boost recovery. We finally discuss rehabilitative protocols based on robotic devices as a tool to promote endogenous plasticity and functional restoration.

Introduction

Following an ischemic insult within the motor cortex, one or more body parts contralateral to the infarct result impaired or paretic. The degree of the motor impairment depends on many factors, such as the extent of the infarct, the identity of the damaged region(s) and the effectiveness of the early medical care. Substantial functional recovery can occur in the first weeks after stroke, mainly due to spontaneous mechanisms (Kwakkel et al., 2004; Cramer, 2008; Darling et al., 2011; Ward, 2011; Grefkes and Fink, 2014). About 26% of stroke survivors are able to carry on everyday activities (Activity of Daily Living or ADLs, i.e., eating, drinking, walking, dressing, bathing, cooking, writing) without any help, but another 26% is forced to shelter in a nursing home (Carmichael, 2005). Impairments of upper and lower limbs are particularly disabling as they impact on the degree of independence in ADLs. Overall, a significant percentage of the patients exhibit persistent disability following ischemic attacks. Therefore, it is critical to increase our knowledge of post-stroke neuroplasticity for implementing novel rehabilitative strategies. In this review we summarize data about plastic reorganizations after injury, both in the ipsilesional and contralesional hemisphere. We also describe non-invasive brain stimulation (NIBS) techniques and robotic devices for stimulating functional recovery in humans and rodent stroke models.

Neuroplasticity After Stroke

The term brain plasticity defines all the modifications in the organization of neural components occurring in the central nervous system during the entire life span of an individual (Sale et al., 2009). Such changes are thought to be highly involved in mechanisms of aging, adaptation to environment and learning. Moreover, neuronal plastic phenomena are likely to be at the basis of adaptive modifications in response to anatomical or functional deficit or brain damage (Nudo, 2006). Ischemic damage causes a dramatic alteration of the entire complex neural network within the affected area. It has been amply demonstrated, by many studies, that the cerebral cortex exhibits spontaneous phenomena of brain plasticity in response to damage (Gerloff et al., 2006; Nudo, 2007). The destruction of neural networks indeed stimulates a reorganization of the connections and this rewiring is highly sensitive to the experience following the damage (Stroemer et al., 1993; Li and Carmichael, 2006). Such plastic phenomena involve particularly the perilesional tissue in the injured hemisphere, but also the contralateral hemisphere, subcortical and spinal regions.

Continue —> Frontiers | Neuroplastic Changes Following Brain Ischemia and their Contribution to Stroke Recovery: Novel Approaches in Neurorehabilitation | Frontiers in Cellular Neuroscience

Figure 3. Example of a novel robotic system that integrates functional grasping, active reaching arm training and bimanual tasks. An example of a novel robotic system that integrates functional grasping, active reaching arm training and bimanual tasks, consisting of: (i) Virtual Reality: software applications composed of rehabilitative and evaluation tasks; (ii) TrackHold: robotic device to support the weight of the user’s limb during tasks execution; (iii) Robotic Hand Exos: active hand exoskeleton to assist grasping tasks; and (iv) Handgrip sensors to support the bilateral grasping training and evaluation (modified from Sgherri et al., 2017).

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[ARTICLE] Hybrid Assistive Neuromuscular Dynamic Stimulation Therapy: A New Strategy for Improving Upper Extremity Function in Patients with Hemiparesis following Stroke – Full Text

Abstract

Hybrid Assistive Neuromuscular Dynamic Stimulation (HANDS) therapy is one of the neurorehabilitation therapeutic approaches that facilitates the use of the paretic upper extremity (UE) in daily life by combining closed-loop electromyography- (EMG-) controlled neuromuscular electrical stimulation (NMES) with a wrist-hand splint. This closed-loop EMG-controlled NMES can change its stimulation intensity in direct proportion to the changes in voluntary generated EMG amplitudes recorded with surface electrodes placed on the target muscle. The stimulation was applied to the paretic finger extensors. Patients wore a wrist-hand splint and carried a portable stimulator in an arm holder for 8 hours during the daytime. The system was active for 8 hours, and patients were instructed to use their paretic hand as much as possible. HANDS therapy was conducted for 3 weeks. The patients were also instructed to practice bimanual activities in their daily lives. Paretic upper extremity motor function improved after 3 weeks of HANDS therapy. Functional improvement of upper extremity motor function and spasticity with HANDS therapy is based on the disinhibition of the affected hemisphere and modulation of reciprocal inhibition. HANDS therapy may offer a promising option for the management of the paretic UE in patients with stroke.

1. Functional Recovery of Upper Extremity Motor Function following Stroke

Stroke is a common health-care problem that causes physical impairment, disability, and problems in social participation. The most common impairment caused by stroke is motor impairment. Motor impairment affects the control of the unilateral upper and lower extremities. Recovery of function in the hemiparetic upper extremity is noted in fewer than 15% of patients after stroke [1].

Patients often compensate for their paretic upper extremity by using their intact upper extremity in the performance of everyday tasks [2]. It is supposed that strong reliance on compensatory overuse of the intact upper extremity inhibits functional recovery of the impaired upper extremity. This may explain the limited improvement of the functional capability of the paretic upper extremity in activities of daily living (ADL).

Principles of motor rehabilitation following stroke have been described as being dose-dependent and task-specific [3]. High-intensity practice and task-specific training are recommended for functional recovery. Several systematic reviews [4, 5] have explored whether high-intensity therapy improves recovery, and the principle that increased intensive training is helpful is widely accepted. Task-specific training is a well-accepted principle in motor rehabilitation. Training should target the goals that are relevant for the needs of the patients and preferably be given in the patient’s own environment.

The goal of upper extremity rehabilitation is to improve the capability of the paretic upper extremity for ADL. Constraint-induced movement therapy (CIMT) has been developed to enhance the forced use of the paretic hand in ADL with reduction of the compensatory overuse of the intact upper extremity. However, to participate in CIMT, the candidates must be able to voluntary extend their fingers and wrist at least 10 degrees, practice for 6 hours daily in a 2-week course, and spend waking hours with their nonparetic hand in a mitt [6].

To counter potential problems inherent in the intensive services needed for CIMT, we developed an alternative therapeutic approach that provides high-intensity training to facilitate the use of the paretic upper extremity in daily living by combining closed-loop electromyography- (EMG-) controlled neuromuscular electrical stimulation (NMES) with a wrist-hand splint for patients with moderate to severe hemiparesis. Fujiwara et al. called this hybrid assistive neuromuscular dynamic stimulation (HANDS) therapy [7].

2. HANDS Therapy

A PubMed literature search was conducted using the MeSH terms stroke, rehabilitation, upper extremity function, and neuromuscular electrical stimulation, and 71 articles were identified. A further search of PubMed with the terms stroke, rehabilitation, upper extremity function, neuromuscular electrical stimulation, and splint identified 4 articles, all regarding HANDS therapy.

HANDS therapy facilitates the use of the paretic upper extremity in daily living by combining closed-loop EMG-controlled NMES with a wrist-hand splint for patients with moderate to severe hemiparesis. This HANDS system is active for 8 hours, and patients are instructed to use their paretic hand as much as possible while wearing the HANDS system. Their nonparetic upper extremity is not restrained. The patients are also instructed to practice bimanual activities in their ADL. All participants in HANDS therapy are admitted, and the length of the intervention is 21 days. They receive 90 minutes of occupational therapy per day, 5 days a week. Each session of occupational therapy consists of gentle stretching exercise of the paretic upper extremity and active muscle reeducation exercise. All participants are instructed how to use their paretic hand in ADL with the HANDS system. Occupational therapists are directed toward participants’ goals and focused on their particular impairments and disabilities; thus, the specific therapy that each patient receives varies [7, 8].

Fujiwara et al. [7, 8] reported the indications for HANDS therapy as follows: () no cognitive deficits; () no pain in the paretic upper extremity; () passive extension range of motion (ROM) greater than 0 degrees of the affected wrist and −10 degrees of the metacarpophalangeal joints; () detectable surface EMG signals in the affected extensor digitorum communis (EDC) or extensor pollicis longus (EPL) when the patient intends to extend their fingers; () ability to raise the paretic hand to the height of the nipple; () scores of Fugl-Meyer test position sense of joints in the glenohumeral joint, elbow, wrist, and thumb of 1 or more; and () the ability to walk without physical assistance in daily life (e.g., including patients who can walk independently with a cane and/or an orthosis). The exclusion criteria were () history of major psychiatric or previous neurological disease, including seizures; () cognitive impairment precluding appropriately giving informed consent or the patient’s Mini Mental Examination Scale score was below 25; () patients with severe pain in the paretic upper extremity; () patients with a pacemaker or other implanted stimulator; and () patients with visuospatial neglect or apraxia.

Previous reports showed that none of the patients experienced any discomfort or significant disability with the HANDS therapy.

2.1. Closed-Loop Electromyography- (EMG-) Controlled Neuromuscular Electrical Stimulation (NMES)

Twenty-nine articles were found in PubMed using the terms stroke, electromyography, neuromuscular electrical stimulation, and upper extremity. Thirteen of 29 articles were on EMG-triggered NMES. Six of 29 articles were on EMG-controlled NMES. Two involved contralaterally controlled electrical stimulation.

EMG-triggered NMES applies preset electrical stimulation when EMG activity reaches a target threshold. The stimulus intensity and duration are determined and not changeable. EMG-controlled NMES applies electrical stimulation during voluntary contraction and changes the stimulation intensity in proportion to the changes in EMG amplitude.

For assistive stimulation, HANDS therapy used closed-loop EMG-controlled NMES, which was developed by Muraoka [9] and commercially available with MURO stimulation (Pacific Supply, Osaka, Japan). This closed-loop EMG-controlled NMES is portable and attaches to the arm (Figure 1). The surface electrodes pick up EMG signals at the target muscle and simultaneously stimulate it in direct proportion to the picked-up EMG signal, with the exception of the 25 ms after delivering each stimulation pulse, in which stimulation artifacts and M wave are observed. The external adjustment unit sets () range of stimulus intensity; () sensitivity of the EMG; () threshold of EMG amplitude that starts stimulation; and () gradient of stimulus intensity change to the change of EMG amplitude. Once these parameters were set with the external adjustment unit, the stimulator memorized these parameters.

Continue —>  Hybrid Assistive Neuromuscular Dynamic Stimulation Therapy: A New Strategy for Improving Upper Extremity Function in Patients with Hemiparesis following Stroke

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