Posts Tagged spasticity

[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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[Abstract+References] Safety and efficacy of letibotulinumtoxinA(BOTULAX®) in treatment of post stroke upper limb spasticity: a randomized, double blind, multi-center, phase III clinical trial

To investigate a new botulinum neurotoxin type A, termed letibotulinumtoxinA(Botulax®) and compare its efficacy and safety for post-stroke upper limb spasticity with that of onabotulinumtoxinA(Botox®).

A prospective, double-blinded, multicenter, randomized controlled clinical study.

Six university hospitals in Korea.

A total of 187 stroke participants with upper limb spasticity.

Two kinds of botulinum neurotoxin type A were used. One set of injection was performed and total injected doses were 309.21±62.48U(Botulax) and 312.64±49.99U(Botox)(P>0.05).

Primary outcome was measured using the modified Ashworth scale for wrist flexors at week 4 and secondary outcome was measured using modified Ashworth scale for wrist flexors, elbow flexors, finger flexors, and thumb flexors as well as Global Assessment in spasticity, Disability Assessment Scale, and Caregiver Burden Scale. Safety measures including adverse events, vital signs and physical examination, and laboratory tests were also monitored.

The mean ages for the Botulax group were 56.81±9.49 and which for the Botox group were 56.93±11.93(P>0.05). In primary outcome, the change in modified Ashworth scale for wrist flexors was -1.45±0.61 in the Botulax group and -1.40±0.57 in the Botox group, and the difference between the two groups was -0.06(95% CI:-0.23–0.12,P>0.05). In secondary outcome, both groups demonstrated significant improvements with respect to modified Ashworth scale, Global Assessment in spasticity, Disability Assessment Scale, and Caregiver Burden Scale (P<0.05), and no significant difference was observed between the two groups (P>0.05). In addition, safety measures showed no significant differences between the two groups (P>0.05).

The efficacy and safety of Botulax were comparable with those of Botox in treatment of post-stoke upper limb spasticity.

 

1. Kanovsky P, Slawek J, Denes Z, . Efficacy and safety of botulinum neurotoxin NT 201 in poststroke upper limb spasticity. Clin Neuropharmacol 2009; 32: 259265. Google Scholar CrossRef, Medline
2. Slawek J, Bogucki A, Reclawowicz D. Botulinum toxin type A for upper limb spasticity following stroke: an open-label study with individualised, flexible injection regimens. Neurol Sci 2005; 26: 3239. Google Scholar CrossRef, Medline
3. Jost WH, Hefter H, Reissig A, . Efficacy and safety of botulinum toxin type A (Dysport) for the treatment of post-stroke arm spasticity: results of the German-Austrian open-label post-marketing surveillance prospective study. J Neurol Sci 2014; 337: 8690. Google Scholar CrossRef, Medline
4. Simpson DM, Alexander DN, O’Brien CF, . Botulinum toxin type A in the treatment of upper extremity spasticity: a randomized, double-blind, placebo-controlled trial. Neurology 1996; 46: 13061310. Google Scholar CrossRef, Medline
5. Brashear A, Gordon MF, Elovic E, . Intramuscular injection of botulinum toxin for the treatment of wrist and finger spasticity after a stroke. N Engl J Med 2002; 347: 395400. Google Scholar CrossRef, Medline
6. Shaw LC, Price CI, van Wijck FM, . Botulinum toxin for the upper limb after stroke (BoTULS) trial: effect on impairment, activity limitation, and pain. Stroke 2011; 42: 13711379. Google Scholar CrossRef, Medline
7. Childers MK, Brashear A, Jozefczyk P, . Dose-dependent response to intramuscular botulinum toxin type A for upper-limb spasticity in patients after a stroke. Arch Phys Med Rehabil 2004; 85: 10631069. Google Scholar CrossRef, Medline
8. Simpson DM, Gracies JM, Yablon SA, . Botulinum neurotoxin versus tizanidine in upper limb spasticity: a placebo-controlled study. J Neurol Neurosurg Psychiatry 2009; 80: 380385. Google Scholar CrossRef, Medline
9. Seo HG, Paik NJ, Lee SU, . Neuronox versus BOTOX in the Treatment of Post-Stroke Upper Limb Spasticity: A Multicenter Randomized Controlled Trial. PLoS One 2015; 10: e0128633. Google Scholar CrossRef
10. Bohannon RW, Smith MB. Interrater reliability of a modified Ashworth scale of muscle spasticity. Phys Ther 1987; 67: 206207. Google Scholar Medline
11. Brashear A, Zafonte R, Corcoran M, . Inter- and intrarater reliability of the Ashworth Scale and the Disability Assessment Scale in patients with upper-limb poststroke spasticity. Arch Phys Med Rehabil 2002; 83: 13491354. Google Scholar CrossRef, Medline
12. Wang HC, Hsieh LF, Chi WC, . Effect of intramuscular botulinum toxin injection on upper limb spasticity in stroke patients. Am J Phys Med Rehabil 2002; 81: 272278. Google Scholar CrossRef, Medline
13. Bhakta BB, Cozens JA, Chamberlain MA, . Impact of botulinum toxin type A on disability and carer burden due to arm spasticity after stroke: a randomised double blind placebo controlled trial. J Neurol Neurosurg Psychiatry 2000; 69: 217221. Google Scholar CrossRef, Medline

Source: Safety and efficacy of letibotulinumtoxinA(BOTULAX®) in treatment of post stroke upper limb spasticity: a randomized, double blind, multi-center, phase III clinical trial – Jan 25, 2017

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[Abstract] Effects of sit-to-stand training combined with transcutaneous electrical stimulation on spasticity, muscle strength and balance ability in patients with stroke: a randomized controlled study

Highlights

  • The effect of sit-to-stand training combined with TENS was evaluated in stroke patients with spastic plantar flexor.
  • TENS followed by sit-to-stand training may improve spasticity, muscle strength and balance.
  • Clinician should consider TENS application prior to sit to stand training for stroke patients with spastic plantar flexor.

Abstract

Sit-to-stand is a fundamental movement of human being for performing mobility and independent activity. However, Stroke people symptoms experience difficulty in conducting the sit-to-stand due to paralysis and especially ankle spasticity. Recently, transcutaneous electrical- stimulation (TENS) is used to reduce pain but also to manage spasticity.

The purpose of this study was to determine

  1. whether TENS would lead to ankle spasticity reduction and (
  2. whether sit-to-stand training combined with TENS would improve spasticity, muscle strength and balance ability in stroke patients.

Forty-stroke patients were recruited and were randomly divided into two groups: TENS group (n = 20) and sham group (n = 20). All participants underwent 30-sessions of sit-to-stand training (for 15-minutes, five-times per week for 6-weeks). Prior to each training session, 30-minutes of TENS over the peroneal nerve was given in TENS group, whereas sham group received non-electrically stimulated TENS for the same amount of time. Composite-Spasticity-Score was used to assess spasticity level of ankle plantar-flexors. Isometric strength in the extensor of hip, knee and ankle were measured by handhelddynamometer. Postural-sway distance was measured using a force platform.

The spasticity score in the TENS group (2.6 ± 0.8) improved significantly greater than the sham group (0.7 ± 0.8, p < 0.05). The muscle strength of hip extensor in the TENS group (2.7 ± 1.1 kg) was significantly higher than the sham group (1.0 ± 0.8 kg, p < 0.05). Significant improvement in postural-sway was observed in the TENS group compared to the sham group (p < 0.05).

Thus, sit-to-stand training combined with TENS may be used to improve the spasticity, balance function and muscle strength in stroke patients.

Source: Effects of sit-to-stand training combined with transcutaneous electrical stimulation on spasticity, muscle strength and balance ability in patients with stroke: a randomized controlled study – Gait & Posture

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[Abstract] Combined Effect Of Botulinum Toxin And Splinting On Motor Components And Function Of People With Stroke  

Abstract

Background and objective: Spasticity is one of the problems following stroke. Due to this increase in muscle tone, patients are confronted to problems in motor control and difficulties in activities of daily living and complications such as shortness and contracture. The aim of this study was to examine the effects of Simultaneous use of both splint and botulinum toxin-A (BTX-A) injection on spasticity, range of motion and upper extremity function in a 3-month period.

Methods: The design of this study was a comparison between 3 groups of interventions, conducted in rehabilitation clinics in Tehran. Sixty people with chronic stroke were recruited. Based on the inclusion criteria, a total of 39 stroke patients after completing the consent forms were entered to intervention groups; splint or botulinum toxin injection or combined splint/botulinum toxin injection. They were followed up about 3 months and the evaluations were done monthly. Goniometry was the method to measure range of motion, and Modified Ashworth scale was used to examine the spasticity and the upper extremity function was scored based on Fugl-Meyer assessment.   Statistical analysis was done using SPSS 17. And ANOVAs was used for comparison between groups and times.  Significance was set at 0.05.

Results: All outcome measures improved within each group but the differences between splint group and BTX-A group and the BTX-A-splint group was not significant in most outcomes during 3 periods (first evaluation until end of the first month, the end of first month until the end of second month, the end of second month until the end of the third month) (p> 0 / 05). The results also showed that the changes in elbow`s spasticity {p= 0.05} and wrist`s spasticity {p= 0.007} and upper extremity function { p = 0.04} were obvious between the three groups over the 3-months and the difference in the group of combined use of botulinum toxin and splint was more than other groups.

Conclusion: In this study, the effects of botulinum toxin injection and Volar-Dorsal Wrist/Hand Immobilization splint and the combined use of botulinum injection and splint were obvious in all groups but was not significantly different between the interventions in a 3-month follow-up.

Source: Combined Effect Of Botulinum Toxin And Splinting On Motor Components And Function Of People With Stroke | Shamili | Advances in Bioscience and Clinical Medicine

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[Abstract] Breakthroughs in the spasticity management: Are non-pharmacological treatments the future?

Highlights

  • Spasticity can cause a severe disability and challenge the rehabilitation process.
  • A successful treatment of spasticity depends on a pathophysiologic assessment.
  • The main therapeutic options include physiotherapy and pharmacological treatments.
  • Non-pharmacologic approaches may reduce spasticity and improve quality of life.

Abstract

The present paper aims at providing an objective narrative review of the existing non-pharmacological treatments for spasticity. Whereas pharmacologic and conventional physiotherapy approaches result well effective in managing spasticity due to stroke, multiple sclerosis, traumatic brain injury, cerebral palsy and incomplete spinal cord injury, the real usefulness of the non-pharmacological ones is still debated. We performed a narrative literature review of the contribution of non-pharmacological treatments to spasticity management, focusing on the role of non-invasive neurostimulation protocols (NINM). Spasticity therapeutic options available to the physicians include various pharmacological and non-pharmacological approaches (including NINM and vibration therapy), aimed at achieving functional goals for patients and their caregivers. A successful treatment of spasticity depends on a clear comprehension of the underlying pathophysiology, the natural history, and the impact on patient’s performances. Even though further studies aimed at validating non-pharmacological treatments for spasticity should be fostered, there is growing evidence supporting the usefulness of non-pharmacologic approaches in significantly helping conventional treatments (physiotherapy and drugs) to reduce spasticity and improving patient’s quality of life. Hence, non-pharmacological treatments should be considered as a crucial part of an effective management of spasticity.

Source: Breakthroughs in the spasticity management: Are non-pharmacological treatments the future? – Journal of Clinical Neuroscience

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[Poster] A Toolkit for Objective Clinical Outcome Measures of Muscle Tone – Archives of Physical Medicine and Rehabilitation

To evaluate a wearable sensor-based toolkit for quantifying muscle tone in patients with upper motor neuron syndrome (UMNS).

Source: A Toolkit for Objective Clinical Outcome Measures of Muscle Tone – Archives of Physical Medicine and Rehabilitation

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[Abstract] Breakthroughs in the spasticity management: Are non-pharmacological treatments the future?

 

Highlights

    Spasticity can cause a severe disability and challenge the rehabilitation process.
    A successful treatment of spasticity depends on a pathophysiologic assessment.
    The main therapeutic options include physiotherapy and pharmacological treatments.
    Non-pharmacologic approaches may reduce spasticity and improve quality of life.

Abstract

The present paper aims at providing an objective narrative review of the existing non-pharmacological treatments for spasticity. Whereas pharmacologic and conventional physiotherapy approaches result well effective in managing spasticity due to stroke, multiple sclerosis, traumatic brain injury, cerebral palsy and incomplete spinal cord injury, the real usefulness of the non-pharmacological ones is still debated.

We performed a narrative literature review of the contribution of non-pharmacological treatments to spasticity management, focusing on the role of non-invasive neurostimulation protocols (NINM). Spasticity therapeutic options available to the physicians include various pharmacological and non-pharmacological approaches (including NINM and vibration therapy), aimed at achieving functional goals for patients and their caregivers. A successful treatment of spasticity depends on a clear comprehension of the underlying pathophysiology, the natural history, and the impact on patient’s performances.

Even though further studies aimed at validating non-pharmacological treatments for spasticity should be fostered, there is growing evidence supporting the usefulness of non-pharmacologic approaches in significantly helping conventional treatments (physiotherapy and drugs) to reduce spasticity and improving patient’s quality of life.

Hence, non-pharmacological treatments should be considered as a crucial part of an effective management of spasticity.

Source: Breakthroughs in the spasticity management: Are non-pharmacological treatments the future?

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[ARTICLE] Efficacy and safety of oral baclofen in the management of spasticity: A rationale for intrathecal baclofen – Full Text

Abstract

Oral baclofen has long been a mainstay in the management of spasticity. This review looks at the clinical evidence for the efficacy and safety of oral baclofen in patients with spasticity of any origin or severity, to determine whether there is a rationale for the use of intrathecal baclofen. Results suggest that oral baclofen may be effective in many patients with spasticity, regardless of the underlying disease or severity, and that it is at least comparable with other antispasmodic agents. However, adverse effects, such as muscle weakness, nausea, somnolence and paraesthesia, are common with oral baclofen, affecting between 25% and 75% of patients, and limiting its usefulness. Intrathecal baclofen may be an effective alternative as the drug is delivered directly into the cerebrospinal fluid, thus bypassing the blood-brain barrier and thereby optimizing the efficacy of baclofen while minimizing drug-related side-effects. Intrathecal baclofen is a viable option in patients who experience intolerable side-effects or who fail to respond to the maximum recommended dose of oral baclofen.

Introduction

Although the exact prevalence is unknown, it is estimated that more than 12 million people worldwide could be affected by spasticity (1), and that 12–27% of these have disabling spasticity, depending on the aetiology (2). Substantial evidence demonstrates that spasticity has a negative impact on patients, causing physical impairment (e.g. pain, pressure sores, contractures), limitation of activities, dependence on caregivers, restricted participation in family and social life, and decreased overall quality of life (3, 4).

Numerous definitions for spasticity exist (5), although that provided by Pandyan et al. (6) has been advocated during recent years: “disordered sensorimotor control resulting from an upper motor neuron lesion, presenting as intermittent or sustained involuntary activation of muscles”. Spasticity is a common complication of upper motor neurone syndrome, and can occur when areas controlling movement are damaged, most often by brain injury disorders, such as or cerebral palsy (CP), traumatic brain injury (BI) or stroke, or by spinal cord disorders, such as spinal cord injury (SCI) or multiple sclerosis (MS) (7). Although heterogeneous, the causes of spasticity share a common pathophysiology, in that the damage disrupts the pathways that regulate activity in alpha motor neurones, causing a change in the balance of signals between the nervous system and the muscles. This imbalance leads to increased activity (excitability) in the muscles, resulting in overactive segmental reflexes. Normally when a muscle is rapidly stretched out, a stretch reflex is triggered and the muscle contracts to maintain muscle length and limb position. To allow smooth, non-jerky, coordinated movement, the segmental reflexes must be inhibited to allow the muscle to relax (i.e. stretch). The main neurotransmitter to achieve this is gamma aminobutyric acid (GABA), which is released by neurones in the spinal cord via descending inhibitory impulses from the brain. However, if the descending inhibitory impulses from the brain (and thus GABA) are cut off through disease or injury, inhibition becomes insufficient; instead, excessive muscular contraction during the muscle stretch takes place, resulting in abnormal muscle tone (hypertonicity).

The severity of spasticity varies from mild to severe according to the level of muscle tone (measured by the Ashworth scale or a modified Ashworth scale in most studies) and the level of disability in performing daily activities (8–10). The use of oral medication to treat spasticity is indicated when spasticity interferes with daily functioning, i.e. causes pain, disturbs sleep or affects activities of daily life. In addition, persistent muscular stiffness and spasms can lead to contracture (permanent stiffness of the muscle, tendon or joint, with decreased range of motion) that can be painful and disabling. Thus, treatment aims to reduce muscle tone in order to facilitate movement and limit contracture. However, some patients rely on excess muscle tone when transferring or ambulating, or to maintain posture. Therefore, the use of antispasmodic drugs needs to be tailored to each patient’s specific needs, to find the correct balance. Commonly-used oral drugs include baclofen, tizanidine, diazepam, and dantrolene, which have differing modes of action, but all are aimed at reducing muscle tone and/or spasms (11).

Oral baclofen is used more frequently than other antispasmodic agents to treat spasticity (8). Baclofen is a GABA-agonist that is thought to selectively bind to presynaptic GABA-B receptors, resulting in hyperpolarization of motor horn cells (12) and a subsequent reduction in the hyperactivity of muscle stretch reflexes, clonus, and cutaneous reflexes that elicit muscle spasms (13). Although widely used, baclofen is mainly water soluble and so does not readily cross the blood-brain barrier (14). As a result, patients may require a high dose to treat their spasticity effectively, which can cause intolerable side-effects (15). As an alternative, baclofen can be delivered directly to the cerebrospinal fluid (CSF) in the intrathecal space, bypassing the blood-brain barrier entirely. This allows a much lower dose to be used to achieve similar CSF concentrations as oral baclofen; it has been determined that the intrathecal baclofen (ITB) dose is 100–1,000 times smaller than the oral daily dose (16), which means that a higher CSF concentration can be achieved at a lower plasma concentration than would be achieved with an oral medication (17, 18). As a result, the central nervous system side-effects of oral baclofen (e.g. sedation, drowsiness, headache) may be reduced (12). The fact that baclofen is only slightly lipid soluble means that baclofen remains in the CSF after ITB therapy, with a relatively long half-life (90 min) (19). There is a 4:1 gradient in drug distribution between the caudal and rostral parts of the spinal cord, favouring high levels of action at the spinal level vs the brain and thus further decreasing cerebral side-effects (20). In addition, animal studies have shown that there is a steep gradient of baclofen along the spinal axis, meaning that during slow intrathecal infusion (20 µl/h) most of the baclofen seems to remain around the catheter tip used for the CSF delivery (21). The clinical implication of this is that the catheter position in relation to the targeted spinal cord segment may be critical to efficacy.

This review aims to systematically evaluate the available evidence for oral baclofen,in order to determine: (i) the efficacy of oral baclofen in spasticity treatment in comparison with placebo or active comparators; (ii) the associated complications or adverse events of oral baclofen; (iii) whether the dosage of oral baclofen changes with the disease severity and duration of spasticity. The results are expected to provide a useful overview of the role of oral baclofen in the management of spasticity, no matter the origin or severity of the condition, and could indicate when intrathecal administration should be considered….

Continue —> Journal of Rehabilitation Medicine – Efficacy and safety of oral baclofen in the management of spasticity: A rationale for intrathecal baclofen – HTML

Fig. 1. PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) flow diagram of included/excluded studies.

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[ARTICLE] Efficacy of Short-Term Robot-Assisted Rehabilitation in Patients With Hand Paralysis After Stroke – Full Text

Background: We evaluated the effectiveness of robot-assisted motion and activity in additional to physiotherapy (PT) and occupational therapy (OT) on stroke patients with hand paralysis. Methods: A randomized controlled trial was conducted. Thirty-two patients, 34.4% female (mean ± SD age: 68.9 ± 11.6 years), with hand paralysis after stroke participated. The experimental group received 30 minutes of passive mobilization of the hand through the robotic device Gloreha (Brescia, Italy), and the control group received an additional 30 minutes of PT and OT for 3 consecutive weeks (3 d/wk) in addition to traditional rehabilitation. Outcomes included the National Institutes of Health Stroke Scale (NIHSS), Modified Ashworth Scale (MAS), Barthel Index (BI), Motricity Index (MI), short version of the Disabilities of the Arm, Shoulder and Hand (QuickDASH), and the visual analog scale (VAS) measurements. All measures were collected at baseline and end of the intervention (3 weeks). Results: A significant effect of time interaction existed for NIHSS, BI, MI, and QuickDASH, after stroke immediately after the interventions (all, P < .001). The experimental group had a greater reduction in pain compared with the control group at the end of the intervention, a reduction of 11.3 mm compared with 3.7 mm, using the 100-mm VAS scale. Conclusions: In the treatment of pain and spasticity in hand paralysis after stroke, robot-assisted mobilization performed in conjunction with traditional PT and OT is as effective as traditional rehabilitation.

Stroke (or cerebrovascular accident) is a sudden ischemic or hemorrhagic episode which causes a disturbed generation and integration of neural commands from the sensorimotor31 areas of the cortex. As a consequence, the ability to selectively activate muscle tissues for performing movement is reduced.26 Sixty percent of those individuals who survive a stroke exhibit a sensorimotor deficit of one or both hands and may benefit from rehabilitation to maximize recovery of the upper extremity.23,25 Restoration of arm and hand motility is essential for the independent performance of daily activities.23,26 A prompt and effective rehabilitation approach is essential28 to obtain recovery of an impaired limb to prevent tendon shortening, spasticity, and pain.2

Recent technologies have facilitated the use of robots as tools to assist patients in the rehabilitation process, thus maximizing patient outcomes.4 Several groups have developed robotic tools for upper limb rehabilitation of the shoulder and elbow.27 These robotic tools assist the patient with carrying out exercise protocols and may help restore upper limb mobility.22,26 The complexity of wrist and finger articulations had delayed the development of dedicated rehabilitation robots until 2003 when the first tool based on continuous passive motion (CPM) was presented followed by several other solutions, with various levels of complexity and functionality.3

A recent review on the mechanisms for motor relearning reported factors such as attention and stimuli (reinforcement) are crucial during learning which indicates that motor relearning can take place with patients with neurological disorders even when only the sensorial passive stimulation is applied.30 In addition, another review reported the benefits of CPM for stretching and upper limb passive mobilization for patients with stroke but that CPM treatment requires further research.40

Among robotic devices, Gloreha (Figure 1),5,10 with its compliant mechanical transmission, may represent an easily applied innovative solution to rehabilitation, because the hand can perform grasp and release activities wearing the device by mean of a flexible and light orthosis. Our objective of this study was to determine the efficacy of robot-assisted motion in addition to traditional physiotherapy (PT) and occupational therapy (OT) compared with additional time spent in PT and OT on stroke patients with hand paralysis on function, motor strength, spasticity, and pain.

Figure 1. Wearable glove/orthosis.

Continue —> Efficacy of Short-Term Robot-Assisted Rehabilitation in Patients With Hand Paralysis After Stroke – Feb 16, 2017

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[ARTICLE] Effect of early use of AbobotulinumtoxinA after stroke on spasticity progression: Protocol for a randomised controlled pilot study in adult subjects with moderate to severe upper limb spasticity (ONTIME pilot) – Full Text

Abstract

Introduction

Approximately 15 million people suffer a stroke annually, up to 40% of which may develop spasticity, which can result in impaired limb function, pain and associated involuntary movements affecting motor control.

Robust clinical data on spasticity progression, associated symptoms development and functional impairment is scarce. Additionally, maximal duration of muscle tone reduction following botulinum toxin type A (BoNT-A) injections remains undetermined. The ONTIME pilot study aims to explore these issues and evaluate whether abobotulinumtoxinA 500 U (Dysport®; Ipsen) administered intramuscularly within 12 weeks following stroke delays the appearance or progression of symptomatic (disabling) upper limb spasticity (ULS).

Methods

ONTIME is a 28-week, phase 4, randomised, double-blind, placebo-controlled, exploratory pilot study initiated at four centres across Malaysia, the Philippines, Singapore and Thailand. Subjects (n = 42) with moderate to severe ULS (modified Ashworth scale [MAS] score ≥2) in elbow flexors or pronators, wrist flexors, or finger flexors will be recruited. Subjects will be randomised 2:1 to abobotulinumtoxinA 500 U or placebo (single dose 2–12 weeks after first-ever stroke).

Primary efficacy will be measured by time between initial injection and visit at which reinjection criteria (MAS score ≥2 in the primary targeted muscle group and appearance or reappearance of symptomatic ULS) are met. Follow-up visits will be 4-weekly to a maximum of 28 weeks.

Discussion

This pilot study will facilitate the design and sample size calculation of further confirmatory studies, and is expected to provide insights into the optimal management of post-stroke patients, including timing of BoNT-A therapy and follow-up duration.

1. Introduction

An estimated 15 million people suffer a stroke annually [1]; of whom, up to 40% develop post-stroke spasticity, a state of velocity-dependent increase in tonic stretch reflexes (‘muscle tone’) with exaggerated tendon jerks [2] most commonly affecting upper limbs [3]; [4]; [5]; [6] ;  [7]. Post-stroke spasticity impedes active and passive functioning of affected limb(s), impairs activities of daily living and requires long-term treatment; associated healthcare costs are up to four-fold greater than for stroke survivors without spasticity [7]. Furthermore, spasticity may involve pain and involuntary movements, interfering with dressing, gait, balance and walking speed, and can disrupt rehabilitation [8]. Without functional improvement, secondary musculoskeletal complications such as contractures and deformity may develop [9].

Data on the proportion of patients with post-stroke spasticity developing disability are scarce. One survey (N = 140) reported a prevalence of 17% spasticity and 4% disabling spasticity with a year [4]. Upper limb involvement and age <65 years were associated with disabling spasticity in this study [4]. In other studies, over a third of individuals developed spasticity within a year, including 20% with severe spasticity [10] ;  [11], suggesting higher rates of disabling spasticity than those reported by Lundström et al. [4].

Studies evaluating the timeframe for developing spasticity symptoms post-stroke are also few, with small cohorts (around 100 patients), but suggest the prevalence and severity of spasticity increases within a year post-stroke [5]; [6]; [10]; [11]; [12] ;  [13]. Certain studies indicate that spasticity symptoms and muscle tone changes are apparent in up to 25% of stroke victims within 2 weeks [3]; [5] ;  [14]. One study reported increased muscle tone as an early risk factor for developing severe disabling spasticity, particularly if it affected more than two joints, or was associated with a modified Ashworth scale (MAS) score ≥2 in one affected joint within 6 weeks post-stroke [14]. Indeed, spasticity may persist [15], and the severity of upper limb spasticity (ULS) may increase over time, most commonly affecting anti-gravity muscles, during the first 2 weeks and at 3 months post-stroke [5].

AbobotulinumtoxinA is an effective focal intervention for reducing ULS [16] and coupled with neurorehabilitation is recommended in standard clinical practice [17] ;  [18]. Treatment with botulinum toxin A (BoNT-A) is generally delayed in post-stroke spasticity until patients show clinical signs of increased muscle tone, usually about 3 months following stroke [19], despite evidence that symptoms begin much earlier.

Recent studies aimed to evaluate whether earlier post-stroke treatment with BoNT-A may prevent disabling spasticity development [15]; [19] ;  [20] and demonstrate that BoNT-A administered within 3 months provides sustained improvement in muscle tone. However, there is a paucity of robust clinical data on spasticity progression timeframes, associated symptom development, functional impairment, and maximal duration of muscle tone reduction with BoNT-A.

The ONTIME pilot study explores these foregoing issues to establish whether treatment with abobotulinumtoxinA (Dysport®) within 2–12 weeks post-stroke might delay symptomatic or disabling spasticity development, and to assess the duration of this effect. Importantly, this study incorporates composite measure of active and passive functionality, involuntary movements and pain.

Fig. 1

Continue —> Effect of early use of AbobotulinumtoxinA after stroke on spasticity progression: Protocol for a randomised controlled pilot study in adult subjects with moderate to severe upper limb spasticity (ONTIME pilot)

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