Posts Tagged spasticity

[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

, , , , , ,

Leave a comment

[Abstract] A Randomized Controlled Study: Effectiveness of Functional Electrical Stimulation on Wrist and Finger Flexor Spasticity in Hemiplegia

Aim

The objective of this study was to investigate the effectiveness of functional electrical stimulation (FES) applied to the wrist and finger extensors for wrist flexor spasticity in hemiplegic patients.

Methods

Thirty stroke patients treated as inpatients were included in the study. Patients were randomly divided into study and control groups. FES was applied to the study group. Wrist range of movement, the Modified Ashworth Scale (MAS), Rivermead Motor Assessment (RMA), Brunnstrom (BS) hand neurophysiological staging, Barthel Index (BI), and Upper Extremity Function Test (UEFT) are outcome measures.

Results

There was no significant difference regarding range of motion (ROM) and BI values on admission between the groups. A significant difference was found in favor of the study group for these values at discharge. In the assessment within groups, there was no significant difference between admission and discharge RMA, BS hand, and UEFT scores in the control group, but there was a significant difference between the admission and discharge values for these parameters in the study group. Both groups showed improvement in MAS values on internal assessment.

Conclusion

It was determined that FES application is an effective method to reduce spasticity and to improve ROM, motor, and functional outcomes in hemiplegic wrist flexor spasticity.

 

Source: A Randomized Controlled Study: Effectiveness of Functional Electrical Stimulation on Wrist and Finger Flexor Spasticity in Hemiplegia – Journal of Stroke and Cerebrovascular Diseases

, , , , , , , , , , ,

Leave a comment

[ARTICLE] The Effects of Navigated Repetitive Transcranial Magnetic Simulation and Brunnstrom Movement Therapy on Upper Extremity Proprioceptive Sense and Spasticity in Stroke Patients: A Double-Blind Randomized Trial – Full Text PDF

Abstract

Purpose: The purpose of this study is to investigate the effects of various treatments (repetitive transcranial magnetic stimulation and Brunnstrom movement therapy) on upper extremity proprioceptive sense and spasticity.

Methods: Twenty-one stroke patients were included in the study. The treatment group (Group 1; n=10) was administered navigated real repetitive transcranial magnetic stimulation (rTMS), and the control group (Group 2; n=11) was administered sham rTMS by the first researcher. The patients in both groups had upper extremity exercises according to Brunnstrom movement therapy (BMT). The patients were assessed using the Brunnstrom recovery stages (BRS), proprioceptive sense assessment, and the modified Ashworth scale (MAS).

Results: Between the treatment group and control group patients, there were no significant statistical differences obtained from pre-treatment and postreatment tenth day, first month, and third month by BRS wrist, hand, and upper extremity stages. The intragroup comparison of the treatment group patients revealed a statistically significant difference between the pre-treatment and post-treatment third month BRS-hand and BRS-upper extremity stages.The pretreatment and postreatment tenth day and first month evaluations of the wrist proprioceptive sense of the groups presented a significant difference. There was no statistically significant difference between the groups in terms of MAS scores before and after treatment evaluations.

Conclusion: The rTMS and BMT approaches that were implemented in the study affected the proprioceptive sense of the wrist after the treatment and in the early period but did not change spasticity.

Keywords: Repetitive transcranial magnetic stimulation, stroke, Brunnstrom recovery stages, proprioceptive sense, spasticity

INTRODUCTION

Proprioceptive sense is the individual’s ability to perceive the position and the motion of his/her body segments in the space via somatosensorial impulses sent by the receptors in the skin, muscles, and joints (1). Researchers have stated that the proprioceptive sense, which is the awareness sense of the body, consists of three fundamental senses: kinesthesia, joint position sense, and neuromuscular control (2). The proprioceptive sense plays a crucial role in carrying out and controlling daily activities, maintaining posture and balance, joint stability, and motor learning (3, 4). Neuromuscular control is affected by proprioceptive inefficiencies apart from motor dysfunctions. It has been shown that proprioceptive knowledge is of extreme importance for the neural control of motion and that the upper extremity proprioceptive sense is commonly decreased or evanished following stroke (5). It has been explained that the proprioceptive deficit incidence rate is 50-65% in stroke patients, which affects daily activities and quality of life negatively (6, 7). It has been stated that proprioceptive and motor deficits have different recovery rates in the first six months following stroke (8). In stroke patients, sensorimotor learning calls for a sound somatosensorial impulse, which is possible through sensorimotor rehabilitation (9). The Bobath, Brunnstrom, Johnstone, and Rood proprioceptive neuromuscular facilitation techniques and the motor learning method, commonly utilized by physiotherapists, are based upon treating sensorimotor functions (10). There exist several recent studies that report that the pain-free, non-invasive transcranial magnetic stimulation (rTMS) application decreases spasticity or that it has no effect (11-13). Stroke rehabilitation is provided by decreasing the transcallosal inhibition from the unaffected motor cortex to the affected motor cortex via 1 Hz rTMS applied on the motor cortex (14, 15). Whereas there is a limited number of studies in the literature with various results on the effects of rTMS and physiotherapy combination on spasticity, a study dealing with the effect of rTMS and physiotherapy combination on proprioceptive sense has not been found. This study was planned to investigate the effect of rTMS and Brunnstrom movement therapy (BMT) on upper extremity proprioceptive sense and spasticity (11, 12).

Full Text PDF

, , , , , , , , ,

Leave a comment

[WEB SITE] What Is Spasticity – Saebo

What is Spasticity?

Spasticity is a neuromuscular condition usually caused by damage to the portion of the brain or spinal cord that controls voluntary movement. The damage causes a change in the balance of signals between the nervous system and the muscles. It is typically found in people with cerebral palsy, traumatic brain injury, stroke, multiple sclerosis, and spinal cord injury.

Charley horse is an understatement.

Spasticity is often described as tight, stiff muscles or spasms that may make movement, posture, and balance difficult. It negatively affects muscles and joints of the extremities, and is particularly harmful to growing children. Individuals with mild spasticity may experience muscle tightness whereas severe spasticity may produce painful, uncontrollable spasms of the extremities; most commonly the legs and arms. This can interfere with functional recovery and curtail rehabilitation efforts.

Unintended consequences.

Spasticity can be disabling and if left untreated, or sub-optimally managed, it may lead to adverse effects such as:

  • Contractures
  • Muscle and joint deformitiesv
  • Urinary tract infections
  • Chronic constipation
  • Fever or other systemic illnesses
  • Pressure sores
  • Overactive reflexes
  • Pain
  • Decreased functional abilities and delayed motor development
  • Difficulty with care and hygiene
  • Abnormal posture
  • Bone and joint deformities

Loosening the grip.

Common treatment interventions for spasticity vary from conservative (therapy) to more aggressive (surgery). Typically, a variety of treatment options are used simultaneously to maximize results. Current spasticity treatment options may include the following:

  • Oral medications
  • Injectable medications
  • Stretching
  • Orthoses
  • Casting
  • Electrotherapeutics
  • Cryotherapy
  • Surgery

Source: What Is Spasticity | Saebo

,

Leave a comment

[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

, , , , ,

Leave a comment

[Abstract] Spasticity Management: The Current State of Transcranial Neuromodulation

Abstract

This narrative review aims to provide an objective view of the non-invasive neuromodulation (NINM) protocols available for treating spasticity, including repetitive transcranial magnetic stimulation (rTMS) and transcranial direct current stimulation (tDCS). On the basis of the relevant randomized controlled trials, we infer that NINM is more effective in reducing spasticity when combined with the conventional therapies than used as a stand-alone treatment. However, the magnitude of NINM aftereffects depends significantly on the applied hemisphere and the underlying pathology. Being in line with these arguments, low-frequency rTMS and cathodal-tDCS over the unaffected hemisphere are more effective in reducing spasticity than high-frequency rTMS and anodal-tDCS over the affected hemisphere in chronic post-stroke. However, most of the studies are heterogeneous in the stimulation setup, patient selection, follow-up duration, and the availability of the sham operation. Therefore, the available data on the usefulness of NINM in reducing spasticity need to be confirmed by further larger and multicentric randomized controlled trials to gather evidence on the efficiency of NINM regimens in reducing spasticity in various neurologic conditions.

Source: Spasticity Management: The Current State of Transcranial Neuromodulation

, , , , , , , ,

Leave a comment

[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

, , , ,

Leave a comment

[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

, , , , , , ,

Leave a comment

[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

, , , , , , , , ,

Leave a comment

[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

, , , , , , , ,

Leave a comment

%d bloggers like this: