Archive for category 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

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[ARTICLE] Assessment and treatment of spastic equinovarus foot after stroke: Guidance from the Mont-Godinne interdisciplinary group – Full Text

Objective: To present interdisciplinary practical guidance for the assessment and treatment of spastic equinovarus foot after stroke.

Results: Clinical examination and diagnostic nerve block with anaesthetics determine the relative role of the factors leading to spastic equinovarus foot after stroke: calf spasticity, triceps surae – Achilles tendon complex shortening and dorsiflexor muscles weakness and/or imbalance. Diagnostic nerve block is a mandatory step in determining the cause(s) of, and the most appropriate treatment(s) for, spastic equinovarus foot. Based on interdisciplinary discussion, and according to a patient-oriented goal approach, a medical and/or surgical treatment plan is proposed in association with a rehabilitation programme. Spasticity is treated with botulinum toxin or phenol–alcohol chemodenervation and neurotomy, shortening is treated by stretching and muscle-tendon lengthening, and weakness is treated by ankle-foot orthosis, functional electrical stimulation and tendon transfer. These treatments are frequently combined.

Conclusion: Based on 20 years of interdisciplinary expertise of management of the spastic foot, guidance was established to clarify a complex problem in order to help clinicians treat spastic equinovarus foot. This work should be the first step in a more global international consensus.

Introduction

Stroke is the third most common cause of death and the primary cause of severe disability in industrialized countries. Following stroke, approximately 80% of patients regain walking function with decreased gait velocity and asymmetrical gait pattern (1). Spastic equinovarus foot (SEVF) is one of the most common disabling deformities observed among hemiplegic patients. SEVF is frequently associated with other kinematic gait abnormalities, such as stiff knee gait, genu recurvatum, and painful claw toes. SEVF deformity forces the patient to increase their hip and knee flexion in the swing phase. If they are unable to do this (e.g. if they have associated stiff knee gait), the patient will present a hip circumbduction in the swing phase. Correction of such equinus may therefore improve distal as well as proximal gait disturbances.

SEVF deformity has 4 main causes (2, 3). The first is spasticity of the calf muscles (soleus, gastrocnemius, tibialis posterior, flexor digitorum and flexor hallucis longus muscles), responsible for SEVF in the stance phase of gait and for painful toe curling with callosities on the pulp and dorsum of the toes. The peroneus longus and brevis muscles may also be spastic (often with clonus), but such spasticity is useful to limit the varus and stabilize the ankle. Secondly, the spastic muscles have a tendency to remain in a shortened position for prolonged periods, which, in turn, results in soft-tissue changes and contractures, leading to a fixed deformity (4). Thirdly, weakness of the ankle dorsiflexor muscles (tibialis anterior, extensor digitorum and hallucis muscles) as well as the peroneus longus and brevis muscles is responsible for drop-foot in the swing phase of gait. Such weakness is often emphasized by triceps spastic co-contraction and/or contracture. The weakness also affects the triceps surae muscles, leading to a lack of propulsion at the end of the stance phase of gait. Lastly, an imbalance between the tibialis anterior and the peroneus muscles leads to varus of the hind-foot in the swing phase, as peroneus activation must compensate for physiological varus positioning related to contraction of the tibialis anterior. In such a case, the foot will be placed in an unstable varus position during the swing phase and at the beginning of the stance phase.

The respective role of the main causes of SEVF (spasticity, shortening, weakness, and imbalance) varies from patient to patient, and therapeutic decisions are therefore challenging. Indeed, as emphasized by Fuller, the causes of SEVF are varied and complex, due to a variety of deforming forces, and thus a single procedure does not exist to correct all deformities (3). Hence there is a need for guidance and guidelines.

Treatments for SEVF described in the literature are multimodal and include rehabilitation, orthosis, botulinum toxin (BoNT-A) injections, alcohol and phenol nerve blocks, functional neurosurgery (selective neurotomy and intrathecal baclofen therapy) and orthopaedic surgery (tendon transfer, tendon lengthening and bone surgery) (5). SEVF rehabilitation programmes include strengthening of the tibialis anterior and peroneus muscles, electrical stimulation, stretching of the triceps surae to reduce spasticity and prevent contracture, and gait and balance training. Modern therapeutic approaches, such as task-oriented strategy and treadmill with bodyweight support, are promoted. Several publications support the effectiveness of these treatments in SEVF (6–8). However, only 3 studies have compared different treatment options (9–11). A systematic review of surgical correction in adult patients with stroke emphasized the need to compare treatments in order to generate evidence on which to base algorithms (8). In fact, no practical guidelines are available for use in daily practice. Evidence regarding choice of treatment is poor, thus therapeutic decision-making is based on professional personal preferences and beliefs rather than on scientific evidence. An interdisciplinary approach with a physical medicine and rehabilitation (PMR) specialist and rehabilitation team, neurosurgeon, and orthopaedic surgeon is therefore mandatory in order to optimize treatments.

The aim of this paper is to present and discuss the Mont-Godinne interdisciplinary guidance (Fig. 1), based on the existing literature and on 20 years of experience of an interdisciplinary medical and surgical approach to SEVF.

Continue —> Journal of Rehabilitation Medicine – Assessment and treatment of spastic equinovarus foot after stroke: Guidance from the Mont-Godinne interdisciplinary group – HTML

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[ARTICLE] Influence of physician empathy on the outcome of botulinum toxin treatment for upper limb spasticity in patients with chronic stroke: A cohort study – Full Text

Abstract

Objective: To examine the relationship between patient-rated physician empathy and outcome of botulinum toxin treatment for post-stroke upper limb spasticity.

Design: Cohort study.

Subjects: Twenty chronic stroke patients with upper limb spasticity.

Methods: All patients received incobotulinumtoxinA injection in at least one muscle for each of the following patterns: flexed elbow, flexed wrist and clenched fist. Each treatment was performed by 1 of 5 physiatrists with equivalent clinical experience. Patient-rated physician empathy was quantified with the Consultation and Relational Empathy Measure immediately after botulinum toxin treatment. Patients were evaluated before and at 4 weeks after botulinum toxin treatment by means of the following outcome measures: Modified Ashworth Scale; Wolf Motor Function Test; Disability Assessment Scale; Goal Attainment Scaling.

Results: Ordinal regression analysis showed a significant influence of patient-rated physician empathy (independent variable) on the outcome (dependent variables) of botulinum toxin treatment at 4 weeks after injection, as measured by Goal Attainment Scaling (p < 0.001).

Conclusion: These findings support the hypothesis that patient-rated physician empathy may influence the outcome of botulinum toxin treatment in chronic stroke patients with upper limb spasticity as measured by Goal Attainment Scaling.

Introduction

Stroke is a leading cause of adult disability (1, 2). Damage to the descending tracts and sensory-motor networks results in the positive and negative signs of the upper motor neurone syndrome (UMNS) (1–3). The upper limb is commonly involved after stroke, with up to 69% of patients having arm weakness on admission to hospital (4). Recovery of upper limb function has been found to correlate with the degree of initial paresis and its topical distribution according to the cortico-motoneuronal representation of arm movements (5–9).

Spasticity is a main feature of UMNS. It is defined as a state of increased muscle tone with exaggerated reflexes characterized by a velocity-dependent increase in resistance to passive movement (10). Upper limb spasticity has been found to be associated with reduced arm function, low levels of independence and high burden of direct care costs during the first year post-stroke (11). It affects nearly half of patients with initial impaired arm function, with a prevalence varying from 17% to 38% of all patients at one year post-stroke (11). Up to 13% of patients with stroke need some form of spasticity treatment (drug therapy, physical therapy or other rehabilitation approaches) within 6–12 months post-onset (11, 12). Botulinum toxin type A (BoNT-A) has been proven safe and effective for reducing upper limb spasticity and improving arm passive function in adult patients (13, 14). While current literature reports highly patient-specific potential gains in function after BoNT-A treatment, there is inadequate evidence to determine the efficacy of BoNT-A in improving active function associated with adult upper limb spasticity (13).

Empathy refers to the ability to understand and share the feelings, thoughts or attitudes of another person (15). It is an essential component of the physician-patient relationship and a key dimension of patient-centred care (15, 16). This is even more important in rehabilitation medicine, where persons with disabilities often report encountering attitudinal and environmental barriers when trying to obtain rehabilitative care and express the need for better communication with their healthcare providers (17).

To the best of our knowledge, no previous research has investigated the influence of physician empathy on patient outcome after spasticity treatment. The aim of this study was to examine the relationship between patient-rated physician empathy and clinical outcome of BoNT-A treatment for upper limb spasticity due to chronic stroke. […]

Continue —> Journal of Rehabilitation Medicine – Influence of physician empathy on the outcome of botulinum toxin treatment for upper limb spasticity in patients with chronic stroke: A cohort study – HTML

 

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[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

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[Abstract] Electro-acupuncture for post-stroke spasticity: a systematic review and meta-analysis

Abstract

Objective

To evaluate the effects and safety of electro-acupuncture (EA) for stroke patients with spasticity.

Data Sources

Five English (PubMed, EMBASE, CINAHL, Cochrane Central Register of Controlled Trials and AMED) and four Chinese databases (CBM, CNKI, CQVIP and Wanfang) were searched from their inception to September 2016.

Data Selection

Randomized controlled trials were included if they measured spasticity with Modified Ashworth Scale in stroke patients and investigated the add-on effects of electro-acupuncture to routine pharmacotherapy and rehabilitation therapies.

Data Extraction

Information on patients, study design, treatment details and outcomes assessing spasticity severity, motor function and activity of daily living were extracted.

Data Synthesis

In total, 22 trials met the search criteria and were included involving 1,425 participants. The estimated add-on effects of EA to reduce spasticity in upper limb measured by MAS (SMD: -0.57[-0.84, -0.29]) and improve overall motor function measured by FMA (MD: 10.60[8.67, 12.53]) were significant. It was also found that for spasticity in lower limb, lower-limb motor function and activity of daily living, significant add-on effects of EA were also shown (SMD: -0.88[-1.42, -0.35], MD:4.42[0.06, 8.78] and MD: 6.85[3.64, 10.05] respectively), though with high heterogeneity. For upper-limb motor function, no significant add-on effects of EA was received.

Conclusions

Electro-acupuncture combined with conventional routine care has the potential of reducing spasticity in upper and lower limb and improving overall and lower extremity motor function and activity of daily living for spasticity patients within 180 days post stroke. Further studies of high methodological and reporting quality are needed to confirm the effects and safety of electro-acupuncture, and to explore the adequate and optimal protocol of EA for post-stroke spasticity incorporating a group of comprehensive outcome measures in different populations.

Source: Electro-acupuncture for post-stroke spasticity: a systematic review and meta-analysis – Archives of Physical Medicine and Rehabilitation

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[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).

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[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

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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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[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

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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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