Posts Tagged spasticity

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

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

Randomized controlled study.

Inpatient rehabilitation center of a teaching hospital.

Sixty-nine patients with foot drop.

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

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

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

1. Brewer L, Horgan F, Hickey A, Stroke rehabilitation: recent advances and future therapies. QJM 2013; 106: 1125. Google Scholar CrossRef, Medline
2. Bethoux F, Rogers HL, Nolan KJ, The effects of peroneal nerve functional electrical stimulation versus ankle-foot orthosis in patients with chronic stroke: a randomized controlled trial. Neurorehabil Neural Repair 2014; 28: 688697. Google Scholar Link
3. O’Dell MW, Dunning K, Kluding P, Response and prediction of improvement in gait speed from functional electrical stimulation in persons with poststroke drop foot. PM R 2014; 6: 587601; quiz 601. Google Scholar CrossRef, Medline
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5. Samuelkamaleshkumar S, Reethajanetsureka S, Pauljebaraj P, Mirror therapy enhances motor performance in the paretic upper limb after stroke: a pilot randomized controlled trial. Arch Phys Med Rehabil 2014; 95: 20002005. Google Scholar CrossRef, Medline
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8. Stein C, Fritsch CG, Robinson C, Effects of electrical stimulation in spastic muscles after stroke: systematic review and meta-analysis of randomized controlled trials. Stroke 2015; 46: 21972205. Google Scholar CrossRef, Medline
9. Knutson JS, Fu MJ, Sheffler LR, Neuromuscular electrical stimulation for motor restoration in hemiplegia. Phys Med Rehabil Clin N Am 2015; 26: 729745. Google Scholar CrossRef, Medline
10. Sabut SK, Sikdar C, Kumar R, Functional electrical stimulation of dorsiflexor muscle: effects on dorsiflexor strength, plantarflexor spasticity, and motor recovery in stroke patients. NeuroRehabilitation 2011; 29: 393400. Google Scholar Medline
11. You G, Liang H, Yan T. Functional electrical stimulation early after stroke improves lower limb motor function and ability in activities of daily living. NeuroRehabilitation 2014; 35: 381389. Google Scholar Medline
12. Kojima K, Ikuno K, Morii Y, Feasibility study of a combined treatment of electromyography-triggered neuromuscular stimulation and mirror therapy in stroke patients: a randomized crossover trial. NeuroRehabilitation 2014; 34: 235244. Google Scholar Medline
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15. Lee D, Lee G, Jeong J. Mirror Therapy with Neuromuscular Electrical Stimulation for improving motor function of stroke survivors: a pilot randomized clinical study. Technol Health Care 2016; 24: 503511. Google Scholar CrossRef, Medline
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18. Lee HJ, Cho KH, Lee WH. The effects of body weight support treadmill training with power-assisted functional electrical stimulation on functional movement and gait in stroke patients. Am J Phys Med Rehabil 2013; 92: 10511059. Google Scholar CrossRef, Medline
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20. Sawner KA, LaVigne JM, Brunnstrom S. Brunnstrom’s movement therapy in hemiplegia: a neurophysiological approach. 2nd ed. Philadelphia, PA: Lippincott, 1992. Google Scholar
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24. Bakhtiary AH, Fatemy E. Does electrical stimulation reduce spasticity after stroke? A randomized controlled study. Clin Rehabil 2008; 22: 418425. Google Scholar Link
25. Sütbeyaz S, Yavuzer G, Sezer N, Mirror therapy enhances lower-extremity motor recovery and motor functioning after stroke: a randomized controlled trial. Arch Phys Med Rehabil 2007; 88: 555559. Google Scholar CrossRef, Medline
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28. Gondin J, Brocca L, Bellinzona E, Neuromuscular electrical stimulation training induces atypical adaptations of the human skeletal muscle phenotype: a functional and proteomic analysis. J Appl Physiol 2011; 110: 433450. Google Scholar CrossRef, Medline
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Source: Effects of mirror therapy combined with neuromuscular electrical stimulation on motor recovery of lower limbs and walking ability of patients with stroke: a randomized controlled studyClinical Rehabilitation – Qun Xu, Feng Guo, Hassan M Abo Salem, Hong Chen, Xiaolin Huang, 2017

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[ARTICLE] Practice patterns for spasticity management with phenol neurolysis – Full Text HTML

Abstract

Objective: To present practice patterns for phenol neurolysis procedures conducted for spasticity management.

Design: A retrospective review of 185 persons with spasticity who underwent phenol neurolysis procedures (n = 293) at an academic rehabilitation hospital and clinic. Patient demographics, concomitant spasticity treatments, and procedure relevant information were collected.

Results: The cohort included 71.9% males and 61.6% inpatient procedures. Neurological diagnoses included stroke (41.0%), traumatic brain injury (28.6%) and spinal cord injury (24.3%). Musculoskeletal diagnoses included spastic hemiplegia or paresis (51.3%), tetraplegia (38.4) and paraplegia (9.2%). At the time of phenol neurolysis, most patients (77.5%) received concomitant pharmacological treatments for spasticity. Injection guidance modalities included electrical stimulation and ultrasound (69.3%) or ultrasound only (27.3%). A mean of 3.48 ml of phenol were injected per nerve and 10.95 ml of phenol were used per procedure. Most commonly injected nerves included the obturator nerve (35.8%) and sciatic branches to the hamstrings and adductor magnus (27.0%). Post-phenol neurolysis assessment was recorded in 54.9% of encounters, in which 84.5% reported subjective benefit. Post-procedure adverse events included pain (4.0%), swelling and inflammation (2.7%), dysaesthesia (0.7%) and hypotension (0.7%).

Conclusion: Phenol neurolysis is currently used to reduce spasticity for various functional goals, including preventing contractures and improving gait. Depending on the pattern of spasticity displayed, numerous peripheral nerves in the upper and lower extremities can be targeted for treatment with phenol neurolysis. Further research into its role in spasticity management, including studies exploring its cost-effectiveness and pharmacological and side-effects compared with other treatment options are needed.

Introduction

Characterized by hyperexcitable stretch reflexes that increase muscle tonicity and exaggerate tendon jerks, spasticity is a common motor disorder that follows a variety of central nervous system insults (1). Implicated neurological insults most often include stroke, traumatic brain injury (TBI) or spinal cord injury (SCI). Spasticity is often associated with various complications including joint contractures, muscle shortening and postural deformities (1) that lead to multiple impairments. Early goal-directed spasticity management is instrumental in helping increase the likelihood of good outcomes and limiting complications (1, 2). Unfortunately, a lack of universally standardized management and an abundance of therapeutic options make spasticity management a challenging task.

Currently, spasticity is frequently managed through a combination of therapeutic modalities, pharmaceutical options and surgical procedures (3). Pharmaceutical options include medications delivered orally, via local injections, or through intrathecal pumps. Oral medications, including baclofen and tizanidine, help decrease spasticity (3). However, systemic side-effects, such as generalized muscle weakness, sedation, confusion, and hypotension, preclude the use of higher dosages that might be warranted for control of moderate-to-severe spasticity (3, 4). Intrathecal baclofen pump (ITB) is often indicated in treating severe and/or diffuse spasticity as a means to deliver high-dosage baclofen with less concern for systemic side-effects (4). Although ITB treatment is very effective, numerous complications and the requirement for commitment to maintenance associated with this treatment makes it favourable only for some patients with severe spasticity (4, 5).

Chemoneurolysis via localized injections can help provide focal spasticity relief (1, 3, 6). In addition, the use of single-event multi-level chemoneurolysis helps treat several areas of muscle spasticity, each with varying severities (7). Medications used in chemo-neurolysis procedures include botulinum neurotoxin (BoNT), phenol, and alcohol neurolysis (3–7). Compared with phenol and the understudied alcohol neurolysis, BoNT usage in treating spasticity is documented extensively in the literature with regards to pharmacodynamics, adverse effects and clinical benefits (7–9). However, the response to chemodenervation with BoNT often requires 3–5 days to generate spasticity benefit, which generally lasts approximately 3 months. Although clinical standards permit repeating chemodenervation every 3 months, the majority of patients with spasticity prefer an increased frequency for maintaining clinical benefit (10–12). BoNT injections are associated with significant costs, and repeated injections are often further restricted by financial feasibility. In the USA, depending on the insurance being used, the approved dosage of BoNT is only 400–600 units of every 3 months. These limitations prevent the sole utility of chemodenervation for a multi-pattern treatment, e.g. elbow flexion, clenched fist, stiff knee gait, and equinovarus of the foot. Consequently, phenol neurolysis (PN) and BoNT are used in complement, with PN frequently reserved for proximal nerves and BoNT used for distal musculature.

In contrast, PN produces an almost-immediate effect that manifests within minutes of injection, which may last as long as 6 months depending on the dosage used (1, 13). In addition, PN is significantly less expensive. PN may also be re-injected before 3 months, unlike BoNT. However, the safety and efficacy of PN is less-commonly documented in the literature than BoNT chemodenervation. PN also requires a higher level of expertise to administer, and has a worse side-effect profile, which includes hypotension, prolonged pain, dysaesthesias, site inflammation, and joint fibrosis (1, 13, 14). These disadvantages for phenol usage are associated with safety concerns relative to neurotoxins, thus making BoNT a vastly more popular option for chemoneurolysis. Phenol is therefore being used increasingly less in the USA and is poorly documented in the spasticity literature. Given its advantages, PN may be superior to chemodenervation with BoNT in certain clinical scenarios. Thus, the primary purpose of the current study is to describe the utilization pattern of PN at a single site.

 

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[Abstract] The Effect of Modified Constraint-Induced Movement Therapy on Spasticity and Motor Function of the Affected Arm in Patients with Chronic Stroke

Purpose: The purpose of this study was to explore the effect of modified constraint-induced movement therapy (CIMT) in a real-world clinical setting on spasticity and functional use of the affected arm and hand in patients with spastic chronic hemiplegia.

Method: A prospective consecutive quasi-experimental study design was used. Twenty patients with spastic hemiplegia (aged 22–67 years) were tested before and after 2-week modified CIMT in an outpatient rehabilitation clinic and at 6 months. The Modified Ashworth Scale (MAS), active range of motion (AROM), grip strength, Motor Activity Log (MAL), Sollerman hand function test, and Box and Block Test (BBT) were used as outcome measures.

Results: Reductions (p<0.05–0.001) in spasticity (MAS) were seen both after the 2-week training period and at 6-month follow-up. Improvements were also seen in AROM (median change of elbow extension 5°, dorsiflexion of hand 10°), grip strength (20 Newton), and functional use after the 2-week training period (MAL: 1 point; Sollerman test: 8 points; BBT: 4 blocks). The improvements persisted at 6-month follow-up, except for scores on the Sollerman hand function test, which improved further.

Conclusion: Our study suggests that modified CIMT in an outpatient clinic may reduce spasticity and increase functional use of the affected arm in spastic chronic hemiplegia, with improvements persisting at 6 months.

Source: The Effect of Modified Constraint-Induced Movement Therapy on Spasticity and Motor Function of the Affected Arm in Patients with Chronic Stroke | Physiotherapy Canada

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[Abstract] Duration of Treatment Effect of IncobotulinumtoxinA in Upper Limb Spasticity (P4.036)

ABSTRACT

Objective: To assess, the duration of treatment effect for incobotulinumtoxinA treatment intervals using a pooled analysis of 2 phase 3 clinical studies in upper-limb post-stroke spasticity (ULPSS).

Background: The efficacy and safety of incobotulinumtoxinA in ULPSS has been confirmed in 2 phase 3 studies. Study 0410 included a randomized placebo-controlled period and an open-label extension (OLEX). OLEX reinjection intervals were flexible (≥12 week intervals with doses ≤400U). Study 3001 included fixed 12-week treatment intervals (TIs). In study 0410, investigators and subjects mutually determined the need for re-injection on the basis of pre-specified criteria (eg, Ashworth scale scores, investigator’s clinical impression).

Design/Methods: All TIs between 2 consecutive incobotulinumtoxinA injections were included, except TIs prior to the end of study visit and those with doses <300U. Outliers and factors other than a medical need for re-injection (eg, visit scheduling) were accounted for using duration thresholds applied during the analysis; the number of subjects with ≥1 TI above a threshold was calculated.

Results: A total of 347/437 incobotulinumtoxinA TIs met the inclusion criteria (range of re-injection intervals observed: 9–49 weeks). Over half (54.8%) of the re-injections were administered at week ≥14. The mean incobotulinumtoxinA TI was 15.46 weeks (standard devation: 4.63 weeks). A majority of subjects (59.1%) had ≥1 TI with re-injection at week ≥16; 33.1% of subjects had 1, 22.1% had 2 and 3.9% had 3. Many subjects (42.5%) had ≥1 TI with re­-injection at week ≥18.

Conclusions: These results demonstrate variability in the duration of treatment effect, which supports the use of flexible and individualized dosing intervals for the treatment of ULPSS. The duration of treatment effect was ≥14 weeks after most treatments; however, a considerable proportion of patients experienced effects lasting up to 20 weeks.

Source: Duration of Treatment Effect of IncobotulinumtoxinA in Upper Limb Spasticity (P4.036)

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[ARTICLE] Practice patterns for spasticity management with phenol neurolysis – HTML

Abstract

Objective: To present practice patterns for phenol neurolysis procedures conducted for spasticity management.

Design: A retrospective review of 185 persons with spasticity who underwent phenol neurolysis procedures (n = 293) at an academic rehabilitation hospital and clinic. Patient demographics, concomitant spasticity treatments, and procedure relevant information were collected.

Results: The cohort included 71.9% males and 61.6% inpatient procedures. Neurological diagnoses included stroke (41.0%), traumatic brain injury (28.6%) and spinal cord injury (24.3%). Musculoskeletal diagnoses included spastic hemiplegia or paresis (51.3%), tetraplegia (38.4) and paraplegia (9.2%). At the time of phenol neurolysis, most patients (77.5%) received concomitant pharmacological treatments for spasticity. Injection guidance modalities included electrical stimulation and ultrasound (69.3%) or ultrasound only (27.3%). A mean of 3.48 ml of phenol were injected per nerve and 10.95 ml of phenol were used per procedure. Most commonly injected nerves included the obturator nerve (35.8%) and sciatic branches to the hamstrings and adductor magnus (27.0%). Post-phenol neurolysis assessment was recorded in 54.9% of encounters, in which 84.5% reported subjective benefit. Post-procedure adverse events included pain (4.0%), swelling and inflammation (2.7%), dysaesthesia (0.7%) and hypotension (0.7%).

Conclusion: Phenol neurolysis is currently used to reduce spasticity for various functional goals, including preventing contractures and improving gait. Depending on the pattern of spasticity displayed, numerous peripheral nerves in the upper and lower extremities can be targeted for treatment with phenol neurolysis. Further research into its role in spasticity management, including studies exploring its cost-effectiveness and pharmacological and side-effects compared with other treatment options are needed.

Introduction

Characterized by hyperexcitable stretch reflexes that increase muscle tonicity and exaggerate tendon jerks, spasticity is a common motor disorder that follows a variety of central nervous system insults (1). Implicated neurological insults most often include stroke, traumatic brain injury (TBI) or spinal cord injury (SCI). Spasticity is often associated with various complications including joint contractures, muscle shortening and postural deformities (1) that lead to multiple impairments. Early goal-directed spasticity management is instrumental in helping increase the likelihood of good outcomes and limiting complications (1, 2). Unfortunately, a lack of universally standardized management and an abundance of therapeutic options make spasticity management a challenging task.

Currently, spasticity is frequently managed through a combination of therapeutic modalities, pharmaceutical options and surgical procedures (3). Pharmaceutical options include medications delivered orally, via local injections, or through intrathecal pumps. Oral medications, including baclofen and tizanidine, help decrease spasticity (3). However, systemic side-effects, such as generalized muscle weakness, sedation, confusion, and hypotension, preclude the use of higher dosages that might be warranted for control of moderate-to-severe spasticity (3, 4). Intrathecal baclofen pump (ITB) is often indicated in treating severe and/or diffuse spasticity as a means to deliver high-dosage baclofen with less concern for systemic side-effects (4). Although ITB treatment is very effective, numerous complications and the requirement for commitment to maintenance associated with this treatment makes it favourable only for some patients with severe spasticity (4, 5).

Chemoneurolysis via localized injections can help provide focal spasticity relief (1, 3, 6). In addition, the use of single-event multi-level chemoneurolysis helps treat several areas of muscle spasticity, each with varying severities (7). Medications used in chemo-neurolysis procedures include botulinum neurotoxin (BoNT), phenol, and alcohol neurolysis (3–7). Compared with phenol and the understudied alcohol neurolysis, BoNT usage in treating spasticity is documented extensively in the literature with regards to pharmacodynamics, adverse effects and clinical benefits (7–9). However, the response to chemodenervation with BoNT often requires 3–5 days to generate spasticity benefit, which generally lasts approximately 3 months. Although clinical standards permit repeating chemodenervation every 3 months, the majority of patients with spasticity prefer an increased frequency for maintaining clinical benefit (10–12). BoNT injections are associated with significant costs, and repeated injections are often further restricted by financial feasibility. In the USA, depending on the insurance being used, the approved dosage of BoNT is only 400–600 units of every 3 months. These limitations prevent the sole utility of chemodenervation for a multi-pattern treatment, e.g. elbow flexion, clenched fist, stiff knee gait, and equinovarus of the foot. Consequently, phenol neurolysis (PN) and BoNT are used in complement, with PN frequently reserved for proximal nerves and BoNT used for distal musculature.

In contrast, PN produces an almost-immediate effect that manifests within minutes of injection, which may last as long as 6 months depending on the dosage used (1, 13). In addition, PN is significantly less expensive. PN may also be re-injected before 3 months, unlike BoNT. However, the safety and efficacy of PN is less-commonly documented in the literature than BoNT chemodenervation. PN also requires a higher level of expertise to administer, and has a worse side-effect profile, which includes hypotension, prolonged pain, dysaesthesias, site inflammation, and joint fibrosis (1, 13, 14). These disadvantages for phenol usage are associated with safety concerns relative to neurotoxins, thus making BoNT a vastly more popular option for chemoneurolysis. Phenol is therefore being used increasingly less in the USA and is poorly documented in the spasticity literature. Given its advantages, PN may be superior to chemodenervation with BoNT in certain clinical scenarios. Thus, the primary purpose of the current study is to describe the utilization pattern of PN at a single site. […]

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[WEB SITE] How to PERMANENTLY Treat Post Stroke Spasticity

The Complete Guide to Treating Post Stroke Spasticity – for Good!

The Complete Guide to Treating Post Stroke Spasticity – for Good!

Post stroke spasticity is the most common post stroke side effect, and it’s likely that you’ve never heard the whole truth about it.

Most likely, you were told that there’s something wrong with your muscles, and Botox can fix it.

While this is partially true, it omits more effective and permanent solutions to spasticity.

There is tons of hope for treating spasticity – even severe spasticity in paralyzed muscles.

Today, we’re sharing the most valuable way to fix this frustrating problem.

Spasticity as Brain-Muscle Miscommunication

Before, you’ve probably heard spasticity explained in relation to your muscles.

Spasticity causes your muscles to become tightened, so it’s natural to focus on your muscles as what needs to be fixed. But spasticity is actually caused by miscommunication between your brain and your muscles.

Normally your muscles are in constant communication with your brain about how much tension they’re feeling, and the brain has to constantly monitor this tension to prevent tearing. Your brain continuously sends out messages telling your muscles when to contract and relax.

When a stroke damages part of the brain responsible for muscle control, this communication is thrown off. The damaged part of your brain no longer receives the messages that your muscles are trying to send, and as a result, your brain no longer tells them when to contract or relax.

So, your muscles keep themselves in a constant state of contraction in order to protect themselves.

That’s the cause of spasticity from the muscular perspective.

However, there’s a second layer to spasticity that no one talks about. Spasticity is also caused by miscommunication from your spinal cord.

The OTHER Cause of Spasticity

While your muscles are always in communication with your brain, they’re also in communication with your spinal cord.

Usually the spinal cord takes the messages from your muscles and sends them up to the brain. But since the brain is no longer reading those messages, your affected muscles have no one to talk to.

So the spinal cord takes over.

But the spinal cord doesn’t know how to properly operate your muscles. It really only has one goal: to prevent your muscles from tearing. In order to do that, your spinal cord sends signals to keep your muscles in a constant state of contraction, which is what causes spasticity.

Your spinal cord only has the best intentions – to prevent your muscles from tearing – but it’s frustrating because now your muscles are painfully stiff.

Let’s look at some temporary and permanent treatment options to fix this issue and alleviate your spasticity.

How to Temporarily Treat Spasticity

There are temporary ways to treat spasticity, which includes locally administered or orally taken drugs.

Locally administered drugs are injected into the affected muscles and help reduce pain, increase movement, and curb potential bone and joint problems.

Orally taken drugs offer the same benefits, but they are not site-specific and will affect all the muscles in your body.

As with most drugs in Western society, they only treat the symptom, not the underlying cause. This means that drugs are only a short-term solution.

So how can you treat the underlying cause?

With the help of your good ol’ friend neuroplasticity.

How to Permanently Reduce Spasticity

Neuroplasticity is your long-term, permanent solution to overcoming spasticity.

When a stroke damages part of the brain responsible for motor function, it decreases the number of brain cells dedicated to moving your affected limbs.

Neuroplasticity comes into play by rewiring your brain and dedicating more brain cells to controlling your affected limbs.

In order for this rewiring to occur, you have to repeat your rehab exercises over and over. The more you repeat the movement, the better the spasticity will subside and movement will improve.

It’s like paving new roads. The more you reinforce those new roads, the stronger they’ll become.

Putting in hard work is essential.

5 Ways to Activate Neuroplasticity and Treat Spasticity

If spasticity is causing you pain, then using temporary solutions in the meantime can help alleviate the barriers keeping you from your rehab exercises.

Since rehab exercise is the only permanent solution to spasticity, getting yourself to participate is crucial.

Here are 5 ways to maximize your benefit from rehab exercise and reduce spasticity:

There’s one thing these methods all have in common: Repetition.

No matter which option you choose, be sure to create an at-home rehabilitation regimen that utilizes a high number of repetitions.

You’ll get better faster this way because it’s the only way to retrain your brain to relax your spastic muscles – permanently.

3 Ways to Treat Spasticity When You Can’t Move Your Muscles

Sometimes muscles become so stiff with spasticity that it feels like they’re paralyzed.

The following 3 methods can help reduce spasticity in paralyzed muscles:

Practice these methods repetitively and you can regain movement in paralyzed muscles.

Yes, it’s possible to regain movement in paralyzed muscles! Read a success story on that here.

Then, once you’ve regained some movement, you can use any of the previous 5 methods to keep improving.

Spasticity as a Surprising Sign of Recovery

And that’s a wrap!

You are now aware that spasticity is caused by miscommunication between your brain and your muscles…

And this should bring you tons hope that your spasticity is treatable because it means that your muscles are still trying to communicate with your brain!

Your body hasn’t given up, and neither should you.

There are tons of success stories of stroke survivors who regained way more movement than doctors ever thought possible. Don’t let someone else’s limiting beliefs limit your recovery.

Even if you have no movement in your spastic muscles, keep trying by focusing on high repetition and taking small steps.

Eventually, your spasticity will start to improve – for good.

Source: How to PERMANENTLY Treat Post Stroke Spasticity – Flint Rehab

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[WEB SITE] Spasticity, Motor Recovery, and Neural Plasticity after Stroke – Full Text

Spasticity and weakness (spastic paresis) are the primary motor impairments after stroke and impose significant challenges for treatment and patient care. Spasticity emerges and disappears in the course of complete motor recovery. Spasticity and motor recovery are both related to neural plasticity after stroke. However, the relation between the two remains poorly understood among clinicians and researchers. Recovery of strength and motor function is mainly attributed to cortical plastic reorganization in the early recovery phase, while reticulospinal (RS) hyperexcitability as a result of maladaptive plasticity, is the most plausible mechanism for post-stroke spasticity. It is important to differentiate and understand that motor recovery and spasticity have different underlying mechanisms. Facilitation and modulation of neural plasticity through rehabilitative strategies, such as early interventions with repetitive goal-oriented intensive therapy, appropriate non-invasive brain stimulation, and pharmacological agents, are the key to promote motor recovery. Individualized rehabilitation protocols could be developed to utilize or avoid the maladaptive plasticity, such as RS hyperexcitability, in the course of motor recovery. Aggressive and appropriate spasticity management with botulinum toxin therapy is an example of how to create a transient plastic state of the neuromotor system that allows motor re-learning and recovery in chronic stages.

Introduction

According to the CDC, approximately 800,000 people have a stroke every year in the United States. The continued care of seven million stroke survivors costs the nation approximately $38.6 billion annually. Spasticity and weakness (i.e., spastic paresis) are the primary motor impairments and impose significant challenges for patient care. Weakness is the primary contributor to impairment in chronic stroke (1). Spasticity is present in about 20–40% stroke survivors (2). Spasticity not only has downstream effects on the patient’s quality of life but also lays substantial burdens on the caregivers and society (2).

Clinically, poststroke spasticity is easily recognized as a phenomenon of velocity-dependent increase in tonic stretch reflexes (“muscle tone”) with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex (3). Though underlying mechanisms of spasticity remain poorly understood, it is well accepted that there is hyperexcitability of the stretch reflex in spasticity (47). Accumulated evidence from animal (8) and human studies (918) supports supraspinal origins of stretch reflex hyperexcitability. In particular, reticulospinal (RS) hyperexcitability resulted from loss of balanced inhibitory, and excitatory descending RS projections after stroke is the most plausible mechanism for poststroke spasticity (19). On the other hand, animal studies have strongly supported the possible role of RS pathways in motor recovery (2036), while recent studies with stroke survivors have demonstrated that RS pathways may not always be beneficial (3738). The relation between spasticity and motor recovery and the role of plastic changes after stroke in this relation, particularly RS hyperexcitability, remain poorly understood among clinicians and researchers. Thus, management of spasticity and facilitation of motor recovery remain clinical challenges. This review is organized into the following sessions to understand this relation and its implication in clinical management.

• Poststroke spasticity and motor recovery are mediated by different mechanisms

• Motor recovery are mediated by cortical plastic reorganizations (spontaneous or via intervention)

• Reticulospinal hyperexcitability as a result of maladaptive plastic changes is the most plausible mechanism for spasticity

• Possible roles of RS hyperexcitability in motor recovery

• An example of spasticity reduction for facilitation of motor recovery […]

Continue —> Frontiers | Spasticity, Motor Recovery, and Neural Plasticity after Stroke | Neurology

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[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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[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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