Archive for category spasticity

[ARTICLE] ADULT SPASTICITY INTERNATIONAL REGISTRY STUDY: METHODOLOGY AND BASELINE PATIENT, HEALTHCARE PROVIDER, AND CAREGIVER CHARACTERISTICS – Full Text PDF

Objective: The main aim of this study was to determine
the utilization patterns and effectiveness of onabotulinumtoxinA (Botox®) for treatment of spasticity in clinical practice.

Design: An international, multicentre, prospective, observational study at selected sites in North America, Europe, and Asia.

Patients: Adult patients with newly diagnosed or established focal spasticity, including those who had previously received treatment with onabotulinumtoxinA.

Methods: Patients were treated with onabotulinumtoxinA, approximately every 12 weeks, according to their physician’s usual clinical practice over a period of up to 96 weeks, with a final follow-up interview at 108 weeks. Patient, physician and caregiver data were collected.

Results: Baseline characteristics are reported. Of the 745 patients enrolled by 75 healthcare providers from 54 sites, 474 patients had previously received onabotulinumtoxinA treatment for spasticity. Lower limb spasticity was more common than upper limb spasticity, with stroke the most common underlying aetiology. The Short-Form 12 (SF-12) health survey scores showed that patients’ spasticity had a greater perceived impact on physical rather than mental aspects.

Conclusion: The data collected in this study will guide the development of administration strategies to optimize the effectiveness of onabotulinumtoxinA in the management of spasticity of various underlying
aetiologies.

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[Abstract] Efficacy and safety of botulinum toxin type A for upper limb spasticity after stroke or traumatic brain injury: a systematic review with meta-analysis.

Abstract

INTRODUCTION:

Muscle spasticity is a positive symptom after stroke and traumatic brain injury. Botulinum toxin type A (BoNT-A) injection is widely used for treating post stroke and traumatic brain injury spasticity. This study aimed to evaluate efficacy and safety of BoNT-A for upper limb spasticity after stroke and traumatic brain injury and investigate reliability and conclusiveness of available evidence for BoNT-A intervention.

EVIDENCE ACQUISITION:

We searched electronic databases from inception to September 10 of 2016. Randomized controlled trials comparing the effectiveness between BoNT-A and placebo in stroke or traumatic brain injury adults with upper limb spasticity were included. Reliability and conclusiveness of the available evidence were examined with trial sequential analysis.

EVIDENCE SYNTHESIS:

From 489 citations identified, 22 studies were included, reporting results for 1804 participants. A statistically significant decrease of muscle tone was observed at each time point after BoNT-A injection compared to placebo (SMD at week 4=-0.98, 95% CI: -1.28 to -0.68; I2=66%, P=0.004; SMD at week 6=-0.85, 95% CI: -1.11 to -0.59, I2=1.2%, P=0.409; SMD at week 8=-0.87, 95% CI: -1.15 to -0.6, I2=0%, P=0.713; SMD at week 12=-0.67, 95% CI: -0.88 to -0.46, I2=0%, P=0.896; and SMD over week 12=-0.73, 95% CI: -1.21 to -0.24, I2=63.5%, P=0.065).Trial sequential analysis showed that as of year 2004 sufficient evidence had been accrued to show significant benefit of BoNT-A four weeks after injection over placebo control. BoNT-A treatment also significantly reduced Disability Assessment Scale Score than placebo at 4, 6 and 12-week follow-up period (WMD=-0.33, 95% CI: -0.63 to -0.03, I2=60%, P=0.114; WMD=-0.54, 95% CI: -0.74 to -0.33, I2= 0%, P=0.596 and WMD=-0.3, 95% CI: -0.45 to -0.14, I2=0%, P=0.426 respectively), and significantly increased patients’ global assessment score at week 4 and 6 after injection (SMD=0.56, 95% CI: 0.28 to 0.83; I2=0%, P=0.681 and SMD=1.11, 95% CI: 0.4 to 1.77; I2=72.8%, P=0.025 respectively). No statistical difference was observed in the frequency of adverse events between BoNT-A and placebo group (RR=1.36, 95% CI [0.82, 2.27]; I2=0%, P=0.619).

CONCLUSIONS:

As compared with placebo, BoNT-A injections have beneficial effects with improved muscle tone and well-tolerated treatment for patients with upper limb spasticity post stroke or traumatic brain injury.

Source: Efficacy and safety of botulinum toxin type A for upper limb spasticity after stroke or traumatic brain injury: a systematic review with meta-analy… – PubMed – NCBI

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[ARTICLE] Rehabilitation plus OnabotulinumtoxinA Improves Motor Function over OnabotulinumtoxinA Alone in Post-Stroke Upper Limb Spasticity: A Single-Blind, Randomized Trial – Full Text HTML

Abstract

Background: OnabotulinumtoxinA (BoNT-A) can temporarily decrease spasticity following stroke, but whether there is an associated improvement in upper limb function is less clear. This study measured the benefit of adding weekly rehabilitation to a background of BoNT-A treatments for chronic upper limb spasticity following stroke. Methods: This was a multi-center clinical trial. Thirty-one patients with post-stroke upper limb spasticity were treated with BoNT-A. They were then randomly assigned to 24 weeks of weekly upper limb rehabilitation or no rehabilitation. They were injected up to two times, and followed for 24 weeks. The primary outcome was change in the Fugl–Meyer upper extremity score, which measures motor function, sensation, range of motion, coordination, and speed. Results: The ‘rehab’ group significantly improved on the Fugl–Meyer upper extremity score (Visit 1 = 60, Visit 5 = 67) while the ‘no rehab’ group did not improve (Visit 1 = 59, Visit 5 = 59; p = 0.006). This improvement was largely driven by the upper extremity “movement” subscale, which showed that the ‘rehab’ group was improving (Visit 1 = 33, Visit 5 = 37) while the ‘no rehab’ group remained virtually unchanged (Visit 1 = 34, Visit 5 = 33; p = 0.034). Conclusions: Following injection of BoNT-A, adding a program of rehabilitation improved motor recovery compared to an injected group with no rehabilitation.

1. Introduction

While several blinded and open-label studies have demonstrated the ability of botulinum toxin to temporarily decrease spasticity following stroke, as measured by standard assessments such as the Modified Ashworth Scale [1,2,3,4,5,6,7,8], the ability of botulinum toxin to improve upper limb function following stroke is less clear, with some studies [1,3,4,5,6,7,8], though not all [2,7], reporting functional improvement. Two recent meta-analyses of randomized controlled trials demonstrated that botulinum toxin treatment resulted in a moderate improvement in upper limb function [9,10]. Despite large clinical trials [2,3,11] and FDA approval, the exact timing, use of adjunct rehabilitation, and continuation of lifelong botulinum toxin treatment remains unclear [12,13].
A recent Cochrane Review included three randomized clinical trials for post-stroke spasticity involving 91 participants [14]. It aimed to determine the efficacy of multidisciplinary rehabilitation programs following treatment with botulinum toxin, and found some evidence supporting modified constraint-induced movement therapy and dynamic elbow splinting. There have been varied study designs exploring rehabilitation in persons after the injection of botulinum toxin or a placebo [13,15], rehabilitation in persons after the injection of botulinum toxin or no injection [16], or rehabilitation after the injection of botulinum toxin with no control condition [17]. As the use of botulinum toxin expands and is beneficial in reducing spasticity and costs [18], the benefit of adding upper limb rehabilitation continues to be questioned. We designed this multi-center, randomized, single-blind clinical trial to assess improvement in patient sensory and motor outcome following the injection of onabotulinumtoxinA (BoNT-A), comparing the effects of rehabilitation versus no rehabilitation, using the upper extremity portion of the Fugl–Meyer Assessment of Sensorimotor Recovery After Stroke [19] as the primary outcome measure. While patients could not be blinded to their randomization to receive additional rehabilitation versus no rehabilitation, the assessments of all of the outcome measures were performed by evaluators blinded to rehabilitation assignment in this single-blind design.

2. Results

Thirty-one patients with post-stroke upper limb spasticity were enrolled, with 29 completing the study (Figure 1). The strokes occurred an average of 6 years prior to study entry, with a range of 6 months to 16½ years. The upper extremity postures treated included flexed elbow, pronated forearm, flexed wrist, flexed fingers, and clenched fist, and were evenly distributed between the treatment groups (the initial dose of BoNT-A administered was left up to the clinician’s judgment based on the amount of spasticity present, and did not differ between groups). One participant (‘no rehab’, injected at Visits 1 and 3A) left the study after Visit 3A due to a deterioration in general health and an inability to travel to study visits. A second participant (‘no rehab’, injected at Visits 1 and 3A) left the study after Visit 4 due to a fall with a broken affected wrist. All of the participants were injected at Visit 1, 19 were injected at Visit 3 (8 ‘rehab’; 11 ‘no rehab’), and 7 were injected at Visit 3A (3 ‘rehab’; 4 ‘no rehab’). Those participants who did not receive injections at Visits 3 or 3A had a level of spasticity that either did not meet the injection criteria due to an Ashworth score of <2 in the wrist (and/or fingers) or one that was felt to be too low to warrant injection. Table 1 provides a description of each group with regard to age, sex, race, whether the stroke occurred in the dominant hemisphere, and clinical measures. At baseline, the treatment groups did not differ on any demographic or clinical variables. […]

Continue—>  Toxins | Free Full-Text | Rehabilitation plus OnabotulinumtoxinA Improves Motor Function over OnabotulinumtoxinA Alone in Post-Stroke Upper Limb Spasticity: A Single-Blind, Randomized Trial | HTML

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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.

 

Continue —> Journal of Rehabilitation Medicine – Practice patterns for spasticity management with phenol neurolysis – HTML

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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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[Abstract+References] Does the method of botulinum neurotoxin injection for limb spasticity affect outcomes? A systematic review 

 

To systematically review randomized controlled trials of botulinum neurotoxin for limb spasticity to determine whether different injection techniques affect spasticity outcomes.

MEDLINE, EMBASE, CINAHL, and Cochrane Central Register of Controlled Trials electronic databases were searched for English language human randomized controlled trials from 1990 to 13 May 2016. Studies were assessed in duplicate for data extraction and risk of bias using the Physiotherapy Evidence Database scale and graded according to Sackett’s levels of evidence.

Nine of 347 studies screened met selection criteria. Four categories of botulinum neurotoxin injection techniques were identified: (1) injection localization technique; (2) injection site selection; (3) injectate volume; (4) injection volume and site selection. There is level 1 evidence that: ultrasound, electromyography, and electrostimulation are superior to manual needle placement; endplate injections improve outcomes vs. multisite quadrant injections; motor point injections are equivalent to multisite injections; high volume injections are similar to low volume injections; and high volume injections distant from the endplate are more efficacious than low volumes closer to the endplate.

Level 1 evidence exists for differences in treatment outcomes using specific botulinum neurotoxin injection techniques. Findings are based on single studies that require independent replication and further study.

 

1. Francisco GEVaughn ABotulinum toxin in upper limb. Am J Phys Med Rehabil 2002; 81(5): 355363Google Scholar CrossRefMedline
2. Moher DLiberati ATetzlaff JAltman DGPreferred reporting items for systematic reviews and meta-analyses: The PRISMA statement. PLoS Med 2009; 6(7): e1000097Google Scholar CrossRefMedline
3. Snow BJTsui JKBhatt MHVarelas MHashimoto SACalne DBTreatment of spasticity with botulinum toxin: A double-blind study. Ann Neurol 1990; 28(4): 512515Google Scholar CrossRefMedline
4. Moher DJadad ARNichol GPenman MTugwell PWalsh SAssessing the quality of randomized controlled trials: An annotated bibliography of scales and checklists. Control Clin Trials 1995; 16(1): 6273.Google Scholar CrossRefMedline
5. Higgins JPTGreen S. Cochrane Handbook for Systematic Reviews of Interventions Version 5.1.0 [updated March 2011]. The Cochrane Collaboration2011Google Scholar
6. Moseley AMHerbert RDSherrington CMaher CGEvidence for physiotherapy practice: A survey of the Physiotherapy Evidence Database (PEDro). Aust J Physiother 2002; 48(1): 4349Google Scholar CrossRefMedline
7. Lui JSarai MMills PBChemodenervation for treatment of limb spasticity following spinal cord injury: A systematic review. Spinal Cord 2015; 53(4): 252264Google Scholar CrossRefMedline
8. Mills PBFung CKTravlos AKrassioukov ANonpharmacologic management of orthostatic hypotension: A systematic review. Arch Phys Med Rehabil 2015; 96(2): 366375.e6Google Scholar CrossRefMedline
9. Centre for Evidence-Based Medicine. Reflections on David Sackett’s time at the Centre for Evidence-Based Medicine. Available at: www.cebm.net/ (accessed 15 March 2015).
10. Eng JTeasell RMiller W, . Spinal cord injury rehabilitation evidence: Method of the SCIRE systematic review. Top Spinal Cord Inj Rehabil 2007; 13(1): 110Google Scholar CrossRefMedline
11. Picelli ATamburin SBonetti P, . Botulinum toxin type A injection into the gastrocnemius muscle for spastic equinus in adults with stroke: A randomized controlled trial comparing manual needle placement, electrical stimulation and ultrasonography-guided injection techniques. Am J Phys Med Rehabil 2012; 91(11): 957964Google Scholar CrossRefMedline
12. Picelli ALobba DMidiri A, . Botulinum toxin injection into the forearm muscles for wrist and fingers spastic overactivity in adults with chronic stroke: A randomized controlled trial comparing three injection techniques. Clin Rehabil 2014; 28(3): 232242Google Scholar Link
13. Ploumis AVarvarousis DKonitsiotis SBeris AEffectiveness of botulinum toxin injection with and without needle electromyographic guidance for the treatment of spasticity in hemiplegic patients: A randomized controlled trial. Disabil Rehabil 2014; 36(4): 313318Google Scholar CrossRefMedline
14. Santamato AMicello MFPanza F, . Can botulinum toxin type A injection technique influence the clinical outcome of patients with post-stroke upper limb spasticity? A randomized controlled trial comparing manual needle placement and ultrasound-guided injection techniques. J Neurol Sci 2014; 347(1–2): 3943Google Scholar CrossRefMedline
15. Gracies JMLugassy MWeisz DJVecchio MFlanagan SSimpson DMBotulinum toxin dilution and endplate targeting in spasticity: A double-blind controlled study. Arch Phys Med Rehabil 2009; 90(1): 916.e2Google Scholar CrossRefMedline
16. Childers MKPt DLHenry HComparision of two injection techniques using botulinum toxin in spastic hemiplegia. Am J Phys Med Rehabil 1996; 75(6): 462469Google Scholar CrossRefMedline
17. Im SPark JHSon SKShin J-ECho SHPark G-YDoes botulinum toxin injection site determine outcome in post-stroke plantarflexion spasticity? Comparison study of two injection sites in the gastrocnemius muscle: A randomized double-blind controlled trial. Clin Rehabil 2014; 28(6): 604613Google Scholar Link
18. Mayer NHWhyte JWannstedt GEllis CComparative impact of 2 botulinum toxin injection techniques for elbow flexor hypertonia. Arch Phys Med Rehabil 2008; 89(5): 982987Google Scholar CrossRefMedline
19. Picelli ABonetti PFontana C, . Accuracy of botulinum toxin type A injection into the gastrocnemius muscle of adults with spastic equinus: Manual needle placement and electrical stimulation guidance compared using ultrasonography. J Rehabil Med 2012; 44(5): 450452Google Scholar CrossRefMedline
20. Deshpande SGormley MECarey JRMuscle fiber orientation in muscles commonly injected with botulinum toxin: An anatomical pilot study. Neurotox Res 2006; 9(2–3): 115120Google Scholar CrossRefMedline
21. Braddom R. Physical Medicine and Rehabilitation. Philadelphia, PAElsevier Saunders2011180pp. Google Scholar
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Source: Does the method of botulinum neurotoxin injection for limb spasticity affect outcomes? A systematic reviewClinical Rehabilitation – Aaron K Chan, Heather Finlayson, Patricia B Mills, 2017

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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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