Archive for category Spasticity

[Abstract] When does spasticity in the upper limb develop after a first stroke? A nationwide observational study on 861 stroke patients

Highlights

  • The post-stroke spasticity of upper limb can cause significant functional impairment.
  • This study for spasticity was a nationwide multicenter study in South Korea.
  • The median time to develop upper limb spasticity after stroke onset was 34 days.
  • The 13% of post-stroke spasticity cases developed after 90 days from onset.

Abstract

This study investigated the time taken for upper extremity spasticity to develop and its regional difference after first-ever stroke onset in a nationwide multicenter study in South Korea. The retrospective observational study included 861 individuals with post-stroke spasticity in the upper limbs. Spasticity in the upper extremity joints was defined as a modified Ashworth Scale score ≥1. The median time to develop upper limb spasticity after stroke onset was 34 days. 12% of post-stroke spasticity cases developed between 2 months and 3 months and 13% developed after 3 months from onset. At the time of diagnosis of spasticity, most patients showed only a slight increase in muscle tone, which was observed most frequently in the elbow, followed by the wrist, and fingers. Younger stroke survivors were more spastic, and the severity of spasticity increased with time. Approximately half of the patients with post-stroke spasticity developed spasticity during the first month. However, post-stroke spasticity can develop more than 3 months after stroke onset. Therefore, it is important to assess spasticity, even in the chronic state.

via When does spasticity in the upper limb develop after a first stroke? A nationwide observational study on 861 stroke patients – Journal of Clinical Neuroscience

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[WEB SITE] Botox® Injection: Not Just for Celebrities’ Furrows and Wrinkles – Lower Extremity Review Magazine

Not at all: Plantar fasciitis is now a proven therapeutic target for onabotulinumtoxinA. Consider its potential value for your patients.

By Benn Jason Scott Boshell, MSc, BSc (Hons)

When people hear the word “Botox,”a their immediate associations might be with facial injection as an anti-wrinkle treatment or magazine gossip on the latest celebrity to suffer a “botch job” from one-too-many injections. Prior to the modern use of this acetylcholine-blocking neurotoxin, no one other than medical professionals who used it to treat their patients really knew what Botox is. Injections were originally used to treat neurological conditions that result in spastic paralysis, such as cerebral palsy.

In addition to managing neurological conditions and, more recently, for aesthetic enhancement, Botox is now being used to treat musculoskeletal disorders. One of these conditions is plantar fasciitis, the subject of this narrative review of the literature.b

a. Botox, the registered trade name of onabotulinumtoxinA, is used in this article for ease of reading.

b. Treatment of plantar fasciitis is not a US Food and Drug Administration-approved indication for Botox®.

How can Botox injection treat plantar fasciitis?

Botox is a neurotoxin that blocks release of the neurotransmitter acetylcholine in overactive muscles. Motor neurons release acetylcholine to activate muscles at the neuromuscular junction; Botox, when injected, causes relaxation of muscles and other local soft tissue.

A body of evidence identifies tightness in calf muscles as a causative factor in plantar fasciitis.1-5 Botox injection into the calf aims to relax contracture in calf muscles, thus reducing tensile strain on the plantar fascia as a result of muscle relaxation. Additionally, Botox can be injected into the muscles of the foot to achieve the same effect.

What is the evidence for Botox injection?

Key Messages

  • Botox injection into the calf aims to relax contracture in calf muscles, thus reducing tensile strain on the plantar fascia. Botox can also be injected into muscles of the foot for the same effect.
  • Improvement in plantar fasciitis pain after Botox injection has been reported to be sustained over the long term.
  • Major adverse effects of Botox are uncommon when injections are administered by a qualified clinician.

Several clinical studies have looked at the effectiveness of Botox injection for treating plantar fasciitis.

Botox injection compared with corticosteroid injection (2013). Elizondo-Rodriguez and co-workers’ level-1, double-blind, randomized controlled trial compared Botox injection to corticosteroid injection for the treatment of plantar fasciitis.6The study randomized participants into 2 groups:

  • Group 1 (19 participants) received a Botox injection and were instructed on performing plantar fascia stretching exercises.
  • Group 2 (17 partcipants) received a corticosteroid injection and the same instructions on plantar fascia stretching exercises.

Results of treatment were recorded at 2 weeks and at 1, 2, 4, and 6 months. No significant improvement was seen in either group after the initial 2-week review. However, both groups showed significant improvement in pain scores at 1 month. At 2-, 4-, and 6-months follow-up, the Botox group had significantly better pain scores than the corticosteroid group. At the final, 6-month review, the average pain score in the Botox group was 1.1 (on a scale of 1 to 10, with 10 the “worst pain”), a reduction from 7.1 (difference of 6 points); in the corticosteroid group, the average pain score was 3.8, a reduction from 7.7 (difference of 3.9 points).

Elizondo-Rodriguez therefore concluded that Botox injection is superior to corticosteroid injection for the treatment of plantar fasciitis over the short term and mid-term. A limitation of this study is that patients were not followed over a longer period; it is not known, therefore, whether participants would have maintained their improved pain scores 12 months’ posttreatment. Longer follow-up would help ascertain whether Botox is also successful in the long-term management of plantar fasciitis.

A particular point of interest from the Elizondo-Rodriguez study is that Botox was not injected into or around the plantar fascia but into the gastrocnemius and soleus muscles. Following injection, calf muscles went into a state of relaxation, due to the effect of Botox. It is believed that this relaxation reduced additional strain on the plantar fascia that results from increased calf-muscle tension. One could argue that this approach seeks to address the purported cause of plantar fasciitis—unlike corticosteroid injection, which aims to treat symptoms.

Figure 1: Medial (a) and plantar (b) views of the injection entry point for study patients. This is at the distal aspect of the plantar-medial aspect of the calcaneus where the plantar fascia is proximal and the flexor digitorum brevis is adjacent. The X marks the most common spot injected for patients based on their maximum point tenderness. The circle around the X is a 1.5-cm radius where some patients received their injection based on their maximum point of tenderness (used with permission from reference 12).

Botox injection compared with corticosteroid injection (2012). Díaz-Llopis and colleagues also compared Botox injection with corticosteroid injection.7 Their study was likewise a randomized, controlled trial, with 28 patients in each group. As in the Elizondo-Rodriguez study,6 Díaz-Llopis found both that Botox and corticosteroid injections were successful at 1-month review; however, the difference between the 2 treatments grew at 6 months, with the Botox group continuing to improve while the steroid group grew slightly worse.

Long-term follow-up of sustained effects of Botox injection (2013). The lead Díaz-Llopis investigator and a different group of co-workers8 returned to the findings of the original Díaz-Llopis study,7 conducting a 12-month follow-up of the 2012 Botox group to determine whether reported improvements were sustained over the long term, which they were. Their findings provide evidence to support the use of Botox injection as a long-term treatment option.

(Notably, the site of the Botox injection in the 2012 Díaz-Llopis study differed from the site used in the Elizondo-Rodriguez study. Instead of injecting into calf muscles, Díaz-Llopis injected Botox into the plantar fascia attachment to the heel bone and further along the arch of the foot; they decided to use this technique based on a 2005 study by Babcock and co-workers.9 By using the same injection technique that Babcock used, Díaz-Llopis and colleagues were able to determine whether they would achieve similar success.)

Botox injection compared with corticosteroid injection (2018). In a randomized, controlled trial reported this year, Roca and co-workers found Botox superior to corticosteroid injection.10

Botox injection compared with placebo. Babcock and colleagues compared Botox injection and placebo in a double-blind, randomized, placebo-controlled study in 27 patients with plantar fasciitis.9 Results were recorded at 3 weeks and 8 weeks; improvement observed in the Botox group was significantly greater than in the placebo group. The strength of the study was limited by short-term follow-up.

Other studies have also compared Botox injection with placebo and found Botox to be significantly more effective.11,12 Ahmad and colleagues,12 in a double-blind, randomized, controlled trial of 50 patients (25 in each group) found Botox injection to be significantly superior to placebo at 6-month and 12-month reviews (Figure 1). The Botox group also showed significant reduction in plantar fascia thickness, which demonstrated healing of the degenerative plantar fascia—a finding not seen in the control group. A further benefit of Botox injection in this study was that it did not reduce heel fat-pad thickness, a commonly reported complication of corticosteroid injection.

Conversely, a similar study that compared Botox injection and placebo found only a marginal difference in improvement between the 2 groups:13 63.1% of the Botox group perceived improvement compared to 55% of the placebo group.

Botox injection compared with extracorporeal shockwave therapy (ESWT). Roca and co-workers’ study14 is interesting because ESWT has become an established, successful treatment option for plantar fasciitis.15 Because Botox injection is considered a novel treatment with less evidence of effectiveness, comparing it with an established treatment can be considered a good test of its effectiveness.

The Roca study randomized patients to 2 groups, 36 in each group. The researchers found both treatments effective—i.e., both demonstrated improved pain scores after treatment. However, ESWT came out on top, producing a greater reduction in pain than Botox injection.

A limitation of this study is that the researchers reviewed patients only 1 to 2 months after treatment. As noted, previous studies of Botox injection demonstrate continued improvement in pain score with more time. It is possible that the Botox group would have seen greater improvement in pain score if the researchers had reviewed that group at 6 and 12 months (although the same possibility can be considered for the ESWT group).

Are there risks to Botox injection?

Botox injection is generally safe; major adverse effects are uncommon when injection is administered by a suitably qualified clinician. There is a possibility (although highly unlikely) that the effect of botulinum toxin will spread to other parts of the body and cause botulism-like signs and symptoms, including:

  • muscle weakness all over the body
  • vision problems
  • difficulty speaking or swallowing
  • difficulty breathing
  • loss of bladder control.

Can a verdict be brought?

Overall, it appears that the evidence for Botox injection as a treatment for plantar fasciitis is sufficiently strong to support its use. Nearly all current studies of moderate- to high-quality  demonstrate significant success with this treatment option.

Despite that conclusion, Botox injection is not a commonly used treatment option and—in the United Kingdom—is not widely available for treating plantar fasciitis; in the United States, Botox injection is not indicated by the Food and Drug Administration for treating plantar fasciitis. Nevertheless, Botox injection deserves greater study and consideration for its applicability to clinical practice for treating plantar fasciitis. This therapy might replace commonly used corticosteroid injection for plantar fasciitis, which has 1) a lower success rate over the long term and 2) an increased risk of harmful effects, including plantar fascia rupture.

The most effective Botox injection technique remains in question. In most studies, plantar fascia and surrounding tissue were injected directly; in some, calf muscles were injected. To determine which technique is better, it will be necessary to conduct a head-to-head trial of these 2 techniques.

Benn Jason Scott Boshell MSc, BSc (Hons) is clinical lead podiatrist at Hatt Health & Movement Clinic, Devizes, United Kingdom.

Source:
https://lermagazine.com/article/botox-injection-not-just-for-celebrities-furrows-and-wrinkles

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[Abstract + References] Effect of Transcutaneous Electrical Nerve Stimulation on Spasticity in Adults With Stroke: A Systematic Review and Meta-analysis

Abstract

Objectives

(1) To determine the effect of transcutaneous electrical nerve stimulation (TENS) on poststroke spasticity. (2) To determine the effect of different parameters (intensity, frequency, duration) of TENS on spasticity reduction in adults with stroke. (3) To determine the influence of time since stroke on the effectiveness of TENS on spasticity.

Data Sources

PubMed, PEDro, CINAHL, Web of Science, CENTRAL, and EMBASE databases were searched from inception to March 2017.

Study Selection

Randomized controlled trial (RCT), quasi-RCT, and non-RCT were included if (1) they evaluated the effects of TENS for the management of spasticity in participants with acute or subacute or chronic stroke using clinical and neurophysiological tools; and (2) TENS was delivered either alone or as an adjunct to other treatments.

Data Extraction

Two authors independently screened and extracted data from 15 of the 829 studies retrieved through the search using a pilot tested pro forma. Disagreements were resolved through discussion with other authors. Quality of studies was assessed using Cochrane risk of bias criteria.

Data Synthesis

Meta-analysis was performed using a random-effects model that showed (1) TENS along with other physical therapy treatments was more effective in reducing spasticity in the lower limbs compared to placebo TENS (SMD −0.64; 95% confidence interval [95% CI], −0.98 to −0.31; P=.0001; I2=17%); and (2) TENS, when administered along with other physical therapy treatments, was effective in reducing spasticity when compared to other physical therapy interventions alone (SMD −0.83; 95% CI, −1.51 to −0.15; P=.02; I2=27%). There were limited studies to evaluate the effectiveness of TENS for upper limb spasticity.

Conclusion

There is strong evidence that TENS as an adjunct is effective in reducing lower limb spasticity when applied for more than 30 minutes over nerve or muscle belly in chronic stroke survivors (review protocol registered at PROSPERO: CRD42015020151)

References

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  2. Wissel, J., Manack, A., Brainin, M. Toward an epidemiology of poststroke spasticity. Neurology. 2013;80:S13–S19
  3. Watkins, C.L., Leathley, M.J., Gregson, J.M., Smith, T.L., Moore, A.P. Prevalence of spasticity post stroke. Clin Rehabil. 2002;16:515–522
  4. Doan, Q.V., Brashear, A., Gillard, P.J. et al, Relationship between disability and health-related quality of life and caregiver burden in patients with upper limb poststroke spasticity. PM R. 2012;4:4–10
  5. Lundström, E., Smits, A., Borg, J., Terént, A. Four-fold increase in direct costs of stroke survivors with without spasticity the first year after the event. Stroke. 2010;41:319–324
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  7. Thibaut, A., Laureys, S., Gosseries, O., Chatelle, C., Ziegler, E. Spasticity after stroke: physiology, assessment and treatment. Brain Inj. 2013;9052:1–13
  8. Richardson, D. Physical therapy in spasticity. Eur J Neurol. 2002;9:17–22
  9. Malas, B., Kacen, M. Orthotic management in patients with stroke. Top Stroke Rehabil. 2001;7:38–45
  10. Lehmann, J.F., Esselman, P.C., Ko, M.J., Smith, J.C., deLateur, B.J., Dralle, A.J. Plastic ankle-foot orthoses: evaluation of function. Arch Phys Med Rehabil. 1983;64:402–407
  11. Barnes, M.P. Medical management of spasticity in stroke. Age Ageing. 2001;30:13–16
  12. Kocabas, H. Comparison of phenol and alcohol neurolysis of tibial nerve motor branches to the gastrocnemius muscle for treatment of spastic foot after stroke: a randomized controlled pilot study.Eur J Phys Rehabil Med. 2010;46:5–10
  13. Fukuhara, T., Kamata, I. Selective posterior rhizotomy for painful spasticity in the lower limbs of hemiplegic patients after stroke: report of two cases. Neurosurgery. 2004;54:1268–1273
  14. Sheean, G., McGuire, J.R. Spastic hypertonia and movement disorders: pathophysiology, clinical presentation, and quantification. PM R. 2009;1:827–833
  15. Martins, F.L., Carvalho, L.C., Silva, C.C., Brasileiro, J.S., Souza, T.O., Lindquist, A.R. Immediate effects of TENS and cryotherapy in the reflex excitability and voluntary activity in hemiparetic subjects: a randomized crossover trial. Rev Bras Fisioter. 2012;16:337–344
  16. Kim, T.H., In, T.S., Cho, H. Task-related training combined with transcutaneous electrical nerve stimulation promotes upper limb functions in patients with chronic stroke. Tohoku J Exp Med. 2013;231:93–100
  17. Tinazzi, M., Zarattini, S., Valeriani, M. et al, Long-lasting modulation of human motor cortex following prolonged transcutaneous electrical nerve stimulation (TENS) of forearm muscles: evidence of reciprocal inhibition and facilitation. Exp Brain Res. 2005;161:457–464
  18. Yan, T., Hui-Chan, C.W. Transcutaneous electrical stimulation on acupuncture points improves muscle function in subjects after acute stroke: a randomized controlled trial. J Rehabil Med. 2009;41:312–316
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  20. Sonde, L., Kalimo, H., Viitanen, M. Stimulation with high-frequency TENS — effects on lower limb spasticity after stroke. Adv Physiother. 2000;2:183–187
  21. Jung, K.-S., In, T.-S., Cho, H. Effects of sit-to-stand training combined with transcutaneous electrical stimulation on spasticity, muscle strength and balance ability in patients with stroke: a randomized controlled study. Gait Posture. 2017;54:183–187
  22. Picelli, A., Dambruoso, F., Bronzato, M. et al, Efficacy of therapeutic ultrasound and transcutaneous electrical nerve stimulation compared with botulinum toxin type A in the treatment of spastic equinus in adults with chronic stroke: a pilot randomized controlled trial. Top Stroke Rehabil. 2014;21:S8–S16
  23. Sonde, L., Gip, C., Fernaeus, S.E., Nilsson, C.G., Viitanen, M. Stimulation with low frequency (1.7 Hz) transcutaneous electric nerve stimulation (low-tens) increases motor function of the post-stroke paretic arm. Scand J Rehabil Med. 1998;30:95–99
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  33. Hussain, T., Mohammad, H. The effect of transcutaneous electrical nerve stimulation (TENS) combined with Bobath on post stroke spasticity. A randomized controlled study. J Neurol Sci. 2013;4:22–29
  34. Park, J., Seo, D., Choi, W., Lee, S. The effects of exercise with tens on spasticity, balance, and gait in patients with chronic stroke: a randomized controlled trial. Med Sci Monit. 2014;20:1890–1896
  35. Laddha, D., Ganesh, G.S., Pattnaik, M., Mohanty, P., Mishra, C. Effect of transcutaneous electrical nerve stimulation on plantar flexor muscle spasticity and walking speed in stroke patients. Physiother Res Int. 2016;21:247–256
  36. Hui-Chan, C.W., Levin, M.F. Stretch reflex latencies in spastic hemiparetic subjects are prolonged after transcutaneous electrical nerve stimulation. Can J Neurol Sci. 1993;20:97–106
  37. Karakoyun, A., Boyraz, İ., Gunduz, R., Karamercan, A., Ozgirgin, N. Electrophysiological and clinical evaluation of the effects of transcutaneous electrical nerve stimulation on the spasticity in the hemiplegic stroke patients. J Phys Ther Sci. 2015;27:3407–3411
  38. Koyama, S., Tanabe, S., Takeda, K., Sakurai, H., Kanada, Y. Modulation of spinal inhibitory reflexes depends on the frequency of transcutaneous electrical nerve stimulation in spastic stroke survivors.Somatosens Mot Res. 2016;33:8–15
  39. Okuma, Y., Lee, R.G. Reciprocal inhibition in hemiplegia: correlation with clinical features and recovery. Can J Neurol Sci. 1996;23:15–23
  40. Sommerfeld, D.K., Gripenstedt, U., Welmer, A.-K. Spasticity after stroke. Am J Phys Med Rehabil. 2012;91:814–820
  41. Fernández-Tenorio, E., Serrano-Muñoz, D., Avendaño-Coy, J., Gómez-Soriano, J. Transcutaneous electrical nerve stimulation for spasticity: a systematic review. Neurologia. 2016; (pii: S0213-4853(16)30111-6)
  42. Kwong, P.W., Ng, G.Y., Chung, R.C., Ng, S.S. Transcutaneous electrical nerve stimulation improves walking capacity and reduces spasticity in stroke survivors: a systematic review and meta-analysis.Clin Rehabil. 2018;32:1203–1219

source:
https://www.archives-pmr.org/article/S0003-9993(18)31455-2/abstract

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[Abstract] Effectiveness of botulinum toxin treatment for upper limb spasticity after stroke over different ICF domains: a systematic review and meta-analysis.

Abstract

Objective

To provide a comprehensive overview of reported effects and scientific robustness of botulinum toxin (BoNT) treatment regarding the main clinical goals related to post-stroke upper limb spasticity, using the ICF classification.

Data sources

Embase.com, PubMed, Wiley/Cochrane Library, and Ebsco/CINAHL were searched from inception up to 16 May 2018.

Study Selection

Randomized controlled trials comparing upper limb BoNT injections with a control intervention in stroke patients were included. A total of 1212 unique records were screened by two independent reviewers. Forty trials were identified, including 2718 stroke patients.

Data Extraction

Outcome data were pooled according to assessment timing (i.e. 4-8 and 12 weeks after injection), and categorized into six main clinical goals (i.e. spasticity-related pain, involuntary movements, passive joint motion, care ability, arm and hand use, and standing and walking performance). Sensitivity analyses were performed for the influence of study and intervention characteristics, involvement of pharmaceutical industry, and publication bias.

Data Synthesis

Robust evidence is shown for the effectiveness of BoNT in reducing resistance to passive movement, as measured with the (Modified) Ashworth Score, and improving self-care ability for the affected hand and arm after intervention (p<0.005) and at follow-up (p<0.005). In addition, robust evidence is shown for the absence of effect on ‘arm-hand capacity’ at follow-up. BoNT significantly reduced ‘involuntary movements’, ‘spasticity-related pain’, and ‘carer burden’, and improved ‘passive range of motion’, while no evidence was found for ‘arm and hand use’ after intervention.

Conclusions

In view of the robustness of current evidence, no further trials are needed to investigate BoNT for its favourable effects on resistance to passive movement of the spastic wrist and fingers, and on self-care. No trials are needed to further confirm the lack of effects of BoNT on arm-hand capacity, whereas additional trials are needed to establish the suggested favourable effects of BoNT on other ‘body functions’ which may result in clinically meaningful outcomes at ‘activity’ and ‘participation’ levels.

via Effectiveness of botulinum toxin treatment for upper limb spasticity after stroke over different ICF domains: a systematic review and meta-analysis – Archives of Physical Medicine and Rehabilitation

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[ARTICLE] Effectiveness of Robot-Assisted Upper Limb Training on Spasticity, Function and Muscle Activity in Chronic Stroke Patients Treated With Botulinum Toxin: A Randomized Single-Blinded Controlled Trial

Abstract

Background: The combined use of Robot-assisted UL training and Botulinum toxin (BoNT) appear to be a promising therapeutic synergism to improve UL function in chronic stroke patients.

Objective: To evaluate the effects of Robot-assisted UL training on UL spasticity, function, muscle strength and the electromyographic UL muscles activity in chronic stroke patients treated with Botulinum toxin.

Methods: This single-blind, randomized, controlled trial involved 32 chronic stroke outpatients with UL spastic hemiparesis. The experimental group (n = 16) received robot-assisted UL training and BoNT treatment. The control group (n = 16) received conventional treatment combined with BoNT treatment. Training protocols lasted for 5 weeks (45 min/session, two sessions/week). Before and after rehabilitation, a blinded rater evaluated patients. The primary outcome was the Modified Ashworth Scale (MAS). Secondary outcomes were the Fugl-Meyer Assessment Scale (FMA) and the Medical Research Council Scale (MRC). The electromyographic activity of 5 UL muscles during the “hand-to-mouth” task was explored only in the experimental group and 14 healthy age-matched controls using a surface Electromyography (EMGs).

Results: No significant between-group differences on the MAS and FMA were measured. The experimental group reported significantly greater improvements on UL muscle strength (p = 0.004; Cohen’s d = 0.49), shoulder abduction (p = 0.039; Cohen’s d = 0.42), external rotation (p = 0.019; Cohen’s d = 0.72), and elbow flexion (p = 0.043; Cohen’s d = 1.15) than the control group. Preliminary observation of muscular activity showed a different enhancement of the biceps brachii activation after the robot-assisted training.

Conclusions: Robot-assisted training is as effective as conventional training on muscle tone reduction when combined with Botulinum toxin in chronic stroke patients with UL spasticity. However, only the robot-assisted UL training contributed to improving muscle strength. The single-group analysis and the qualitative inspection of sEMG data performed in the experimental group showed improvement in the agonist muscles activity during the hand-to-mouth task.

Clinical Trial Registration: www.ClinicalTrials.gov, identifier: NCT03590314

Introduction

Upper limb (UL) sensorimotor impairments are one of the major determinants of long-term disability in stroke survivors (). Several disturbances are the manifestation of UL impairments after stroke (i.e., muscle weakness, changes in muscle tone, joint disturbances, impaired motor control). However, spasticity and weakness are the primary reason for rehabilitative intervention in the chronic stages (). Historically, spasticity refers to a velocity-dependent increase in tonic stretch reflexes with exaggerated tendon jerks resulting from hyperexcitability of the stretch reflex () while weakness is the loss of the ability to generate the normal amount of force.

From 7 to 38% of post-stroke patients complain of UL spasticity in the first year (). The pathophysiology of spasticity is complicated, and new knowledge has progressively challenged this definition. Processes involving central and peripheral mechanisms contribute to the spastic movement disorder resulting in abnormal regulation of tonic stretch reflex and increased muscle resistance of the passively stretched muscle and deficits in agonist and antagonist coactivation (). The resulting immobilization of the muscle at a fixed length for a prolonged time induces secondary biomechanical and viscoelastic properties changes in muscles and soft tissues, and pain (). These peripheral mechanisms, in turn, leads to further stiffness, and viscoelastic muscle changes (). Whether the muscular properties changes may be adaptive and secondary to paresis are uncertain. However, the management of UL spasticity should combine treatment of both the neurogenic and peripheral components of spasticity ().

UL weakness after stroke is prevalent in both acute and chronic phases of recovery (). It is a determinant of UL function in ADLs and other negative consequences such as bone mineral content (), atrophy and altered muscle pattern of activation. Literature supports UL strengthening training effectiveness for all levels of impairment and in all stages of recovery (). However, a small number of trials have been performed in chronic subgroup patients, and there is still controversy in including this procedure in UL rehabilitation ().

Botulinum toxin (BoNT) injection in carefully selected muscles is a valuable treatment for spastic muscles in stroke patients improving deficits in agonist and antagonist coactivation, facilitating agonist recruitment and increasing active range of motion (). However, improvements in UL activity or performance is modest (). With a view of improving UL function after stroke, moderate to high-quality evidence support combining BoNT treatment with other rehabilitation procedures (). Specifically, the integration of robotics in the UL rehabilitation holds promise for developing high-intensity, repetitive, task-specific, interactive treatment of upper limb (). The combined use of these procedures to compensate for their limitations has been studied in only one pilot RCT reporting positive results in UL function (Fugl-Meyer UL Assessment scale) and muscular activation pattern (). With the limits of the small sample, the results support the value of combining high-intensity UL training by robotics and BoNT treatment in patients with UL spastic paresis.

Clinical scales are currently used to assess the rehabilitation treatment effects, but these outcome measures may suffer from some drawbacks that can be overcome by instrumental assessment as subjectivity, limited sensitivity, and the lack of information on the underlying training effects on motor control (). Instrumental assessment, such as surface electromyography (sEMG) during a functional task execution allows assessing abnormal activation of spastic muscles and deficits of voluntary movements in patients with stroke.

Moreover, the hand-to-mouth task is representative of Activities of Daily Life (ADL) such as eating and drinking. Kinematic analysis of the hand-to-mouth task has been widely used to assess UL functions in individuals affected by neurological diseases showing adequate to more than adequate test-retest reliability in healthy subjects (). The task involves flexing the elbow a slightly flexing the shoulder against gravity, and it is considered to be a paradigmatic functional task for the assessment of spasticity and strength deficits on the elbow muscles (). Although sEMG has been reported to be a useful assessment procedure to detect muscle activity improvement after rehabilitation, limited results have been reported ().

The primary aim of this study was to explore the therapeutic synergisms of combined robot-assisted upper limb training and BoNT treatment on upper limb spasticity. The secondary aim was to evaluate the treatment effects on UL function, muscle strength, and the electromyographic activity of UL muscles during a functional task.

The combined treatment would contribute to decrease UL spasticity and improve function through a combination of training effects between BoNT neurolysis and the robotic treatment. A reduction of muscle tone would parallel improvement in muscle strength ought to the high-intensity, repetitive and task-specific robotic training. Since spasticity is associated with abnormal activation of shortening muscles and deficits in voluntary movement of the UL, the sEMG assessment would target these impairments ().

Materials and Methods

Trial Design

A single-blind RCT with two parallel group is reported. The primary endpoint was the changes in UL spasticity while the secondary endpoints were changes in UL function, muscle strength and the electromyographic activity of UL muscles during a functional task. The study was conducted according to the tenets of the Declaration of Helsinki, the guidelines for Good Clinical Practice, and the Consolidated Standards of Reporting Trials (CONSORT), approved by the local Ethics Committee “Nucleo ricerca clinica–Research and Biostatistic Support Unit” (prog n.2366), and registered at clinical trial (NCT03590314).

Patients

Chronic post-stroke patients with upper-limb spasticity referred to the Neurorehabilitation Unit (AOUI Verona) and the Physical Medicine and Rehabilitation Section, “OORR” Hospital (University of Foggia) were assessed for eligibility.

Inclusion criteria were: age > 18 years, diagnosis of ischemic or hemorrhagic first-ever stroke as documented by a computerized tomography scan or magnetic resonance imaging, at least 6 months since stroke, Modified Ashworth Scale (MAS) score (shoulder and elbow) ≤ 3 and ≥1+ (), BoNT injection within the previous 12 weeks of at least one of muscles of the affected upper limb, Mini-Mental State Examination (MMSE) score ≥24 () and Trunk Control Test score = 100/100 ().

Exclusion criteria were: any rehabilitation intervention in the 3 months before recruitment, bilateral cerebrovascular lesion, severe neuropsychologic impairment (global aphasia, severe attention deficit or neglect), joint orthopedic disorders.

All participants were informed regarding the experimental nature of the study. Informed consent was obtained from all subjects. The local ethics committee approved the study.

Interventions

Each patient underwent a BoNT injection in the paretic limb. The dose of BoNT injected into the target muscle was based on the severity of spasticity in each case. Different commercial formulations of BoNT were used according to the pharmaceutical portfolio contracts of our Hospitals (Onabotulinumtoxin A, Abobotulinumtoxin A, and Incobotulinumtoxin A). The dose, volume and number of injection sites were set accordingly. A Logiq ® Book XP portable ultrasound system (GE Healthcare; Chalfont St. Giles, UK) was used to inject BoNT into the target muscle.

Before the start of the study authors designed the experimental (EG) and the control group (CG) protocols. Two physiotherapists, one for each group, carried out the rehabilitation procedures. Patients of both groups received ten individual sessions (45 min/session, two sessions/week, five consecutive weeks). Treatments were performed in the rehabilitative gym of the G. B. Rossi University Hospital Neurological Rehabilitation Unit, or “OORR” Hospital.

Robot-Assisted UL Training

The Robot-assisted UL Training group was treated using the electromechanical device Armotion (Reha Technology, Olten, Switzerland). It is an end-effector device that allows goal-directed arm movements in a bi-dimensional space with visual feedback. It offers different training modalities such as passive, active, passive-active, perturbative, and assistive modes. The robot can move, drive or oppose the patient’s movement and allows creating a personalized treatment, varying parameters such as some repetitions, execution speed, resistance degree of motion. The exercises available from the software are supported by games that facilitate the functional use of the paretic arm (). The robot is equipped with a control system called “impedance control” that modulates the robot movements for adapting to the motor behavior of the patient’s upper limb. The joints involved in the exercises were the shoulder and the elbow, is the wrist fixed to the device.

The Robot-assisted UL Training consisted of passive mobilization and stretching exercises for affected UL (10 min) followed by robot-assisted exercises (35 min). Four types of exercises contained within the Armotion software and amount of repetitions were selected as follows: (i) “Collect the coins” (45–75 coins/10 min), (ii) “Drive the car” (15–25 laps/10 min), (iii) “Wash the dishes” (40–60 repetitions/10 min), and (iv) “Burst the balloons” (100–150 balloons/5 min) (Figure 1). All exercises were oriented to achieving several goals in various directions, emphasizing the elbow flexion-extension and reaching movement. The robot allows participants to execute the exercises through an “assisted as needed” control strategy. For increment the difficulty, we have varied the assisted and non-assisted modality, increasing the number of repetitions over the study period.

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Figure 1
The upper limb robot-assisted training setting.

Conventional Training

The conventional training consisted of UL passive mobilization and stretching (10 min) followed by UL exercises (35 min) that incorporated single or multi-joint movements for the scapula, shoulder, and elbow, performed in different positions (i.e., supine and standing position). The increase of difficulty and progression of intensity were obtained by increasing ROM, repetitions and performing movements against gravity or slight resistance (). Training parameters were recorded on the patient’s log. […]

 

Continue —>  Effectiveness of Robot-Assisted Upper Limb Training on Spasticity, Function and Muscle Activity in Chronic Stroke Patients Treated With Botulinum Toxin: A Randomized Single-Blinded Controlled Trial

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[Abstract] Effectiveness of static stretching positioning on post-stroke upper-limb spasticity and mobility: Systematic review with meta-analysis

Abstract

OBJECTIVE:

To systematically review the effects of static stretching with positioning orthoses or simple positioning combined or not with other therapies on upper-limb spasticity and mobility in adults after stroke.

METHODS:

This meta-analysis was conducted according to PRISMA guidelines and registered at PROSPERO. MEDLINE (Pubmed), Embase, Cochrane CENTRAL, Scopus and PEDro databases were searched from inception to January 2018 for articles. Two independent researchers extracted data, assessed the methodological quality and rated the quality of evidence of studies.

RESULTS:

Three studies (57 participants) were included in the spasticity meta-analysis and 7 (210 participants) in the mobility meta-analysis. Static stretching with positioning orthoses reduced wrist-flexor spasticity as compared with no therapy (mean difference [MD]=-1.89, 95% confidence interval [CI] -2.44 to -1.34; I2 79%, P<0.001). No data were available concerning the spasticity of other muscles. Static stretching with simple positioning, combined or not with other therapies, was not better than conventional physiotherapy in preventing loss of mobility of shoulder external rotation (MD=3.50, 95% CI -3.45 to 10.45; I2 54.7%, P=0.32), shoulder flexion (MD=-1.20, 95% CI -8.95 to 6.55; I2 0%, P=0.76) or wrist extension (MD=-0.32, 95% CI -6.98 to 5.75; I238.5%, P=0.92). No data were available concerning the mobility of other joints.

CONCLUSION:

This meta-analysis revealed very low-quality evidence that static stretching with positioning orthoses reduces wrist flexion spasticity after stroke as compared with no therapy. Furthermore, we found low-quality evidence that static stretching by simple positioning is not better than conventional physiotherapy for preventing loss of mobility in the shoulder and wrist. Considering the limited number of studies devoted to this issue in post-stroke survivors, further randomized clinical trials are still needed.

 

via Effectiveness of static stretching positioning on post-stroke upper-limb spasticity and mobility: Systematic review with meta-analysis. – PubMed – NCBI

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[Powerpoint] What is spasticity?

Δεν υπάρχει διαθέσιμη περιγραφή για τη φωτογραφία.
Δεν υπάρχει διαθέσιμη περιγραφή για τη φωτογραφία.Δεν υπάρχει διαθέσιμη περιγραφή για τη φωτογραφία.Η εικόνα ίσως περιέχει: κείμενο που λέει "Spasticity resulted from loss of descending, fascilitatory a inhibitory influences that act on la interneuron inhibition. Resiprocal inhibition mediated through la interneuron inhibition requires fascilitation from higher centres. With injury to CNS the interneuron is unable to shut off antagonist muscle firing with resultant increased velocity dependent resistance to movement. The combination of both decrease inhibition, increased depolarization state of cell membrane, decrease action potential threshold for nerve signal conduction thus increase activity of structures innervated by the affected nerves."
+27

 

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[ARTICLE] Effectiveness of Robot-Assisted Upper Limb Training on Spasticity, Function and Muscle Activity in Chronic Stroke Patients Treated With Botulinum Toxin: A Randomized Single-Blinded Controlled Trial – Full Text

Background: The combined use of Robot-assisted UL training and Botulinum toxin (BoNT) appear to be a promising therapeutic synergism to improve UL function in chronic stroke patients.

Objective: To evaluate the effects of Robot-assisted UL training on UL spasticity, function, muscle strength and the electromyographic UL muscles activity in chronic stroke patients treated with Botulinum toxin.

Methods: This single-blind, randomized, controlled trial involved 32 chronic stroke outpatients with UL spastic hemiparesis. The experimental group (n = 16) received robot-assisted UL training and BoNT treatment. The control group (n = 16) received conventional treatment combined with BoNT treatment. Training protocols lasted for 5 weeks (45 min/session, two sessions/week). Before and after rehabilitation, a blinded rater evaluated patients. The primary outcome was the Modified Ashworth Scale (MAS). Secondary outcomes were the Fugl-Meyer Assessment Scale (FMA) and the Medical Research Council Scale (MRC). The electromyographic activity of 5 UL muscles during the “hand-to-mouth” task was explored only in the experimental group and 14 healthy age-matched controls using a surface Electromyography (EMGs).

Results: No significant between-group differences on the MAS and FMA were measured. The experimental group reported significantly greater improvements on UL muscle strength (p = 0.004; Cohen’s d = 0.49), shoulder abduction (p = 0.039; Cohen’s d = 0.42), external rotation (p = 0.019; Cohen’s d = 0.72), and elbow flexion (p = 0.043; Cohen’s d = 1.15) than the control group. Preliminary observation of muscular activity showed a different enhancement of the biceps brachii activation after the robot-assisted training.

Conclusions: Robot-assisted training is as effective as conventional training on muscle tone reduction when combined with Botulinum toxin in chronic stroke patients with UL spasticity. However, only the robot-assisted UL training contributed to improving muscle strength. The single-group analysis and the qualitative inspection of sEMG data performed in the experimental group showed improvement in the agonist muscles activity during the hand-to-mouth task.

Introduction

Upper limb (UL) sensorimotor impairments are one of the major determinants of long-term disability in stroke survivors (1). Several disturbances are the manifestation of UL impairments after stroke (i.e., muscle weakness, changes in muscle tone, joint disturbances, impaired motor control). However, spasticity and weakness are the primary reason for rehabilitative intervention in the chronic stages (13). Historically, spasticity refers to a velocity-dependent increase in tonic stretch reflexes with exaggerated tendon jerks resulting from hyperexcitability of the stretch reflex (4) while weakness is the loss of the ability to generate the normal amount of force.

From 7 to 38% of post-stroke patients complain of UL spasticity in the first year (5). The pathophysiology of spasticity is complicated, and new knowledge has progressively challenged this definition. Processes involving central and peripheral mechanisms contribute to the spastic movement disorder resulting in abnormal regulation of tonic stretch reflex and increased muscle resistance of the passively stretched muscle and deficits in agonist and antagonist coactivation (67). The resulting immobilization of the muscle at a fixed length for a prolonged time induces secondary biomechanical and viscoelastic properties changes in muscles and soft tissues, and pain (811). These peripheral mechanisms, in turn, leads to further stiffness, and viscoelastic muscle changes (28). Whether the muscular properties changes may be adaptive and secondary to paresis are uncertain. However, the management of UL spasticity should combine treatment of both the neurogenic and peripheral components of spasticity (910).

UL weakness after stroke is prevalent in both acute and chronic phases of recovery (3). It is a determinant of UL function in ADLs and other negative consequences such as bone mineral content (3), atrophy and altered muscle pattern of activation. Literature supports UL strengthening training effectiveness for all levels of impairment and in all stages of recovery (3). However, a small number of trials have been performed in chronic subgroup patients, and there is still controversy in including this procedure in UL rehabilitation (3).

Botulinum toxin (BoNT) injection in carefully selected muscles is a valuable treatment for spastic muscles in stroke patients improving deficits in agonist and antagonist coactivation, facilitating agonist recruitment and increasing active range of motion (681214). However, improvements in UL activity or performance is modest (13). With a view of improving UL function after stroke, moderate to high-quality evidence support combining BoNT treatment with other rehabilitation procedures (1915). Specifically, the integration of robotics in the UL rehabilitation holds promise for developing high-intensity, repetitive, task-specific, interactive treatment of upper limb (15). The combined use of these procedures to compensate for their limitations has been studied in only one pilot RCT reporting positive results in UL function (Fugl-Meyer UL Assessment scale) and muscular activation pattern (16). With the limits of the small sample, the results support the value of combining high-intensity UL training by robotics and BoNT treatment in patients with UL spastic paresis.

Clinical scales are currently used to assess the rehabilitation treatment effects, but these outcome measures may suffer from some drawbacks that can be overcome by instrumental assessment as subjectivity, limited sensitivity, and the lack of information on the underlying training effects on motor control (17). Instrumental assessment, such as surface electromyography (sEMG) during a functional task execution allows assessing abnormal activation of spastic muscles and deficits of voluntary movements in patients with stroke.

Moreover, the hand-to-mouth task is representative of Activities of Daily Life (ADL) such as eating and drinking. Kinematic analysis of the hand-to-mouth task has been widely used to assess UL functions in individuals affected by neurological diseases showing adequate to more than adequate test-retest reliability in healthy subjects (1819). The task involves flexing the elbow a slightly flexing the shoulder against gravity, and it is considered to be a paradigmatic functional task for the assessment of spasticity and strength deficits on the elbow muscles (1720). Although sEMG has been reported to be a useful assessment procedure to detect muscle activity improvement after rehabilitation, limited results have been reported (1621).

The primary aim of this study was to explore the therapeutic synergisms of combined robot-assisted upper limb training and BoNT treatment on upper limb spasticity. The secondary aim was to evaluate the treatment effects on UL function, muscle strength, and the electromyographic activity of UL muscles during a functional task.

The combined treatment would contribute to decrease UL spasticity and improve function through a combination of training effects between BoNT neurolysis and the robotic treatment. A reduction of muscle tone would parallel improvement in muscle strength ought to the high-intensity, repetitive and task-specific robotic training. Since spasticity is associated with abnormal activation of shortening muscles and deficits in voluntary movement of the UL, the sEMG assessment would target these impairments (281115).

Materials and Methods

Trial Design

A single-blind RCT with two parallel group is reported. The primary endpoint was the changes in UL spasticity while the secondary endpoints were changes in UL function, muscle strength and the electromyographic activity of UL muscles during a functional task. The study was conducted according to the tenets of the Declaration of Helsinki, the guidelines for Good Clinical Practice, and the Consolidated Standards of Reporting Trials (CONSORT), approved by the local Ethics Committee “Nucleo ricerca clinica–Research and Biostatistic Support Unit” (prog n.2366), and registered at clinical trial (NCT03590314).

Patients

Chronic post-stroke patients with upper-limb spasticity referred to the Neurorehabilitation Unit (AOUI Verona) and the Physical Medicine and Rehabilitation Section, “OORR” Hospital (University of Foggia) were assessed for eligibility.

Inclusion criteria were: age > 18 years, diagnosis of ischemic or hemorrhagic first-ever stroke as documented by a computerized tomography scan or magnetic resonance imaging, at least 6 months since stroke, Modified Ashworth Scale (MAS) score (shoulder and elbow) ≤ 3 and ≥1+ (22), BoNT injection within the previous 12 weeks of at least one of muscles of the affected upper limb, Mini-Mental State Examination (MMSE) score ≥24 (23) and Trunk Control Test score = 100/100 (24).

Exclusion criteria were: any rehabilitation intervention in the 3 months before recruitment, bilateral cerebrovascular lesion, severe neuropsychologic impairment (global aphasia, severe attention deficit or neglect), joint orthopedic disorders.

All participants were informed regarding the experimental nature of the study. Informed consent was obtained from all subjects. The local ethics committee approved the study.

Interventions

Each patient underwent a BoNT injection in the paretic limb. The dose of BoNT injected into the target muscle was based on the severity of spasticity in each case. Different commercial formulations of BoNT were used according to the pharmaceutical portfolio contracts of our Hospitals (Onabotulinumtoxin A, Abobotulinumtoxin A, and Incobotulinumtoxin A). The dose, volume and number of injection sites were set accordingly. A Logiq ® Book XP portable ultrasound system (GE Healthcare; Chalfont St. Giles, UK) was used to inject BoNT into the target muscle.

Before the start of the study authors designed the experimental (EG) and the control group (CG) protocols. Two physiotherapists, one for each group, carried out the rehabilitation procedures. Patients of both groups received ten individual sessions (45 min/session, two sessions/week, five consecutive weeks). Treatments were performed in the rehabilitative gym of the G. B. Rossi University Hospital Neurological Rehabilitation Unit, or “OORR” Hospital.

Robot-Assisted UL Training

The Robot-assisted UL Training group was treated using the electromechanical device Armotion (Reha Technology, Olten, Switzerland). It is an end-effector device that allows goal-directed arm movements in a bi-dimensional space with visual feedback. It offers different training modalities such as passive, active, passive-active, perturbative, and assistive modes. The robot can move, drive or oppose the patient’s movement and allows creating a personalized treatment, varying parameters such as some repetitions, execution speed, resistance degree of motion. The exercises available from the software are supported by games that facilitate the functional use of the paretic arm (25). The robot is equipped with a control system called “impedance control” that modulates the robot movements for adapting to the motor behavior of the patient’s upper limb. The joints involved in the exercises were the shoulder and the elbow, is the wrist fixed to the device.

The Robot-assisted UL Training consisted of passive mobilization and stretching exercises for affected UL (10 min) followed by robot-assisted exercises (35 min). Four types of exercises contained within the Armotion software and amount of repetitions were selected as follows: (i) “Collect the coins” (45–75 coins/10 min), (ii) “Drive the car” (15–25 laps/10 min), (iii) “Wash the dishes” (40–60 repetitions/10 min), and (iv) “Burst the balloons” (100–150 balloons/5 min) (Figure 1). All exercises were oriented to achieving several goals in various directions, emphasizing the elbow flexion-extension and reaching movement. The robot allows participants to execute the exercises through an “assisted as needed” control strategy. For increment the difficulty, we have varied the assisted and non-assisted modality, increasing the number of repetitions over the study period.[…]

 

Figure 1. The upper limb robot-assisted training setting.

Continue —> Frontiers | Effectiveness of Robot-Assisted Upper Limb Training on Spasticity, Function and Muscle Activity in Chronic Stroke Patients Treated With Botulinum Toxin: A Randomized Single-Blinded Controlled Trial | Neurology

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[WEB SITE] Nonpharmacologic Approaches to Spasticity Management

Drug therapies alone are not considered sufficient for the treatment of spasticity, and the general consensus supports a broader therapeutic strategy.

Drug therapies alone are not considered sufficient for the treatment of spasticity, and the general consensus supports a broader therapeutic strategy.

Spasticity, defined as a velocity-dependent increase in muscle tone caused by the increased excitability of the muscle stretch reflex, is a challenging symptom that frequently accompanies severe neurological conditions including stroke, multiple sclerosis (MS), cerebral palsy (CP), and spinal cord injury.1 The mechanisms of spasticity are complex, involving an inhibitory/excitatory disruption to the spinal network that heightens muscle activity and spinal reflex responses as a result of compensatory structural neuronal reorganization to central nervous system damage or injury.1,2 The original site of the disrupted signal depends on the cause of central nervous system damage; stroke spasticity originates from the cerebral cortex, whereas spasticity associated with MS and spinal cord injury originates in the spinal cord.

The Role of Nonpharmacologic Therapies

Pharmacologic interventions including oral and injected drugs are a mainstay of spasticity management; however, drug therapies alone are not considered sufficient, and the general consensus supports a broader therapeutic strategy.2 “Spasticity management usually requires a multimodal approach, using nonpharmacological and pharmacological treatment strategies,” Patricia Branco Mills, MHSc, MD, FRCPC, physical medicine and rehabilitation specialist at GF Strong Rehabilitation Centre in Vancouver, British Columbia, Canada, told Neurology Advisor. “The goals are generally to improve function, quality of life, and medical/health status through a transdisciplinary, holistic approach,” Dr Mills said.

In a 2017 review of new technologic advances in neurorehabilitative treatments for spasticity, Naro and colleagues2 emphasized that physical therapy and occupational therapy should be included in any rehabilitation program for focal or generalized spasticity, with other therapies added to achieve optimal results. In a review of spasticity management in stroke, Francois Bethoux, MD,3 reported that because of complications associated with drug and surgical treatment that may exacerbate functional performance through weakness and compensatory hypertonia in weakened limbs, treatment should rely on nonpharmacologic approaches used either before or adjunctively to these strategies.3 In addition to PT, he pointed to multiple other modalities, including ultrasound, thermotherapy, neuromuscular electrical stimulation and muscle strengthening exercises applied to an agonist muscle, and robotic devices for stretching and movement training, as important to a treatment plan.3

Noninvasive Neuromodulation Therapies

Noninvasive neuromodulation therapies designed to modify neuroplastic mechanisms for better adaptive muscle responses via the application of electromagnetic stimuli in conjunction with weak currents and or biochemical agents show potential for reducing spasticity across a number of conditions.

Repetitive transcranial magnetic stimulation (rTMS) involving the indirect application of magnetic pulses in a repeating pattern to induce cortical excitability, has demonstrated more consistent magnitude and duration of benefits in studies of spasticity. In patients with MS, this modality, applied at high frequency (5 Hz, 900 pulses per 15-minute session) to the primary motor region of the brain for 10 sessions over the course of 2 weeks, improved lower limb spasticity for a week to a month after application in patients with relapsing remitting MS.4

Leo et al4 reported that several studies demonstrated that low-frequency rTMS applied to the healthy brain hemisphere reduced chronic stroke-associated upper limb spasticity for up to 1 month posttreatment, whereas high-frequency rTMS showed only limited benefits. It has also demonstrated lasting inhibitory aftereffects on corticospinal motor output that make it especially effective in conjunction with physical conditioning or other therapies for MS spasticity.4

Transcranial direct current stimulation (tDCS) is a method of direct application of low-amplitude current to the brain via rubber electrodes (with saline-dampened sponges) adhered to the scalp to induce excitability. The treatment exerts a neuromodulating effect on neuronal firing rates and plasticity with potential to restore normal balance of the polarity of the neurons. A few sham-controlled studies showed improved Modified Ashworth Scale scores and decreased lower limb spasticity after tDCS administered 5 times per week for 20 minutes, at a setting of 1 mA, for 1 to 4 weeks for patients with stroke as well as MS and CP.4 There were no complications, and adverse effects were minimal.4 A second review by the same group reported only short-term benefits of tDCS in MS and CP and concluded that the evidence in support of tDCS for spasticity was unconvincing, particularly when compared with more significant results from rTMS.

Other Noninvasive Therapies

Lacey Bromley, PT, DPT, NCS, MSCS, a physical therapist from Susan Bennett PT and Associates and a consultant in MS therapeutic strategies, explained that several inhibitory techniques can also be employed to reduce spasticity for a short period. “These include prolonged stretching of the spastic muscle (30-60 seconds), prolonged cold of the spastic muscle, biofeedback techniques, and cutaneous electric stimulation on the opposing muscle. However, these strategies will only reduce the tone temporarily.”

“We have had success utilizing [functional electrical stimulation] on the common peroneal nerve, which innervates the anterior tibialis muscle,” she told Neurology Advisor, referring to the task-directed stimulation therapy that, similar to neuromuscular electrical stimulation, delivers small impulses directly to the affected nerves to force muscle contraction that produces functional movement. Both therapies have demonstrated reductions in spasticity in CP, spinal cord injury, and stroke.2

A wide range of nonpharmacologic therapies and devices are under investigation for spasticity. Their benefits, however, rely largely on the hemisphere of application and the underlying mechanisms, which will require further study for better results.4 Dr Mills observed that many modalities that show promise include targeted exercises, casting/splints, and electromagnetic devices. “Given that pharmacological options can have side effects that patients want to avoid or minimize, there should be a high priority on investigating nonpharmacological treatment strategies that can be used on their own or to improve the effects of pharmacological strategies when given in combination,” Dr Mills said.

References

  1. Mukherjee A, Chakravarty A. Spasticity mechanisms – for the clinicianFront Neurol.2010;1:149.
  2. Naro A, Leo A, Russo M, et al. Breakthroughs in the spasticity management: Are non-pharmacological treatments the future?J Clin Neurosci. 2017;39:16-27.
  3. Bethoux F. Spasticity management after strokePhys Med Rehab Clin N Am. 2015;26:625-639.
  4. Leo A, Naro A, Molonia F, et al. Spasticity management: the current state of transcranial neuromodulationPM R. 2017;9(10):1020-1029.

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[NEWS] People with Spasticity or Dystonia May Become Immune to Botox Treatment – Rehab Managment

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Orange and botox

Botulinum toxin type A (aka Botox) is used as a treatment among people with dystonia or spasticity. Some people who receive this treatment may develop resistance to it, according to a study published recently in Neurology.

The study included nearly 600 patients with dystonia or spasticity who had been receiving botulinum toxin type A for about 3 to 5 years.

The researchers found that about 15% of the patients developed an immune response that made the treatment less effective or ineffective.

“People may be able to lessen their chances of developing this response by making sure the dose of the drug in each injection is as low as possible, the time between injections is not shortened, and booster injections are avoided,” says study author Dr. Philipp Albrecht, in a news release from the American Academy of Neurology.

Albrecht is a member of the medical faculty at Heinrich Heine University in Dusseldorf, Germany.

According to the American Association of Neurological Surgeons (AANS), spasticity is a condition in which certain muscles are continuously contracted, which can interfere with normal movement and speech. Spasticity is usually caused by damage to the portion of the brain or spinal cord that controls voluntary movement.

Dystonia is a complex neurological disorder characterized by involuntary muscle contractions. As many as 250,000 people in the United States have dystonia, making it the third most common movement disorder after essential tremor and Parkinson’s disease, the AANS says, per the release.

[Source(s): American Academy of Neurology, HealthDay]

 

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