Cortical activity modulation by botulinum toxin type A in patients with post-stroke arm spasticity: Real and imagined hand movement

Veverka, Tomáš; Hluštı́k, Petr; Hok, Pavel; Otruba, Pavel; Tüdös, Zbyněk; Zapletalová, Jana; Krobot, Alois; Kaňovský, Petr

doi:10.1016/j.jns.2014.09.009

Cited by 19 publications

(21 citation statements)

References 55 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…There was a significant transient decrease in the global MAS score at W4, when the pharmacological peripheral effect of BoNT-A is assumed to be maximal, and a subsequent increase in the global MAS score at further follow-up (W11). In contrast to our previous BoNT-A-studies (15, 16, 20), there was a significant change in the global MAS score from baseline to W11, when BoNT-A is expected to wane from the neuromuscular junctions (43). Namely, some improvement of spasticity persisted by the end of the study, even though local BoNT-A effect should have disappeared.…”

Section: Discussioncontrasting

confidence: 99%

“…It has been previously demonstrated that brain activation during motor imagery is strongly influenced by the proprioceptive information related to the pre-existing configuration of the limbs (64). After successful treatment of PSS, the internal models (predictions) of the upper limb are likely to adapt to the newly reduced flow of afferent information, which could, in turn, reduce the occurrence of unnecessary fMRI activation during motor imagery, as was observed with actual movement (15). Similar effects on overt and imagined upper limb movement were observed in Parkinson disease patients before and after treatment with L-DOPA (65, 66).…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Botulinum Toxin Modulates Posterior Parietal Cortex Activation in Post-stroke Spasticity of the Upper Limb

Veverka¹,

Hok²,

Otruba³

et al. 2019

Front. Neurol.

Self Cite

View full text Add to dashboard Cite

Post-stroke spasticity (PSS) is effectively treated with intramuscular botulinum toxin type A (BoNT-A), although the clinical improvement is likely mediated by changes at the central nervous system level. Using functional magnetic resonance imaging (fMRI) of the brain, this study aims to confirm and locate BoNT-A-related changes during motor imagery with the impaired hand in severe PSS. Temporary alterations in primary and secondary sensorimotor representation of the impaired upper limb were expected. Thirty chronic stroke patients with upper limb PSS undergoing comprehensive treatment including physiotherapy and indicated for BoNT treatment were investigated. A change in PSS of the upper limb was assessed with the modified Ashworth scale (MAS). fMRI and clinical assessments were performed before (W0) and 4 weeks (W4) and 11 weeks (W11) after BoNT-A application. fMRI data were acquired using 1.5-Tesla scanners during imagery of finger-thumb opposition sequences with the impaired hand. At the group level, we separately modeled (1) average activation at each time point with the MAS score and age at W0 as covariates; and (2) within-subject effect of BoNT-A and the effect of time since W0 as independent variables. Comprehensive treatment of PSS with BoNT-A significantly decreased PSS of the upper limb with a maximal effect at W4. Task-related fMRI prior to treatment (W0) showed extensive activation of bilateral frontoparietal sensorimotor cortical areas, bilateral cerebellum, and contralesional basal ganglia and thalamus. After BoNT-A application (W4), the activation extent decreased globally, mostly in the bilateral parietal cortices and cerebellum, but returned close to baseline at W11. The intra-subject contrast revealed a significant BoNT-A effect, manifesting as a transient decrease in the activation of the ipsilesional intraparietal sulcus and superior parietal lobule. We demonstrate that BoNT-A treatment of PSS of the upper limb is associated with transient changes in the ipsilesional posterior parietal cortex, possibly resulting from temporarily altered sensorimotor upper limb representations.

show abstract

Section: Discussioncontrasting

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Botulinum Toxin Modulates Posterior Parietal Cortex Activation in Post-stroke Spasticity of the Upper Limb

Veverka¹,

Hok²,

Otruba³

et al. 2019

Front. Neurol.

Self Cite

View full text Add to dashboard Cite

show abstract

“…However, early treatment may modify disease progression before secondary local biomechanical changes occur [ 22 , 23 , 24 ]. Disease modification at the level of cortical reorganization was demonstrated through functional magnetic resonance imaging in BoNT-A therapy for chronic PSS [ 25 ], suggesting preventive potential—and a possible paradigm shift towards early intervention. As spasticity is a form of maladaptive plasticity that progresses over time [ 13 , 26 ], early therapeutic intervention may provide an opportunity to prevent or reduce neurological changes leading to disabling spasticity [ 23 ].…”

Section: Discussionmentioning

confidence: 99%

Early AbobotulinumtoxinA (Dysport®) in Post-Stroke Adult Upper Limb Spasticity: ONTIME Pilot Study

Rosales

Balcaitiene

Berard

et al. 2018

Toxins

View full text Add to dashboard Cite

The ONTIME study investigated whether early post-stroke abobotulinumtoxinA injection delays appearance or progression of upper limb spasticity (ULS) symptoms. ONTIME (NCT02321436) was a 28-week, exploratory, double-blind, randomized, placebo-controlled study of abobotulinumtoxinA 500U in patients with ULS (Modified Ashworth Scale [MAS] score ≥ 2) 2–12 weeks post-stroke. Patients were either symptomatic or asymptomatic (only increased MAS) at baseline. Primary efficacy outcome measure: time between injection and visit at which re-injection criteria were met (MAS ≥ 2 and ≥1, sign of symptomatic spasticity: pain, involuntary movements, impaired active or passive function). Forty-two patients were randomized (abobotulinumtoxinA 500U: n = 28; placebo: n = 14) with median 5.86 weeks since stroke. Median time to reach re-injection criteria was significantly longer for abobotulinumtoxinA (156 days) than placebo (32 days; log-rank: p = 0.0176; Wilcoxon: p = 0.0480). Eleven (39.3%) patients receiving abobotulinumtoxinA did not require re-injection for ≥28 weeks versus two (14.3%) in placebo group. In this exploratory study, early abobotulinumtoxinA treatment significantly delayed time to reach re-injection criteria compared with placebo in patients with post-stroke ULS. These findings suggest an optimal time for post-stroke spasticity management and help determine the design and sample sizes for larger confirmatory studies.

show abstract

“…Importantly, comprehensive treatment in stroke patients also requires regular physiotherapy, therefore, the reported effects of BoNT-A are usually combined with the effects of physiotherapy [106]. As this is the recommended treatment approach, application of BoNT-A without physiotherapy would be unethical and, therefore, their effects have usually been studied together [107][108][109][110][111][112][113] but see [114,115]. Despite a wide range of structural lesions that lead to spasticity, the following paragraphs illustrate that changes observed in spasticity seem to be much more uniform than observations in dystonia.…”

Section: Spasticitymentioning

confidence: 99%

The Central Effects of Botulinum Toxin in Dystonia and Spasticity

Hok

Veverka

Hluštı́k

et al. 2021

Toxins

Self Cite

View full text Add to dashboard Cite

In dystonic and spastic movement disorders, however different in their pathophysiological mechanisms, a similar impairment of sensorimotor control with special emphasis on afferentation is assumed. Peripheral intervention on afferent inputs evokes plastic changes within the central sensorimotor system. Intramuscular application of botulinum toxin type A (BoNT-A) is a standard evidence-based treatment for both conditions. Apart from its peripheral action on muscle spindles, a growing body of evidence suggests that BoNT-A effects could also be mediated by changes at the central level including cerebral cortex. We review recent studies employing electrophysiology and neuroimaging to investigate how intramuscular application of BoNT-A influences cortical reorganization. Based on such data, BoNT-A becomes gradually accepted as a promising tool to correct the maladaptive plastic changes within the sensorimotor cortex. In summary, electrophysiology and especially neuroimaging studies with BoNT-A further our understanding of pathophysiology underlying dystonic and spastic movement disorders and may consequently help develop novel treatment strategies based on neural plasticity.

show abstract

Cortical activity modulation by botulinum toxin type A in patients with post-stroke arm spasticity: Real and imagined hand movement

Cited by 19 publications

References 55 publications

Botulinum Toxin Modulates Posterior Parietal Cortex Activation in Post-stroke Spasticity of the Upper Limb

Botulinum Toxin Modulates Posterior Parietal Cortex Activation in Post-stroke Spasticity of the Upper Limb

Early AbobotulinumtoxinA (Dysport®) in Post-Stroke Adult Upper Limb Spasticity: ONTIME Pilot Study

The Central Effects of Botulinum Toxin in Dystonia and Spasticity

Contact Info

Product

Resources

About