The Use of Botulinum Toxin in Spasticity

Spasticity is a prevalent disabling clinical symptom for children with cerebral palsy. Treatment of spasticity with botulinum toxin in children with cerebral palsy was first reported in 1993. Botulinum toxin provides a focal, controlled muscle weakness with reduction in spasticity. Interpretation of the literature is difficult because of the paucity of reliable measures of spasticity and challenges with measuring meaningful functional changes in children with disabilities. This study documents the effects of botulinum toxin A injections into the gastrocnemius muscles in children with spastic diplegia. Outcomes are evaluated across all 5 domains of the National Centers for Medical and Rehabilitation Research domains of medical rehabilitation. A randomized, double-masked, placebo-controlled design was applied to 33 children with spastic diplegia with a mean age of 5.5 and Gross Motor Function Classification System Levels of I through III. Participants received either 12 U/kg botulinum toxin A or placebo saline injections to bilateral gastrocnemius muscles. Outcomes were measured at baseline and 3, 8, 12, and 24 weeks after injection. Significant decreases in the electromyographic representation of spasticity were documented 3 weeks after botulinum toxin A treatment. A significant decrease in viscoelastic aspects of spasticity was present at 8 weeks, and subsequent increases in dorsiflexion range were documented at 12 weeks for the botulinum toxin A group. Improvement was found in performance goals at 12 weeks and in maximum voluntary torque and gross motor function at 24 weeks for the botulinum toxin A. There were no significant differences between groups in satisfaction with performance goals, energy expenditure, Ashworth scores, or frequency of adverse effects. The safety profile of 12 U/kg of botulinum toxin A is excellent. Although physiologic and mechanical effects of treatment with botulinum toxin A were documented with functional improvement at 6 months, family satisfaction with outcomes were no different. Communication is needed to ensure realistic expectations of treatment.

There is considerable evidence that injection of botulinum toxin (BTX) into muscles with spastic overactivity reduces resistance to passive movement in joints supplied by the injected muscles. The demonstration of improvement in active performance of the paretic limbs has been only anecdotal to date, and represents the most difficult challenge in research on BTX therapy in spastic paralysis. Data are reviewed that indicate several neurophysiological actions of BTX, other than the blocking of acetylcholine release at the neuromuscular ending: effects on the central nervous system, including retrograde axonal transport, reduced motoneuronal excitability, action on central synapses such as decreased Renshaw inhibition and increased presynaptic inhibition; action on gamma motoneuronal endings; action on most active terminals; spread of BTX to neighboring muscles; spread of BTX effects to remote muscles. Several of these neurophysiological actions are likely to contribute to improvement in active movements, as they may antagonize the primary mechanisms of functional impairment in patients with spastic paralysis: weakness, spastic cocontraction, spastic dystonia, and muscle shortening. We review the evidence for reduction of spastic cocontraction in both the injected muscle and its antagonist, and for improvement of antagonist weakness after BTX injection. The capacity of intramuscular BTX to reduce spastic dystonia and lengthen shortened muscles is also discussed based on prior literature. When injected into the more overactive of a pair of spastic antagonists around a joint, BTX should affect all the main mechanisms impairing active function around the joint.

Motor deficits are the most common impairment acutely after stroke and persist in nearly half of all patients.1,2 Although much focus is on hemiparesis in this setting, injury to the motor system does not produce a homogenous clinical syndrome. Instead, weakness may be accompanied by other negative findings such as slowness and fatigue and by positive findings such as synkinesia and spasticity. Spasticity is a state of increased tone with exaggerated reflexes resulting from upper motor neuron injury. It is a condition of many contrasts. Reduced activity in one area, the descending motor tracts, results in increased activity in another area, the skeletal muscles. Spasticity is common across neurological conditions, yet accurate measurement is difficult. It is associated …

To examine the benefits of high intensity ambulatory rehabilitation programmes over usual care following botulinum toxin A (BoNT-A) for post-stroke spasticity in Australian adults. Prospective single centre, controlled clinical trial. Fifty-nine adults, median 61 years old and 2.5 years following stroke. PARTICIPANTS were dichotomised into high intensity ambulatory rehabilitation programmes (≥ 3 × 1-h weekly sessions for approximately 10 weeks) or usual care programmes (≤ 2 × 1-h weekly sessions) following BoNT-A injections for spasticity. A blinded assessor completed outcomes at 0 (baseline), 6, 12 and 24 weeks. Primary endpoints: proportion of participants achieving ≥ 50% of their goals (using Goal Attainment Scaling: GAS) and GAS T-score change at 12 weeks. Modified Ashworth Scale (MAS), participant satisfaction, activity/participation measures and caregiver burden. Both groups showed significant improvement in goal attainment and participant satisfaction up to 24 weeks, with no overall between-group significant differences. There was, however, a statistical trend (p = 0.052) for participants to achieve more upper limb goals in the high intensity therapy group. GAS and satisfaction benefits persisted beyond the duration of spasticity reduction as measured by MAS. While patient-centred outcomes following BoNT-A injections for post-stroke spasticity were not influenced by intensity of ambulatory rehabilitation programmes, there was a trend for high intensity therapy to be associated with greater upper limb goal attainment. This suggests that the effects of more intensive therapy may be a modifier of the 'black box' of rehabilitation; however, further research is required to evaluate this effect and determine which elements of therapy programmes optimise post-BoNT-A outcomes.

Quantitative Assessment of Limb Motion by Inertial Sensors Before and After Botulinum Toxin for Spasticity

To study the location and verification of motor points (MP) of the upper limbs for targeting botulinum toxin (BT) type A injections in the treatment of spasticity. Twenty healthy people were examined. Using electromyography a complete study of the muscles of the upper limbs was conducted. Anatomical localization of MP was performed. The location of MP is identical and does not depend on sex, age and the dominant limb. Tables and maps of MP locations are presented. MP in the flexor muscles of the arm were identified. A surface map with MP location was created. This data may improve the clinical efficacy and feasibility of MP targeting, when injecting BT in spasticity.

The long-term risk of stroke increases with age, and stroke is a common cause of disability in the community. Spasticity is considered a significantly disabling impairment that develops in people who have had a stroke. The burden of care is higher in stroke survivors who have spasticity when compared with stroke survivors without spasticity with regard to treatment costs, quality of life, and caregiver burden. To assess if pharmacological interventions for spasticity are more effective than no intervention, normal practice, or control at improving function following stroke. We searched the Cochrane Stroke Group Trials Register (May 2016), the Cochrane Central Register of Controlled Trials (CENTRAL, 2016, Issue 5), MEDLINE (1946 to May 2016), Embase (2008 to May 2016), CINAHL (1982 to May 2016), AMED (1985 to May 2016), and eight further databases and trial registers. In an effort to identify further studies, we undertook handsearches of reference lists and contacted study authors and commercial companies. We included randomised controlled trials (RCTs) that compared any systemically acting or locally acting drug versus placebo, control, or comparative drug with the aim of treating spasticity. Two review authors independently assessed the studies for inclusion and extracted the data. We assessed the included studies for both quality and risk of bias. We contacted study authors to request further information when necessary. We included seven RCTs with a total 403 participants. We found a high risk of bias in all but one RCT. Two of the seven RCTs assessed a systemic drug versus placebo. We pooled data on an indirect measure of spasticity (160 participants) from these two studies but found no significant effect (odds ratio (OR) 1.66, 95% confidence interval (CI) 0.21 to 13.07; I2 = 85%). We identified a significant risk of adverse events per participant occurring in the treatment group versus placebo group (risk ratio (RR) 1.65, 95% CI 1.12 to 2.42; 160 participants; I2 = 0%). Only one of these studies used a functional outcome measure, and we found no significant difference between groups.Of the other five studies, two assessed a systemic drug versus another systemic drug, one assessed a systemic drug versus local drug, and the final two assessed a local drug versus another local drug. The lack of high-quality RCTs limited our ability to make specific conclusions. Evidence is insufficient to determine if systemic antispasmodics are effective at improving function following stroke.

This is a protocol for a Cochrane Review (Intervention). The objectives are as follows: Primary To determine if pharmacological interventions for spasticity are more effective than no intervention, normal practice or control at improving function following stroke. Secondary To determine if pharmacological interventions for spasticity after stroke are more effective than no intervention, normal practice or control at: preventing secondary complications such as pain and contractures; decreasing spasticity at an impairment level. To determine if global antispasmodic interventions are more effective than local treatments at improving function after stroke. To determine if early administration of pharmacological interventions for spasticity (before six months) are more effective than late administration (after six months) of pharmacological intervention at improving function after stroke. To determine the side effects of the use of pharmacological interventions against placebo. To determine whether there is a difference between using pharmacological interventions for spasticity compared with no intervention, normal practice or control at improving function of the arm or leg following stroke.

To investigate the benefits of the focal use of botulinum toxin in spasticity in the forearm seen after incomplete spinal cord injury. A single case study with standardized assessment before and at three-week intervals after injection. EMG-guided selective injection of botulinum toxin. A 23-year-old man, 18 months post injury. Rivermead Motor Assessment; grip strength; Jebsen hand tests; visual analogue scale; Ashworth spasticity scale. Weakness was seen as expected with some functional losses, but the patient made gains in the areas of concern: shaking hands, typing, using the hand to drink. These gains were sustained at 12 weeks. Selective use of botulinum toxin to weaken muscles can lead to functional benefit.

Botulinum toxin for spasticity after stroke or non-progressive brain lesion

Botulinum toxin for spasticity after stroke.

Botulinum toxin for spasticity after stroke or non-progressive brain lesion

This review of the long-term management of spasticity addresses some of the clinical dilemmas in the management of patients with chronic disability. As it is important for clinicians to have clear objectives in patient treatment, the available treatment strategies are set out. Why is it important to treat spastic patients and what treatment does one use? When should one consider a change in the strategy and why is it necessary to have a clear discharge policy from the service to avoid serious logistic problems? The review reiterates the role of physical treatment in the management and thereafter the maintenance of patients with spasticity. There are now a number of good papers on the use of botulinum toxin in spasticity, but this review sets out their context in clinical management and briefly mentions the use of phenol nerve blockade and intrathecal baclofen in clinical practice. Finally, how does one justify the use of an agent regarded as expensive? It is important to use outcome measures that are valid and sensitive to change, and an example is given of ways of demonstrating benefit.

The brain is continually reorganizing (plasticity). Plastic changes within the sensorimotor system are not only beneficial (adaptive plasticity) but may even worsen function (maladaptive plasticity). Conditions such as dystonia and poststroke spasticity (PSS) that interfere with motor performance could be attributed to maladaptive plasticity. Botulinum toxin (BoNT) has been proven to be safe and effective in treating various hyperfunctional cholinergic states. Beside the well-known neuromuscular junction site of action, BoNT also exerts effects through supraspinal mechanisms and can even affect cortical reorganization. The hypothesis of central reorganization following BoNT treatment has been supported by studies using neurophysiological and imaging methods in patients with focal dystonia and PSS. The growing evidence of BoNT-related central (remote) effects make BoNT injections a promising tool to favorably affect maladaptive changes even at the cortical level.

In July 2024, the U.S. Department of Veterans Affairs (VA) and U.S. Department of Defense (DOD) released a joint update of their 2019 clinical practice guideline (CPG) for the management of stroke rehabilitation. This synopsis is a condensed version of the 2024 CPG, highlighting the key aspects of the guideline development process and describing the major recommendations. The VA/DOD Evidence-Based Practice Work Group convened a joint VA/DOD guideline development work group (WG) that included clinical stakeholders and conformed to the Institute of Medicine's tenets for trustworthy CPGs. The guideline WG conducted a patient focus group, developed key questions, and systematically searched and evaluated the literature (English-language publications from 1 July 2018 to 2 May 2023). The GRADE (Grading of Recommendations Assessment, Development and Evaluation) system was used to evaluate the evidence. The WG developed 47 recommendations along with algorithms for stroke rehabilitation in the inpatient and outpatient settings. Stakeholders outside the WG reviewed the CPG before approval by the VA/DOD Evidence-Based Practice Work Group. This synopsis summarizes where evidence is strongest to support guidelines in crucial areas relevant to primary care physicians: transition to community (case management, psychosocial or behavioral interventions); motor therapy (task-specific practice, mirror therapy, rhythmic auditory stimulation, electrical stimulation, botulinum toxin for spasticity); dysphagia, aphasia, and cognition (chin tuck against resistance, respiratory muscle strength training); and mental health (selective serotonin reuptake inhibitor use, psychotherapy, mindfulness-based therapies for treatment but not prevention of depression).