[ARTICLE] Spotlight on botulinum toxin and its potential in the treatment of stroke-related spasticity – Full Text HTML/PDF

Abstract: Poststroke spasticity affects up to one-half of stroke patients and has debilitating effects, contributing to diminished activities of daily living, quality of life, pain, and functional impairments. Botulinum toxin (BoNT) is proven to be safe and effective in the treatment of focal poststroke spasticity. The aim of this review is to highlight BoNT and its potential in the treatment of upper and lower limb poststroke spasticity. We review evidence for the efficacy of BoNT type A and B formulations and address considerations of optimal injection technique, patient and caregiver satisfaction, and potential adverse effects of BoNT.

Introduction

Spasticity is a velocity-dependent increase in muscle tone as a part of the upper motor neuron syndrome and is seen in a wide variety of neurologic diseases including stroke.¹ Poststroke spasticity can develop as early as 1 week after stroke,² and it is estimated to occur in up to one-half of stroke survivors.³ The most frequent predictors of spasticity include weakness and reduced motor control.² Long-term spasticity may lead to tendon contractures and limb deformities that can cause significant pain and functional impairment. Depending on the location of the spasticity, this can impact mobility, activities of daily living such as toileting, dressing, and transferring, and quality of life (QoL) and increase the dependence on caregivers.⁴

The aim of the treatment in poststroke spasticity is focused on muscle limb overactivity reduction. Treatment modalities are used to alleviate spasticity including physical therapy, systemic and intrathecal medications, and surgery. Systemic medications can be helpful if spasticity is generalized. Agents such as baclofen (gamma-aminobutyric acid [GABA]-B receptor agonist) diazepam (GABA-A receptor agonist), dantrolene (decreases calcium release from skeletal muscle sarcoplasmic reticulum), or tizanidine (TZD; alpha-2 adrenergic receptor agonist) often have systemic side effects such as dry mouth, dizziness, sedation, or generalized weakness.⁵ After several months of treatment, tolerance may develop to systemic medications.

Chemodenervation and neurolytic procedures with alcohol or phenol may be utilized as second-line management. These techniques are more localized and are injected perineurally to destroy the nerve causing spasticity. The effect may be limited by partial nerve regeneration and adverse effects such as bladder, bowel, and sexual dysfunction.⁶ Intrathecal baclofen acts on GABA receptors in the lumbar spinal cord and may improve walking speed and functional mobility in poststroke spasticity. However, this therapy is invasive and limited by side effects including nausea, vomiting, and urinary retention. Overdosing may lead to death.^7,8

The aim of this review is to highlight botulinum toxin (BoNT) and its potential in the treatment of upper and lower limb poststroke spasticity. Optimal treatment may include BoNT injections into focal muscles in conjunction with an integrated multidisciplinary team approach and intensive rehabilitation programs or to help utilize affected muscles.⁹ Higher-intensity rehabilitation programs (≥3 1-hour weekly session for ~10 weeks) may help patients achieve more upper limb goals following BoNT injections for spasticity when compared with usual care programs (≤2 1-hour weekly sessions).¹⁰ A recent consensus panel of 44 neurologists and physiatrists with experience in BoNT therapy recommended starting a rehabilitation program during the first week after BoNT injection therapy.¹¹

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[Abstract] Botulinum Toxin Injection and Rehabilitation for Neurosurgical Patients with Spasticity.

Abstract

Objectives

Spasticity gives rise to impairment in motor functions and activities of daily living. Botulinum toxin (BTX) can be injected to temporarily paralyze the affected muscles, which provides a window of opportunity for rehabilitation. We present our 2.5-year experience with BTX injection and a patient-specific rehabilitation program provided by a multidisciplinary team, which consists of neurosurgeons, nurses, physiotherapists, occupational therapists and prosthetic orthotists.

Methodology

It is a retrospective study of prospectively collected data in a local hospital including twenty-two patients suffering from spasticity. Outcome measures include goal attainment, caregiver burden and biomechanical assessment by Modified Ashworth Scale and Modified Tardieu Scale (MTS).

Results

OnabotulinumtoxinA injection together with rehabilitation facilitates the attainment of patient-centred physical goals in daily activities. It reduces caregiver burden. Spasticity is reduced particularly for finger and wrist flexors as well as hip adductors. Responses of ankle plantarflexors are less satisfactory which may be due to inadequate dosages. Initial improvement in the R2 component of the MTS for ankle plantarflexors and hip adductors may be attributable to the application of ankle-foot orthosis and abduction pillow.

Conclusions

Multidisciplinary management for spasticity is feasible within our healthcare setting and our promising findings indicate its wider adoption in this locality.

Source: Botulinum Toxin Injection and Rehabilitation for Neurosurgical Patients with Spasticity – See – Surgical Practice – Wiley Online Library

[ARTICLE] Safety and efficacy of incobotulinumtoxinA as a potential treatment for poststroke spasticity – Full Text HTML/PDF

Abstract: Spasticity is a common disabling symptom for several neurological conditions. Botulinum toxin type A injection represents the gold standard treatment for focal spasticity after stroke showing efficacy, reversibility, and low prevalence of complications. In recent years, incobotulinumtoxinA, a new Botulinum toxin type A free of complexing proteins, has been used for treating several movement disorders with safety and efficacy. IncobotulinumtoxinA is currently approved for treating spasticity of the upper limb in stroke survivors, even if several studies described the use also in lower limb muscles. In the present review article, we examine the safety and effectiveness of incobotulinumtoxinA for the treatment of spasticity after stroke.

Introduction

Spasticity with muscle paresis and loss of dexterity represents one of the most common and discomforting complications affecting stroke survivors. It can have a disabling effect on stroke patients through pain and reduced mobility, affecting quality of life, and can be highly detrimental to daily functioning. Previous studies, based on the estimates of health care professionals, suggested that the prevalence of poststroke spasticity was ~60%, even if this value can be lower than the real value considering the difficulties in measuring spasticity routinely in rehabilitative settings.¹

In a recent study, conducted in a clinical setting, 39% of patients with first-ever stroke were spastic after 12 months.² Lundström et al reported that an estimated prevalence of spasticity 1 year after the first-ever stroke was 17% and that it was more prevalent in the upper limb than in the lower limb.³

In another study, spasticity was present in only 19% of the 95 subjects investigated 3 months after stroke.⁴ The same group of authors reported that 13 subjects out of 63 displayed spasticity after 18 months of stroke.⁵

There is no consensus concerning the number of patients developing spasticity. The discrepancies about the prevalence of spasticity onset after stroke might be related to various study settings and samples as well as the difficulty to measure and to identify its early development, discriminating between spastic-dystonia, muscle contracture, increase of stiffness, and other biomechanical factors. It is known that spastic hypertone can be responsible for motor impairments and activity limitations as well as for forced limb posture and pain at rest and during passive movements. The degree of spasticity may change according to the position of the patients, the task being performed, and the presence of aggravating factors such as pressure ulcers, skin infections, or urinary tract infections. Therefore, considering the variability of clinical features of stroke survivors, the assessment of spasticity is difficult as well as the need for treatment. In fact, for example, it has also been suggested that for stroke patients, the overactivity of leg extensor muscles enables them to support their body, standing position, and stance phase of gait cycle but interferes with knee flexion during the swing phase, so in this case, a botulinum toxin (BoNT) injection into rectus femoris or vastus intermedius muscles can be useful to reduce this impairment.⁶

Spasticity is also divided into generalized and focal when few muscles are involved. This type of classification can influence the choice of treatment considering not only the therapy but also the aim to improve limb posture and body image, to apply splinting, to consent hygiene, to increase passive articular range of motion, to walk and stand, to decrease pain and discomfort, to reduce the burden of care, or to prevent contracture. The purpose of this review article is to evaluate the effectiveness of the employment of incobotulinumtoxinA, a recent marked formulation of botulinum toxin type A (BoNT-A), to reduce spasticity in stroke survivors through an analysis of published clinical studies.

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[ARTICLE] Hemiparetic gait and changes in functional performance due to OnabotulinumtoxinA injection to lower limb muscles

Highlights

• Measurement of temporal spatial gait parameters helps assess function in hemiparetic patients.
• Dynamic EMG is valuable in the selection of muscles in hemiparetic gait.
• Gait parameters showed significant increase in walking velocity and cadence after OnabotA injection to ankle muscles.
• Average of 320 (± 107) units of OnabotA injection to selected ankle muscles enhances functional ambulation in hemiparetic gait.

Abstract

Objective: To review gait alterations and evaluate the effects of OnabotulinumtoxinA on spatiotemporal walking parameters of patients with hemiparetic gait.

Design: Retrospective pre- and post-intervention analysis.

Setting: Gait analysis laboratory in a tertiary level rehabilitation hospital.

Participants: 42 patients with hemiparesis. 19 males and 23 females, age 18-78 years were included.

Intervention: Spatiotemporal parameters collected before and within 4 to 10 weeks after OnabotA injection to the ankle muscles. Data was recorded at self-selected velocity on a 12 meter instrumented walkway. The most common muscles injected were medial and lateral gastrocnemius, soleus and tibialis posterior. Average total OnabotulinumtoxinA dose was 320±107 units.

Main Outcome: Spatiotemporal parameters of walking assessed before (T0) and within 4 to 10 weeks post injection (T1). Paired t-test was used to compare pre- and post-intervention data. A sequential Holm-Bonferroni procedure was used to adjust for multiple comparisons and minimize the risk of type I error. Statistical significance was set at p<0.05.

Results: Statistically significant increases were seen for walking velocity (20%) (T0=0.40±0.26 m/s and T1=0.48±0.29 m/s; p=0.006), and increased cadence (T0=63.48±23.93 steps/min, and T1=70.88±23.65 steps/min; p=0.006) following OnabotulinumtoxinA injections.

Conclusion: This study demonstrates that injection of OnabotulinumtoxinA 320 units to ankle muscles selected with the aid of dynamic electromyography can significantly increase gait velocity and enhance functional ambulation in adults with hemiparesis due to upper motor neuron syndrome.

μέσω Hemiparetic gait and changes in functional performance due to OnabotulinumtoxinA injection to lower limb muscles.