Assessment: Botulinum Neurotoxin for the Treatment of Spasticity (An Evidence-Based Review) (original) (raw)
Related papers
Neurology, 2008
Objective: To perform an evidence-based review of the safety and efficacy of botulinum neurotoxin (BoNT) in the treatment of movement disorders.Methods: A literature search was performed including MEDLINE and Current Contents for therapeutic articles relevant to BoNT and selected movement disorders. Authors reviewed, abstracted, and classified articles based on American Academy of Neurology criteria (Class I–IV).Results: The highest quality literature available for the respective indications was as follows: blepharospasm (two Class II studies); hemifacial spasm (one Class II and one Class III study); cervical dystonia (seven Class I studies); focal upper extremity dystonia (one Class I and three Class II studies); focal lower extremity dystonia (one Class II study); laryngeal dystonia (one Class I study); motor tics (one Class II study); and upper extremity essential tremor (two Class II studies).Recommendations: Botulinum neurotoxin should be offered as a treatment option for the t...
Dystonia, Spasticity and Botulinum Toxin Therapy: Rationale, Evidences and Clinical Context
InTech eBooks, 2012
Dystonia-The Many Facets 84 2. BoNT: Peripheral blockade and beyond There are two kinds of BoNT (type A [BoNT-A: onabotulinumtoxinA or Botox ® , abobotulinumtoxinA or Dysport ® and incobotulinumtoxinA or Xeomin ® ], and type B [BoNT-B: rimabotulinumtoxinB or Neurobloc ® /Myobloc ® ]) t h a t h a v e b e e n p r o v e n t o b e s a f e a n d effective in treating various hyperfunctional cholinergic states. Their therapeutic applications range from various forms of muscle hyperactivity (e.g. dystonia, spasticity, spasms, tremors, and tics), autonomic hyperactivity (e.g. drooling, hyperhidrosis and bladder overactivity) and cosmesis (e.g. frown lines and "crow's feet). BoNT is more effective in blocking active neuromuscular junctions(9), and this effect can be enhanced by electric stimulation of the peripheral nerve(10). This toxin disrupts neurotransmission by cleavage of pre-synaptic vesicle fusion proteins; SNAP-25 for BoNT-A and synaptobrevin for BoNT-B, effectively blocking release of acetylcholine to the neuromuscular junctions and induce chemodenervation. The BoNT-A initially binds presynaptically (via the heavy chain attachment domain) and enters neurons by binding to the synaptic vesicle protein SV2(11). The toxin then undergoes internalization by vesicle endocytosis and translocation into the cytosol, to eventually exert its light chain proteolytic activity(12). After injection, the BoNT complex dissociates and diffuses into the target tissues. Toxin spread is a fast and active phenomenon that is driven by BoNT dose, dilution, needle size, and injection technique among others(13). Subclinical effects of BoNT on endplates far away from the injected sites can be demonstrated by increased jitter in single-fiber electromyography (SFEMG) in animals(3,14) and humans(15-16). Clinically not relevant for the moment and taken with a cautious stand because of the high animal doses applied, BoNT may undergo retrograde axonal transport, possibly transcytosed to afferent neurons, in which it cleaves its substrate SNAP-25. BoNT-truncated SNAP-25 appears not only at the injection site but also in distant regions that project to the infusion area. This retrograde spread was blocked by colchicine, pointing to a likely involvement of microtubule-dependent axonal transport(17). BoNTalso affects the cholinergically mediated intrafusal fibers of muscle spindles, parallel to that of extrafusal fibers , implying an important functional effect (see a review on the subject by Rosales and Dressler, 2010[4]). In healthy, dystonic or spastic adults, the effect on muscle spindles appear to be more prolonged than that in extrafusal fibers, and whether one applies studies using the tonic vibration reflex (TVR)(18-19); or the transcranial magnetic stimulation(20). Since the gamma-motor-neurons are unable to activate the intrafusal fibers with BoNT-A, the muscle spindle output via the afferent axons will be reduced, and because muscle activity is supported by afferent feedback, there may be reduced alpha-motorneuron drive(3). These events imply that there could be potential modulation of central motor programs following BoNT-A(21). In fact, recent BoNT-A studies in dystonia and spasticity have shown evidences of modifications in the cortical and subcortical levels(22-24); including plasticity changes(25). 3. BoNT for dystonia 3.1 Rationale Dystonia is a multi-level system disorder where involvement spans from the peripheral (muscular) to the segmental and suprasegmental levels (brainstem, basal ganglia and cortex)(4,26). Muscle hypertonus/spasms in dystonia are relieved by chemodenervation procedures that include muscle-based injections (i.e. muscle afferent block [MAB] and www.intechopen.com Dystonia, Spasticty and Botulinum Toxin Therapy
Treatment of focal dystonias with botulinum neurotoxin
Toxicon, 2009
This is a review on the use of injections of botulinum toxin for the treatment of focal dystonias. Disorders covered include cranial dystonia, cervical dystonia, spasmodic dysphonia, and focal hand dystonia. Considered are clinical aspects, alternative treatment strategies and principles of use of botulinum toxin injections.
Neurology, 2016
To update the 2008 American Academy of Neurology (AAN) guidelines regarding botulinum neurotoxin for blepharospasm, cervical dystonia (CD), headache, and adult spasticity. We searched the literature for relevant articles and classified them using 2004 AAN criteria. Blepharospasm: OnabotulinumtoxinA (onaBoNT-A) and incobotulinumtoxinA (incoBoNT-A) are probably effective and should be considered (Level B). AbobotulinumtoxinA (aboBoNT-A) is possibly effective and may be considered (Level C). CD: AboBoNT-A and rimabotulinumtoxinB (rimaBoNT-B) are established as effective and should be offered (Level A), and onaBoNT-A and incoBoNT-A are probably effective and should be considered (Level B). Adult spasticity: AboBoNT-A, incoBoNT-A, and onaBoNT-A are established as effective and should be offered (Level A), and rimaBoNT-B is probably effective and should be considered (Level B), for upper limb spasticity. AboBoNT-A and onaBoNT-A are established as effective and should be offered (Level A) ...
Botulinum toxin therapy of dystonia
Journal of Neural Transmission, 2020
Botulinum toxin (BT) is used to treat a large number of muscle hyperactivity syndromes. Its use in dystonia, however, is still one of the most important indications for BT therapy. When BT is injected into dystonic muscles, it produces a peripheral paresis which is localised, well controllable and follows a distinct and predictable time course of around 3 months. Adverse effects are always transient and usually mild, long-term application is safe. With this profile BT can be used to treat cranial dystonia, cervical dystonia and limb dystonia including writer's and musician's cramps. The recent introduction of BT high dose therapy also allows to treat more widespread dystonia including segmental and generalised dystonia. BT can easily be combined with other anti-dystonic treatments such as deep brain stimulation and intrathecal baclofen application. Best treatment results are obtained when BT therapy is integrated in the multimodal and long-term 'multilayer concept of treatment of dystonia'. The biggest challenge for the future will be to deliver state of the art BT therapy to all dystonia patients in need, regardless of whether they live in developed countries or beyond.
Localized injections of botulinum toxin for the treatment of focal dystonia and hemifacial spasm
Movement Disorders, 1987
Medical treatment of dystonia usually results in an incomplete response and is frequently unsuccessful. Peripheral surgical therapy is available for some focal dystonias, but may only offer temporary relief and may have unacceptable complications. We have used local injections of botulinum toxin into the appropriate muscles for treatment of disabling focal or segmental dystonia in 93 patients with torticollis, blepharospasm, oromandibular dystonia (OMD), limb dystonia, lingual dystonia, and dystonia adductor dysphonia, in addition to four patients with hemifacial spasm. Significant relief of motor symptoms was seen in 69% of the patients with blepharospasm and 64% of patients with torticollis; 74% of the latter group with pain experience relief. Relief of symptoms was noted in most patients with OMD and limb dystonia, and all with lingual dystonia, dystonic adductor spastic dysphonia, and those with hemifacial spasm. Benefit averaged 2½-3 months initially; however some patients experienced longer relief with subsequent injections. Adverse effects were transient, although 2 patients developed antibodies against the toxin, and we documented evidence for distant effects in others. This approach of chemically weakening contracting muscles in focal dystonia offers many advantages over pharmacotherapy and surgical therapy. Additional experience is needed to explore the proper doses, and potential for long term adverse effects.
Botulinum toxin A in the treatment of spasticity – An open label study
Journal of Back and Musculoskeletal Rehabilitation, 2002
To assess the efficacy of botulinum toxin type A in spasticity in upper-motor neuron syndromes. Methods: Twenty-three patients with spasticity resulted from stroke-related hemiplegia, transverse myelitis and multiple sclerosis took part in the study. Following the history and physical examinations of the patients, injections of botulinum toxin-A were applied. The dose ranged from 80 to 400 mouse unit (MU) depending on the size of the muscle injected. In all patients, spasticity, spasms and pain were measured using the Ashworth Scale, Spasm Frequency Score, and Visual Analogue Scale prior to the therapy, at the 1st week, 1st month and 3rd month of the therapy. Results: In all patients, botulinum toxin type A led to a significant decrease in spasticity, spasms and pain after the 1st week, 1st and 3 rd months of the treatment when compared to the baseline values (p < 0.001). No significant side effects or complications were observed. Conclusion: Our results have demonstrated that botulinum toxin type A is effective in the management of patients with spasticity due to stroke-related hemiplegia, transverse myelitis and multiple sclerosis, without major adverse effects.