But botox DOES NOTHING TO CURE SPASTICITY!
I'm 18 years post stroke and the spasticity hasn't diminished one bit!
Obviously these researchers don't think much of the ridiculous opinion of Dr. William M. Landau!
Spasticity After Stroke: Why Bother? Aug. 2004)
The latest here:
Botulinum Toxin Injections for Stroke Rehabilitation
Stroke affects around 800,000 Americans every year, and has a variety of sequelae across many organ systems.1 Often, strokes can result in chronic paresis and spasticity, which are significant contributors to long-term disability.2 Patients with hemiparesis can experience mild to severe gait dysfunctions that can leave them unable to ambulate or function normally.3 Post-stroke spasticity of the lower extremities can lead to equinovarus deformity that makes ambulation difficult and impairs balance and a normal gait cycle.4 Spastic hemiparesis can also contribute to these gait dysfunctions and can affect walking velocity due to atypical muscle activation, causing an increase in tonic stretch reflexes and muscle hypertonicity.3,5
Treatments for spastic hemiparesis vary from oral antispasticity medications, shock wave therapy, botulinum toxin injections and many more.6 Ultrasound-guided botulinum toxin injections have increased in popularity due to the ability for focal injection and the absence of side effects—such as sedation—which are prevalent with generalized antispasticity medications.7 Use of both botulinum toxin A and B injections for chemodenervation has proven effective(NOT TRUE! It doesn't cure spasticity!) in treatment of spasticity in adults and children.8
AbobotulinumtoxinA (aboBoNT-A; Dysport, Galderma Laboratories) is FDA approved for use in treatment of hypertonic muscles in spastic paresis. Botulinum toxin is a neurotoxin produced by Clostridium botulinum, a spore-forming Bacillus bacterium that is gram-positive and anaerobic.9 The heavy chain of the toxin binds to the receptors on the presynaptic surface of cholinergic nerve terminals and are taken into the cell. The disulfide bond between the heavy and light chains is broken, and the light chain interacts with SNARE (soluble N-ethylmaleimide–sensitive factor attachment) proteins.5,9 This prevents fusion and exocytosis of the acetylcholine vesicles into the synaptic terminal. The onset of action is between 24 and 72 hours, but the binding is irreversible, so effects remain until two to three months later when new nerve terminals and synaptic contacts are created.9 This time line allows for more targeted treatments in stroke patients, as injection frequency can be tailored to a patient’s needs.
In 2003, a class I study examined calf muscle hypertonicity and aboBoNT-A effects on walking rehabilitation. A total of 234 participants who had previous strokes received different doses of aboBoNT-A over 12 weeks. Investigators measured stepping rate and two-minute walking distance, as well as calf spasticity, limb pain and use of walking aids. They found small but significant improvements across the measured parameters, concluding that botulinum toxin injections are a safe and helpful form of rehabilitation therapy.10
A paper published in 2021 examined repeated aboBoNT-A injections effects on walking velocity in people with spastic hemiparesis.11 The study was conducted on adults with hemiparesis; the treatment involved one intramuscular injection of 1,000 to 1,500 units of aboBoNT-A or placebo. Participants were between 18 and 80 years of age with spastic hemiparesis and only one brain injury or stroke prior to study enrollment. They had comfortable barefoot walking velocities of 0.1 to 0.8 meters per second (with 0.1-0.4 meters per second considered to be household ambulators, and 0.4-0.8 considered as limited ambulators). The injection was given in the gastrocnemius–soleus muscle complex, with additional injections in other muscles, depending on the clinician’s judgment. The study ran for up to 18 months with five injections. Results varied based on the number of injections, as expected, but overall the comfortable barefoot walking velocities had a mean improvement of 0.14 meters per second.11 This improvement moved many of the participants from the household ambulation category into community ambulators.
Botulinum toxin injections are widely accepted in their use for post-stroke spasticity. However, dosing and frequency are not standardized, and more studies need to establish treatment algorithms and clinical guidelines.12 Although botulinum toxin therapy should be highly specialized to the patient due to varying levels of post-stroke spasticity, guidelines would help decrease iatrogenic conditions. A study published in 2021 examined the increase of high doses of botulinum toxin A administration and the risks for severe side effects.13 The study concluded that doses up to 840 units were effective and safe, although the American-European Consensus Conference recommended that doses do not exceed 600 units.14 The investigators also said higher doses may be applicable in certain patients, but recognized that more studies need to be done in this area to enable safer use of the injections and better patient outcomes.13
Overall, botulinum toxin injections have been proven to help with spasticity and muscle tone in stroke patients. Current studies have focused specifically on improved spasticity and hypertonicity but less on quality of life and functional improvements.4 In a systematic review published in 2018, investigators recognized the need for studies that examine botulinum toxin’s ability to improve functional outcomes.4,12 Spasticity is just one variable in the overall rehabilitation of post-stroke patients. To establish the positive impact of botulinum toxin on overall rehabilitation of the lower limb, further research must be done.
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