Posts Tagged Botox

[NEWS] Botox is Now Approved for Lower-Limb Spasticity in Children

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The US Food and Drug Administration (FDA) has approved onabotulinumtoxinA (Botox, Allergan) to ease lower-limb spasticity in children and adolescents aged 2 years to 17 years, excluding spasticity caused by cerebral palsy (CP), Allergan announces.

“Lower limb spasticity can impact many aspects of a child’s life and have a drastic influence on their overall development and quality of life,” David Nicholson, Allergan’s chief research and development officer, says in a news release.

The FDA approved Botox for lower-limb spasticity on the basis of safety and efficacy data from a phase 3 study involving more than 300 children aged 2 years or older with lower-limb spasticity.

Participants in the trial had CP, but the approved indication excludes lower-limb spasticity caused by CP, owing to marketing exclusivity by another company, according to Allergan.

The approved recommended dose per treatment session is 4 to 8 units/kg divided among affected muscles of the lower limb. The total dose for pediatric patients should not exceed 8 units/kg body weight, or 300 units, whichever is lower.

When treating both lower limbs or upper and lower limbs in combination, the total dose for pediatric patients should not exceed 10 units/kg, or 340 units, whichever is lower, in a 3-month interval, the company states.

“Pediatric lower limb spasticity inhibits normal muscular movement and function and can result in delayed or impaired motor development, as well as difficulty with posture and positioning,” Mark Gormley, Jr, MD, of Gillette Children’s Specialty Healthcare–St. Paul, comments, in the release.

“Botox has a well-established safety and efficacy profile, and supports children and adolescents successfully manage both their upper and lower limb spasticity,” said Gormley.

Botox was approved for pediatric upper-limb spasticity in June.

[Source: Medscape]

 

via Botox is Now Approved for Lower-Limb Spasticity in Children – Rehab Managment

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[WEB SITE] Medical Device as Post-Stroke Spasticity Reducer Shows Promise

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An investigational, non-invasive medical device shows promise as a possible treatment for spasticity in patients who have experienced a stroke, Feinstein Institutes for Medical Research scientists report.

Their study, published in Springer Nature’s Bioelectronic Medicine, suggests that trans-spinal direct current stimulation and peripheral nerve direct current stimulation significantly reduced upper limb spasticity in participants who experienced a stroke.

Spasticity is a residual inability of the brain to control muscle tone. It increases muscle stiffness, which inhibits movement of the hands, arms, and legs; can affect the face and throat; and sometimes causes pain.

Efforts to treat upper limb spasticity have focused on intensive, repetitive, activity-dependent learning; however, it is common to experience residual spasticity despite aggressive therapy. When spasticity continues to worsen and causes pain, the standard-of-care is botox (botulinum toxin) injection, according to a media release from Feinstein Institutes for Medical Research.

“Spasticity is a persistent and common inhibitor of movement in patients with chronic stroke, and it has been a great hurdle as we continue to use intensive training to assist motor recovery,” says Bruce T. Volpe, MD, professor at the Feinstein Institutes and lead author of the paper, in the release.

“The surprise in these clinical results were the improved motor functions that apparently occurred with the focused treatment only of spasticity. We are eager to start a trial that couples motor training and anti-spasticity treatment.”

The treatment involves passing a direct electrical current across the spinal cord with a skin surface electrode, known as trans-spinal direct current stimulation (tsDCS), and adding a peripheral direct current stimulation (pDCS) in the paralyzed upper limb. There are additional benefits to patients when tsDCS is combined with pDCS.

Volpe, along with a team that includes Johanna Chang, MS, Alexandra Paget-Blanc, BS, and Maira Saul, MD, employed this device in patients with chronic stroke and hemiparesis to test whether treatment would decrease upper limb spasticity. The trial was a single-blind cross-over design study.

Twenty six participants were treated with five consecutive days of 20 minutes of active, paired tsDCS+pDCS. The participants received both active and sham stimulation conditions, but were not told the order of stimulation.

The device used in the trial was PathMaker Neurosystems Inc’s MyoRegulator, a non-invasive device designed to provide simultaneous, non-invasive stimulation intended to suppress hyperexcitable spinal neurons involved with spasticity.

The results demonstrated that the active treatment condition significantly reduced upper limb spasticity for up to five weeks and these patient responders saw significant improvements in motor function, the release explains.

[Source(s): Feinstein Institutes for Medical Research, PR Newswire]

 

via Medical Device as Post-Stroke Spasticity Reducer Shows Promise – Rehab Managment

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[NEWS] People with Spasticity or Dystonia May Become Immune to Botox Treatment – Rehab Managment

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Botulinum toxin type A (aka Botox) is used as a treatment among people with dystonia or spasticity. Some people who receive this treatment may develop resistance to it, according to a study published recently in Neurology.

The study included nearly 600 patients with dystonia or spasticity who had been receiving botulinum toxin type A for about 3 to 5 years.

The researchers found that about 15% of the patients developed an immune response that made the treatment less effective or ineffective.

“People may be able to lessen their chances of developing this response by making sure the dose of the drug in each injection is as low as possible, the time between injections is not shortened, and booster injections are avoided,” says study author Dr. Philipp Albrecht, in a news release from the American Academy of Neurology.

Albrecht is a member of the medical faculty at Heinrich Heine University in Dusseldorf, Germany.

According to the American Association of Neurological Surgeons (AANS), spasticity is a condition in which certain muscles are continuously contracted, which can interfere with normal movement and speech. Spasticity is usually caused by damage to the portion of the brain or spinal cord that controls voluntary movement.

Dystonia is a complex neurological disorder characterized by involuntary muscle contractions. As many as 250,000 people in the United States have dystonia, making it the third most common movement disorder after essential tremor and Parkinson’s disease, the AANS says, per the release.

[Source(s): American Academy of Neurology, HealthDay]

 

via People with Spasticity or Dystonia May Become Immune to Botox Treatment – Rehab Managment

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[WEB SITE] What is clonus? Everything you need to know

Clonus is a neurological condition that occurs when nerve cells that control the muscles are damaged. This damage causes involuntary muscle contractions or spasms.

Clonus spasms often occur in a rhythmic pattern. Symptoms are common in a few different muscles, especially in the extremities. These include the:

  • ankles
  • knees
  • calves
  • wrists
  • jaw
  • biceps

Damaged nerves can cause muscles to misfire, leading to involuntary contractions, muscle tightness, and pain.

Clonus can cause a muscle to pulse for an extended period. This pulsing can lead to muscle fatigue, which may make it difficult for a person to use the muscle later.

Clonus can make everyday activities strenuous and can even be debilitating. In this article, learn more about the causes and treatment.

Causes

Nerve cells in muscles causing clonus

Damaged nerve cells cause clonus.

While researchers do not understand the exact cause of clonus, it appears to be due to damaged nerve passageways in the brain.

A number of chronic conditions are associated with clonus. As these conditions require specialized treatment, the outcome may vary in each case.

Conditions associated with clonus include:

Multiple sclerosis (MS) is an autoimmune disorder that attacks the protective sheath around the nerves. The resulting damage disrupts the nerve signals in the brain.

A stroke starves a part of the brain of oxygen, usually due to a blood clot. A stroke may cause clonus if it damages the area in the brain that controls movement.

Infections, such as meningitis or encephalitis, can damage brain cells or nerves if they become severe.

Major injuries, such as head trauma from a major accident, may also damage the nerves in the brain or spinal cord.

Serotonin syndrome is a potentially dangerous reaction that occurs if too much serotonin builds up in the body. This buildup could be due to drug abuse, but it may also be caused by taking high doses of medications or mixing certain medical drugs.

A brain tumor that pushes against the motor neurons in the brain or causes these areas to swell may lead to clonus.

Other causes of clonus include anything that has the potential to affect the nerves or brain cells, including:

  • cerebral palsy
  • Lou Gehrig’s disease
  • anoxic brain injury
  • hereditary spastic paraparesis
  • kidney or liver failure
  • overdoses of drugs such as Tramadol, which is a strong painkiller

Clonus tests

Clonus may be diagnosed using an MRI scan.

An MRI scan may be used to diagnose clonus.

To diagnose clonus, doctors may first physically examine the area that is most affected. If a muscle contracts while a person is in the doctor’s office, they may monitor the contraction to see how fast the muscle is pulsing and how many times it contracts before stopping.

Doctors will then order a specific series of tests to help them confirm the diagnosis. They may use magnetic resonance imaging (MRI) to check for damage to the cells or nerves.

Blood tests may also help identify markers for various conditions associated with clonus.

A physical test may also help doctors identify clonus. During this test, they will ask the person to quickly flex their foot, so their toes are pointing upward and then hold the muscle there.

This may cause a sustained pulsing in the ankle. A series of these pulses may indicate clonus. Doctors do not rely on this test to diagnose clonus, but it can help point them in the right direction during the diagnostic process.

Treatment

Treatment for clonus varies depending on the underlying cause. Doctors may try many different treatment methods before finding the one that works best for each person.

Medications

Sedative medications and muscle relaxers help reduce clonus symptoms. Doctors often recommend these drugs in the first instance for people experiencing clonus.

Medications that may help with clonus contractions include:

  • baclofen (Lioresal)
  • dantrolene (Dantrium)
  • tizanidine (Zanaflex)
  • gabapentin (Neurotonin)
  • diazepam (Valium)
  • clonazepam (Klonopin)

Sedatives and anti-spasticity medications can cause drowsiness or sleepiness. People taking these medications should not drive a car or operate heavy machinery.

Other side effects may include mental confusion, lightheadedness, or even trouble walking. A person should discuss these side effects with a doctor, especially if they are likely to disrupt a person’s work or everyday activities.

Other treatments

Clonus may be treated with physical therapy.

Physical therapy may help treat clonus.

Other than medication, treatments that may help reduce clonus include:

Physical therapy

Working with a physical therapist to stretch or exercise the muscles may help increase the range of motion in the damaged area. Some therapists may recommend wrist or ankle splints for some people as they can provide structure and improve stability, reducing the risk of accidents.

Botox injections

Some people with clonus respond well to Botox injections. Botox therapy involves injecting specific toxins to paralyze muscles in the area. The effects of Botox injections wear off over time so a person will require repeat injections on a regular basis.

Surgery

Surgery is often the last resort. During a procedure to treat clonus, surgeons will cut away parts of the nerve that are causing abnormal muscle movements, which should relieve symptoms.

Home remedies

While medical treatments for clonus are important, home remedies can be valuable in supporting these efforts.

Using heat packs or taking warm baths may relieve pain, while applying cold packs may help reduce muscle aches. Stretching and yoga may help promote an increased range of motion.

Some people may also find a magnesium supplement or magnesium salt bath helps relax the muscles. People should speak to a doctor before trying magnesium, as it may interact with other medications.

Outlook

The outlook for clonus may vary according to the underlying cause. Where a sudden injury or illness causes clonus and muscle spasms, the symptoms will likely go away over time or respond well to physical therapy.

Chronic conditions such as multiple sclerosis, meningitis, or a stroke may require long-term treatments for symptom management.

Clonus may sometimes get worse if the underlying condition progresses. Many people find they can manage symptoms by working closely with a doctor and physical therapist.

via Clonus: Definition, causes, tests, and treatment

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[Abstract] Efficacy and safety of NABOTA in post-stroke upper limb spasticity: A phase 3 multicenter, double-blinded, randomized controlled trial

Highlights

A phase III clinical trial was performed for a novel botulinum toxin A, NABOTA, on post-stroke upper limb spasticity.

NABOTA demonstrated non-inferiority on efficacy and safety compared to onabotulinum toxin A (Botox).

NABOTA may serve as an alternative for treatment of post-stroke upper limb spasticity using botulinum toxin A.

Abstract

Botulinum toxin A is widely used in the clinics to reduce spasticity and improve upper limb function for post-stroke patients. Efficacy and safety of a new botulinum toxin type A, NABOTA (DWP450) in post-stroke upper limb spasticity was evaluated in comparison with Botox (onabotulinum toxin A). A total of 197 patients with post-stroke upper limb spasticity were included in this study and randomly assigned to NABOTA group (n = 99) or Botox group (n = 98). Wrist flexors with modified Ashworth Scale (MAS) grade 2 or greater, and elbow flexors, thumb flexors and finger flexors with MAS 1 or greater were injected with either drug. The primary outcome was the change of wrist flexor MAS between baseline and 4 weeks post-injection. MAS of each injected muscle, Disability Assessment Scale (DAS), and Caregiver Burden Scale were also assessed at baseline and 4, 8, and 12 weeks after the injection. Global Assessment Scale (GAS) was evaluated on the last visit at 12 weeks. The change of MAS for wrist flexor between baseline and 4 weeks post-injection was − 1.44 ± 0.72 in the NABOTA group and − 1.46 ± 0.77 in the Botox group. The difference of change between both groups was 0.0129 (95% confidence interval − 0.2062–0.2319), within the non-inferiority margin of 0.45. Both groups showed significant improvements regarding MAS of all injected muscles, DAS, and Caregiver Burden Scale at all follow-up periods. There were no significant differences in all secondary outcome measures between the two groups. NABOTA demonstrated non-inferior efficacy and safety for improving upper limb spasticity in stroke patients compared to Botox.

 

via Efficacy and safety of NABOTA in post-stroke upper limb spasticity: A phase 3 multicenter, double-blinded, randomized controlled trial – ScienceDirect

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[Abstract+References] Safety and efficacy of letibotulinumtoxinA(BOTULAX®) in treatment of post stroke upper limb spasticity: a randomized, double blind, multi-center, phase III clinical trial

To investigate a new botulinum neurotoxin type A, termed letibotulinumtoxinA(Botulax®) and compare its efficacy and safety for post-stroke upper limb spasticity with that of onabotulinumtoxinA(Botox®).

A prospective, double-blinded, multicenter, randomized controlled clinical study.

Six university hospitals in Korea.

A total of 187 stroke participants with upper limb spasticity.

Two kinds of botulinum neurotoxin type A were used. One set of injection was performed and total injected doses were 309.21±62.48U(Botulax) and 312.64±49.99U(Botox)(P>0.05).

Primary outcome was measured using the modified Ashworth scale for wrist flexors at week 4 and secondary outcome was measured using modified Ashworth scale for wrist flexors, elbow flexors, finger flexors, and thumb flexors as well as Global Assessment in spasticity, Disability Assessment Scale, and Caregiver Burden Scale. Safety measures including adverse events, vital signs and physical examination, and laboratory tests were also monitored.

The mean ages for the Botulax group were 56.81±9.49 and which for the Botox group were 56.93±11.93(P>0.05). In primary outcome, the change in modified Ashworth scale for wrist flexors was -1.45±0.61 in the Botulax group and -1.40±0.57 in the Botox group, and the difference between the two groups was -0.06(95% CI:-0.23–0.12,P>0.05). In secondary outcome, both groups demonstrated significant improvements with respect to modified Ashworth scale, Global Assessment in spasticity, Disability Assessment Scale, and Caregiver Burden Scale (P<0.05), and no significant difference was observed between the two groups (P>0.05). In addition, safety measures showed no significant differences between the two groups (P>0.05).

The efficacy and safety of Botulax were comparable with those of Botox in treatment of post-stoke upper limb spasticity.

 

1. Kanovsky P, Slawek J, Denes Z, . Efficacy and safety of botulinum neurotoxin NT 201 in poststroke upper limb spasticity. Clin Neuropharmacol 2009; 32: 259265. Google Scholar CrossRef, Medline
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3. Jost WH, Hefter H, Reissig A, . Efficacy and safety of botulinum toxin type A (Dysport) for the treatment of post-stroke arm spasticity: results of the German-Austrian open-label post-marketing surveillance prospective study. J Neurol Sci 2014; 337: 8690. Google Scholar CrossRef, Medline
4. Simpson DM, Alexander DN, O’Brien CF, . Botulinum toxin type A in the treatment of upper extremity spasticity: a randomized, double-blind, placebo-controlled trial. Neurology 1996; 46: 13061310. Google Scholar CrossRef, Medline
5. Brashear A, Gordon MF, Elovic E, . Intramuscular injection of botulinum toxin for the treatment of wrist and finger spasticity after a stroke. N Engl J Med 2002; 347: 395400. Google Scholar CrossRef, Medline
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8. Simpson DM, Gracies JM, Yablon SA, . Botulinum neurotoxin versus tizanidine in upper limb spasticity: a placebo-controlled study. J Neurol Neurosurg Psychiatry 2009; 80: 380385. Google Scholar CrossRef, Medline
9. Seo HG, Paik NJ, Lee SU, . Neuronox versus BOTOX in the Treatment of Post-Stroke Upper Limb Spasticity: A Multicenter Randomized Controlled Trial. PLoS One 2015; 10: e0128633. Google Scholar CrossRef
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Source: Safety and efficacy of letibotulinumtoxinA(BOTULAX®) in treatment of post stroke upper limb spasticity: a randomized, double blind, multi-center, phase III clinical trial – Jan 25, 2017

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[VIDEO] Botox Injections for Stroke & Spasticity Recovery – YouTube

Δημοσιεύτηκε στις 12 Μαΐ 2012

Sarah Abrusley discusses her recovery from a 2007 stroke and how Botox injections have relaxed the muscle tone and spasticity she was suffering in her left arm and hand. She is under the care of Dr. Andrea Toomer of Culicchia Neurological Clinic in New Orleans.

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[WEB SITE] New wearable electronic device could revolutionise treatment for stroke patients

Stroke patients are starting a trial of a new electronic device to recover movement and control of their hand.

Neuroscientists at Newcastle University have developed the device, the size of a mobile phone, which delivers a series of small electrical shocks followed by an audible click to strengthen brain and spinal connections.

The experts believe this could revolutionise treatment for patients, providing a wearable solution to the effects of stroke.

Following successful work in primates and healthy human subjects, the Newcastle University team are now working with colleagues at the prestigious Institute of Neurosciences, Kolkata, India, to start the clinical trial. Involving 150 stroke patients, the aim of the study is to see whether it leads to improved hand and arm control.

Stuart Baker, Professor of Movement Neuroscience at Newcastle University who has led the work said: “We were astonished to find that a small electric shock and the sound of a click had the potential to change the brain’s connections. However, our previous research in primates changed our thinking about how we could activate these pathways, leading to our study in humans.”

Recovering hand control

Publishing today in the Journal of Neuroscience, the team report on the development of the miniaturised device and its success in healthy patients at strengthening connections in the reticulospinal tract, one of the signal pathways between the brain and spinal cord.

This is important for patients as when people have a stroke they often lose the major pathway found in all mammals connecting the brain to spinal cord. The team’s previous work in primates showed that after a stroke they can adapt and use a different, more primitive pathway, the reticulospinal tract, to recover.

However, their recovery tends to be imbalanced with more connections made to flexors, the muscles that close the hand, than extensors, those that open the hand. This imbalance is also seen in stroke patients as typically, even after a period of recuperation, they find that they still have weakness of the extensor muscles preventing them opening their fist which leads to the distinctive curled hand.

Partial paralysis of the arms, typically on just one side, is common after stroke, and can affect someone’s ability to wash, dress or feed themselves. Only about 15% of stroke patients spontaneously recover the use of their hand and arm, with many people left facing the rest of their lives with a severe level of disability.

Senior author of the paper, Professor Baker added: “We have developed a miniaturised device which delivers an audible click followed by a weak electric shock to the arm muscle to strengthen the brain’s connections. This means the stroke patients in the trial are wearing an earpiece and a pad on the arm, each linked by wires to the device so that the click and shock can be continually delivered to them.

“We think that if they wear this for 4 hours a day we will be able to see a permanent improvement in their extensor muscle connections which will help them gain control on their hand.”

Improving connections

The techniques to strengthen brain connections using paired stimuli are well documented, but until now this has needed bulky equipment, with a mains electric supply.

The research published today is a proof of concept in human subjects and comes directly out of the team’s work on primates. In the paper they report how they pair a click in a headphone with an electric shock to a muscle to induce the changes in connections either strengthening or weakening reflexes depending on the sequence selected. They demonstrated that wearing the portable electronic device for seven hours strengthened the signal pathway in more than half of the subjects (15 out of 25).

Professor Stuart Baker added: “We would never have thought of using audible clicks unless we had the recordings from primates to show us that this might work. Furthermore, it is our earlier work in primates which shows that the connections we are changing are definitely involved in stroke recovery.”

The work has been funded through a Milstein Award from the Medical Research Council and the Wellcome Trust.

The clinical trial is just starting at the Institute of Neurosciences, Kolkata, India. The country has a higher rate of stroke than Western countries which can affect people at a younger age meaning there is a large number of patients. The Institute has strong collaborative links with Newcastle University enabling a carefully controlled clinical trial with results expected at the end of this year.

A patient’s perspective

Chris Blower, 30, is a third year Biomedical Sciences student at Newcastle University and he had a stroke when he was a child after open heart surgery. He describes his thoughts on the research:

I had a stroke at the age of seven. The immediate effect was paralysis of the right-hand side of my body, which caused slurred speech, loss of bowel control and an inability to move unaided. Though I have recovered from these immediate effects, I am now feeling the longer term effects of stroke; slow, limited and difficult movement of my right arm and leg.

My situation is not unique and many stroke survivors have similar long-term effects to mine. Professor Baker’s work may be able to help people in my position regain some, if not all, motor control of their arm and hand. His research shows that, in stroke, the brains motor pathway to the spinal cord is damaged and that an evolutionarily older signal pathway could be ‘piggybacked’ and used instead. With electrical stimulation, exercise and an audible cue the brain can be taught to use this older pathway instead.

This gives me a lot of hope for stroke survivors. My wrist and fingers pull in, closing my hand into a fist, but with the device Professor Baker is proposing my brain could be re-taught to use my muscles and pull back, opening my hand out. The options presented to me so far, by doctors, have been Botox injections and surgery; Botox in my arm would weaken the muscles closing my hand and allow my fingers to spread, surgery would do the same thing by moving the tendons in my arm. Professor Baker’s electrical stimulations is certainly a more appealing option, to me, as it seems to be a permanent solution that would not require an operation on my arm.

I was invited to look around the animal house and observe a macaque monkey undergoing a test and this has made me think about my own stroke and the effect it has had on my life.

I have never seen anything like this before and I didn’t know what to expect. The macaque monkey that I observed was calmly carrying out finger manipulation tests while electrodes monitored the cells of her spinal cord.

Although this procedure requires electrodes to be placed into the brain and spine of the animal, Professor Baker explained how the monkey had been practicing and learning this test for two years before the monitoring equipment was attached. In this way the testing has become routine before it had even started and the animal was in no pain or distress, even at the sight of a stranger (me).

The animals’ calm, placid temperaments carry over to their living spaces; with lots of windows, natural light and high up spaces the macaques are able to see all around them and along the corridors. This means that they aren’t feeling threatened when people approach and are comfortable enough that even a stranger (me, again) can approach and say ‘hello’.

From my tour of the animal house at the Institute of Neuroscience I saw animals in calm, healthy conditions, to which the tests were just a part of their daily routine. Animal testing is controversial but I think that the work of Professor Baker and his team is important in helping people who have suffered stroke and other life-changing trauma to regain their independence and, often, their lives.

Source: Newcastle University

Source: New wearable electronic device could revolutionise treatment for stroke patients

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[BOOK] Botulinum Neurotoxin Injection Manual (2015) [PDF]- Alter, Katharine – Free Medical Books

Source: Botulinum Neurotoxin Injection Manual (2015) [PDF]- Alter, Katharine | Free Medical Books

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[ARTICLE] OnabotulinumtoxinA Improves Pain in Patients with Post-Stroke Spasticity: Findings from a Randomized, Double-Blind, Placebo-Controlled Trial – Full Text HTML/PDF

Abstract

Context

Patients with post-stroke spasticity (PSS) commonly experience pain in affected limbs, which may impact quality of life.

Objectives

To assess onabotulinumtoxinA for pain in patients with PSS from the BOTOX® Economic Spasticity Trial, a multicenter, randomized, double-blind, placebo-controlled trial.

Methods

Patients with PSS (N=273) were randomized to 22- to 34-weeks double-blind treatment with onabotulinumtoxinA + standard care (SC) or placebo injection + SC and were eligible to receive open-label onabotulinumtoxinA up to 52 weeks. Assessments included change from baseline on the 11-point pain numeric rating scale, proportion of patients with baseline pain ≥4 achieving ≥30% and ≥50% improvement in pain, and pain interference with work at week 12, end of double-blind treatment, and week 52.

Results

At baseline, most patients (74.3%) experienced pain and 47.4% had pain ≥4 (pain subgroup). Mean pain reduction from baseline at week 12 was significantly greater with onabotulinumtoxinA + SC (–0.77, 95% CI –1.14 to –0.40) than placebo + SC (–0.13, 95% CI –0.51 to 0.24; P < 0.05). Higher proportions of patients in the pain subgroup achieved ≥30% and ≥50% reductions in pain at week 12 with onabotulinumtoxinA + SC (53.7% and 37.0%, respectively) compared with placebo (28.8% and 18.6%, respectively;P<0.05). Reductions in pain were sustained through week 52. Compared with placebo + SC, onabotulinumtoxinA consistently reduced pain interference with work.

Conclusion

This is the first randomized, placebo-controlled trial demonstrating statistically significant and clinically meaningful reductions in pain and pain interference with work with onabotulinumtoxinA in patients with PSS.


Introduction

Pain prevalence varies widely (10–70%) among post-stroke patients 1, 2, 3 and 4. Several mechanisms may contribute to this range (e.g., peripheral nerve damage, soft tissue trauma, central post-stroke pain, complex regional pain syndrome 5, 6, 7 and 8). Spasticity and pain are factors contributing to “learned non-use” of the affected limb and are often disabling, interfering with daily activities, sleep, walking, physiotherapy, leisure activities, and ultimately affecting patients’ quality of life 9, 10 and 11.

In randomized, double-blind, placebo-controlled trials, onabotulinumtoxinA has been shown to significantly reduce excess muscle tone and decrease disability among patients with upper-limb spasticity 12 and 13, and to further reduce spasms and improve gait in patients with lower-limb spasticity 14 and 15. OnabotulinumtoxinA is effective at reducing pain in patients with cervical dystonia and chronic migraine 16. Prospective open-label studies have shown that onabotulinumtoxinA can reduce pain in patients with post-stroke spasticity (PSS) 8, 17 and 18. However, the efficacy of onabotulinumtoxinA in reducing pain in patients with PSS has not been demonstrated in a large, randomized, placebo-controlled study.

The BOTOX® Economic Spasticity Trial (BEST) was a prospective clinical trial designed to compare the efficacy of onabotulinumtoxinA or placebo (in addition to standard care [SC]) in helping patients with PSS achieve their personal functional goals 19. Here we present results from BEST comparing the effectiveness of onabotulinumtoxinA + SC versus placebo + SC on pain.

Continue —> OnabotulinumtoxinA Improves Pain in Patients with Post-Stroke Spasticity: Findings from a Randomized, Double-Blind, Placebo-Controlled Trial

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