Archive for category Spasticity
The U.S. Food and Drug Administration (FDA) has approved a label expansion of BOTOX to include eight new muscles for the treatment of upper limb spasticity in adults, Allergan, an AbbVie company, announces in a media release.
The new muscles for treatment include additional muscles of the elbow and forearm (brachialis, brachioradialis, pronator teres, and pronator quadratus), as well as intrinsic hand muscles (lumbricals and interossei) and thumb muscles (flexor pollicis brevis and opponens pollicis). The label now includes the use of ultrasound as a muscle localization technique in adult spasticity, the release explains.
“Today’s announcement is especially important because spasticity is a disabling neurological condition that can have a significant impact on a patient’s quality of life. This label expansion not only adds to our rich history in neurotoxin science, but also reinforces the role of BOTOX in upper limb spasticity treatment. BOTOX provides an evidence-based dosing strategy to meet the clinical needs of providers and their patients.”
— Mitchell F. Brin, MD, Senior Vice President, Chief Scientific Officer, BOTOX & Neurotoxins, AbbVie
Helps Reduce Muscle Stiffness
Spasticity in adults is commonly caused by stroke, multiple sclerosis, spinal cord injury, cerebral palsy, and traumatic brain injury. Individuals with spasticity experience stiffness in the muscles of their upper and/or lower limbs, and may have difficulty with voluntary control. Upper limb spasticity can manifest as a bent elbow, an arm pressed against the chest, or a curled-in hand with a clenched fist, significantly hindering the patient’s ability to perform everyday activities. This can result in difficulty with posture and positioning, and severely interfere with normal muscular movement and function.
BOTOX has been proven to significantly reduce muscle stiffness and is indicated for the treatment of spasticity in patients 2 years of age and older. This expanded BOTOX dosing guidance provides physicians the ability to treat based on clinical assessment of a patient’s spasticity and anatomy while staying within the BOTOX maximum cumulative dose of 400 Units in a 3-month period in adults. BOTOX has not been shown to improve upper extremity functional abilities or range of motion at a joint affected by a fixed contracture. The safety profile of BOTOX in adult upper limb spasticity remains the same, with the most common adverse reactions including nausea, fatigue, bronchitis, pain in extremity and muscular weakness, the release continues.
“BOTOX has demonstrated efficacy and safety for spasticity management at clinically proven doses. This label expansion offers physicians and their patients living with spasticity another important tool as part of a comprehensive treatment plan for spasticity management.”
— Kimberly Heckert, MD, Director, Spasticity Management Fellowship, Thomas Jefferson University of Philadelphia
Hemiparesis following stroke is often accompanied by spasticity. Spasticity is one factor among the multiple components of the upper motor neuron syndrome that contributes to movement impairment. However, the specific contribution of spasticity is difficult to isolate and quantify. We propose a new method of quantification and evaluation of the impact of spasticity on the quality of movement following stroke.
Spasticity was assessed using the Tonic Stretch Reflex Threshold (TSRT). TSRT was analyzed in relation to stochastic models of motion to quantify the deviation of the hemiparetic upper limb motion from the normal motion patterns during a reaching task. Specifically, we assessed the impact of spasticity in the elbow flexors on reaching motion patterns using two distinct measures of the ‘distance’ between pathological and normal movement, (a) the bidirectional Kullback–Liebler divergence (BKLD) and (b) Hellinger’s distance (HD). These measures differ in their sensitivity to different confounding variables. Motor impairment was assessed clinically by the Fugl-Meyer assessment scale for the upper extremity (FMA-UE). Forty-two first-event stroke patients in the subacute phase and 13 healthy controls of similar age participated in the study. Elbow motion was analyzed in the context of repeated reach-to-grasp movements towards four differently located targets. Log-BKLD and HD along with movement time, final elbow extension angle, mean elbow velocity, peak elbow velocity, and the number of velocity peaks of the elbow motion were computed.
Upper limb kinematics in patients with lower FMA-UE scores (greater impairment) showed greater deviation from normality when the distance between impaired and normal elbow motion was analyzed either with the BKLD or HD measures. The severity of spasticity, reflected by the TSRT, was related to the distance between impaired and normal elbow motion analyzed with either distance measure. Mean elbow velocity differed between targets, however HD was not sensitive to target location. This may point at effects of spasticity on motion quality that go beyond effects on velocity.
The two methods for analyzing pathological movement post-stroke provide new options for studying the relationship between spasticity and movement quality under different spatiotemporal constraints.
Stroke is one of the leading causes of long-term motor disability . Most individuals with stroke present upper limb sensorimotor deficits that persist into the chronic stage (more than 6 months following the onset of stroke) [1, 2]. Spasticity, a sensorimotor disorder characterized by a velocity-dependent increase in muscle resistance stemming from hyperexcitability of the dysregulated muscle-spindle activity and stretch-reflex arc, is a prevalent sensorimotor deficit following stroke [3,4,5]. As many as 20–50% of patients develop spasticity during the first year after the event . Objective and accurate quantification of spasticity and its effects on voluntary motion is important for guiding rehabilitation of the affected limbs.
While there are several clinical measures of spasticity, controversy remains about the most appropriate ones [7, 8]. Moreover, current measures are not sufficient for determining relationships between spasticity, movement deficits, and functional ability [9, 10]. To establish the effects of spasticity on voluntary motion, prior work has attempted to identify the relationship between the amount of hypertonicity measured at rest and movement disruption of voluntarily activated muscle [10,11,12]. One of the commonly used measures of spasticity is the Modified Ashworth Scale (MAS), which grades the resistance felt during passive stretching of muscles on a 6-point ordinal scale [13, 14]. A major drawback of the MAS is that the passive resistance during stretch characterizes only one aspect of the spasticity phenomenon (i.e., amount of hypertonia at rest). In addition, the scale has low resolution and poor-to-good test–retest reliability [13, 14].
Altered muscle resistance at rest may not be the only reason for disruption in voluntary movement . The Tonic Stretch Reflex Threshold (TSRT) identifies where in the biomechanical joint range abnormal muscle resistance begins to contribute to disrupted muscle activation patterns and kinematics [16, 17] providing more specific information about how spasticity and movement deficits are related. TSRT can be determined objectively using the Montreal Spasticity Measure device . The relationship of the TSRT angle with spasticity is based on the threshold control theory of motor control proposed by Feldman [19, 20]. According to the threshold control theory, voluntary movement is generated by regulating the spatial thresholds (of muscle length), at which muscle activation begins. The TSRT, i.e., the spatial threshold at zero velocity, is extrapolated based on the linear regression through measurements representing dynamic spatial thresholds evoked at different stretch velocities.
Upper limb recovery following damage to the brain refers to behavioral restitution (restoring premorbid movement patterns), to which spontaneous restitution is the main contributor. Improvements in upper limb function can also occur through behavioral compensation in which the system accomplishes functional tasks using altered movement patterns . Standard clinical measures of upper limb function do not capture movement quality in a precise manner and therefore are inadequate for differentiating between restitution and compensation . Measurement of movement kinematics and kinetics were suggested as the best way to address this problem. Although some guidelines are available regarding metrics used to characterize motor recovery , there is no consensus about how to identify the relationship between spasticity and motor dysfunction. Spasticity is affected by movement velocity and by multiple factors that are difficult to control, such as fatigue, secondary tasks, posture, psychological stress, and time of the day. The variability resulting from these aspects together with the inherent variability of human motion, especially during slow movement, which is typical in people with stroke, complicate the measurement of the effects of spasticity on kinematics. Therefore, a measure that can integrate the spatial and temporal aspects of motion while accounting for motion variability is required.
Stochastic models (based on random variables) offer a comprehensive yet parsimonious representation of motion data. They can capture complex, multi-dimensional, spatiotemporal phenomena while accounting for variability. These features lend stochastic models coupled with a stochastic distance measure (a distance measure between stochastic models) potential advantages over the more commonly used point measures (e.g., mean) for quantifying the effects of spasticity on voluntary motion. However, as the computation of stochastic distance measures is typically more complex, their benefits must be verified. There are several stochastic distance measures that differ according to the characteristics of the differences they capture and the ease of their computation for diverse distributions. Gaussian mixture models (GMMs) are particularly attractive stochastic models for motion representation, since they are easily adapted for spatiotemporal data representation and have standard efficient methods for parameter estimation based on maximum-likelihood estimators via the expectation–maximization algorithm  or Bayesian estimation . Two examples of commonly used stochastic measures suitable for measuring distances between GMMs, are the bidirectional Kullback–Leibler divergence (BKLD) and Hellinger’s distance (HD) [26,27,28]. Selecting an appropriate stochastic distance measure is complex since different measures quantify different aspects of dissimilarity between distributions, and thus, are influenced differently by data attributes. HD seems particularly worth exploring in addition to KLD in the context of quantifying the influence of spasticity on voluntary motion. It offers a different perspective regarding the distance between models, and it can rectify some of the shortcomings of the KLD (and BKLD). GMMs, KLD and HD and their shortcomings are described in Appendix 1.
Davidowitz et al.  have recently proposed using GMMs and BKLD for quantifying the effects of spasticity (measured by the resistance to passive movement, as reflected in the MAS score) on kinematics of voluntary motion. In a cohort of 16 participants with stroke, spasticity measured by the MAS explained the BKLD of the elbow motion models of reaching movement from nearest neighbor models of healthy individuals. Deviations in individuals with stroke with higher spasticity levels were greater (larger BKLD) than those in individuals with mild spasticity. In the current study, we advanced this effort in two directions. First, we quantified the threshold angle of spasticity using TSRT. In addition, we compared two stochastic distance measures, BKLD and HD, and analyzed the advantages of each for measuring the effects of spasticity on voluntary movement. We hypothesized that both distance measures would be related to TSRT and that differences between the measured distances would highlight different aspects of spasticity, due to the variant sensitivity of BKLD and HD to different confounding variables. Preliminary results have been presented in abstract form [30, 31]. […]
Many stroke survivors suffer from spasticity in their affected hand, causing them to present with a clenched fist. Spasticity is a condition of muscle stiffness and is caused by miscommunication from the brain to the affected hand. Hand spasticity also interferes with limb positioning, grasping, self-care and other activities of daily living.
Table of contents
The general aspects of the spasticity in the hand
- Muscles appear stiff because the signals to the muscles are sent incorrectly through the damaged part of the brain.
- When a muscle is affected by spasticity, the limbs seem more stiff the faster it is moved.
- Spasticity is seen in a number of different conditions including cerebral palsy, traumatic brain injury, spinal cord injury, stroke and multiple sclerosis.
- People may have difficulty moving from one position to another.
There are a few different spasticity treatment options. These treatments can be both temporary or permanent.
One temporary option would be getting a botox injection to the hand. Botox is a medication that is used to relax the muscles. Botox usually lasts about 3 months before it wears off.
2. Utilizing hand splints(orthosis)
Another way to treat spasticity is by utilizing hand splints(orthosis). If someone keeps their hand clenched all day, their muscles will start to shorten, causing them to become very tight. If the hand is in a clenched position for too long without being stretched, it can cause contractures. Contractures can be very painful and can require surgery to release them. In order to prevent contractures, it is important to stretch out the muscles. Neofect provides a variety of hand orthosis for stroke recovery according to the hand movement level.
3. Rewire pathways in the brain through Neuroplasticity
In order to treat spasticity in a more permanent way, one would have to retrain the brain in order to prevent miscommunication from the brain to the hand. Reorganization of surviving central nervous system elements supports behavioral recovery.
Stroke survivors can rewire the pathways in the brain. This process is known as Neuroplasticity. Neuroplasticity is the ability of the brain to rewire itself even in injured areas by performing repetitive tasks and movements. Repetition helps stimulate neuroplasticity and strengthen new neural connections that are growing. The main goal of task oriented/repetitive rehab activity is to enhance neuroplasticity as well as support behavioral and functional recovery like opening the hand.
Now that you know using a hand splint or stroke recovery equipment is one of the ways to treat hand spasticity, you might be wondering which hand splint to use. Here are a few things to consider before choosing a hand splint. Refer to the image below to find the right hand splint for you.
Neofect Extender is a positioning tool for those with mind spasticity or weakness. With customizable tension straps, the extender helps reduce spasticity by encouraging the fingers into an extended open hand position. The finger strapping can also be reserved to support a secure grip while holding an object.
Neofect Extender Plus has a lightweight ergonomic design that features gliding elastic finger strapping which mimics the natural movement of the extensor tendons of the fingers. The proprietary tension system gently extends the client’s fingers and thumb following grasping. Thick industrial strength velcro allows for the tension to be adjusted for each fingers as well as the MCPs and wrist. The palm is exposed to increase breathability and ease when putting the glove on.
Neofect Finger Splint is a finger positioning tool for those who have moderate to severe hand spasticity. The splint prevents deformity and shortening of the fingers caused by spasticity.
A great way to provide a long passive stretch is by utilizing Neofect’s hand orthosis. These are functional gloves for stroke survivors that are used to minimize spasticity, maintain functional grasp as well as prevent stiffness. To find out more about the Neofect Hand Orthosis please call us at 888-623-8947 or email us at email@example.com.
Posted by Debbie Overman
Ipsen announces findings from a new US healthcare database analysis to assess the current treatment patterns of adults living with spasticity in a real-life setting.
The analysis focused on the proportion of people living with active spasticity who received botulinum neurotoxin type A (BoNT-A) treatment. The abstract, Analysis of US Commercial Claims to Understand Patient Treatment Pathways in Spasticity, was presented recently during the International Society of Physical and Rehabilitation Medicine (ISPRM) 2021 Congress.
Spasticity is usually caused by damage to the parts of the brain or spinal cord that control voluntary movement, leading to a change in the balance of signals between the nervous system and the muscles, which results in increased activity in the muscles. When injected into specific muscles of people living with movement disorders, BoNT injections cause temporary muscle relaxation, which can ease symptoms and aid rehabilitation. BoNT-A injections are considered as a recommended first-line treatment for adults living with spasticity in several countries, including the US, a media release from Ipsen explains.
Ipsen analyzed data from two large US commercial claims databases: IBM Watson’s MarketScan and the IQVIA Anonymous Longitudinal Patient Data (APLD) database:
- A total of 4,974,859 records were accessed in the MarketScan database, and 10,685,964 records in the IQVIA database.
- Spasticity was identified from the two sources using International Classification of Disease (ICD) codes for spastic conditions (eg, monoplegia, diplegia, hemiplegia and contracture).
- This revealed 126,465 and 1,151,127 people living with spasticity in the MarketScan and IQVIA databases, respectively.
- In the MarketScan database, only 5,111 people living with spasticity (4%) were treated with BoNT-A. In the IQVIA database, an even smaller percentage were treated with BoNT-A (31,176 patients, 3%).
“While effective treatment of spasticity requires a multidisciplinary approach, which may involve a combination of exercise, physical therapy, medication, or surgery, it is concerning to see that many people living with spasticity in the US are not receiving a recommended first-line treatment. The pandemic has been disruptive to the management of spasticity; these new data have, however, put a spotlight on the broader issues in the treatment of this condition that pre-date the pandemic.”
— Isabelle Bocher-Pianka, Chief Patient Affairs Officer at Ipsen
“We need to address barriers to treatment and find innovative ways to address the access issues in the treatment of this debilitating condition. Despite being a recommended first-line treatment, these data highlight a significant disconnect between the patient journey and the guidelines, since BoNT-A is only used for a small proportion of people living with spasticity in the US and this is likely to be true in other parts of the world.”
— Dr Alberto Esquenazi, Sheerr Gait and Motion Analysis Laboratory, MossRehab
“Poor control of spasticity can result in the breakthrough of painful symptoms such as muscle stiffness, spasms and involuntary contractions, which means the person living with spasticity may find it difficult to walk or perform certain tasks. These data show there is an urgent need to build on these findings and gather further insights into the underlying reasons for this disconnect.”
— Dr. Andreas Lysandropoulos, Vice President, Head of Global Medical Affairs Neuroscience at Ipsen
[Source(s): Ipsen, Business Wire]
Posted by Debbie Overman
Revance Therapeutics Inc announces positive topline data from its JUNIPER Phase 2, randomized, double-blind, placebo-controlled, multi-center clinical trial of its investigational drug candidate DaxibotulinumtoxinA for Injection for the treatment of adults with moderate to severe upper limb spasticity.
The JUNIPER study was designed to evaluate the efficacy and safety of DaxibotulinumtoxinA for Injection for adults with upper limb spasticity after stroke or traumatic brain injury and to identify a dose to advance into a Phase 3 program. Three doses (250 units, 375 units, 500 units) were studied, and subjects were randomized in a 1:1:1:1 ratio across the active doses or placebo.
The trial was originally designed to include 128 subjects. Due to the ongoing COVID-19 challenges related to continued subject enrollment and the scheduling of in-person study visits, Revance made the decision in June 2020 to curtail enrollment at 83 subjects, according to a media release from Revance Therapeutics Inc.
“As an investigator in the JUNIPER trial, I am delighted to see the efficacy and safety data that will support the advancement of DaxibotulinumtoxinA for Injection in adult upper limb spasticity. What impresses me most is the duration of effect covering at least 24-weeks across all dose groups studied, while also being well tolerated.
“The need for longer duration botulinum toxin treatments for upper limb spasticity is considerable, as the frequent re-emergence of symptoms around 12 weeks continues to be a painful, costly and a time-consuming burden for patients. The data indicates that DaxibotulinumtoxinA for Injection has the potential to reduce the frequency of adult upper limb spasticity treatments by up to 50% annually, delivering meaningful pharmacoeconomic benefits, improvement in patients’ quality of life, and the opportunity to expand treatment care.”
— Atul Patel, MD, MHSA, Medical Director, Kansas Institute of Research
About the JUNIPER Study
The company’s JUNIPER study was a Phase 2, randomized, double-blind, placebo-controlled, parallel group, dose-ranging, multi-center trial to evaluate the efficacy and safety of DaxibotulinumtoxinA for Injection for the treatment of adult upper limb spasticity in adults following stroke or traumatic brain injury. The study was conducted at 30 sites in the United States and has enrolled 83 male and female patients between the age of 18 to 75 years old.
Patients were randomized into one of four treatment groups: 275 units, 350 units, 500 units and placebo. The study was designed to run up to 36 weeks, with two co-primary outcome measures: mean change from baseline in muscle tone measured with the MAS in SMG of the elbow, wrist, or finger flexors at Week 6; and mean score of the PGIC at Week 6. The first 73 subjects, who were dosed before enrollment was paused in March due to the COVID-19 pandemic, were followed up for 36 weeks, and the succeeding 10 subjects were followed up to Week 12.
The study’s co-primary endpoints were improvement from baseline in the Modified Ashworth Score (MAS) and the Physician Global Impression of Change (PGIC) score at Week 6. In the JUNIPER study, proof of concept was demonstrated with all three doses being numerically higher than placebo for the improvement in the MAS score, with the 500-unit dose demonstrating a clinically meaningful and statistically significant reduction from baseline in muscle tone versus placebo (p=0.0488). Additionally, each of the three doses demonstrated a numerical improvement compared with placebo on the PGIC assessment but did not reach statistical significance with the reduced enrollment.
On a key secondary endpoint, DaxibotulinumtoxinA for Injection delivered a median duration of at least 24 weeks across all three doses. Duration of effect was defined as the time from injection (in weeks) until the loss of improvement as measured by the MAS (for the suprahypertonic muscle group or SMG) and the PGIC, or a request for retreatment by the subject.
All three doses of DaxibotulinumtoxinA for Injection were generally safe and well tolerated with no increase in the incidence of adverse events observed in the higher dose treatment groups. The majority of treatment-related adverse events were mild or moderate in severity and were similar to or lower than those reported in prior botulinum toxin studies in adult upper limb spasticity, the release continues.
“I am very proud of our team and their efforts to successfully complete our Phase 2 trial during what has proven to be a very challenging time for trial enrollment and follow up. Although we reduced the subject enrollment size in response to COVID-19 concerns, we were able to generate sufficient data to inform our dosing strategy for our Phase 3 program, while also demonstrating a long duration profile that is consistent across our therapeutic and aesthetic clinical programs.
“Our next step is to schedule an end-of-Phase 2 meeting with the FDA prior to finalizing a Phase 3 program. I want to thank the patients, investigators, CROs and the Revance team for their time and commitment in making this trial possible.”
— Mark J. Foley, President and Chief Executive Officer at Revance
[Source(s): Revance Therapeutics Inc, Business Wire]
[Abstract] A New Definition of Poststroke Spasticity and the Interference of Spasticity With Motor Recovery From Acute to Chronic Stages
The relationship of poststroke spasticity and motor recovery can be confusing. “True” motor recovery refers to return of motor behaviors to prestroke state with the same end-effectors and temporo-spatial pattern. This requires neural recovery and repair, and presumably occurs mainly in the acute and subacute stages. However, according to the International Classification of Functioning, Disability and Health, motor recovery after stroke is also defined as “improvement in performance of functional tasks,” i.e., functional recovery, which is mainly mediated by compensatory mechanisms. Therefore, stroke survivors can execute motor tasks in spite of disordered motor control and the presence of spasticity. Spasticity interferes with execution of normal motor behaviors (“true” motor recovery), throughout the evolution of stroke from acute to chronic stages. Spasticity reduction does not affect functional recovery in the acute and subacute stages; however, appropriate management of spasticity could lead to improvement of motor function, that is, functional recovery, during the chronic stage of stroke. We assert that spasticity results from upregulation of medial cortico-reticulo-spinal pathways that are disinhibited due to damage of the motor cortex or corticobulbar pathways. Spasticity emerges as a manifestation of maladaptive plasticity in the early stages of recovery and can persist into the chronic stage. It coexists and shares similar pathophysiological processes with related motor impairments, such as abnormal force control, muscle coactivation and motor synergies, and diffuse interlimb muscle activation. Accordingly, we propose a new definition of spasticity to better account for its pathophysiology and the complex nuances of different definitions of motor recovery.
What are the Brunnstrom Stages of Stroke Recovery?
The brunnstrom stages is one of the most well-known stroke recovery stages which is also known as the Brunnstrom approach. The Brunnstrom stages was developed by physical therapist Signe Brunnstrom in the 1960’s. When a stroke occurs, typically it affects one side of the body. The Brunnstrom approach describes the sequence of motor development and reorganization of the brain after stroke. So you can check the status of your stroke recovery through the Brunnstrom stages.
You can think of it as a built in organizational system. Our brain automatically recruits lower functioning reflexes, just to get any movement. Then it begins to sort out what is useful and what connections we need to build at a higher level.
It’s also a way to know what movement actions to take advantage of during your post stroke rehabilitation.
Table of contents
- Stage 1: Flaccidity
- Stage 2: Spasticity Appears
- Stage 3: Increased Spasticity
- Stage 4: Decreased Spasticity
- Stage 5: Spasticity Continues to Decrease
- Stage 6: Spasticity Disappears and Coordination Reappears
- How long will it take to recover from stroke?
What to do for Stroke Rehabilitation or stroke recovery in each stage
During this stage the muscles on your affected side aren’t able to move and they might feel limp and floppy.
What can I do during this stage?
Passive range of motion is one of the most important exercises you can do in this stage. Passive simply means that you are using your other arm to assist with movement or someone else is moving your arm for you.
The main reason to complete these exercises is that it increases sensory input to the brain. Right now, there aren’t any signals being sent from the brain to the muscle to activate it, but you can send signals from the skin and muscles about touch and movement to the brain and remind your brain that your affected side is awake and ready to learn again!
In this stage, muscles may begin to tighten reflexively and have difficulty relaxing. This is called spasticity. This movement is usually involuntary and in response to an outside stimulus, such as a poke. The brain is still having a difficult time sending any signals to the muscles for voluntary movement.
What can I do in this stage?
Passive range of motion continues to be key in this stage. With spasticity, even passive movement can be challenging. When we don’t move a joint, the tendons start to stiffen and can make movement even more difficult in the future. Think of it as the hinge of a door that can get rusty and hard to open over time if it’s not taken care of. Oil your joints with movement either passive or active-assisted range of motion.
Active-assisted range of motion is a combination of passive and active range of motion. You might be able to activate your shoulder muscles to lift your arm up, but not all the way. For active assisted range of motion, you want to activate the muscle as much as you can and then use your unaffected hand to move the joint through the full range of motion.
During this stage, certain muscles might tighten more and can be more difficult to relax. Multiple muscles might fire together when we try to move our affected side. This is called a muscle synergy and we can use our synergies to complete an activity if we understand it.
What can I do in this stage?
In addition to keeping up with your passive or active-assistive range of motion exercises, it’s important to understand your synergies so you can use them purposefully. The more we can send signals from the brain to the muscle the stronger those signals become, and the best way to increase the amount of signals is to incorporate your exercises into the things you already do during the day.
There are two typical synergy patterns in this stage: the flexor synergy and the extensor synergy. A flexor synergy at the arm would have the shoulder rotating outward, at the same time the elbow flexes and forearm rotates out. Think about the movement that happens when you try to touch the ear on the same side of your body.
An extensor synergy is opposite: the shoulder rotates inward, the elbow straightens, and the forearm rotates downward. Think about the movement that would happen if the back of your hand touched the inside of your opposite knee.
If we know that these are the muscles that want to fire together, we can use it to help function. For instance, you might be working on feeding yourself, but struggling to reach your mouth. If you think about moving your shoulder does it help move your elbow and get closer to your mouth? Little shifts in thinking can help you be more successful, which will help encourage you to keep going!
During this stage of motor recovery, the involuntary muscle tightness (spasticity) starts to decrease. Your brain is more successful at sending signals to specific muscles to activate. You’re still likely to use muscle synergies, but you’re able to move outside of them as well.
What can I do in this stage?
This is when we want to focus on isolating movements and strengthening those connections in the brain to certain muscles with active range of motion exercises. Repetition is critical for neural-reorganization. We can’t repair the damage that was done to the brain after stroke, but we can teach a different area of the brain to do its job. We want to do movements outside of our muscle synergies to improve how our brain sends signals.
During this stage of motor recovery, the signals from the brain to the muscle are even more successful and the muscle tightening of spasticity is minimal, allowing your affected side after stroke to move more complexly.
What can I do in this stage?
Strengthening is the key ingredient in this stage. We’ve seen a progression in the stages, but also in the treatment. We’ve started with passive range of motion, then moved to active assisted range of motion, then active range of motion within synergies, then isolating muscles. Now it’s time to add resistance to movement. Add small weights or use a household item like a half-full water bottle to your exercises. Incorporate theraband or theraputty to your daily routine.
During this stage of motor recovery, spasticity disappears completely and coordination quickly begins to improve. During this stage motor control is almost fully restored!
What can I do in this stage?
Continue strengthening the muscles that need strengthening and add coordination exercises that incorporate both sides of the body: golfing, shuffling cards, etc. If there’s something you used to do that you want to get back to doing, practice it. Your brain will be motivated to practice the coordination required for an exciting activity.
As much as we’d like for there to be a clear cut answer, every person is different. Some may see more rapid progress in days, weeks, or months after stroke. It might take years for others. Some people may some may spend more time than they would like to on a stage.
We do know that recovery has no end date. Some stroke patients and stroke survivors(stroke victims) might not have an occupational therapist or rehabilitation program to follow. Each day is a new opportunity to look at where we’re at and take action to get to where we want to be. The Brunnstrom approach gives us roadmap.
Has a stroke left you or your loved one struggling to regain full functionality in your arm or hand? Introducing the Neofect Smart Rehab, a biofeedback training device.
Repetition is the key to increase mobility. Neofect Smart Rehab encourages repetition in a fun, engaging way through interactive gamified training games, challenging you to improve arm and hand function through neuroplasticity which is the brain’s ability to retrain itself after an injury. Through repetition, you can strengthen other pathways in the brain to improve the use of your affected side.
- Post-stroke spasticity can make it difficult to stretch, move, and accomplish everyday tasks.
- Modifying your home, working with an occupational therapist, practicing daily exercises, and using mobility aids can help you manage spasticity.
- Treatments, such as injections and medications, can help reduce long-term damage from spasticity.
Strokes occur when blood flow to the arteries in the brain become blocked, or (in more serious cases) leak or burst. This causes trauma to the brain and spinal cord, which can lead to other symptoms.
Between 25 percent and 43 percent of people will experience a condition called spasticity in the first year after a stroke, according to the American Stroke Association.
Spasticity causes muscles to become stiff and tight, making it difficult to stretch, move, and take care of everyday tasks.
Fortunately, treatments and lifestyle adjustments can help reduce the severity of the condition and its impact on your life.
Read on to learn more about spasticity and ways to manage it.
A stroke can damage the part of the brain that controls the signals to the muscles. If that happens, you may experience spasticity, or an abnormal increase in muscle tone.
It can cause your muscles to get stiff, tight, and painful, causing you to be unable to move fluidly.
That, in turn, can affect the way you speak, move, and walk. Your muscles may remain contracted in certain positions, like a bent wrist, clenched fist, or tucking your thumb into your palm, according to the American Association of Neurological Surgeons.
Other ways spasticity can affect the body after a stroke include:
- tight knees
- tension in the fingers
- bending your foot at an angle
- weakness in a foot, causing it to drag when walking
- bending your arm and holding it tight against the chest
- curling in the toes
Spasticity tends to be more common in younger people who have a stroke, according to the American Stroke Association. Strokes that are caused by a bleed can also increase the risk of spasticity.
Treatment options for spasticity after a stroke depend on the severity of your symptoms. Your doctor may also suggest trying a variety of treatments and management strategies at the same time.
Here are some common treatment options, according to the American Stroke Association:
- exercise and stretching
- muscle braces
- injections of certain medications, such botulinum toxin (Botox)
- oral medications, such as baclofen, diazepam, tizanidine, and dantrolene sodium
- intrathecal baclofen therapy (ITB)
There are also lifestyle changes people can make to reduce the symptoms of spasticity after a stroke.
While spasticity can be painful, there are ways to reduce symptoms of the condition and improve your quality of life.
Here are seven tips for living with spasticity:
1. Exercise or stretch the affected limbs
One of the best things you can do for spasticity after a stroke is to keep the affected limbs moving.
Regularly exercising these areas can help ease tightness, prevent muscles from shortening, and maintain your full range of motion.
A physical therapist or occupational therapist can show you exercises that may help your post-stroke spasticity.
2. Adjust your posture
Try to avoid staying in one position too long if you’re coping with spasticity after a stroke. That can cause muscles and joints to get stiff and sore.
Caregivers should aim to help people with spasticity switch positions every 1–2 hours to help keep the body limber.
3. Support affected limbs
Providing extra support for affected limbs can also keep you more comfortable and reduce the effects of spasticity. For example, try not to let your arm or leg fall off the side of the bed or wheelchair.
Be especially mindful when lying down. Placing your affected arm or leg under your body when resting can worsen spasticity.
Lying on your back can help keep your limbs in a more comfortable position. If you prefer to lie on your side, avoid putting the weight on the side that the stroke affected.
Special braces can help support limbs and prevent spasticity from getting worse.
4. Adapt your home
Making adjustments around the home can make it easier for people with spasticity to move around and accomplish tasks.
Here are some ways you can adapt your home, according to the American Stroke Association:
- install ramps to doorways
- add grab bars to the bathroom
- install raised toilet seats
- place a bench in your tub or shower
- use plastic adhesive strips on the bottom of your tub
5. Ask for support
People with spasticity, along with their caregivers, can find it helpful to seek support from family, friends, and other loved ones. They can encourage active movement and help with tasks around the home.
It can also be a great way to bond and enjoy time together. If your loved one is stretching, for instance, try stretching with them for encouragement.
6. Work with an occupational therapist
Occupational therapists help people with disabilities and health conditions learn new ways of performing everyday tasks more easily.
This may mean learning to get dressed with the opposite hand, or modifying eating habits. While learning something new is always a journey, staying positive can help make the process easier.
7. Use mobility aids
If spasticity has made it difficult to get around after a stroke, using mobility aids can help you move more easily. Common mobility aids include:
Talk with an occupational therapist to see if a mobility aid can be helpful for you.
Spasticity often occurs between 3 and 6 weeks after a stroke, according to research from 2018. The muscular symptoms of spasticity have been shown to continue increasing at 6 months after a stroke.
If left untreated, spasticity can cause permanent shrinking and contracting of the muscles, along with joints locked into single positions.
While there’s no cure for post-stroke spasticity, treatments and lifestyle changes can help reduce symptoms and maintain your range of motion.
At least a quarter of people will develop spasticity after a stroke. The condition can cause tight, stiff muscles and reduce your mobility.
You can manage symptoms and improve your quality of life with spasticity by modifying your home, practicing daily exercises, working with an occupational therapist, and using mobility aids.
Treatments can also help prevent long-term damage from spasticity. Talk with a doctor to see if medication or injections are right for you.
[ARTICLE] Goal attainment: a clinically meaningful measure of success of Botulinum Toxin-A treatment for lower limb spasticity in ambulatory patients – Full Text
The objectives of this study were: (1) to evaluate whether Botulinum toxin type A (BoNT-A) treatment for lower limb spasticity leads to patient goal attainment and identify factors associated with positive goal attainment, and (2) to assess the effect of BoNT-A treatment on patients’ gait.
Retrospective cohort study between June 2014 and February 2019.
Public outpatient spasticity clinic in a tertiary hospital.
Thirty patients (50% female, average age 50.5 years) with lower limb spasticity of heterogenous aetiologies (96.7% cerebral ± spinal origin and 3.3% isolated spinal origin). 73.3% of patients had previously received BoNT-A treatment.
BoNT-A injection to lower limb muscles.
Main outcome measures
The primary outcome measure was goal attainment measured using the Goal Attainment Scale (GAS). The Modified Ashworth Scale (MAS) was used to assess spasticity. Gait was characterised by spatiotemporal parameters.
Fifty-six treatment episodes were analysed and showed BoNT-A treatment resulted in a significant reduction in spasticity (pre-treatment MAS = 3.18±0.73; post-treatment MAS = 2.27±0.89, p<0.001) with no associated change in gait parameters. Logistic regression revealed most patients (74.1%) achieved all of their goals with younger patients having a high likelihood of goal attainment regardless of their gait profile identified by latent profile analysis of the gait parameters. Patients considered to have a low functioning gait profile demonstrated a significantly greater likelihood of goal attainment than the patients of the other gait profiles combined (OR= 45.6, 95% CI= 1.3 to 1602.1; p=0.036). Chronic spasticity, pre-treatment severity of spasticity (MAS) and its reduction were not associated with likelihood of goal attainment.
The success and efficacy of BoNT-A treatment in improving patient perceived gait quality and reducing the negative symptoms of spasticity was best measured using the GAS. The study emphasises the importance of measuring patient goals as a clinical outcome. Gait parameters were most informative when used collectively to classify patients on the basis of their overall gait profile which assisted in identifying differences between patients’ likelihood of goal attainment following treatment.
Spasticity, a sequelae of numerous neurological disorders, is characterised by a velocity dependent increase in muscle tone that results in resistance to passive movement, involuntary muscle spasms and contractions (1, 2). Lower limb spasticity can result in disabling consequences including pain, spasm, altered posture, deformity of the foot and ankle, and impairment of gait and mobility (3, 4). The impact on gait and mobility is associated with loss of function and independence, higher morbidity including falls and fracture (3) and premature residential aged care placement (5-7). Prevention and management of lower limb spasticity and sequelae is therefore an important focus of neurological rehabilitation.
Previous research has demonstrated the positive effects of focal injections of the neurotoxic protein botulinum toxin A (BoNT-A) in treating spasticity and it is now a widely accepted treatment modality (8-18). Studies investigating the effect of BoNT-A on lower limb spasticity have concentrated on outcomes including gait, safe and independent mobility, and activities of daily living (3, 8-10, 13-15, 17, 19-27). To date, the evidence regarding the benefit of BoNT-A mediated reduction in lower limb spasticity on functional outcomes remains inconsistent (20).
In clinical practice the indications and objectives for BoNT-A treatment of lower limb spasticity are diverse and patient specific, as are the patient’s priorities and expectations of the treatment. Rehabilitation-centred frameworks should therefore include a meaningful patient focused purpose for BoNT-A treatment, beyond reducing spasticity itself (28), by identifying patient needs, priorities and goals and tailoring treatment towards addressing and achieving these.
Few previous studies examining BoNT-A treatment for lower limb spasticity have reported the nature of patient goals, examined goal attainment outcomes or investigated factors associated with the likelihood of goal attainment (15, 29-31). A better understanding of such relationships is of clinical value, may guide patient selection and help predict positive treatment outcomes. Hence, the primary aim of this study was to evaluate the attainment of patients’ self-identified treatment goals, and factors associated with the likelihood of patient goal attainment. A secondary aim was to assess the effect of BoNT-A treatment on the gait of patients with lower limb spasticity.[…]
[Abstract] The clinical effect of Kinesio taping and modified constraint-induced movement therapy on upper extremity function and spasticity in patients with stroke: a randomized controlled pilot study
BACKGROUND: Spasticity and impaired hand function are common complication in patients with stroke, and it pose negative impact on quality of life.
AIM: We aimed to assess the effect of the combined administration of kinesio taping (KT) and modified constraint-induced movement therapy (mCIMT) on upper extremity function and spasticity in hemiplegic patients with stroke.
DESIGN: A randomized controlled pilot study.
SETTING: A hospital center.
POPULATION: Patient of stroke with hemiplegia for 3-12 months
METHODS: 35 patients were enrolled and allocated into three groups, including the sham KT and mCIMT group, KT group, or KT and mCIMT group. The KT, sham KT, and mCIMT serve as additional therapies (5 days/week for 3 weeks) besides regular rehabilitation (5 days/week for 6 weeks). KT was applied over the dorsal side of the affected hand, while mCIMT was applied to restrain the unaffected upper extremity. The outcomes included the modified Tardieu scale (mTS), Brunnstrom stage, Box and Block Test (BBT), Fugl-Meyer assessment for the upper extremity (FMA-UE), and Stroke Impact Scale version 3.0. Measurements were taken at baseline, immediately after intervention (third week), and 3 weeks later (sixth week).
RESULTS: Between baseline and the third week, within-group comparisons yielded significant improvement in the wrist and hand parts of the FMA and BBT of the Sham KT and mCIMT group (p=0.007-0.035); in the hand part of the FMA, BBT, and mTS degree (p=0.005-0.024) of the KT group; and in the Brunnstrom stage of the wrist, FMAUE, BBT, and mTS degrees (p=0.005-0.032) of the KT and mCIMT group. Between baseline and the sixth week, there was significant difference in the proximal part of the FMA and mTS degree in groups with KT, but an additional improvement on the Brunnstrom stage of the wrist was noted in the KT and mCIMT group.
CONCLUSIONS: KT benefits patients with stroke in spasticity reduction and upper extremity function. The combination of KT and mCIMT provides extra benefit in motor performance with a more long-lasting effect.
CLINICAL REHABILITATION IMPACT: Kinesio taping could act as potential adjuvant therapy in patient of stroke with hemiplegia.