[WEB SITE] Seizures Follow Similar Path Regardless of Speed

Summary: By capturing a cell by cell view of seizures propagating through a mouse brain, researchers discovered neurons fire in a sequential pattern, regardless of how quickly the seizure occurs. The findings confirm seizures are not a result of neurons going haywire.

Source: Columbia University.

Of the 50 million people who suffer from epilepsy worldwide, a third fail to respond to medication. As the search for better drugs continues, researchers are still trying to make sense of how seizures start and spread.

In a new study in Cell Reports, researchers at Columbia University come a step closer by showing that the neurons of mice undergoing seizures fire off in a sequential pattern no matter how quickly the seizure propagates — a finding that confirms seizures are not the result of neurons randomly going haywire.

“This is good news,” said the study’s senior author, Dr. Rafael Yuste, a neuroscientist at Columbia. “It means that local neuronal circuits matter, and that targeting the right cells may stop or even prevent some types of brain seizure.”

To induce the seizures, researchers injected a tiny area of cortex in awake mice with two types of drugs–one that increases neuronal firing and another that blocks the inhibitory interneurons that control information flow between cells. Recording the seizures as they rippled outward, researchers found that cells in the mouse’s brain systematically fired one after the other. Under both models, the seizure spread across the top layer of cortex in a wave-like pattern before descending into its lower layers.

Unexpectedly, they found that whether the seizure lasted 10 seconds or 30 seconds, it followed the same route, like a commuter stuck in traffic. The concept of neurons firing in a reliable pattern no matter how fast the seizure is traveling is illustrated on the cover of Cell Reports, drawn by the study’s lead author, Dr. Michael Wenzel.

“The basic pattern of a string stretched between two hands stays the same whether the hands move closer together or farther away,” he says. “Just as neurons maintain their relative firing patterns regardless of how slowly or quickly the seizure unfolds.”

Researchers were able to get a cell-by-cell view of a seizure propagating through a mouse’s brain using high-speed calcium imaging that allowed them to zoom in 100 times closer than electrode techniques used on the human brain.

Image shows brain.

Researchers were able to get a cell-by-cell view of a seizure propagating through a mouse’s brain using high-speed calcium imaging that allowed them to zoom in 100 times closer than electrode techniques used on the human brain. NeuroscienceNews.com image is in the public domain.

It may be the first time that researchers have watched a seizure unfold at this level of detail, and their findings suggest that inhibitory neurons may be a promising area of future research, said Dr. Catherine Schevon, a neurology professor at Columbia University Medical Center who was not involved in the research.

“The role of inhibitory restraint in seizure development is an area that few have studied at micrometer scale,” she said. “This could be a useful treatment target for future drug development or stem cell interneuron implants.”

Source: Seizures Follow Similar Path Regardless of Speed – Neuroscience News

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[WEB SITE] Brain Training: Improve Your Neuroplasticity in 9 Easy Steps

Can we improve our capacity for creativity, memory and analysis through brain training exercises? Do online brain training games really work? The simple answer to these questions is yes; we can improve the brain’s ability to function, and we can actually reshape the physical structure of our brains through neuroplasticity training exercises.

Happily in improving your brain’s ability to function, it is not necessary to pay for expensive online games, that ultimately add nothing to the quality of your life. These nine training tips are free to engage in, will improve your brain’s function, and entice you to live life to its fullest!

How We Can Increase Brain Function As We Age

A study of randomly chosen individuals age 57-71 showed improved brain function after just 12 hours of strategic brain training exercises. Using MRIs of the participants brains both before and after, researchers saw upwards of an 8% improvement in blood flow and other indices that indicate improved brain function.

Improved brain function included improved ability to strategize, remember and draw big-picture conclusions from lengthy texts of information.

Remarkably, in a follow up study using MRIs again on the participants, researchers found that the benefits derived from the single training session were still in place one year later. Enhanced synaptic plasticity means that we can think faster, listen better, respond to situations faster and concentrate with greater focus. Creativity is enhanced as well.

MRI of the Brain

By Nevit Dilmen (Own work)(http://creativecommons.org/licenses/by-sa/3.0)], via Wikimedia Commons
By Nevit Dilmen (Own work)(http://creativecommons.org/licenses/by-sa/3.0)%5D, via Wikimedia Commons

[…]

more —> Brain Training: Improve Your Neuroplasticity in 9 Easy Steps | HealDove

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[ARTICLE] A randomised controlled cross-over double-blind pilot study protocol on THC:CBD oromucosal spray efficacy as an add-on therapy for post-stroke spasticity – Full Text

Abstract

Introduction Stroke is the most disabling neurological disorder and often causes spasticity. Transmucosal cannabinoids (tetrahydrocannabinol and cannabidiol (THC:CBD), Sativex) is currently available to treat spasticity-associated symptoms in patients with multiple sclerosis. Cannabinoids are being considered useful also in the treatment of pain, nausea and epilepsy, but may bear and increased risk for cardiovascular events. Spasticity is often assessed with subjective and clinical rating scales, which are unable to measure the increased excitability of the monosynaptic reflex, considered the hallmark of spasticity. The neurophysiological assessment of the stretch reflex provides a precise and objective method to measure spasticity. We propose a novel study to understand if Sativex could be useful in reducing spasticity in stroke survivors and investigating tolerability and safety by accurate cardiovascular monitoring.

Methods and analysis We will recruit 50 patients with spasticity following stroke to take THC:CBD in a double-blind placebo-controlled cross-over study. Spasticity will be assessed with a numeric rating scale for spasticity, the modified Ashworth scale and with the electromyographical recording of the stretch reflex. The cardiovascular risk will be assessed prior to inclusion. Blood pressure, heart rate, number of daily spasms, bladder function, sleep disruption and adverse events will be monitored throughout the study. A mixed-model analysis of variance will be used to compare the stretch reflex amplitude between the time points; semiquantitative measures will be compared using the Mann-Whitney test (THC:CBD vs placebo) and Wilcoxon test (baseline vs treatment).

Introduction

Stroke is one of the most disabling neurological disease and frequently determines important chronic consequences such as spasticity. Prevalence of poststroke spasticity ranges from 4% to 42.6%, with the prevalence of disabling spasticity ranging from 2% to 13%.1 Treatment of poststroke spasticity is based on rehabilitation, local injection of botulinum toxin (BoNT) in the affected muscles for focal spasticity and/or use of classic oral drugs such as tizanidine, baclofen, thiocolchicoside and benzodiazepines, which are not always effective and have a good number of possible side effects.

The transmucosal administration of delta-9-tetrahydrocannabinol and cannabidiol (THC and CBD at 1:1 ratio oromucosal spray, Sativex) is able to reduce spasticity acting on endocannabinoid receptors CB1and CB2. This novel drug has been licensed after an extensive clinical trial programme2–4 in adult patients with multiple sclerosis who have shown no significant benefit from other antispasmodic drugs. More than 45 000 patient/years of exposure since its approval in more than 15 EU countries support their antispasticity effectiveness and safety profile in this indication.5 Besides improving spasticity, cannabinoids can be beneficial in reducing pain, chemotherapy-induced nausea and vomiting; moreover, they contribute to reducing seizures and to lowering eye pressure in glaucoma.6Cannabinoids can also exert psychological effects by lowering anxiety levels and inducing sedation or euphoria. Marijuana, which is the main source of cannabinoids, is declared illegal in many countries mostly because of the risk of abuse, dependence and withdrawal syndrome, related to the effect of its high amounts of THC. Several reports support an increased ischaemic stroke risk related to relevant abuse of smoked marijuana7–17 as well as synthetic cannabinoids.18–20 Ischaemic stroke following cannabis involves more frequently basal ganglia and cerebellum where CB1 and CB2 receptors show a higher expression.13

The ‘French Association of the Regional Abuse and Dependence Monitoring Centres Working Group on Cannabis Complications’ warns about the increased cardiovascular risk related to the use of herbal cannabis, mostly consisting of acute coronary syndromes and peripheral arteriopathies, potentially leading to life-threatening conditions.21 The detrimental consequences of cannabinoids could be attributed to the increase in heart rate22 as well as arterial spasms also in the context of a reversible cerebral vasoconstriction syndrome,23 but also vasculitis, postural hypotension and cardioembolism.24

On the other side, some studies support a beneficial effect on stroke evolution of cannabinoid receptors stimulation. In fact, cannabinoid-mediated activation of CB1 and CB2 receptors reduces inflammation and neuronal injury in acute ischaemic stroke.25 Activation of CB2 receptors shows protective effects after ischaemic injury26 and inhibits atherosclerotic plaque progression.27 28

To our knowledge, no correlations have been reported between haemorrhagic stroke and cannabinoids intake. In our opinion, the modification of blood pressure is the most important cannabinoid effect that should be taken into account in patients with a previous haemorrhagic stroke or predisposed to intracranial bleeding. Cannabinoids are indeed capable of inducing blood pressure fluctuations in a specific triphasic pattern (low-high-low) potentially harmful if the patient is with bleeding risk.29Ischaemic disease is not included among THC:CBD oromucosal spray contraindications. However, considering that, to our knowledge, no study has been performed with THC:CBD oromucosal spray on post-stroke spasticity, we believe that a particular caution should be used in stroke patients.

The decision of which method of measure is considered as end point is a major issue in studies involving spasticity. The definition of spasticity provided by Lance is one of the most precise and reliable, focusing on the stretch reflex as the neurophysiological equivalent of spasticity.30 Probably because of technical complexity and required expertise, neurophysiological approaches are rarely adopted. Clinical rating scales such as the modified Ashworth scale (MAS)31 or subjective scores such as the numeric rating scale (NRS) for spasticity are being widely used.32 33 Recent evidence supports the idea that MAS and NRS are indeed useful to quickly rate spasticity in a clinical setting, however NRS provide a very variable and imprecise assessment of many symptoms related to spasticity, but where spasticity itself is probably only a common factor.34 The adoption of stretch reflex as the most appropriate neurophysiological measure of spasticity increases the specificity and reduces the variability of the end point and is particularly suitable for clinical trials.

Our proposal is therefore to assess the efficacy of THC:CBD oromucosal spray in patients with spasticity following stroke as add-on to first-line antispasticity medications with an experimental pilot randomised placebo-controlled cross-over clinical trial using the stretch reflex as primary outcome measure. Prior to inclusion in the study, we propose strict selection criteria in order to reduce the risk of relevant side effects. […]

Continue —>  A randomised controlled cross-over double-blind pilot study protocol on THC:CBD oromucosal spray efficacy as an add-on therapy for post-stroke spasticity | BMJ Open

 

Graphical representation of the study protocol, particularly depicting the cross-over design and the time points. THC/CBD, tetrahydrocannabinol/cannabidiol.

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[BLOG POST] Tired After a Stroke? Understanding Post-Stroke Fatigue | Saebo

Feeling tired is a normal part of life. Whether you didn’t get a good night of sleep or wore yourself out with a busy day or an exerting activity, your body can only handle so much before you start to feel the physical effects of being tired. In cases like these, all you need to do is rest in order to feel re-charged and rejuvenated. But for individuals who have suffered from a stroke, it’s not that easy.

Fatigue after a stroke is common, and it’s different from simply feeling tired. Post-stroke fatigue can make somebody feel like they completely lack energy or strength, with a persistent feeling of being tired or weary. Unlike typical tiredness, a nap or sleeping longer at night won’t solve things. If you are experiencing post-stroke fatigue, it is important to consult with your doctor so you can take the proper steps to start feeling better and more energized.

 

What is Post-Stroke Fatigue?

Post-stroke fatigue can occur after a mild or severe stroke, and roughly 40 to 70 percent of stroke patients experience this “invisible symptom.” It’s a particularly frustrating side effect of a stroke because it can make you feel completely exhausted and off your game, which in turn makes recovering from the stroke seem even more difficult.

Those who experience post-stroke fatigue can feel like they are not in control of their recovery, as it’s hard for them to muster the energy to participate in their rehab activities or normal day-to-day functions. Many individuals with post-stroke fatigue initially confuse it with “being tired,” but post-stroke fatigue is not the same thing as just being tired. It can come out of nowhere, without warning, and rest isn’t always the solution.

Post-stroke fatigue is draining both physically and emotionally/mentally, and the severity of the stroke does not seem to correlate to the severity of the fatigue. Even a mild stroke can result in extreme post-stroke fatigue, and even if you suffered a stroke some time ago and feel as if you’ve made a full recovery, post-stroke fatigue can still impact you.

 

What Causes Post-Stroke Fatigue?

 

Experts aren’t entirely sure what causes post-stroke fatigue because there has been limited research on the subject.Medical conditions like diabetes and heart disease can play a role, as can any pre-existing fatigue issues an individual had before suffering from a stroke. In addition to fatigue, sleep apnea is another issue reported by stroke survivors, so it’s possible there is some sort of link between the two, though nothing has been proven.

Survivors often feel stressed or depressed about the stroke afterwards, from worrying about the recovery process to being concerned with their symptoms. Stress and the mental demands that come with it can lead to fatigue. There are a lot of unknowns about the cause of post-stress fatigue, but one thing is certain: a stroke takes a big toll on a person’s body, and many stroke survivors feel severe fatigue as a result.

 

How Do You Tell if You Have Post-Stroke Fatigue?

Remember that there’s a difference between feeling tired and having post-stroke fatigue. The latter will give you afeeling of complete exhaustion; you will lack all energy and feel extremely weary. You will probably feel like you have to rest every day, or even multiple times a day. This can make it difficult to accomplish things, whether it’s something as simple as spending time with family, running errands, or even attending your post-stroke therapy sessions.

Until you feel the type of exhaustion that comes with post-stroke fatigue it’s difficult to explain, so don’t feel frustrated if your friends and family don’t understand why you’re struggling. If you think you have post-stroke fatigue, don’t hesitate to consult with your doctor.

 

Tips to Increase Your Energy

The first step in combating post-stroke fatigue is to discuss it with your doctor. Let them know what you’ve been feeling. Your doctor will probably start the process by making sure you’ve had an up-to-date physical. With that information, your doctor can rule out other potential causes for your fatigue or determine if your fatigue might stem from your medication.

It goes without saying, but try to take naps if time allows. Naps won’t cure you of your fatigue long term, but resting when you feel run down can help you feel more refreshed, even if only for a short while.

Do your best to relax. Don’t let your post-stroke fatigue, or any other side effects of your stroke, get you down. Stay positive! Being stressed or tense will only sap you of more energy. A positive attitude goes a long way in feeling upbeat and energetic. Try to get back into the swing of things by returning to your pre-stroke routines. Simple things like staying active and involved with friends and family can yield big benefits.

Yes, it will seem overwhelming at times. Suffering from a stroke, dealing with the aftermath, and having no energy on top of it can be tough, but celebrate your successes. Take baby steps, and be proud of the progress you’ve made. Focus on what you’ve accomplished during your recovery so far, rather than dread what’s left to be done.

 

Tired of Being Tired

Post-stroke fatigue is a daunting condition, and many people who are recovering from a stroke might not even realize they have it, instead thinking they are simply tired. If you’ve had a stroke and find yourself feeling sapped of your energy on a consistent basis, talk to your doctor. There’s a chance you have post-stroke fatigue. You’re not alone; 40 to 70 percent of stroke survivors experience this kind of exhaustion.

By speaking with the proper medical professionals, making it a point to rest as often as possible, and having a positive mindset, you can combat the constant drowsiness and work on returning to your pre-stroke energy levels.

Source: Tired After a Stroke? Understanding Post-Stroke Fatigue | Saebo

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[WEB SITE] Real-world data confirms clinical effectiveness of Zebinix®  

Real-world data confirms clinical effectiveness of Zebinix® (eslicarbazepine acetate) for the treatment of partial-onset epilepsy in adults

  • Eslicarbazepine acetate data shows seizure freedom in 41.3% of patients at 12 months, and retention rates of 73.4%.1
  • Results from the Euro-Esli study presented 5th September 2017 at the 32ndInternational Epilepsy Congress (IEC) in Barcelona, Spain.1

Bial and Eisai have announced data confirming the effectiveness and tolerability of Zebinix® (eslicarbazepine acetate) in routine clinical practice, thereby complementing evidence from clinical trials.[i] The Euro-Esli study is an exploratory pooled analysis of data from 14 European clinical practice studies, analysing data of 2,058 patients aged between 14-88 years old with partial-onset seizures (POS), with or without secondary generalisation.1 Full results were presented at the IEC in Barcelona, Spain.1

“It is most reassuring to see similar efficacy results with eslicarbazepine acetate in a routine clinical setting compared to that of clinical trials; we can be confident that this treatment is effective amongst the diversity of our ‘real’ epilepsy patients,” explains Dr Vicente Villanueva, Neurologist and Epileptologist, Hospital Universitario y Politécnico La Fe, Valencia, Spain. “Real-world studies like the Euro-Esli study are important because they provide significant insight into how a drug performs in a routine medical setting, allowing us to assess the drug, to ultimately improve patient outcomes.”

Epilepsy is one of the most common neurological conditions in the world, affecting approximately six million people in Europe.2 An epileptic seizure is a clinical manifestation of the condition, thought to result from an abnormal discharge of a set of neurons in the brain.[ii] Seizures can vary in manifestation, from brief lapses of attention to severe and prolonged convulsions.[iii] Depending on the type, seizures may involve one part of the body or the whole body, and may affect consciousness.3 Seizures can also vary in frequency from less than one per year, to several per day.3 Epilepsy has many possible causes but often the cause is unknown.3

The Euro-Esli study (in over 2,000 patients with epilepsy) showed that at 3, 6 and 12 months, seizure freedom rates in patients aged 14-88 years treated with eslicarbazepine acetate were 30.6%, 38.3% and 41.3% respectively. Retention rates were 95.4%, 86.6% and 73.4% and responder rates were 60.9%, 70.5% and 75.6%, respectively.1 There were significant reductions from baseline to final visit in monthly frequencies of total (mean reduction 44.1%), simple partial (78.8%), complex partial (53.1%) and secondarily generalised (80.0%) seizures (p<0.001 for all).1 Adverse events were reported for 34.0% of patients and led to discontinuation of 13.6% of patients.1 The most frequently reported adverse events were dizziness (6.7%), fatigue (5.4%) and somnolence (5.1%).1

These results improve our knowledge and understanding around the use of eslicarbazepine acetate in routine clinical practice and strengthen Bial’s commitment to developing and delivering beneficial treatment options for people living with epilepsy António Portela, CEO of Bial

These data underscore our commitment to our anti-epileptic drug product portfolio. We will continue to invest both in clinical trials and the generation of real-world evidence to improve the lives of patients living with epilepsy
Neil West, Vice President EMEA, Global Neurology Business Unit at Eisai

Eslicarbazepine acetate is indicated as monotherapy in the treatment of POS, with or without secondary generalisation, in adults with newly diagnosed epilepsy; and as adjunctive therapy in adults, adolescents, and children aged above six years, with POS with or without secondary generalisation.[iv]

About the Euro-Esli study1

The Euro-Esli study was a large, exploratory, pooled analysis of real-world data from 14 European clinical practice studies, including data from 2,058 patients (52.1% male; mean age 44 years; mean epilepsy duration 20.9 years). Retention and effectiveness were assessed after 3, 6 and 12 months of treatment with eslicarbazepine acetate. Effectiveness assessments comprised percentage reduction from baseline in monthly seizure frequency, responder rate (≥50% seizure frequency reduction) and seizure freedom rate (seizure freedom at least since prior visit). Safety and tolerability were assessed by evaluating adverse events (AEs).

REFERENCES

[i] Villanueva V, et al. (2017) A European audit of real-world use of eslicarbazepine acetate as a treatment for partial-onset seizures: the Euro-Esli study. International Epilepsy Congress (IEC) 2017; Barcelona, Spain, Poster p0918

[ii] World Health Organization. (2010) Epilepsy in The WHO European Region: Fostering Epilepsy Care in Europe. Cruquius, Paswerk Bedrijven. Available from: www.ibe-epilepsy.org/downloads/EURO%20Report%20160510.pdf [Accessed August 2017].

[iii] World Health Organization. (2017) Epilepsy Fact Sheet. Available from: www.who.int/mediacentre/factsheets/fs999/en/ [Accessed August 2017].

[iv] Eisai. (2017) Zebinix® (eslicarbazepine acetate) Summary of Product Characteristics. Available from: www.ema.europa.eu/docs/en_GB/document_library/EPAR_-_Product_Information/human/000988/WC500047225.pdf  [Accessed August 2017].

[v] Hebeisen S, et al. (2015) Eslicarbazepine and the enhancement of slow inactivation of voltage-gated sodium channels: A comparison with carbamazepine, oxcarbazepine and lacosamide. Neuropharmacology. 89, 122-135

[vi] Elger C, et al. (2007) Eslicarbazepine acetate: A double-blind, add-on, placebo-controlled exploratory trial in adult patients with partial-onset seizures. Epilepsia. 48, 497-504.

[vii] Elger C, et al. (2009) Efficacy and safety of eslicarbazepine acetate as adjunctive treatment in adults with refractory partial onset seizures: A randomised, double-blind, placebo-controlled, parallel-group phase III study.Epilepsia. 50, 454-63.

[viii] Ben-Menachem E, et al. (2010) Eslicarbazepine acetate as adjunctive therapy in adult patients with partial epilepsy. Epilepsy Research. 89(2-3), 278-85.

[ix] Gil-Nagel A, et al. (2009) Efficacy and safety of 800 and 1200 mg eslicarbazepine acetate as adjunctive treatment in adults with refractory partial-onset seizures. Acta Neurologica Scandinavica. 120, 281-87.

Source: Real-world data confirms clinical effectiveness of Zebinix® | ACNR | Online Neurology Journal

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[BLOG POST] How to Prevent or Minimize the Plateau Phase After a Stroke – Saebo

The rehabilitation process throughout the first several months of stroke recovery can be confusing and often daunting, with peaks and valleys that either encourage or slow the healing process. Varying levels of paralysis are common, and adjusting to ongoing therapy requires a shift in mindset and a complete lifestyle overhaul.

Yet, some of the most significant improvements often occur during these early days, reflecting the initial plasticity of the brain. Therefore, gaining momentum during this neurologically progressive time is key to facing the often-frustrating period ahead—a stage known as a plateau. During this stage, it may feel as if the initial spike in progress was the end of successful rehabilitation and that no further improvement is possible. But for some, the plateauing phase is quite common and even to be expected, and understanding this will help both the patient and caregivers to avoid losing hope, motivation, and persistence during this difficult time.

Are plateaus real?

Over the past two decades, research has reaffirmed the frequency and common intricacies of plateauing in newer stroke patients. In the past, it was more likely for doctors to assume that patients only regained motor function in the first few months after a stroke, and that once the plateau occurred, ongoing exercises and therapy were ineffective.

However, recently published reports now show that patients can regain motor recovery and function up to 23 years after a stroke. Medical professionals are now finding that this complex recovery period often continues to occur for months and even years after a patient has left rehab—and primarily resumes only if patients and caretakers build a recovery planand have access to evidence-based technology to prevent the plateau phase after leaving traditional rehabilitation. Designing a home-exercise program, often by upgrading the previous inpatient therapeutic regimen, is the key to maintaining progress or restarting growth if the plateau phase has begun.

What causes a plateau?

When a stroke occurs, a specific area of the brain suffers an infarction, obstructing the blood supply and killing the functionality of a section of the brain. Though this specific area is not recoverable, the area directly surrounding the infarction-impacted region still holds potential for rehabilitation. In the moments directly after the stroke, however, the area simply does not work.

During the initial healing phase known as the subacute phase, which is usually the first three to six months after the stroke, the most consistent and encouraging signs of progress occur in these regions. This natural healing stage often takes place when patients are being coached along in rehab; but if the plateau stage occurs towards the end of  the natural healing phase, it’s common for patients to be sent home for a shift in care.

For this group of patients, this is a difficult transition for several reasons: familiar exercises must be altered and adjusted, the home routine requires greater adaptability, and patients face the discouragement of no longer seeing an uptick in progress, often deterring patients and caretakers from pushing on. Progressing through the discouragement is more easily accomplished when patients and caretakers understand the plateau stage. A solid plan of ongoing, managed care is necessary for continuing to bolster the still-developing parts of the mind.

It’s not the patients that have plateaued, rather treatment options have plateaued them.

It is important to keep in mind that traditional therapy that isn’t evidence-based can be ineffective and can actually causea plateau. Sometimes a patient’s recovery is only as good as the therapist, and if the therapist isn’t modifying the treatment to the patient’s specific needs and incorporating the latest proven interventions because they haven’t been trained or educated, the patient will most likely plateau. If the therapist is well educated on the latest advances and interventions in stroke recovery the patient has a much better chance of avoiding the plateau phase. So, a plateau phase may not be an absolute, it’s a possibility.

How can you overcome a plateau?

After reassuring research, the medical community confirms that working with a managed care professional with a series of ongoing exercises does promote improvement in a stroke patient’s long-term recovery. When signs of recovery seem to stall altogether, here are a few common practices for jumpstarting at-home care.

Saebo Rehabilitation Devices

The brain’s cortical plasticity is a key component in this stage of recovery, and Saebo offers several tools for employing this factor. Motor function and utilization of the hands can be continuously developed with the assistance of the SaeboGlove or SaeboFlex, easing therapy at home with minimal assistance and instruction. The SaeboFlex and SaeboGlove include a proprietary tension system that encourages the extension and grasping strength of the hands of healing stroke patients. This action simultaneously supports brain growth and reprogramming, encouraging the plasticity of the mind through task-oriented exercises.

If patients are unable to functionally use their affected hand, they will develop learned non-use and will eventually reach the plateau phase due to avoidance. The SaeboFlex and and SaeboGlove are two tools that may prevent or minimize the plateau phase and allow patients to engage their affected hand in functional tasks that would otherwise be impossible.

Constraint-Induced Movement Therapy

Similar to the SaeboGlove and SaeboFlex’s use of cortical plasticity, Constraint-Induced Movement Therapy (CIMT) encourages the regrowth of neurological pathways damaged during a stroke. This promotes more meticulous use of the affected hand. By keeping the functional hand from taking full responsibility for daily tasks—usually with a mitt—this method involves preference of the developing side of the brain. Though CIMT is an intensive process, which must be guided and supervised for several-hour stretches at a time, positive results may be seen for years to come.

At-Home Exercises

Maintaining a regimen of exercises that both meets the needs of ongoing recovery and the patient’s comfort is essential to progressing past the plateau stage after traditional rehab. The factor of neuroplasticity allows the brain to constantly adapt, but persistence and regularity is key. When followed correctly, an increase in motor function and strength is probable in many patients. Continuing physical exercise assists with many aspects of the healing process, supporting flexibility, coordination, and balance. Though physical activity does not prevent the occurrence of a second stroke, it will keep the body in key health for recovery.

Staying Motivated

During the difficult transition to home care, supportive family and medical professionals are the vital factor in helping patients maintain motivation and feel guided toward success. As a patient is just beginning the rehabilitation process, it is almost solely in the hands of the assistant to set the tone of the session, and this mutual understanding will drive the exercises forward, making it easier to set and meet small goals along the way. Roadblocks and frustrations are common, but with a structured and steady plan, these stages will pass and times of progress will return.

Handling Emotional Changes

When difficult emotions arise, it is crucial to realize that this is completely normal. Stroke recovery is a long, often slow process, and frustration, anger, and depression are understandable obstacles to encounter. Know that these feelings and physical plateaus will pass with time when both patients and caretakers allow themselves self-care and patience. It is also helpful for families to keep this in mind, as maintaining a genuinely flexible and positive atmosphere during rehabilitation will help all parties see these changes and efforts as a long-term process.

Keep Moving Forward

When heading into long-term stroke treatment, awareness of evidence-based treatment interventions may prevent or decrease the plateauing stage. But with consistent at-home tools and exercises, progress will return, even if it feels slower than in previous phases. The recently damaged brain is taking the necessary time to heal and regrow, and this requires setting short-term goals and celebrating small victories. Reaching the plateau stage is an opportunity to reconsider the next best way forward with your therapist—progress is still ahead, even if the methods and system require a new outlook.

Source: How to Prevent or Minimize the Plateau Phase After a Stroke | Saebo

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[Congress Abstracts] 2017 Canadian Stroke Congress Abstracts – International Journal of Stroke

 

Visit site and search with Ctrl+F  —> 2017 Canadian Stroke Congress AbstractsInternational Journal of Stroke, 2017

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[ARTICLE] Transcranial direct current stimulation (tDCS) for improving capacity in activities and arm function after stroke: a network meta-analysis of randomised controlled trials – Full Text

Abstract

Background

Transcranial Direct Current Stimulation (tDCS) is an emerging approach for improving capacity in activities of daily living (ADL) and upper limb function after stroke. However, it remains unclear what type of tDCS stimulation is most effective. Our aim was to give an overview of the evidence network regarding the efficacy and safety of tDCS and to estimate the effectiveness of the different stimulation types.

Methods

We performed a systematic review of randomised trials using network meta-analysis (NMA), searching the following databases until 5 July 2016: Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE, EMBASE, CINAHL, AMED, Web of Science, and four other databases. We included studies with adult people with stroke. We compared any kind of active tDCS (anodal, cathodal, or dual, that is applying anodal and cathodal tDCS concurrently) regarding improvement of our primary outcome of ADL capacity, versus control, after stroke. PROSPERO ID: CRD42016042055.

Results

We included 26 studies with 754 participants. Our NMA showed evidence of an effect of cathodal tDCS in improving our primary outcome, that of ADL capacity (standardized mean difference, SMD = 0.42; 95% CI 0.14 to 0.70). tDCS did not improve our secondary outcome, that of arm function, measured by the Fugl-Meyer upper extremity assessment (FM-UE). There was no difference in safety between tDCS and its control interventions, measured by the number of dropouts and adverse events.

Conclusion

Comparing different forms of tDCS shows that cathodal tDCS is the most promising treatment option to improve ADL capacity in people with stroke.

Background

An emerging approach for enhancing neural plasticity and hence rehabilitation outcomes after stroke is non-invasive brain stimulation (NIBS). Several stimulation procedures are available, such as repetitive transcranial magnetic stimulation (rTMS) [1], transcranial direct current stimulation (tDCS) [234], transcranial alternating current stimulation (tACS) [5], and transcranial pulsed ultrasound (TPU) [6]. In recent years a considerable evidence base for NIBS has emerged, especially for rTMS and tDCS.

tDCS is relatively inexpensive, easy to administer and portable, hence constituting an ideal adjuvant therapy during stroke rehabilitation. It works by applying a weak and constant direct current to the brain and has the ability to either enhance or suppress cortical excitability, with effect lasting up to several hours after the stimulation [789]. Hypothetically, this technique makes tDCS a potentially useful tool to modulate neuronal inhibitory and excitatory networks of the affected and the non-affected hemisphere post stroke to enhance, for example, upper limb motor recovery [1011]. Three different stimulation types can be distinguished.

  • In anodal stimulation, the anodal electrode (+) usually is placed over the lesioned brain area and the reference electrode over the contralateral orbit [12]. This leads to subthreshold depolarization, hence promoting neural excitation [3].

  • In cathodal stimulation, the cathode (−) usually is placed over the non-lesioned brain area and the reference electrode over the contralateral orbit [12], leading to subthreshold polarization and hence inhibiting neural activity [3].

  • Dual tDCS means the simultaneous application of anodal and cathodal stimulation [13].

However, the literature does not provide clear guidelines, not only regarding the tDCS type, but also regarding the electrode configuration [14], the amount of current applied and the duration of tDCS, or the question if tDCS should be applied as a standalone therapy or in combination with other treatments, like robot-assisted therapy [15].

Rationale

There is so far conflicting evidence from systematic reviews of randomised controlled trials on the effectiveness of different tDCS approaches after stroke. For example, over the past two decades more than 30 randomised clinical trials have investigated the effects of different tDCS stimulation techniques for stroke, and there are 55 ongoing trials [16]. However, the resulting network of evidence from randomised controlled trials (RCTs) investigating different types of tDCS (i.e., anodal, cathodal or dual) as well as their comparators like sham tDCS, physical rehabilitation or pharmacological agents has not yet been analyzed in a systematic review so far.

A network meta-analysis (NMA), also known as multiple treatment comparison meta-analysis or mixed treatment comparison analysis, allows for a quantitative synthesis of the evidence network. This is made possible by combining direct evidence from head-to-head comparisons of three or more interventions within randomised trials with indirect evidence across randomised trials on the basis of a common comparator [17181920]. Network meta-analysis has many advantages over traditional pairwise meta-analysis, such as visualizing and facilitating the interpretation of the wider picture of the evidence and improving understanding of the relative merits of these different types of neuromodulation when compared to sham tDCS and/or another comparator such as exercise therapy and/or pharmacological agents [2122]. By borrowing strength from indirect evidence to gain certainty about all treatment comparisons, network meta-analysis allows comparative effects that have not been investigated directly in randomised clinical trials to be estimated and ranked [2223].

Objective

The aim of our systematic review with NMA was to give an overview of the evidence network of randomised controlled trials of tDCS (anodal, cathodal, or dual) for improving capacity in activities of daily living (ADL) and upper limb function after stroke, as well as its safety, and to estimate and rank the relative effectiveness of the different stimulation types, while taking into account potentially important treatment effect modifiers.

Continue —>  Transcranial direct current stimulation (tDCS) for improving capacity in activities and arm function after stroke: a network meta-analysis of randomised controlled trials | Journal of NeuroEngineering and Rehabilitation | Full Text

 

Fig. 1 Study flow diagram

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[WEB SITE] Types of Seizures – Epilepsy Ontario

Types of Seizures

There are several different types of seizures. Most seizures can be categorized as either focal or generalized.

1. Focal (or partial) seizures

 Focal (or partial) seizures Section

Focal (or partial) seizures occur when seizure activity is limited to a part of one brain hemisphere. There is a site, or a focus, in the brain where the seizure begins. There are two types of focal seizures:

If you have epilepsy, ask your healthcare provider to explain what type of seizures you have. Learning the names and terms for your seizure type(s) can help you describe it accurately to others.

2. Generalized Seizures

Generalized Seizures Section

Generalized seizures occur when there is widespread seizure activity in the left and right hemispheres of the brain. The different types of generalized seizures are:

Additional Seizure Types

Additional Seizure Types Section

Infantile Spasms
Infantile spasms are a type of epilepsy seizure but they do not fit into the category of focal or generalized seizures.

Psychogenic Non-epileptic Seizures (PNES)
Psychogenic non-epileptic seizures are not due to epilepsy but may look very similar to an epilepsy seizure.

Source: Types of Seizures – Epilepsy Ontario

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[ARTICLE] Post-stroke Rehabilitation Training with a Motor-Imagery-Based Brain-Computer Interface (BCI)-Controlled Hand Exoskeleton: A Randomized Controlled Multicenter Trial – Full Text

Repeated use of brain-computer interfaces (BCIs) providing contingent sensory feedback of brain activity was recently proposed as a rehabilitation approach to restore motor function after stroke or spinal cord lesions. However, there are only a few clinical studies that investigate feasibility and effectiveness of such an approach. Here we report on a placebo-controlled, multicenter clinical trial that investigated whether stroke survivors with severe upper limb (UL) paralysis benefit from 10 BCI training sessions each lasting up to 40 min. A total of 74 patients participated: median time since stroke is 8 months, 25 and 75% quartiles [3.0; 13.0]; median severity of UL paralysis is 4.5 points [0.0; 30.0] as measured by the Action Research Arm Test, ARAT, and 19.5 points [11.0; 40.0] as measured by the Fugl-Meyer Motor Assessment, FMMA. Patients in the BCI group (n = 55) performed motor imagery of opening their affected hand. Motor imagery-related brain electroencephalographic activity was translated into contingent hand exoskeleton-driven opening movements of the affected hand. In a control group (n = 19), hand exoskeleton-driven opening movements of the affected hand were independent of brain electroencephalographic activity. Evaluation of the UL clinical assessments indicated that both groups improved, but only the BCI group showed an improvement in the ARAT’s grasp score from 0 [0.0; 14.0] to 3.0 [0.0; 15.0] points (p < 0.01) and pinch scores from 0.0 [0.0; 7.0] to 1.0 [0.0; 12.0] points (p < 0.01). Upon training completion, 21.8% and 36.4% of the patients in the BCI group improved their ARAT and FMMA scores respectively. The corresponding numbers for the control group were 5.1% (ARAT) and 15.8% (FMMA). These results suggests that adding BCI control to exoskeleton-assisted physical therapy can improve post-stroke rehabilitation outcomes. Both maximum and mean values of the percentage of successfully decoded imagery-related EEG activity, were higher than chance level. A correlation between the classification accuracy and the improvement in the upper extremity function was found. An improvement of motor function was found for patients with different duration, severity and location of the stroke.

Introduction

Motor imagery (Page et al., 2001), or mental practice, attracted considerable interest as a potential neurorehabilitation technique improving motor recovery following stroke (Jackson et al., 2001). According to the Guidelines for adult stroke rehabilitation and recovery (Winstein et al., 2016), mental practice may proof beneficial as an adjunct to upper extremity rehabilitation services (Winstein et al., 2016). Several studies suggest that motor imagery can trigger neuroplasticity in ipsilesional motor cortical areas despite severe paralysis after stroke (Grosse-Wentrup et al., 2011Shih et al., 2012Mokienko et al., 2013bSoekadar et al., 2015).

The effect of motor imagery on motor function and neuroplasticity has been demonstrated in numerous neurophysiological studies in healthy subjects. Motor imagery has been shown to activate the primary motor cortex (M1) and brain structures involved in planning and control of voluntary movements (Shih et al., 2012Mokienko et al., 2013a,bFrolov et al., 2014). For example, it was shown that motor imagery of fist clenching reduces the excitation threshold of motor evoked potentials (MEP) elicited by transcranial magnetic stimulation (TMS) delivered to M1 (Mokienko et al., 2013b).

As motor imagery results in specific modulations of brain electroencephalographic (EEG) signals, e.g., sensorimotor rhythms (SMR) (Pfurtscheller and Aranibar, 1979), it can be used to voluntarily control an external device, e.g., a robot or exoskeleton using a brain-computer interface (BCI) (Nicolas-Alonso and Gomez-Gil, 2012). Such system allowing for voluntary control of an exoskeleton moving a paralyzed limb can be used as an assistive device restoring lost function (Maciejasz et al., 2014). Besides receiving visual feedback, the user receives haptic and kinesthetic feedback which is contingent upon the imagination of a specific movement.

Several BCI studies involving this type of haptic and kinesthetic feedback have demonstrated improvements in clinical parameters of post-stroke motor recovery (Ramos-Murguialday et al., 2013Ang et al., 20142015Ono et al., 2014). The number of subjects with post-stroke upper extremity paresis included in these studies was, however, relatively low [from 12 (Ono et al., 2014) to 32 (Ramos-Murguialday et al., 2013) patients]. As BCI-driven external devices, a haptic knob (Ang et al., 2014), MIT-Manus (Ang et al., 2015), or a custom-made orthotic device (Ramos-Murguialday et al., 2013Ono et al., 2014) were used. Furthermore, several other studies reported on using BCI-driven exoskeletons in patients with post-stroke hand paresis (Biryukova et al., 2016Kotov et al., 2016Mokienko et al., 2016), but these reports did not test for clinical efficacy and did not include a control group. While very promising, it still remains unclear whether BCI training is an effective tool to facilitate motor recovery after stroke or other lesions of the central nervous system (CNS) (Teo and Chew, 2014).

Here we report a randomized and controlled multicenter study investigating whether 10 sessions of BCI-controlled hand-exoskeleton active training after subacute and chronic stroke yields a better clinical outcome than 10 sessions in which hand-exoskeleton induced passive movements were not controlled by motor imagery-related modulations of brain activity. Besides assessing the effect of BCI training on clinical scores such as the ARAT and FMMA, we tested whether improvements in the upper extremity function correlates with the patient’s ability to generate motor imagery-related modulations of EEG activity.[…]

Continue —> Frontiers | Post-stroke Rehabilitation Training with a Motor-Imagery-Based Brain-Computer Interface (BCI)-Controlled Hand Exoskeleton: A Randomized Controlled Multicenter Trial | Neuroscience

 

Figure 1. The subject flow diagram from recruitment through analysis (Consolidated Standards of Reporting Trials flow diagram).

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