Archive for May, 2017

[BLOG POST] Combating Struggles with Acquired Brain Injury

The physical, neurological and emotional challenges that may arise from an acquired brain injury (ABI) are vast. Different causes and injuries create consequences that vary among individuals. Therapists need to be perceptive in order to both address struggles and provide avenues for constructive thinking.

One of the largest hurdles therapists encounter in rehabilitation with individuals who have suffered an ABI is the patient often lacks insight into their own deficits. Their injured brain signals they are fine and can successfully perform activities they used to do before injury, when in fact they may be struggling with anything from orientation and memory to executive function. This is challenging for family members and caregivers and is also is a barrier for treatment if the patient does not come to terms with these new deficits. Although insight typically improves to some degree as the patient progresses, giving the right level and amount of explanation about what has happened and future planning is helpful.

A thorough evaluation should be completed early on to identify cognitive deficits. Once strengths and deficits are identified, treatment can begin. Include tasks to promote gains in deficit areas such as memory and attention, such as deductive and/or abstract reasoning tasks, working memory tasks or word-retrieval activities. Also think about how strengths can be utilized to assist in this processIf a patient’s reading comprehension is better than auditory comprehension, printed information should be used to improve their ability to comprehend spoken information.

Combat common struggles by demonstrating compensatory strategies that aid the individual in participating in life activities. For patients experiencing memory and organization deficits, be prepared with a list of smart phone apps and functions they can use to set alerts for appointments, manage tasks, make lists, etc.

Fatigue is common in individuals recovering from a brain injury. Their brain is working “overtime” to make sense of things, and performing tasks successfully may take a great deal of conscious thought and effort. Assist patients in creating a schedule to work on their cognitive exercises and/or stay active in doing their daily activities, and include rest to help the brain recover. Once the brain begins to fatigue, there is a decrease in function. The patient will notice activities and tasks become harder, and head pain may also occur. This should signal the patient that it’s time to rest.

Lastly, there are things the brain injury survivor can focus on that will help their recovery, including:

  • Accepting their new persona
  • Allowing themselves to make mistakes
  • Striving to keep a positive attitude
  • Remembering they can continue to improve

Continued improvements may be the most important point in keeping your patient motivated. In years past, it was commonly accepted that after a window of about three years, the brain would not have any further recovery. It is now known that neuroplasticity allows for continued recovery over time with focused effort. Different parts of the brain can establish neuropathways and take over functions lost through damage to other parts of the brain.

Area Manager Jean Herauf, SLP has 30+ years’ experience, more than 20 of them with RehabVisions. Jean is active in her clinic’s local brain injury support group and has attended numerous courses over the years, and read a good deal on ABI.

Source: Combating Struggles with Acquired Brain Injury – RehabVisions

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[WEB SITE] Neuroplasticity after Stroke

Neuroplasticity after Stroke

Neuroplasticity after stroke is the #1 thing that every stroke survivor should know about.

If you want to maximize your recovery, then understanding and applying the concept of neuroplasticity to your regimen will help you harness your brain’s full healing potential.

It’s an inspiring phenomenon, so let’s get started.

What Is Neuroplasticity?

The word neuroplasticity is the combination of 2 words: neuron and plasticity. Neurons are the nerve cells in your brain, and plasticity refers to something that is capable of being molded or reorganized.

Therefore, neuroplasticity refers to the process of reorganizing the neurons in your brain. It’s the mechanism that your brain uses to heal from damage and rewire itself.

Rewiring Your Brain after Stroke

After a stroke, certain parts of the brain can become damaged (depending on what type of stroke and where it occurred) and the functions that were once stored in those parts of the brain become impaired. For example, if the part of your brain responsible for motor control on the right side of your body becomes damaged, it will make it hard to move your right arm.

That’s when neuroplasticity comes into play.

Neuroplasticity allows your brain to rewire functions that were once held in damaged areas of the brain over to new, healthy parts of the brain. So with our right arm example, a different, healthy area of your brain is capable of picking up the slack and taking on the task of moving your right arm.

There’s one important requisite for neuroplasticity to occur, however, and it’s repetition.

You need to utilize a high number of repetitions during your rehab exercises, otherewise it won’t work that well.

How to Make Neuroplasticity Work for You

To rewire your brain after stroke, think of it as paving new roads.

If you only put a little effort in, then the new pathways won’t be that strong and they will fade with time. However, if you put a lot of effort in, you can pave a strong, durable road that will last for a long time.

The same goes with your rehab exercises.

The more you practice and repeat an exercise over and over, the stronger those new pathways in your brain become.

Neuroplasticity is nothing without good reinforcement and diligence.

One Last Bit

To really maximize your brain’s healing, you should be aware of all the other elements that go into stroke recovery.

This guide covers all the bases, we hope you find it useful.

Did you know that your brain was capable of such magic?

How will you apply this concept to your rehabilitation?

Leave us a comment below and share your thoughts with us!

Source: Neuroplasticity after Stroke – Flint Rehab

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[WEB SITE] How to PERMANENTLY Treat Post Stroke Spasticity

The Complete Guide to Treating Post Stroke Spasticity – for Good!

The Complete Guide to Treating Post Stroke Spasticity – for Good!

Post stroke spasticity is the most common post stroke side effect, and it’s likely that you’ve never heard the whole truth about it.

Most likely, you were told that there’s something wrong with your muscles, and Botox can fix it.

While this is partially true, it omits more effective and permanent solutions to spasticity.

There is tons of hope for treating spasticity – even severe spasticity in paralyzed muscles.

Today, we’re sharing the most valuable way to fix this frustrating problem.

Spasticity as Brain-Muscle Miscommunication

Before, you’ve probably heard spasticity explained in relation to your muscles.

Spasticity causes your muscles to become tightened, so it’s natural to focus on your muscles as what needs to be fixed. But spasticity is actually caused by miscommunication between your brain and your muscles.

Normally your muscles are in constant communication with your brain about how much tension they’re feeling, and the brain has to constantly monitor this tension to prevent tearing. Your brain continuously sends out messages telling your muscles when to contract and relax.

When a stroke damages part of the brain responsible for muscle control, this communication is thrown off. The damaged part of your brain no longer receives the messages that your muscles are trying to send, and as a result, your brain no longer tells them when to contract or relax.

So, your muscles keep themselves in a constant state of contraction in order to protect themselves.

That’s the cause of spasticity from the muscular perspective.

However, there’s a second layer to spasticity that no one talks about. Spasticity is also caused by miscommunication from your spinal cord.

The OTHER Cause of Spasticity

While your muscles are always in communication with your brain, they’re also in communication with your spinal cord.

Usually the spinal cord takes the messages from your muscles and sends them up to the brain. But since the brain is no longer reading those messages, your affected muscles have no one to talk to.

So the spinal cord takes over.

But the spinal cord doesn’t know how to properly operate your muscles. It really only has one goal: to prevent your muscles from tearing. In order to do that, your spinal cord sends signals to keep your muscles in a constant state of contraction, which is what causes spasticity.

Your spinal cord only has the best intentions – to prevent your muscles from tearing – but it’s frustrating because now your muscles are painfully stiff.

Let’s look at some temporary and permanent treatment options to fix this issue and alleviate your spasticity.

How to Temporarily Treat Spasticity

There are temporary ways to treat spasticity, which includes locally administered or orally taken drugs.

Locally administered drugs are injected into the affected muscles and help reduce pain, increase movement, and curb potential bone and joint problems.

Orally taken drugs offer the same benefits, but they are not site-specific and will affect all the muscles in your body.

As with most drugs in Western society, they only treat the symptom, not the underlying cause. This means that drugs are only a short-term solution.

So how can you treat the underlying cause?

With the help of your good ol’ friend neuroplasticity.

How to Permanently Reduce Spasticity

Neuroplasticity is your long-term, permanent solution to overcoming spasticity.

When a stroke damages part of the brain responsible for motor function, it decreases the number of brain cells dedicated to moving your affected limbs.

Neuroplasticity comes into play by rewiring your brain and dedicating more brain cells to controlling your affected limbs.

In order for this rewiring to occur, you have to repeat your rehab exercises over and over. The more you repeat the movement, the better the spasticity will subside and movement will improve.

It’s like paving new roads. The more you reinforce those new roads, the stronger they’ll become.

Putting in hard work is essential.

5 Ways to Activate Neuroplasticity and Treat Spasticity

If spasticity is causing you pain, then using temporary solutions in the meantime can help alleviate the barriers keeping you from your rehab exercises.

Since rehab exercise is the only permanent solution to spasticity, getting yourself to participate is crucial.

Here are 5 ways to maximize your benefit from rehab exercise and reduce spasticity:

There’s one thing these methods all have in common: Repetition.

No matter which option you choose, be sure to create an at-home rehabilitation regimen that utilizes a high number of repetitions.

You’ll get better faster this way because it’s the only way to retrain your brain to relax your spastic muscles – permanently.

3 Ways to Treat Spasticity When You Can’t Move Your Muscles

Sometimes muscles become so stiff with spasticity that it feels like they’re paralyzed.

The following 3 methods can help reduce spasticity in paralyzed muscles:

Practice these methods repetitively and you can regain movement in paralyzed muscles.

Yes, it’s possible to regain movement in paralyzed muscles! Read a success story on that here.

Then, once you’ve regained some movement, you can use any of the previous 5 methods to keep improving.

Spasticity as a Surprising Sign of Recovery

And that’s a wrap!

You are now aware that spasticity is caused by miscommunication between your brain and your muscles…

And this should bring you tons hope that your spasticity is treatable because it means that your muscles are still trying to communicate with your brain!

Your body hasn’t given up, and neither should you.

There are tons of success stories of stroke survivors who regained way more movement than doctors ever thought possible. Don’t let someone else’s limiting beliefs limit your recovery.

Even if you have no movement in your spastic muscles, keep trying by focusing on high repetition and taking small steps.

Eventually, your spasticity will start to improve – for good.

Source: How to PERMANENTLY Treat Post Stroke Spasticity – Flint Rehab

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[BLOG POST] Recognizing the Signs of PTSD After Stroke

Post-Traumatic Stress Disorder (PTSD) is a condition that runs its victims down emotionally and physically. Though most frequently linked to combat veterans and sexual-assault survivors, PTSD can present itself following any traumatic experience, and that includes medical emergencies. Following a stroke and its resulting medical treatment, it is common for patients to feel overwhelmed.


According to a study published in the journal PLoS ONE in June of 2013, almost one quarter of patients who survive a stroke will suffer from PTSD. Unfortunately, it is common for the symptoms of PTSD following a stroke to go unnoticed; due to the intense nature of physical recovery, the psychological hardship associated with it can lead to increased risk for heart disease or another stroke.


What is PTSD?

After experiencing or witnessing a traumatic event, such as a medical emergency, natural disaster, or an assault, it is difficult to adjust to everyday life again. Some people may struggle with relaxing or sleeping, have flashbacks or unsettling memories, or feel constant anxiety.

This psychological reaction is common and very frustrating. The good news is that it typically diminishes, and life returns to normal over the course of weeks or months, depending on the severity of the event. If a patient is experiencing these mental health symptoms for longer than a few weeks or months, whether constant or in waves, it is possible that they may have PTSD.


Symptoms of PTSD After Stroke

It is important to know the signs and symptoms of PTSD so that you can recognize them in a patient or loved one you are caring for after a stroke. Common symptoms of PTSD include experiencing a traumatic event over and over again, having nightmares, or being unable to stop thinking about it. To add to these extremely uncomfortable experiences, victims can also feel  general, unyielding anxiety and try to avoid reminders of the event that started their suffering. They can also be tortured with feelings of self-doubt or misplaced guilt after a stroke or other traumatic event, a state of hyperarousal, or feeling overly alert.

If you are worried that a patient or family member is suffering from PTSD, ask them questions such as:

  • Are you having nightmares?
  • How are you coping?
  • How does this make you feel?

These questions can help the patient discuss their symptoms and improve the likelihood of psychological recovery.



Transient Ischemic Attack (TIA), also known as a mini stroke, can increase the likelihood of developing PTSD because the fear of having a stroke may become overwhelming. According to a study published in the American Heart Association journal Stroke, about one third of TIA patients develop signs of PTSD. Approximately 14 percent of TIA patients also experience a drop in physical quality of life, with 6.5 percent of patients experiencing a drop in mental quality of life.


Treating PTSD

There are ways to relieve the strain of PTSD. Treatment for PTSD may include medication, psychotherapy, or both. Patients experiencing signs of PTSD should see a trained and qualified mental health professional as treatments may vary from patient to patient.


A mental health provider or psychiatrist may prescribe antidepressants to patients struggling with PTSD. Antidepressants have been shown to relieve the symptoms of anger, sadness, and overwhelming worry better than other available medications.


Sometimes referred to as “talk therapy,” psychotherapy can take place in a one-on-one capacity or in a group setting. Talk therapy is the process of speaking with a mental health professional and can encompass the discussion of PTSD symptoms alone or the effect such symptoms may be having on a patient’s life.

PTSD can sometimes wreak havoc on a person’s social, family, or professional life. To help heal the damage, a mental health professional may combine multiple forms of psychotherapy to address any and all issues a patient may be having with the aftermath of a stroke or TIA. Most often, psychotherapy lasts six to twelve weeks, but it is not unusual for it to take longer to address each patient’s symptoms and struggles. Patients are encouraged to involve family and friends in their recovery because having the extra support can improve the speed and efficiency of mental recovery from a stroke.


Finding Relief

PTSD can plague individuals who experience or witness a traumatic event. Medical emergencies are often traumatic, so it is common for survivors of stroke to suffer from PTSD; survivors of TIA can develop PTSD because they may be scared of suffering another mini stroke or of having a full-fledged stroke.

Symptoms can be very taxing on survivors and heartbreaking for their families to see. Fortunately, there are effective treatments for PTSD, including antidepressants and talk therapy with a mental health professional. If you are experiencing PTSD, it is important that you communicate how you feel with your doctor, family, and friends, as a strong support system can help you find the relief from psychological pain that you deserve.

Source: Recognizing the Signs of PTSD After Stroke | Saebo

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[ARTICLE] Non-Invasive Brain Stimulation to Enhance Upper Limb Motor Practice Poststroke: A Model for Selection of Cortical Site – Full Text

Motor practice is an essential part of upper limb motor recovery following stroke. To be effective, it must be intensive with a high number of repetitions. Despite the time and effort required, gains made from practice alone are often relatively limited, and substantial residual impairment remains. Using non-invasive brain stimulation to modulate cortical excitability prior to practice could enhance the effects of practice and provide greater returns on the investment of time and effort. However, determining which cortical area to target is not trivial. The implications of relevant conceptual frameworks such as Interhemispheric Competition and Bimodal Balance Recovery are discussed. In addition, we introduce the STAC (Structural reserve, Task Attributes, Connectivity) framework, which incorporates patient-, site-, and task-specific factors. An example is provided of how this framework can assist in selecting a cortical region to target for priming prior to reaching practice poststroke. We suggest that this expanded patient-, site-, and task-specific approach provides a useful model for guiding the development of more successful approaches to neuromodulation for enhancing motor recovery after stroke.

Poststroke Arm Impairment

Upper limb motor impairment following stroke is highly prevalent and often persists even after intensive rehabilitation efforts (14). It is also one of the most disabling of stroke sequela, limiting functional independence and precluding return to work and other roles (5).

Upper extremity motor control relies heavily on input transmitted via the corticospinal tract (CST). The CST descends through the posterior limb of the internal capsule, an area vulnerable to middle cerebral artery stroke and in which CST fibers are densely packed. Thus, even a small lesion in this location can have devastating effects on motor function (69). A loss of voluntary wrist and finger extension is particularly common and appears to be related to the extent of CST damage (10). There is also evidence that those who retain wrist extension and have considerable CST sparing are more likely to be responsive to existing therapies (7811).

However, even individuals who lack voluntary wrist and finger extension often retain some ability to move the shoulder and elbow. Unfortunately, only a few stereotyped movement patterns can be performed and these are often not functional. The combination of shoulder flexion with elbow extension that is required for most functional reaching tasks, for example, is frequently lost. Nevertheless, previous studies have demonstrated that reaching practice with trunk restraint can improve unconstrained reaching ability, even in patients who lack wrist and finger extension (1215). Still, a great deal of time and effort is required and the improvements are relatively small.

Non-Invasive Brain Stimulation

Non-invasive brain stimulation offers a potential method of enhancing the effects of practice and thus giving patients greater returns on their investment of time and effort. Approaches to non-invasive brain stimulation are rapidly expanding but generally fall into two major categories: transcranial magnetic stimulation (TMS) and transcranial electrical stimulation [TES; see Ref. (16) for overview of non-invasive techniques for neuromodulation]. These modalities are applied to the scalp overlying a specific cortical area that is being targeted. The level of spatial specificity varies depending on many factors including the modality used (TMS is generally more precise than TES), the stimulation intensity (higher intensity results in a more widespread effect), and the architecture of the underlying tissue. The excitability of the underlying pool of neurons can be modulated by varying stimulation parameters such as the frequency and temporal pattern of the stimuli. Therefore, stimulation can be used to temporarily inhibit or facilitate the underlying cortical area for a sustained period of time after the stimulation ends (usually 20–40 min). In this way, non-invasive brain stimulation could be used to “prime” relevant cortical areas before a bout of practice, potentially enhancing the effects of practice. However, there is little guidance for how such cortical sites might be selected and in which direction (inhibition or facilitation) their activity should be modulated. Conceptual models that could offer such guidance are considered below.

Mechanistic Models to Guide Neuromodulation

Continue —> Frontiers | Non-Invasive Brain Stimulation to Enhance Upper Limb Motor Practice Poststroke: A Model for Selection of Cortical Site | Neurology

Figure 1. On randomly delivered trials, transcranial magnetic stimulation (TMS) perturbation was applied just after a “Go” cue. The effect of this pre-movement perturbation on the speed of the subsequent reaching movement is expressed relative to that in trials with no TMS perturbation. The amount of slowing due to TMS perturbation of the lesioned vs. non-lesioned hemispheres is shown for patients with good structural reserve (left) and patients with poor structural reserve (right).

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[ARTICLE] Functional Electrical Stimulation with Augmented Feedback Training Improves Gait and Functional Performance in Individuals with Chronic Stroke: A Randomized Controlled Trial – Full Text PDF


Purpose: The purpose of this study was to compare the effects of the FES-gait with augmented feedback training to the FES alone on the gait and functional performance in individuals with chronic stroke.

Methods: This study used a pretest and posttest randomized control design. The subjects who signed the agreement were randomly divided into 12 experimental groups and 12 control groups. The experimental groups performed two types of augmented feedback training (knowledge of performance and knowledge of results) together with FES, and the control group performed FES on the TA and GM without augmented feedback and then walked for 30 minutes for 40 meters. Both the experimental groups and the control groups received training five times a week for four weeks.

Results: The groups that received the FES with augmented feedback training significantly showed a greater improvement in single limb support (SLS) and gait velocity than the groups that received FES alone. In addition, timed up and go (TUG) test and six minute walk test (6MWT) showed a significant improvement in the groups that received FES with augmented feedback compared to the groups that received FES alone.

Conclusion: Compared with the existing FES gait training, augmented feedback showed improvements in gait parameters, walking ability, and dynamic balance. The augmented feedback will be an important method that can provide motivation for motor learning to stroke patients.

Full Text PDF

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[ARTICLE] Update on cell therapy for stroke – Full Text


Ischaemic stroke remains a leading cause of death and disability. Current stroke treatment options aim to minimise the damage from a pending stroke during the acute stroke period using intravenous thrombolytics and endovascular thrombectomy; however, there are no currently approved treatment options for reversing neurological damage once a stroke is completed. Preclinical studies suggest that cell therapy may be safe and effective in improving functional outcomes. Several recent clinical trials have reported safety and some improvement in outcomes following cell therapy administration in ischaemic stroke, which are reviewed. Cell therapy may provide a promising new treatment for stroke reducing stroke-related disability. Further investigation is needed to determine specific effects of cell therapy and to optimise cell delivery methods, cell dosing, type of cells used, timing of delivery, infarct size and location of infarct that are likely to benefit from cell therapy.


Until recently, intravenous recombinant tissue plasminogen activator was the only proven effective treatment for acute stroke. Endovascular thrombectomy has now been added to our arsenal for acute stroke treatment following the publication of five randomised trials demonstrating highly significant treatment effects favouring endovascular therapy.1–6 Outcome data support advancements in acute stroke care and neurorehabilitation with a significant increase in stroke survivors over time.7 However, despite these advancements, stroke remains a leading cause of long-term disability.8 For patients with residual deficits after stroke, we have no currently approved therapy for restoring function.

Cell therapy is one approach to enhancing recovery after stroke. In animal models, delivery of several different types of stem cells reduce infarct size and improve functional outcomes.9 Clinical trials of cell therapy completed in the 2000s mostly treating small cohorts of patients with chronic stroke demonstrated adequate safety and a suggestion of efficacy with the use of cell therapy. Kondziolka and colleagues used N-Tera 2 cells derived from a lung metastasis of a human testicular germ cell tumour that when treated with retinoic acid generate postmitotic neurons that maintain a fetal neuronal phenotype indefinitely in vitro (LBS neurons). LBS neurons were stereotactically implanted around the stroke bed of chronic subcortical ischaemic stroke. This study demonstrated safety and feasibility of stereotactic cell implantation, although there was no significant improvement in functional outcomes.10 11 Using a similar stereotactic approach implanting cells into the basal ganglia, Savitz and colleagues transplanted LGE cells (fetal porcine striatum-derived cells, Genvec) in five patients. Two patients showed improvements, but two patients experienced adverse effects including delayed worsening of neurological symptoms and seizure resulting in early termination of the study.12 Bang and colleagues reported the safety and feasibility of intravenous infusion of autologous mesenchymal stem cells (MSCs) with no reported adverse effects in five patients treated with intravenous MSCs. Although they reported some initial motor improvements, at 12 months, there was no significant difference in motor scores.13 These early clinical trials mostly focused on chronic subcortical strokes, but more recent trials are now investigating cell therapy for treatment of both cortical and subcortical infarcts. This review discusses the considerations for design of cell therapy trials and summarises the results of more recent studies.

Continue —> Update on cell therapy for stroke | Stroke and Vascular Neurology

Table 1

Summary of recent human cell therapy trials for stroke

Clinical trial/sponsor Age Time after stroke Additional selection criteria Cell type Route Stroke location Patients (n) Safety results Efficacy results
MASTERS/Athersys 18–83 24–48 hours NIHSS 8–20, infarct 5-100cc, premorbid mRS 0–1 Multistem adult-derived stem cell product Intravenous Cortical 129 Similar SAE at 1 year 22(34%) versus 24 (39%) placebo,
Lower mortality—5 deaths (8%) versus 9deaths (15%) in placebo19
No effect on 90-day Global Stroke Recovery Assessment (mRS 0–2, NIHSS increase by 75%, Barthel Index >95) but trend towards improved outcome with earlier delivery of cells19
InveST/Department of Biotechnology, India 18–75 7–29 days NIHSS >7, GCS >8, BI <50, paretic arm or leg stable >48 hours Autologous marrow-derived stem cells Intravenous 120
(58 cell therapy)
61 AE (33%) and eight deaths versus 60 AEs (36%) and five deaths placebo22 No effect on 180-day Barthel Index Score, mRS shift or score >3, NIHSS, change of infarct volume22
RECOVER-Stroke/Aldagen 30–75 13–19 days NIHSS 7–22, mRS >3 ALDHbrautologous marrow-derived stem cells Intracarotid infusion distal to ophthalmic Anterior circulation ± subcortical 29 IA, 19 sham 12 SAE IA, 11 SAE sham; 0 cell-related SAE23 No difference in mRS, Barthel, NIHSS at 90 days or 1 year
PISCES-II/ReNeuron 40–89 2–13 months Paretic arm with NIHSS motor arm score 2–3 CTX0E03 DP allogeneic human fetal neural stem cells Stereotaxic infusion into ipsilateral putamen 21 Pending Pending
Sanbio 18–75 6–60 months NIHSS>7, mRS 3–4, stable symptoms>3 weeks SB623 allogeneic marrow-derived stem cells transiently transfected with plasmid encoding Notch122 Stereotaxic infusion peri-infarct Subcortical ± cortical component24 18 28 SAE, 0 cell-related SAE25 Improved ESS at 6 months (p<0.01) and 12 months (p<0.001)
Improved NIHSS at 6 months (p<0.01) and 12 months(p<0.001)
Improved Fugl-Meyer at 6 months (p<0.001) and 12 months(p<0.001)25
PISCES/ReNeuron >60, male only 6–60 months Persistent hemiparesis, Stable NIHSS over 4 weeks (Pt 2 CTX0E03 DP allogeneic human neural stem cells Stereotaxic infusion into putamen Subcortical 11 16 SAE (in nine patients), 0 cell-related SAE28 Improved NIHSS at 2 years (p=0.002), No change, Barthel Index, MMSE, Ashworth, mRS28 29
  • AE, Adverse Event; ARAT, Action Research Arm Test; BI, Barthel Index; DP, drug product; ESS, European Stroke Scale; IA, intra-arterially; MASTERS, Multistem Administration for Stroke Treatment and Enhanced Recovery Study; MMSE, Mini-Mental Status Examination; mRS, modified Rankin Score; NIHSS, National Institutes of Health Stroke Scale; PISCES, Pilot Investigation of Stem Cells in Stroke; SAE, Serious aAverse Events.

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[Abstract] Portable and Reconfigurable Wrist Robot Improves Hand Function for Post-Stroke Subjects  


Rehabilitation robots have become increasingly popular for stroke rehabilitation. However, the high cost of robots hampers their implementation on a large scale. This study implements the concept of a modular and reconfigurable robot, reducing its cost and size by adopting different therapeutic end effectors for different training movements using a single robot. The challenge is to increase the robot’s portability and identify appropriate kinds of modular tools and configurations. Because literature on the effectiveness of this kind of rehabilitation robot is still scarce, this paper presents the design of a portable and reconfigurable rehabilitation robot and describes its use with a group of post-stroke patients for wrist and forearm training. Seven stroke subjects received training using a reconfigurable robot for 30 sessions, lasting 30 minutes per session. Post-training, statistical analysis showed significant improvement of 3.29 points (16.20%, p = 0.027) on the Fugl-Meyer Assessment Scale for forearm and wrist components (FMA-FW). Significant improvement of active range of motion (AROM) was detected in both pronation-supination (75.59%, p = 0.018) and wrist flexion-extension (56.12%, p = 0.018) after the training. These preliminary results demonstrate that the developed reconfigurable robot could improve subjects’ wrist and forearm movement.

Source: Portable and Reconfigurable Wrist Robot Improves Hand Function for Post-Stroke Subjects – IEEE Xplore Document

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[ARTICLE] Design and test of an automated version of the modified Jebsen test of hand function using Microsoft Kinect – Full Text



The present paper describes the design and evaluation of an automated version of the Modified Jebsen Test of Hand Function (MJT) based on the Microsoft Kinect sensor.


The MJT was administered twice to 11 chronic stroke subjects with varying degrees of hand function deficits. The test times of the MJT were evaluated manually by a therapist using a stopwatch, and automatically using the Microsoft Kinect sensor. The ground truth times were assessed based on inspection of the video-recordings. The agreement between the methods was evaluated along with the test-retest performance.


The results from Bland-Altman analysis showed better agreement between the ground truth times and the automatic MJT time evaluations compared to the agreement between the ground truth times and the times estimated by the therapist. The results from the test-retest performance showed that the subjects significantly improved their performance in several subtests of the MJT, indicating a practice effect.


The results from the test showed that the Kinect can be used for automating the MJT.


Deficits in motor function, in the form of hemiparesis or hemiplegia, are a frequent consequence of cerebral stroke [1]. Even though motor function may be regained to some extent through intensive rehabilitative training following acute treatment of stroke, deficits in hand function often remain [23]. Following discharge from the rehabilitation unit, patients are typically asked to perform unsupervised self-training in their own home. The lack of supervision during training at home will likely have an impact on the patient’s training compliance and training quality. Therefore, it is important to perform regular evaluations of the patient’s functional level in order to provide useful supervision and to maintain patient motivation. The patients’ performance in a specific motor function test provides valuable insight into whether the training scheme chosen for a patient is effective or it should be changed. Thus, it is very important that the motor function tests being used are objective and reflect the actual functional level of the patient being tested. Several validated motor function tests including assessment of hand function exist, e.g. Jebsen Test of Hand Function [4], Action Research Arm Test [5], Fugl-Meyer Assessment [6], Wolf Motor Function Test (WMFT) [7], Box and Blocks Test [8] and Nine Hole Peg Test [9]. Common for all these tests is that they must be administered by a therapist, which might be a source for variability in the test results, and cause the test results not always to be completely reproducible and objective. In tests including performance time as an outcome measure, e.g. the WMFT, the reaction time of the subject could introduce a bias to the results, as suggested by previous studies [1011]. Likewise, the end time of the test would likely be subjected to a bias, since the examiner has a finite reaction time. Thus, both the reaction time of the examiner and the subject could be potential sources of bias and variability in timed motor function tests. The sensitivity of a motor function test is affected by sources of bias and variability and therefore it is of interest to minimize these, to make detection of even small changes possible.

By automating motor function tests, the objectivity of the tests would be increased. This might also make possible to use the tests at remote sites, without direct supervision, as a part of a tele-rehabilitation service. Finally, automated tests could be administered more frequently. Previous studies have shown that selected parts of the WMFT can be automated by use of motion sensors mounted on the body of healthy subjects [10] and stroke patients [11]. Both systems automated the test by analyzing three-dimensional kinematics data from body-worn sensors (inertial measurement units) mounted on the most affected wrist, arm and shoulder of stroke patients [1011]. Similarly, using inertial measurement unit sensors, Yang et al. (2013) showed that when administering the 10 m walking test, the output from their system was in close agreement with the walking speeds estimated using a stop-watch [12]. These systems require though correct positioning and mounting of the motion sensors [10]. Huang et al. (2012) showed that also a computer vision based approach, consisting of a monitor camera and a Xilinx Virtex II Pro Field Programmable Gate Array (for computation), may be used for automating the WMFT. All participants being tested had to wear a black sweatband on the wrist of the extremity being tested [13]. Another low-price method for capturing the movements of a patient performing a motor function test is the Microsoft Kinect sensor (Kinect). By using a Kinect, the need for body mounted sensors is eliminated, thus lowering the susceptibility to data loss and easing donning and doffing of the system. Furthermore, the Microsoft Kinect sensor is a low-cost commercially available device. In this paper, we describe the design and test of a Kinect based system for automatic evaluation of a standardized, validated motor function test, administered to stroke patients with hand function deficits. The Modified Jebsen Test of Hand Function (MJT) [14], initially proposed by Bovend’Eerdt et al. (2004) as a test for assessment of gross functional dexterity in stroke patients, was selected for automation as this test is easy to administer and takes short time to complete.

Continue —> Design and test of an automated version of the modified Jebsen test of hand function using Microsoft Kinect | Journal of NeuroEngineering and Rehabilitation | Full Text

Fig. 3 The edge of the table was detected in the binary image (lower) produced by thresholding the depth image (upper) into two parts, one part containing all pixels with a depth value lower than a depth level of 300 mm below the surface of the table and the other part containing pixels with depth values above this threshold

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[ARTICLE] Neurofeedback as a form of cognitive rehabilitation therapy following stroke: A systematic review – Full Text

Neurofeedback therapy (NFT) has been used within a number of populations however it has not been applied or thoroughly examined as a form of cognitive rehabilitation within a stroke population.

Objectives for this systematic review included:

  • i) identifying how NFT is utilized to treat cognitive deficits following stroke,
  • ii) examining the strength and quality of evidence to support the use of NFT as a form of cognitive rehabilitation therapy (CRT) and
  • iii) providing recommendations for future investigations.

Searches were conducted using OVID (Medline, Health Star, Embase + Embase Classic) and PubMed databases. Additional searches were completed using the Cochrane Reviews library database, Google Scholar, the University of Toronto online library catalogue, website and select journals. Searches were completed Feb/March 2015 and updated in June/July/Aug 2015. Eight studies were eligible for inclusion in this review.

Studies were eligible for inclusion if they:

  • i) were specific to a stroke population,
  • ii) delivered CRT via a NFT protocol,
  • iii) included participants who were affected by a cognitive deficit(s) following stroke (i.e. memory loss, loss of executive function, speech impairment etc.).

NFT protocols were highly specific and varied within each study. The majority of studies identified improvements in participant cognitive deficits following the initiation of therapy. Reviewers assessed study quality using the Downs and Black Checklist for Measuring Study Quality tool; limited study quality and strength of evidence restricted generalizability of conclusions regarding the use of this therapy to the greater stroke population.

Progression in this field requires further inquiry to strengthen methodology quality and study design. Future investigations should aim to standardize NFT protocols in an effort to understand the dose-response relationship between NFT and improvements in functional outcome. Future investigations should also place a large emphasis on long-term participant follow-up.


In 2011, stroke was identified as the third leading cause of death among Canadians (5.5%, 13 283 deaths), and considered to be the leading cause of neurological disability in Canadian adults [12]. Although stroke occurrence is most common in individuals aged 70 and older, stroke incidence for individuals over the age of 50 has increased by 24% and 13% in individuals over the age of 60, in the last decade [3]. Following a stroke, patients typically enter rehabilitation programs (i.e. physical therapy, occupational therapy, etc.) to address a multitude of physical, emotional and cognitive deficits [45]. Many rehabilitation interventions initiated following stroke primarily target functional motor impairments. In reviewing the literature, few investigations have been published that aim to target cognitive deficits, despite 40% of stroke survivors experiencing a decline in cognitive function (especially memory) following stroke [6].

The brain is a highly complex and organized organ therefore the extent of impairment and deficits that follow stroke are largely dependent on lesion severity and location [7]. Physiologically these impairments are a result of the loss of neuronal circuits and connections linked to the relevant sensory, motor, and cognitive functions [89]. Furthermore, it is thought that the neurological recovery that occurs following a stroke is a direct result of brain plasticity and it’s ability to repair and reorganize [10]. Some evidence exists for the initiation of reparative functions in the brain in as little as a few hours following a stroke [1112]. In respect to recovery trajectories following stroke, ninety-five percent of stroke patients reach their peak language recovery within 6 weeks of a stroke, and within 3 months for hemispatial neglect [1314]. Deficits that do not spontaneously resolve contribute to the large number of individuals requiring long term care following stroke (i.e. rehabilitative therapy) [1516]. Occupational and physical rehabilitation programs target functional and mobility issues however, in addition to these impairments patients experience a wide range of cognitive and neurological deficits. Individuals with impairments of this nature often require cognitive rehabilitation therapy (CRT).

CRT encompasses any intervention targeting the restoration, remediation and adaptation of cognitive functions including: attention, concentration, memory, comprehension, communication, reasoning, problem solving, planning, initiation, judgement, self-monitoring and awareness [17]. CRT can be offered in a variety of settings such as rehabilitation hospitals, community care facilities, private residences as well as the workplace [18]. Although cognitive therapy has been around since the early 19th century, the 1970’s marked the most recent biofeedback movement in CRT [18]. Traditionally used to treat muscular impairments (via electromyography (EMG) feedback) biofeedback has taken on a new form known as neurofeedback therapy (NFT). NFT targets the brain and cognitive functions through the use of electroencephalography (EEG), hence neurofeedback is sometimes referred to as EEG biofeedback [19]. In classical NFT, EEG and brainwave activity is provided as a visual or auditory cue to the user [6]. Using these cues the user can consciously adapt their brainwave activity to reach targeted training thresholds. NFT relies on operant conditioning to stimulate the neuroplastic abilities of the brain [2021]. Physiologically stimulating specific band frequencies over damaged areas stimulates cortical metabolism [19]. NFT is also used to counter excessive slow wave activity (i.e. theta waves and sometimes alpha waves) that typically follow stroke [21]. An alternative form of NFT known as nonlinear dynamical neurofeedback has also been used to restore homeostasis to the brain. This form of NFT requires no conscious effort from the participant to adapt their brainwaves in any particular direction (i.e. the participant maintains a passive role). Modalities like NeurOptimal® utilize Functional Targeting to provide the brain with “… information about itself which allows the brain to assemble it’s own, best organizing strategies moment by moment” [22]. In the context of this review, the studies included herein concern the use of classical NFT only.

To date, NFT has been used extensively to treat cognitive deficits associated with other neurological disorders and illnesses including: mild traumatic brain injury [23], ADD/ADHD [24], Epilepsy [25], Autism Spectrum Disorders [2627], Dyslexia [28], Fibromyalgia [29], Depression [30], and opiate additions [31]. Despite promising NFT outcomes within these populations, NFT has not been thoroughly evaluated for use in a stroke population. The aim of this systematic review was to thoroughly evaluate the available evidence pertinent to understanding the effectiveness of NFT as a form of CRT following stroke. To achieve this objective a number of research questions were established to guide this review:

  1. Among a stroke population, how is NFT utilized to treat cognitive deficits?
  2. Among identified NFT interventions targeting a stroke population, what is the quality and strength of evidence to support the use of NFT as a form of CRT following stroke?
  3. Based on the available NFT evidence for use in stroke populations, what recommendations can be made for future research?


The primary outcome of interest in this review was to identify if cognitive symptom complaints could be ameliorated following the initiation of NFT in a sub-acute and chronic post-stroke population. Secondary outcomes aimed to assess study quality, methodology and strength of support for use of NFT in this population.

Continue —> Neurofeedback as a form of cognitive rehabilitation therapy following stroke: A systematic review

Fig 1. PRISMA flow diagram.

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