Does stroke location predict walk speed response to gait rehabilitation?

This is fucking pathetic that we are still asking questions like these. It means that every stroke survivor is an unregistered clinical trial of one for walking rehabilitation.  Because we have never had an objective stroke damage diagnosis.
https://ueaeprints.uea.ac.uk/55626/1/Does_Stroke_Location_Predict_Walk_Speed_Response_to_Gait_Rehabilitation.pdf
P. Simon Jones 1
, Valerie M. Pomeroy 2
, Jasmine Wang 3
, Gottfried Schlaug 3
, S. Tulasi Marrapu 1
, Sharon Geva 1
, Philip J. Rowe 4
, Elizabeth Chandler 2
,  Andrew  Kerr 4
,  Jean+Claude  Baron 1,5
,  for  the  SWIFT+Cast
investigators.
Affiliations:
1.Stroke Research Group, Dept of Clinical Neuroscienc
es, University of
Cambridge, UK
2.Acquired Brain Injury Rehabilitation Alliance, Scho
ol of Health Sciences,
University of East Anglia, Norwich, UK
3.Department of Neurology, Beth Israel Deaconess Medi
cal Center, Harvard
Medical School Boston, USA.
4.Bioengineering Unit, University of Strathclyde, Gla
sgow, UK.
5.Inserm U894, Sorbonne Paris Cité, Centre Hospitalie
r Sainte+Anne, Paris,
France
Running head: Stroke location and walking rehabilit
ation
Correspondence: 
Jean+Claude Baron
INSERM U894
2 ter rue d'Alésia
75014 Paris, France
tel: (33) (0)1 40788626 
fax: (33) (0)1 45807293 
email: jean+claude.baron@inserm.fr

Abstract
Objectives:  Recovery  of  independent  ambulation  after  stroke  is  a  major  goal.
However, which rehabilitation regimen best benefits each individual is unknown and
decisions are currently made on a subjective basis.  Predictors of response to specific
therapies would guide the type of therapy most appropriate for each patient. Although
lesion topography is a strong predictor of upper limb response, walking involves more
distributed functions.  Earlier studies that assessed the cortico+spinal tract (CST) were
negative, suggesting other structures may be important.
Experimental design: The relationship between lesion topography and response of
walking speed to standard rehabilitation was assessed in 50 adult+onset patients using
both  volumetric measurement  of  CST  lesion  load  and voxel+based  lesion+symptom
mapping (VLSM) to assess non+CST structures. Two functional mobility scales, the
Functional Ambulation Category (FAC) and the Modified Rivermead Mobility Index
(MRMI) were also administered. Performance measures were obtained both at entry
into the study (3+42 days post+stroke) and at the end of a six+week therapy. Baseline
score,  age,  time  since  stroke  onset  and  white  matter  hyperintensities  score  were
included as nuisance covariates in regression models.
Principal  observations:
CST  damage  independently  predicted  response  to therapy for FAC and MRMI, but not for Walk speed. However, using VLSM the latter  was  predicted  by  damage  to  the  putamen, insula,  external  capsule  and neighbouring white matter.
Conclusions:
Walk  speed  response  to  rehabilitation  was  affected by  damage involving the putamen and neighbouring structures but not the CST, while the latter  has  modest  but  significant  impact  on  everyday  functions  of  general mobility and gait. 

Motivating Stroke Rehabilitation Through Music: A Feasibility Study Using Digital Musical Instruments In The Home

Will this motivate your doctor and hospital to create a music stroke protocol? The evidence has been out there for years. Are they that incompetent that no research is ever applied in a clinical setting? Call the hospital president on that question, we need to get rid of the dead wood holding back stroke rehab innovation.

Motivating Stroke Rehabilitation Through Music: A Feasibility Study Using Digital Musical Instruments In The Home

Pedro Kirk1,2, Michael Grierson1, Rebeka Bodak2,3, Lauren Stewart2 Contact: mu101pk@gold.ac.uk 1Department of Computing, Goldsmiths College, University of London, United Kingdom 2Department of Psychology, Goldsmiths College, University of London, United Kingdom 3Department of Clinical Medicine, Aarhus University, Denmark  

 Aim and Hypothesis  The aim of the study was to see if active seated music making could improve upper limb function in the home environment and motivate participants to self-manage their rehabilitation.  
Hypothesis: H1: Entraining to music will motivate stroke survivors to perform exercise on their own in the home environment.  

H2: Active seated reaching activities entraining to the tempo of self-selected backing tracks will show an improvement in the stroke survivor’s physical ability and psychosocial wellbeing.     Background 
o  Every year there are a reported 15 million strokes worldwide with 5 million survivors left with severe disability (World Heart Federation, 2015).  o  Stroke survivors often receive little formal support to help with physical and psychosocial problems post hospitalization (Joice, 2012). o  Recent Research has found that music supported therapy (MST) is effective for stroke rehabilitation (Altenmüller et al., 2009; Amengual et al., 2013; Grau-Sánchez et al., 2013; Schneider et al., 2007) o  There is a lack of research studies evaluating music as a motivational aid for self-management in the home environment.

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Don't do this, your doctor wouldn't approve. This is an ad, not research.
http://healthyreport.info/?aid=2
If you haven’t already heard, Cannabidiol (CBD) is a non-psychoactive component of Cannabis that seems to have a wide range of therapeutic benefits. CBD is naturally occurring in the Hemp plant and according to the United States own government patent #6,630,507 “it supports the nutritional health of aging bodies. Cannabinoids are found to have particular application as neuroprotectants, for example in limiting neurological damage following stroke and trauma, or in the treatment of neurodegenerative diseases, such as Alzheimer’s disease and Parkinson’s disease.”

Some benefits scientists suggest people are getting from Cannabidiol (CBD)

• Reduced feelings of anxiety
• Reversing brain damage caused by alcohol
• Anti-inflammatory, neuro-protective, and anti-oxidant

We decided to see what expert medical doctors and product users had to say about Cannabidiol (CBD), and the results were surprising. In fact, Dr. Sanjay Gupta, a neurosurgeon, a medical professor and an Emmy award-winning chief medical correspondent for CNN concluded “…The science is there. This isn’t anecdotal. We have been terribly and systematically misled for nearly 70 years in the United States.”
For long term health and wellness use, CBD is one of the best ways to keep a body healthy. Studies suggest, for specific ailments, CBD may help in many ways.

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We also learned that most scientists agree that decreasing stress levels play a part in battling cancer, heart disease and other stress related illness.
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In November 2012 Tikun Olam, an Israeli medical cannabis facility, announced a new strain of the plant which has only cannabidiol as an active ingredient, and virtually no THC , providing some of the medicinal benefits of cannabis without euphoria. The Researchers said the cannabis plant, enriched with CBD, “can be used for treating diseases like rheumatoid arthritis,colitis, liver inflammation, heart disease and diabetes.” Cannabis CBD we speak about in this article, is legally derived from the hemp plant.

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Current trends in tai chi for stroke rehabilitation

I took a tai chi class once although I had to modify a lot of the upper arm movements to use the good arm to assist the bad arm into position.
http://www.sciencedirect.com/science/article/pii/S2095754815000241

• Yong Zhang^a,
• Yanzhe Ning^b,
• Hongwei Liu^b,
• Li Zhou^a,
• Yihuai Zou^b,
• Zongheng Li^{a, ,}

 Show more

doi:10.1016/j.jtcms.2014.12.001

Get rights and content

Open Access funded by Beijing University of Chinese Medicine

Under a Creative Commons license

---

Abstract

Background

There are an increasing number of studies focusing on the effect of tai chi for different diseases. As a special form of physical activity, tai chi may be beneficial for the rehabilitation of stroke, a leading cause of disability worldwide.

Objective

This review summarizes the existing literature on the potential benefits of tai chi for stroke rehabilitation and offers recommendations for future research.

Methods

Studies on the biomechanics and physiology of tai chi for stroke rehabilitation are reviewed. Research on tai chi for stroke rehabilitation and related diseases are summarized. Finally, the shortcomings of existing studies and recommendations for future studies are discussed.

Conclusions

Tai chi appears to be beneficial for stroke rehabilitation. But reporting quality of existing studies are sub-optimal. Future trials should define tai chi style, apply rigorous methodology to sample size calculation, randomization, recruiting criteria, and outcome measures. To avoid inadequacies during the research and reporting processes, investigators may wish to follow CONSORT guidelines and refer to well-conducted clinical studies on tai chi.

Sonification of arm movements in stroke rehabilitation: a novel approach in neurologic music therapy

I can't wrap my head around this so would need to see a demonstration. But really impressive for a dissertation. You can even read it in German if you want to.

Sonification of arm movements in stroke rehabilitation: a novel approach in neurologic music therapy

Stroke is one of the leading causes of disabilities worldwide, and the number of affected
patients per year and country is increasing due to the societies growing older. Rehabilitation
of stroke patients remains a challenge, although currently several new training programs are
being investigated, all aiming at an improved efficiency and sustainability of rehabilitation
effects. Some traditional rehabilitation programs lack general acceptance by patients, due to
high demands on the patients' cooperation, which sometimes may be perceived by patients as
frustrating. Yet, even the well established standard physiotherapeutical approaches do not
unambiguously provide evidence of efficacy when it comes to improvement of skilled motor
behavior. Therefore there is an urgent need for innovative, patient motivating, goal directed
and efficient training programs in stroke rehabilitation.
Sonification stands for the usage of non-speech audio conveying otherwise not audible
information. The first sonification device was the Geiger-Müller counter 
which detects electromagnetic radiation and communicates a decay by a click sound.
 In this thesis, stroke patients arm movements in a predefined three dimensional space were sonified. Sonification was then applied to develop and to incorporate musical retraining for the arm affected by the stroke.
The first  experimental study was  conducted  in order to  examine and validate the
effectiveness of a certain type of sonification for a later application in stroke rehabilitation.
To   date,   no  established   sonification-supported   rehabilitation   protocol   strategy   exists.
Therefore a computer program was developed, the “SonicPointer”, to sonify participants'
computer mouse movements in real-time with complex tones. Tone characteristics were
derived from a parameter mapping, invisible and unbeknown to the participants, which was
overlaid on the computer screen. In each trial, a target tone was presented and subjects were
2
instructed to indicate its “origin” with respect to the overlaid parameter mappings on the
screen as quickly and accurately as possible with a mouse click. Due to the participants'
ignorance of the parameter map on the screen, only implicit learning over a series of trials
led to an increase in accuracy in this task. One of the aims of the study was to find out how
sonification parameters should be mapped in space optimally. Twenty-six elderly healthy
participants were tested with this device. Generally, subjects' localizing performance was
better on the tone pitch axis as compared to the tone brightness axis. Furthermore, the
learning curves were steepest and participants were fastest when pitch was mapped onto the
vertical and brightness onto the horizontal axis, suggesting that this is the optimal
constellation for this two-dimensional sonification.
In the second experimental study presented herein we applied the previously acquired
optimal sonification mapping in a newly developed musical sonification therapy designed to
retrain gross-motor functions. Four stroke patients were included in this clinical pre-post
feasibility study and were trained with the musical sonification therapy. Patients' upper
extremity functions and their psychological states were assessed pre and post training with
numerous   standardized   motor   function   tests,   assessments   and   neuropsychological
questionnaires. The four patients were subdivided into two groups. Both groups received
nine days of musical sonification therapy (MG) or a sham sonification movement training
(CG). The only difference between the training protocols was that in the CG no sound was
played back at the patients. During the training, patients started by exploring the acoustic
effects when moving their affected arm in a predefined three-dimensional space. The training
proceeded with increasingly complex tone sequences leading to the patients playing simple
melodies only by moving their impaired arms in the 3D space. The two MG patients
improved in nearly all motor-function tests after the training. Also they reported to be less
impaired by the stroke. The two CG patients did not benefit noticeably from the movement
training.
Since the second feasibility study yielded promising results, - although with limited
statistical power,- a third clinical musical sonification therapy study was run. The setup was
basically the same as in experiment two but this time 25 stroke patients were trained and
tested. An advanced 3D analysis of the arm movement smoothness was developed and
3
included into the pre post-test battery. The 15 MG patients showed significantly reduced
joint pain in the Fugl Meyer Assessment as compared to the control-group after the musical
sonification training. They also reported a trend to have an improved hand function on the
Stroke Impact Scale.
Summarizing the results of the experiments presented in this thesis it can be concluded that
the mapping of sounds in space is crucial for the outcome and a musical sonification can be
applied   as   a   promising   stroke   rehabilitation   tool.   Of   course   the   number   of   patients
investigated   is   limited   and   further   evaluation   and   research   is   necessary.  Furthermore,
different motor tests should be included in future research in order to prevent floor and
ceiling effects.

Computerized Cognitive Rehabilitation of Attention and Executive Function in Acquired Brain Injury: A Systematic Review

Since your doctor is obviously rigorously following all stroke research s/he does not need this review on cognition. But in case s/he doesn't then you could train them on the finer points. Your doctor is really good if they are keeping up with 4931 articles. Send your doctor after what the computerized rehabilitation protocols are. 

Computerized Cognitive Rehabilitation of Attention and Executive Function in Acquired Brain Injury: A Systematic Review

(PMID:26709580)

• Abstract
• Citations
• BioEntities
• Related Articles
• External Links

Bogdanova Y, Yee MK, Ho VT, Cicerone KD

VA Boston Healthcare System, Psychology Research Service (Dr Bogdanova and Mss Yee and Ho); and Department of Psychiatry, Boston University School of Medicine (Dr Bogdanova and Ms Ho), and Boston University School of Public Health (Ms Yee), Boston, Massachusetts; Department of Neuropsychology, JFK-Johnson Rehabilitation Institute, Edison, New Jersey (Dr Cicerone); and Department of Physical Medicine and Rehabilitation, Rutgers Robert Wood Johnson Medical School, Edison, New Jersey (Dr Cicerone).

The Journal of Head Trauma Rehabilitation [2015]

Type: Journal Article

Abstract

Highlight Terms Diseases(1)

Comprehensive review of the use of computerized treatment as a rehabilitation tool for attention and executive function in adults (aged 18 years or older) who suffered an acquired brain injury.Systematic review of empirical research.Two reviewers independently assessed articles using the methodological quality criteria of Cicerone et al. Data extracted included sample size, diagnosis, intervention information, treatment schedule, assessment methods, and outcome measures.A literature review (PubMed, EMBASE, Ovid, Cochrane, PsychINFO, CINAHL) generated a total of 4931 publications. Twenty-eight studies using computerized cognitive interventions targeting attention and executive functions were included in this review. In 23 studies, significant improvements in attention and executive function subsequent to training were reported; in the remaining 5, promising trends were observed.Preliminary evidence suggests improvements in cognitive function following computerized rehabilitation for acquired brain injury populations including traumatic brain injury and stroke. Further studies are needed to address methodological issues (eg, small sample size, inadequate control groups) and to inform development of guidelines and standardized protocols.

Robert Waldinger: What makes a good life? Lessons from the longest study on happiness

It's all about relationships. If I were to look back at when I was 50 the betting would be that I won't be healthy at 80. Of course it took having a stroke to kick me out of my relationship and find happiness with friends.
http://www.ted.com/talks/robert_waldinger_what_makes_a_good_life_lessons_from_the_longest_study_on_happiness/transcript?language=en
Part of the transcript:
Once we had followed our men all the way into their 80s, we wanted to look back at them at midlife and to see if we could predict who was going to grow into a happy, healthy octogenarian and who wasn't. And when we gathered together everything we knew about them at age 50, it wasn't their middle age cholesterol levels that predicted how they were going to grow old. It was how satisfied they were in their relationships. The people who were the most satisfied in their relationships at age 50 were the healthiest at age 80. And good, close relationships seem to buffer us from some of the slings and arrows of getting old. Our most happily partnered men and women reported, in their 80s, that on the days when they had more physical pain, their mood stayed just as happy. But the people who were in unhappy relationships, on the days when they reported more physical pain, it was magnified by more emotional pain.

09:03 And the third big lesson that we learned about relationships and our health is that good relationships don't just protect our bodies, they protect our brains. It turns out that being in a securely attached relationship to another person in your 80s is protective, that the people who are in relationships where they really feel they can count on the other person in times of need, those people's memories stay sharper longer. And the people in relationships where they feel they really can't count on the other one, those are the people who experience earlier memory decline. And those good relationships, they don't have to be smooth all the time. Some of our octogenarian couples could bicker with each other day in and day out, but as long as they felt that they could really count on the other when the going got tough, those arguments didn't take a toll on their memories.

10:00 So this message, that good, close relationships are good for our health and well-being, this is wisdom that's as old as the hills. Why is this so hard to get and so easy to ignore? Well, we're human. What we'd really like is a quick fix, something we can get that'll make our lives good and keep them that way. Relationships are messy and they're complicated and the hard work of tending to family and friends, it's not sexy or glamorous. It's also lifelong. It never ends. The people in our 75-year study who were the happiest in retirement were the people who had actively worked to replace workmates with new playmates. Just like the millennials in that recent survey, many of our men when they were starting out as young adults really believed that fame and wealth and high achievement were what they needed to go after to have a good life. But over and over, over these 75 years, our study has shown that the people who fared the best were the people who leaned in to relationships, with family, with friends, with community.

Prevention of cardiovascular events with antiplatelet treatment: does time of intake matter for aspirin and ADP receptor blockers?

Do you even have a time protocol for your medicine? How long before your doctor changes that based on this research? Never? Do not make changes on your own.
http://www.ncbi.nlm.nih.gov/pubmed/26334227

Sibbing D¹, Gross L, Aradi D.

Author information

Abstract

Long-term evidence supports a clustering of cardiovascular events in the early morning. Several studies have shown that platelet hyper-reactivity to various stimuli is also present at this period of the day. However, the idea of treatment strategies reflecting the circadian variation in platelet reactivity has been largely neglected so far, and this is true despite the huge number of patients being treated with these drugs. Some pharmacodynamic data suggest that early-morning platelet hyper-reactivity may be overcome by shifting aspirin intake to the bedtime. However, there is lack of evidence whether shifting the time of intake or splitting the daily dose of P2Y12-inhibitors with a regular QD dosing (clopidogrel or prasugrel) to the evening would be effective to overcome platelet hyper-reactivity or to suppress the excess of cardiovascular events observed during morning hours. Further research is warranted to clarify whether such a simple and costless effort like dose shifting or splitting may be beneficial to prevent cardiovascular events.

KEYWORDS:

ADP receptors; antiplatelet agents; antiplatelet drugs; clinical trials; platelet pharmacology

PMID:

26334227

[PubMed - in process]

Discharge home after acute stroke: Differences between older and younger patients

Completely and totally the wrong conclusion. The solution you would have to propose is that before your stroke you get a caring and loving spouse. The goal should be 100% return to home. You haven't even identified the problem. The problem is that stroke rehab is a total fucking failure. You solve that by not having to provide very much of it. And that is by researching and creating protocols that stop the neuronal cascade of death in the first week.
http://www.ncbi.nlm.nih.gov/pubmed/26667264

Dutrieux RD¹, van Eijk M, van Mierlo ML, van Heugten CM, Visser-Meily JM, Achterberg WP.

Author information

Abstract

OBJECTIVE:

To identify determinants for discharge destination of older (≥ 70 years) and younger (< 70 years) acute stroke patients.

DESIGN:

Multicentre prospective cohort.

PATIENTS:

A total of 395 patients, within 7 days of clinically evaluated stroke, were included from 6 hospital stroke units.

METHODS:

The main outcome measure was discharge destination (home vs clinical rehabilitation). Independent variables were: demographic factors, stroke characteristics, functional impairments and disabilities, cognition, comorbidity, and premorbid social participation. Multivariate logistic regression analysis established the independent strength of the contribution of possible determinants to discharge destination.

RESULTS:

Seventy-six percent of younger patients were discharged home, compared with 63% of older patients. Most of the younger patients discharged to clinical rehabilitation (71%) had a spouse, whereas only 40% of the older age group discharged to clinical rehabilitation had a spouse. Multivariate analysis showed that, besides National Institutes of Health Stroke Scale and Barthel Index scores, having a spouse was an important determinant for discharge home in the older age group (adjusted odds ratio 4.77, 95% confidence interval 2.01-11.31), but not in the younger age group.

CONCLUSION:

The presence of a spouse is an additional important factor determining discharge home in older stroke patients. It is important to monitor and support informal caregivers in order to provide appropriate care for older community-dwelling stroke patients.

PMID:

26667264

[PubMed - as supplied by publisher]

I'm sure your doctor will never prescribe anything like this to you even though it does promote neurogenesis.

Cannabinoids promote embryonic and adult hippocampus neurogenesis and produce anxiolytic- and antidepressant-like effects

Your doctor can get some here:

Cannabis Oil (Cannabidiol CBD) without a prescription in all 50 United States.

Remember, do nothing without your doctors prescription.

 

Augmenting NMDA receptor signaling boosts experience-dependent neuroplasticity in the adult human brain

You'll have to ask your doctor how much this boosts neuroplasticity and how they are going to test d-cycloserine (DCS) in a stroke protocol to prove it works. When is it going to be available in their clinic?

1. Jennifer K. Forsyth^a,
2. Peter Bachman^b,
3. Daniel H. Mathalon^c,^d,
4. Brian J. Roach^d, and
5. Robert F. Asarnow^a,^e,¹

Author Affiliations

1. Edited by Karin Foerde, New York University, New York, NY, and accepted by the Editorial Board October 28, 2015 (received for review May 12, 2015)

1. Abstract
2. Full Text
3. Authors & Info
4. Figures
5. SI
6. Metrics
7. Related Content
8. PDF
9. PDF + SI

Significance

Experience-dependent plasticity is the capacity of the brain to undergo changes following environmental input and use, and is a primary means through which the adult brain enables new behavior. In the current study, we provide evidence that enhancing signaling at the glutamate N-methyl-d-aspartate receptor (NMDAR) can enhance the mechanism underlying many forms of experience-dependent plasticity (i.e., long-term potentiation of synaptic currents) and also enhance experience-dependent learning in healthy adult humans. This suggests exciting possibilities for manipulating plasticity in adults and has implications for treating neurological and neuropsychiatric disorders in which experience-dependent plasticity is impaired.

Abstract

Experience-dependent plasticity is a fundamental property of the brain. It is critical for everyday function, is impaired in a range of neurological and psychiatric disorders, and frequently depends on long-term potentiation (LTP). Preclinical studies suggest that augmenting N-methyl-d-aspartate receptor (NMDAR) signaling may promote experience-dependent plasticity; however, a lack of noninvasive methods has limited our ability to test this idea in humans until recently. We examined the effects of enhancing NMDAR signaling using d-cycloserine (DCS) on a recently developed LTP EEG paradigm that uses high-frequency visual stimulation (HFvS) to induce neural potentiation in visual cortex neurons, as well as on three cognitive tasks: a weather prediction task (WPT), an information integration task (IIT), and a n-back task. The WPT and IIT are learning tasks that require practice with feedback to reach optimal performance. The n-back assesses working memory. Healthy adults were randomized to receive DCS (100 mg; n = 32) or placebo (n = 33); groups were similar in IQ and demographic characteristics. Participants who received DCS showed enhanced potentiation of neural responses following repetitive HFvS, as well as enhanced performance on the WPT and IIT. Groups did not differ on the n-back. Augmenting NMDAR signaling using DCS therefore enhanced activity-dependent plasticity in human adults, as demonstrated by lasting enhancement of neural potentiation following repetitive HFvS and accelerated acquisition of two learning tasks. Results highlight the utility of considering cellular mechanisms underlying distinct cognitive functions when investigating potential cognitive enhancers.

o get
http://www.pnas.org/content/112/50/15331.abstract

1. Jennifer K. Forsyth^a,
2. Peter Bachman^b,
3. Daniel H. Mathalon^c,^d,
4. Brian J. Roach^d, and
5. Robert F. Asarnow^a,^e,¹

Author Affiliations

1. Edited by Karin Foerde, New York University, New York, NY, and accepted by the Editorial Board October 28, 2015 (received for review May 12, 2015)

1. Abstract
2. Full Text
3. Authors & Info
4. Figures
5. SI
6. Metrics
7. Related Content
8. PDF
9. PDF + SI

Significance

Experience-dependent plasticity is the capacity of the brain to undergo changes following environmental input and use, and is a primary means through which the adult brain enables new behavior. In the current study, we provide evidence that enhancing signaling at the glutamate N-methyl-d-aspartate receptor (NMDAR) can enhance the mechanism underlying many forms of experience-dependent plasticity (i.e., long-term potentiation of synaptic currents) and also enhance experience-dependent learning in healthy adult humans. This suggests exciting possibilities for manipulating plasticity in adults and has implications for treating neurological and neuropsychiatric disorders in which experience-dependent plasticity is impaired.

Abstract

Experience-dependent plasticity is a fundamental property of the brain. It is critical for everyday function, is impaired in a range of neurological and psychiatric disorders, and frequently depends on long-term potentiation (LTP). Preclinical studies suggest that augmenting N-methyl-d-aspartate receptor (NMDAR) signaling may promote experience-dependent plasticity; however, a lack of noninvasive methods has limited our ability to test this idea in humans until recently. We examined the effects of enhancing NMDAR signaling using d-cycloserine (DCS) on a recently developed LTP EEG paradigm that uses high-frequency visual stimulation (HFvS) to induce neural potentiation in visual cortex neurons, as well as on three cognitive tasks: a weather prediction task (WPT), an information integration task (IIT), and a n-back task. The WPT and IIT are learning tasks that require practice with feedback to reach optimal performance. The n-back assesses working memory. Healthy adults were randomized to receive DCS (100 mg; n = 32) or placebo (n = 33); groups were similar in IQ and demographic characteristics. Participants who received DCS showed enhanced potentiation of neural responses following repetitive HFvS, as well as enhanced performance on the WPT and IIT. Groups did not differ on the n-back. Augmenting NMDAR signaling using DCS therefore enhanced activity-dependent plasticity in human adults, as demonstrated by lasting enhancement of neural potentiation following repetitive HFvS and accelerated acquisition of two learning tasks. Results highlight the utility of considering cellular mechanisms underlying distinct cognitive functions when investigating potential cognitive enhancers.

Positron Emission Tomographic Imaging in Stroke Cross-Sectional and Follow-Up Assessment of Amyloid in Ischemic Stroke

So if there was β-amyloid accumulation in the stroke area what difference would it make if that area is dead? Or were they trying to say it was located in the penumbra? If this didn't find anything why exactly is there an increased risk of dementia/Alzheimers after a stroke?
http://stroke.ahajournals.org/content/47/1/113.full?

1. Ramesh Sahathevan, PhD;
2. Thomas Linden, PhD;
3. Victor L. Villemagne, MD;
4. Leonid Churilov, PhD;
5. John V. Ly;
6. Christopher Rowe, MD;
7. Geoffrey Donnan, MD*;
8. Amy Brodtmann, PhD*

+ Author Affiliations

1. From the Florey Institute of Neuroscience and Mental Health, Melbourne, Victoria, Australia (R.S., T.L., L.C., J.V.L., G.D., A.D.); University of Melbourne, Victoria, Australia (R.S., V.L.V., L.C., J.V.L., C.R., G.D., A.D.); Universiti Kebangsaan Malaysia Medical Centre, Bangi, Malaysia (R.S.); Gothenburg University, Gothenburg, Sweden (T.L.); and Austin Hospital PET Centre, Melbourne, Victoria, Australia (V.L.V., C.R.).

1. Correspondence to Amy Brodtmann, PhD, Florey Institute of Neuroscience and Mental Health, Melbourne Brain Centre, 245 Burgundy St, Heidelberg, Victoria 3081, Australia. E-mail agbrod@unimelb.edu.au

1. ↵* Drs Donnan and Brodtmann contributed equally.

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Abstract

Background and Purpose—Cardiovascular risk factors significantly increase the risk of developing Alzheimer disease. A possible mechanism may be via ischemic infarction–driving amyloid deposition. We conducted a study to determine the presence of β-amyloid in infarct, peri-infarct, and hemispheric areas after stroke. We hypothesized that an infarct would trigger β-amyloid deposition, with deposition over time.

Methods—Patients were recruited within 40 days of acute ischemic stroke and imaged with computed tomographic or magnetic resonance imaging and Pittsburgh compound B (11C-PiB) positron emission tomographic scans. Follow-up positron emission tomographic scanning was performed in a subgroup ≤18 months after the stroke event. Standardized uptake value ratios for regions of interest were analyzed after coregistration.

Results—Forty-seven patients were imaged with ¹¹C-PiB positron emission tomography. There was an increase in ¹¹C-PiB accumulation in the stroke area compared with a reference region in the contralesional hemisphere, which was not statistically significant (median difference in standardized uptake value ratio, 0.07 [95% confidence interval, −0.06 to 0.123]; P=0.452). There was no significant increase in the accumulation of ¹¹C-PiB in the peri-infarct region or in the ipsilesional hemisphere (median difference in standardized uptake value ratio, 0.04 [95% confidence interval, −0.02 to 0.10]; P=0.095). We repeated ¹¹C-PiB positron emission tomography in 21 patients and found a significant reduction in accumulation of ¹¹C-PiB between regions of interest (median difference in standardized uptake value ratio, −0.08 [95% confidence interval, −0.23 to −0.03]; P=0.04).

Conclusions—There was no significant increase in ¹¹C-PiB accumulation in or around the infarct. There was no increase in ipsilesional hemispheric ¹¹C-PiB accumulation over time. We found no evidence that infarction leads to sustained or increased β-amyloid deposition ≤18 months after stroke.

PowerDot Wearable Sport Muscle Stimulator

No idea if this would help us or not, so ask your therapist. A bit pricey at $129.99 or 249.99 for two.
https://www.touchofmodern.com/sales/powerdot-dcb34f8c-6593-4a65-a050-a26ff533a120?open=1&utm_source=responsys&utm_medium=email&utm_content=afternoon_email
PowerDot is the solution for any active athlete looking for new ways to work out and recover muscle mass. No matter which active sport you're involved in and whether you’re a busy amateur or a world-record holder, PowerDot can help you improve your sports performance and results. Whether it’s age, genetics or simply lack of time, your muscles can only do so much. With PowerDot, you can give your muscles that extra boost to recover faster and deliver better results for the same effort.

Researchers study neurology of balancing on two legs

If we still do not understand walking then how the hell are our therapists supposed to create a stroke walking protocol to correct our problems in walking? I'm a great example, spasticity that turns my left foot out slightly creates pain in my left foot in various spots and since there is no cure for spasticity, I'm completely screwed.
http://medicalxpress.com/news/2015-12-neurology-legs.html
Walking on two legs is inherently unstable, meaning that the human central nervous system must work hard to maintain balance. Walking motion is maintained by two control approaches—feedforward control, in which the body anticipates possible disturbances to steady walking, and feedback control, when the body reacts to an unseen disturbance to stay upright. The precise mechanisms underlying these control approaches are not yet fully understood.

To uncover variables underpinning feedback control, Tetsuro Funato at the University of Electro-Communications, Tokyo, Japan, together with scientists from Kyoto University, used a technique based on 'uncontrolled manifold analysis' (UCM) —a way of quantifying the behavior of different multi-segmental motion, how their relationships are formed and how they are used in response to disturbances.
Funato and his team gathered data from 11 healthy male participants who were asked to walk steadily on a treadmill. The researchers sped up or slowed down the treadmill abruptly, with consecutive disturbances occurring either frequently (within one walking cycle) or gradually (over a few steps).
The team were interested in the significance of 'intersegmental co-ordination' on walking control - specifically, the interaction of the thigh, shank and foot during motion phases. They compared this with fluctuations in the participants' center of mass, head and limb axis during both steady and disturbed walking.
Their UCM-based results indicated that fluctuations in intersegmental co-ordination were smaller than center of mass, head and limb axis fluctuations. This suggests intersegmental co-ordination may play a significant role in a feedback control of walking by maintaining a continuous cyclic pattern regardless of disturbances.

Explore further: Walking on an incline could help people suffering from knee problems

More information: Tetsuro Funato et al. Validating the feedback control of intersegmental coordination by fluctuation analysis of disturbed walking, Experimental Brain Research (2015). DOI: 10.1007/s00221-015-4216-x

Provided by: University of Electro Communications

Single photon emission computed tomography imaging of cerebral blood flow, blood–brain barrier disruption, and apoptosis time course after focal cerebral ischemia in rats

By following up on this in humans we should be able to calculate the numbers of neurons dying during the neuronal cascade of death in the first week. We already know that 1.9 million die per minute during the actual stroke, which leads to the mantra, 'Time is Brain'. We've known this for ten years and yet our fucking failures of stroke associations have done nothing in those ten years to solve anything in stroke. How many gazillions of dead neurons are our stroke associations responsible for killing?  If we can come up with the number dying the first week we might have a chance of actually getting researchers to solve the problem of stopping the 5 causes of neuronal death. But since we have NO stroke strategy or stroke leadership in any part of stroke no will even attempt to solve this. Your children and grandchildren are fucking screwed if they have a stroke since nothing will be done better than today.
http://wso.sagepub.com/content/11/1/117.abstract?

1. Philippe Garrigue1,2,3
2. Laura Giacomino4
3. Chiara Bucci5
4. Valeria Muzio5
5. Maria A Filannino5
6. Florence Sabatier1,6
7. Françoise Dignat-George1,7
8. Pascale Pisano1,8
9. Benjamin Guillet1,2,3⇑

1. ¹INSERM, INSERM UMR_S1076 VRCM Aix-Marseille Université, France
2. ²APHM, Hôpital La Timone, Service de Radiopharmacie, Marseille, France
3. ³CERIMED, Aix-Marseille Université, Marseille, France
4. ⁴Département Anesthésie-Réanimation adulte, APHM, Aix-Marseille Université, Marseille, France
5. ⁵Advanced Accelerator Applications, Colleretto Giacosa (TO), Italy
6. ⁶APHM, Laboratoire de Culture et Thérapie Cellulaire, INSERM, Hôpital La Conception, Marseille, France
7. ⁷APHM, Hôpital La Conception, Service d’Hématologie, Marseille, France
8. ⁸APHM, Pôle Pharmacie, Marseille, France

1. Benjamin Guillet, Faculté de Pharmacie, 27 Bd Jean Moulin, 13005 Marseille, France. Email: benjamin.guillet@univ-amu.fr

Abstract

Background Cerebral ischemia is a leading cause of disability worldwide and no other effective therapy has been validated to date than intravenous thrombolysis. In this context, many preclinical models have been developed and recent advances in preclinical imaging represent promising tools. Thus, we proposed here to characterize in vivo time profiles of cerebral blood flow, blood–brain barrier disruption and apoptosis following a transient middle cerebral artery occlusion in rats using SPECT/CT imaging.

Methods Rats underwent a 1-h middle cerebral artery occlusion followed by reperfusion. Cerebral blood flow, blood–brain barrier disruption and apoptosis were evaluated by SPECT/CT imaging using respectively ^99mTc-HMPAO, ^99mTc-DTPA and the experimental ^99mTc-Annexin V-128, up to 14 days after middle cerebral artery occlusion. Histological evaluation of apoptosis has been performed using TUNEL method to validate the ^99mTc-Annexin V-128 uptake.

Results ^99mTc-HMPAO cerebral blood flow evaluation showed hypoperfusion during occlusion, partially restored on days 4 and 7 and sustained up to 14 days after middle cerebral artery occlusion. ^99mTc-DTPA SPECT/CT showed a blood–brain barrier disruption starting on day 1 post-middle cerebral artery occlusion, peaking on day 2, with barrier integrity totally restored on day 7. ^99mTc-Annexin V-128 SPECT/CT imaging showed significant positive correlation with TUNEL immunohistochemistry and allowed ischemic-induced apoptosis to be detected from day 2 to day 7, peaking on day 3 after middle cerebral artery occlusion.

Conclusions Using SPECT/CT imaging, we showed that after transient middle cerebral artery occlusion in rat there was a sustained decrease in cerebral blood flow followed by blood–brain barrier disruption preceding meanwhile apoptosis. Rodent SPECT/CT imaging of cerebral blood flow, blood–brain barrier disruption and apoptosis appears to be an efficient tool for evaluating neuroprotective drugs and regenerative therapies against cerebral ischemia and time-windows for therapeutic intervention.

MicroTransponder developing neurostimulation technology to allow tinnitus and stroke victims to re-train their brains

Hell, vagus nerve stimulation for stroke has been known for a long time.

Earlier research on this is here July, 2012;

Nerve stimulation plus standard therapy may accelerate stroke recovery

and here Jan. 2013;

UK docs aim to `rewire` brains of stroke patients

and here - Sept. 2013;

Researchers Find Early Success in New Treatment for Stroke Recovery 

And just when the hell will the research be enough to create a stroke protocol?I bet this will still take 50 years to get rolled out because we have no stroke leadership making sure stroke medical teams are using the latest interventions. Remember you can't even suggest this to your doctor because that would be practicing medicine without a license. Whereas your doctor is probably practicing no medicine for stroke at all and has a license. Ask how your doctor will get you to 100% recovery.
http://medcitynews.com/2015/12/microtransponder-developing-neurostimulation-technology-to-treat-tinnitus-and-stroke-victims/?utm_source=MedCity+News+Subscribers&utm_campaign=0c3fc8bac8-MCN+Daily+Email&utm_medium=email&utm_term=0_5092836c41-0c3fc8bac8-408818725


Dallas-based MicroTransponder is looking to treat neurological conditions with its aired Vagus Nerve Stimulation, which is designed to help patients with tinnitus as well as stroke victims. The company, which has completed clinical studies, recently announced a $5.5 million round of funding (planned to be used to launch the product in Europe) and now have a paper published in the journal Stroke.

For the treatment of tinnitus, chronic ringing in the ears, they have developed what they call the Serenity System. For stroke victims who have upper limb mobility issues, they have created the Vivistim System.

In an interview, CEO Frank McEachern shared about the recent financing and what MicroTransponder is focused on with its technology:
Can you explain how the MicroTransponder technology actually works?
The Vagus Nerve Stimulation is a pacemaker-type device implanted in the chest. A wire reaches the left vagus nerve in the neck. That system implant generates the electrical current that stimulates the vagus nerve. That basic kind of implant has been used for a long time, but for different purposes – to treat epilepsy. It reduces seizures and has been FDA approved.
In terms of what is being implanted, this is something that is not unique, but what’s novel is when we stimulate the vagus nerve, we are taking advantage of the fact that the nerve is part of the learning system. When we stimulate the vagus nerve, it releases some neurotransmitters that makes what happens in the immediate environment important to the brain.

We get a window where we can generate importance to the brain so that we can direct learning. No one has used neurostimulation to direct learning like we have.
Can you elaborate on the issue of tinnitus and how your device really treats this condition?
Tinnitus, ringing in the ear, is not an ear problem. It’s a brain problem. What happens is there is an abnormal circuit in the brain that is hyper-active. In part of the auditory cortex, a bunch of neurons are firing together and it creates a phantom sound. What we do, is we go in and play frequencies outside of the tinnitus frequency and re-normalize that broken circuit.
Although tinnitus is an issue in the brain, originally, the insult occurs in the ear from a loud noise. Right now, it’s the number one disability for someone in the military. What’s happening is there is damage to the cochlea. Each portion of the cochlea will capture a unique feature of frequency. With certain trauma, one part can be damaged. The cochlea matches one-to-one with your auditory cortex, sending input to one part of that cortext – with damage, it doesn’t make that connection and your brain looking for information from neighboring regions.
That’s abornmal, and the result is that a large area of the cortex is communicating between itself, which is faulty. Our device is designed to re-normalize this information transference.
Is there any similarity to shock therapy in how the brain’s system reacts to this?
I wouldn’t compare it to that. Shock therapy disrupts the system, but with this it is focused on the vagus nerve to release these neurotransmitters that make the brain plastic for a temporary period so we can teach it.
Nobody has done this kind of stimulation to direct brain learning. Say you take a drug that affects the same neurotransmitters, it just floods your system which doesn’t allow the brain to make certain events important.
Beyond tinnitus, how does this work for stroke victims?
A person who has had a stroke, they do regular rehab. After a stroke, about four months later, many have recovered upper limb functions, but about half haven’t. It becomes harder to show improvement through other therapies. It’s hard to continue improvement after the first time of growth, you kind of plateau.
With this, each time a patient does a movement, they get a moment of vagus nerve stimulation. It makes the event important. These are basic motions, but the adult brain doesn’t know these functions are important. You need to make new connections, but your brain doesn’t recognize that these basic items are critical and important. They were as a child, but as an a adult, now, we can hijack the system to force these activities to be important again.

Graded Motor Imagery

This site seems quite useful to survivors.  These all should be available from your stroke team if they were any good at all. Only $20 Australian. There is a free 5 login trial on Recognise Do not do this on your own, you know how dangerous thinking is post-stroke
Three parts;
1. Left/Right Discrimination
2. Explicit motor imagery
3. Mirror therapy
http://www.gradedmotorimagery.com/index.html