Effect of Exercise on Neurodegeneration in Neurological Disorders

Demand your doctor find out exactly how much exercise you should be getting. You do want to not be in the 33% of stroke survivors that get dementia.
http://link.springer.com/chapter/10.1007/978-3-319-04111-7_5

• Akhlaq A. Farooqui

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Abstract

Exercise induces neuroprotection not only by increasing blood flow throughout the brain, elevating levels of neurotrophins and neurotransmitters, inducing neurogenesis in the hippocampus, and increasing neuroplasticity, but also by decreasing brain atrophy, reducing neuroinflammation, and oxidative stress. Molecular mechanisms and signal transduction pathways by which exercise exerts its beneficial effects are not fully understood. However, it is becoming increasingly evident that exercise upregulates the expression of BDNF, a growth factor, which promotes synaptic plasticity and cognition. In addition, physical activity reduces blood pressure, obesity, and type II diabetes, which are risk factors for stroke, AD, PD, and depression. In animal models of stroke, AD, PD, and depression, exercise produces beneficial effect by reducing levels of proinflammatory lipid mediators and retarding the accumulation of abnormal proteins, such as β-amyloid in animal models of AD and α-synuculin in animal models of PD.

Social interaction plays a critical role in neurogenesis and recovery after stroke

So everyone should move to a new location immediately after their stroke with no friends or relatives around. Instead of waiting for 6 years to move I should have done it immediately. Same as the environmental enrichment that is proven to be good for you. But do you really think your doctors are going to do something cheap and smart like this?
http://www.nature.com/tp/journal/v4/n1/abs/tp2013128a.html

V R Venna¹, Y Xu¹, S J Doran¹, A Patrizz¹ and L D McCullough^1,2,3

1. ¹Department of Neuroscience, University of Connecticut Health Center, Farmington, CT, USA
2. ²Department of Neurology, University of Connecticut Health Center, Farmington, CT, USA
3. ³The Stroke Center at Hartford Hospital, Hartford, CT, USA

Correspondence: Dr LD McCullough, Department of Neuroscience, University of Connecticut Health Center, 263 Farmington Avenue, Farmington, CT 06030, USA. E-mail: lmccullough@uchc.edu

Received 13 September 2013; Revised 25 November 2013; Accepted 7 December 2013

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Abstract

Stroke survivors often experience social isolation. Social interaction improves quality of life and decreases mortality after stroke. Male mice (20–25 g; C57BL/6N), all initially pair housed, were subjected to middle cerebral artery occlusion (MCAO). Mice were subsequently assigned into one of three housing conditions: (1) Isolated (SI); (2) Paired with their original cage mate who was also subjected to stroke (stroke partner (PH-SP)); or (3) Paired with their original cage mate who underwent sham surgery (healthy partner (PH-HP)). Infarct analysis was performed 72 h after stroke and chronic survival was assessed at day 30. Immediate post-stroke isolation led to a significant increase in infarct size and mortality. Interestingly, mice paired with a healthy partner had significantly lower mortality than mice paired with a stroke partner, despite equivalent infarct damage. To control for changes in infarct size induced by immediate post-stroke isolation, additional cohorts were assessed that remained pair housed for three days after stroke prior to randomization. Levels of brain-derived neurotrophic factor (BDNF) were assessed at 90 days and cell proliferation (in cohorts injected with 5-bromo-2′-deoxyuridine, BrdU) was evaluated at 8 and 90 days after stroke. All mice in the delayed housing protocol had equivalent infarct volumes (SI, PH-HP and PH-SP). Mice paired with a healthy partner showed enhanced behavioral recovery compared with either isolated mice or mice paired with a stroke partner. Behavioral improvements paralleled changes in BDNF levels and neurogenesis. These findings suggest that the social environment has an important role in recovery after ischemic brain injury.

The remarkable impact of yoga breathing for trauma

More proof for you Amy. From the Stanford School of Medicine. You'll have to read and follow the links at the site. See what your doctor is doing about the psychological trauma you have from your stroke.
http://scopeblog.stanford.edu/2014/01/31/the-remarkable-impact-of-yoga-breathing-for-trauma/

The remarkable impact of yoga breathing for trauma

The remarkable impact of yoga breathing for trauma

Vibrostimulation in Bobsleigh

Will this work in stroke rehab?  What does your doctor have to say on vibration in general?
These other possibilities can be used by your doctor to analyze whether this will be useful in your stroke rehab.
1. Effects of whole-body vibration on muscle architecture, muscle strength, and balance in stroke: A randomized controlled trial
2. Vibrating Glove May Enhance Sense of Touch
3. No specific effect of whole-body vibration training in chronic stroke: a double-blind randomized controlled study.
4. Efficacy of whole body vibration exercise in older people: a systematic review
5. Quicker and easier rehabilitation following a stroke - vibration
6. Vibration and stroke rehab
I really don't give a crap, I believe it is necessary for extra sensation and balance.
Its why I got this for my fingers.

7-speed Secret Love Finger Fun Vibator Vibration Massager with Sexy Dice

And the cool bobsled one here;
http://www.lspa.eu/files/research/Journal_of_Sport_Science/zurnals_2011_2.4-12.pdf

Ugis Ciematnieks1, Nauris Keizans1,

Sandis Prusis2, Leonids Cupriks1

1Latvian Academy of Sport Education,

Brivibas str. 333, Riga, LV 1006, Latvia

Phone: +371 67543410, fax. +371 67543480

E-mail: smagatletika@lspa.lv

2Latvian Bobsleigh Federation,

Annas Sakses str. 19, Riga, LV 1014, Latvia

Phone: +371 7517373, fax. +371 7517374

E-mail: latbob@parks.lv

Abstract

Foreign literature contents studies about the general effects of

vibrostimulation on the human work capacity, so we had an interest in local

vibrostimulations application possibilities in the Olympic kind of sport -

bobsleigh. Aim of study was to determine how local vibrostimulation can be

used in bobsleigh and whether it is appropriate. As main methods we used

method of test exercise, vibrostimulation, pedagogical experiment and

method of questionnaire. Study took place in Ventspils Olympic Sports

Center, Latvian bobsleigh team training camp during the sample period

from 12th to 17th July. The study subjects was 26±2 years old, average

weight 99±3kg, their experience aim a high performance sports training

process an average of 6 years (including bobsleigh), n = 10. During all the

camp the athletes took the test exercises - bobsleigh push from standing

position and bobsleigh push from run. In addition we interviewed athletes'

group, which took procedures of vibrostimulation to determine the muscle

senses during and after vibration, as well as areas where the vibration should

not be applied. Processing the experimental results we found that in

bobsleigh push from standing position the mean results of experimental

group remained worse. In bobsleigh push from run results of both groups

deteriorated by 0.02sec (p> 0.05). Comparing the groups the difference was

not reliable at the beginning of the experiment, at the end of the experiment

(tt> te). Processing results of questionnaire found that the athletes feel very

unpleasant during and after vibrostimulation of calves muscle tendons (four

respondents), quadriceps and calves muscle vibrostimulation (three

respondents). Athletes mentioned the fact that just after vibrostimulation

seen quite a feeling of lightness in leg musculature.

 

VIBROSTIMULATION IN BOBSLEIGH’

Real-Time Video Feedback Could Improve Effect of Core Stabilization Exercise in Stroke Patients

Is this enough for your doctor and therapist to add to your stroke protocols?
http://www.alphagalileo.org/ViewItem.aspx?ItemId=138561&CultureCode=en
According to Study Published in Restorative Neurology and Neuroscience
Amsterdam, NL, January 30, 2014 – About 80% of stroke survivors experience hemiparesis, which causes weakness or the inability to move one side of the body. Core stabilization exercise to improve postural stability and independent walking in chronic hemiparetic stroke patients could be enhanced by real-time video feedback, report researchers in Restorative Neurology and Neuroscience.
Stroke is the most common cause of permanent disability in adults. Stroke patients generally show muscle weakness of limbs and trunk on the affected side. Walking performance is often affected by muscle weakness, spasticity, contracture, pain, sensory and visual impairments, and postural instability. One of the main goals of stroke rehabilitation programs is to improve posture and help patients to walk independently and safely. Core stability exercise has been used with success in athletes and orthopedic patients with lower back pain and has also been reported to improve trunk stability in stroke patients, which is essential for balance and extremity use during daily functional activities and higher level tasks.
Researchers hypothesized that that the effects of core stabilization exercise in stroke patients could be enhanced by augmented, or real-time, video feedback. Augmented feedback can provide information to patients regarding their problems while they are performing functional activities by themselves because it contains information on the nature or quality of the movement during performance and includes identification of the correct and incorrect parts of the function activities.
“The augmented reality system provided by video feedback using a computer in a simulator is a powerful mode of augmented feedback. It is delivered to the patient online in a computer-aided instruction program. The system provides real-time feedback as well as a record of the entire performance. The patient can therefore detect errors directly and attempt to correct them on the next trial. However, there is little research on the effect of real-time feedback on postural stability in individuals with chronic hemiparetic stroke during the core stabilization exercises,” explains co-author Byoung-Hee Lee, PT, PhD, of the Department of Physical Therapy, College of Health Welfare, Sahmyook University, Republic of Korea.
This study examined the feasibility of real-time feedback on postural stability and gait performance during core stabilization exercise in 19 patients, who had been diagnosed with chronic hemiparetic stroke six months or more before the study. Importantly, core stabilization exercise minimizes the risks of falls and improves safety during training, critical considerations when working with stroke patients. All of the patients had sufficient cognitive ability to take part in the study and could walk independently with or without a walking aid for at least 15 minutes.
Participants were randomly assigned to an experimental group or a control group. Both groups met three times per week for 30 minutes over six weeks. The participants in the experimental group were provided real-time feedback during core stabilization exercises (bed, wedge, and ball exercises), and those in the control group performed core stabilization exercises without real-time feedback. Balance and gait performance of all participants was assessed before and after the training.
Prior to the six-week period, the control group performed better than the experimental group, but by the end of the period both the gait velocity (walking speed) and stride length showed significantly greater improvement in the experimental group than in the control group. Both groups were also trained on a timed up and go (TUG) test. After training, TUG test improvement was significantly greater in the experimental group compared to the control group.
Lee points out that, “Despite the small number of patients studied, the results clearly demonstrated that real-time feedback enhanced the results achieved through core stabilization exercise training because patients gained a better understanding of the movements as they were performing them. This study represents a step forward in the development of clinical treatment programs that can contribute to recovery of function,” he concludes.

• Full bibliographic information“Core Stabilization Exercise with Real-time Feedback for Chronic Hemiparetic Stroke: A Pilot Randomized Controlled Trial,” by Eunjung Chung, PT, PhD, Byoung-Hee Lee, PT, PhD, and Sujin Hwang, PT, PhD. Restorative Neurology and Neuroscience, DOI http://dx.doi.org/10.3233/RNN-130353. Published by IOS Press online ahead of issue.

Brain function 'boosted for days after reading a novel'

My god, if your doctor and hospital can't afford a book and use this for improved brain function after your stroke, then they are idiots.
http://www.independent.co.uk/news/science/brain-function-boosted-for-days-after-reading-a-novel-9028302.html

Recognising neuroplasticity in musculoskeletal rehabilitation: a basis for greater collaboration between musculoskeletal and neurological physiotherapists

Ask your doctor to find out exactly what strategies will help. They should easily be able to contact the authors on your behalf.
http://www.sciencedirect.com/science/article/pii/S1356689X14000071

• Suzanne J. Snodgrass^, ,
• Nicola R. Heneghan,
• Henry Tsao,
• Peter Stanwell,
• Darren A. Rivett,
• Paulette M. van Vliet

• Discipline of Physiotherapy, School of Health Sciences, The University of Newcastle, Hunter Building, Callaghan, NSW 2308, Australia

Choose an option to locate/access this article:

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Purchase $35.95

• 

---

Abstract

Evidence is emerging for central nervous system (CNS) changes in the presence of musculoskeletal dysfunction and pain. Motor control exercises, and potentially manual therapy, can induce changes in the CNS, yet the focus in musculoskeletal physiotherapy practice is conventionally on movement impairments with less consideration of intervention-induced neuroplastic changes. Studies in healthy individuals and those with neurological dysfunction provide examples of strategies that may also be used to enhance neuroplasticity during the rehabilitation of individuals with musculoskeletal dysfunction, improving the effectiveness of interventions. In this paper, the evidence for neuroplastic changes in patients with musculoskeletal conditions is discussed. The authors compare and contrast neurological and musculoskeletal physiotherapy clinical paradigms in the context of the motor learning principles of experience-dependent plasticity: part and whole practice, repetition, task-specificity and feedback that induces an external focus of attention in the learner. It is proposed that increased collaboration between neurological and musculoskeletal physiotherapists and researchers will facilitate new discoveries on the neurophysiological mechanisms underpinning sensorimotor changes in patients with musculoskeletal dysfunction. This may lead to greater integration of strategies to enhance neuroplasticity in patients treated in musculoskeletal physiotherapy practice.

Hospital wins national award for stroke care - Houston Methodist Sugar Land

What a pile of crap. If you can't provide real information like 30-day deaths and 100% recovery statistics, you just buffalo them with bullshit meaningless statistics. You could meet all these processes and still have a 100% death rate and be praised for that. Totally wrong thing to measure.
Big Whoopee.
http://www.fbherald.com/health/article_63c48900-892b-11e3-98cb-0019bb2963f4.html 

Houston Methodist Sugar Land Hospital has received the American Heart Association and American Stroke Association’s “Get With The Guidelines“ Stroke Gold Plus Quality Achievement Award.
The award recognizes the hospital’s standards for stroke care by following nationally accepted standards and recommendations.
“With a stroke, time lost is brain lost, and the (award) demonstrates Houston Methodist Sugar Land Hospital’s commitment to being one of the top hospitals in the country for providing aggressive, proven stroke care and addressing the important element of time,” said Dr. James Ling, medical director of the stroke program.
The hospital’s system for diagnosis and treatment of stroke patients admitted to the emergency department includes always being equipped to provide brain imaging scans, having neurologists available to conduct patient evaluations, and using clot-busting medications when appropriate.
The hospital also received the association’s “Target: Stroke Honor Roll” for improving stroke care.
It is “commended for its commitment to implementing standards of care and protocols for treating stroke patients,” said Dr. Lee Schwamm, chair of the Get With The Guidelines National Steering Committee. “The full implementation of acute care and secondary prevention recommendations and guidelines is a critical step in saving the lives and improving outcomes of stroke patients.”
The hospital said the award comes at a time of growing need.
“The number of acute ischemic stroke patients eligible for treatment is expected to grow over the next decade due to increasing stroke incidence and a large aging population,” said Janet Leatherwood, chief nursing officer.
Stroke is one of the leading causes of death and serious, long-term disability in the United States, according to the American Heart Association/American Stroke Association.
On average, someone suffers a stroke every 40 seconds, someone dies of a stroke every four minutes and 795,000 people suffer a new or recurrent stroke each year.

Slow reaction time linked with early death

Our researchers should be able to easily replicate this study in stroke survivors to see if the same results occur. Then you could ask your doctor what can be done to speed up your reaction time. And after you pick yourself up off the floor from laughing at the answer you can go home and google your own answer.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=138413&CultureCode=en
Having a slow reaction time in midlife increases risk of having died 15 years later, according to new research published in the journal PLOS ONE.
 Researchers from UCL and the University of Edinburgh looked at data from more than 5,000 participants (age 20 to 59) collected from the Third National Health and Nutrition Examination Survey (NHANES-III) in the US. At the start of the study in 1990s, participants visited an examination centre and had their reaction times measured. The task was very simple – they had to press a button when they saw an image appear on a computer screen. Over the next 15 years, they were followed to record who had died and who survived.
A total of 378 (7.4%) people in the sample died, but those with slower reaction times were 25% more likely to have died (from any cause) compared to those with average reaction times. This remained the case after the researchers had accounted for the participants’ age, sex, ethnic group, socio-economic background and lifestyle factors into account. There was no relationship between reaction time and death from cancer or respiratory problems.
Lead researcher Dr Gareth Hagger-Johnson, from the UCL Department of Epidemiology and Public Health, said: “Reaction time is thought to reflect a basic aspect of the central nervous system and speed of information processing is considered a basic cognitive ability (mental skill). Our research shows that a simple test of reaction time in adulthood can predict survival, independently of age, sex, ethnic group and socio-economic background. Reaction time may indicate how well our central nervous and other systems in the body are working. People who are consistently slow to respond to new information may go on to experience problems that increase their risk of early death. In the future, we may be able to use reaction times to monitor health and survival. For now, a healthy lifestyle is the best thing people can do in order to live longer”.

• Full bibliographic informationThe paper, "Reaction time and mortality from the major causes of death: The NHANES-III study”, will be published in the journal PLOS ONE on January 29th (5pm EST).

Low Levels of Pro-inflammatory Agent Help Cognition in Rats

I would expect this to be a great line of stroke research but there is no great stroke association to ask if this is being researched in humans. We just may never know the answer to such a simple question.
http://www.biosciencetechnology.com/news/2014/01/low-levels-pro-inflammatory-agent-help-cognition-rats?#.UulmfhDljXY
Although inflammation is frequently a cause of disease in the body, research from The University of Texas Health Science Center at San Antonio indicates that low levels of a pro-inflammatory cytokine in the brain are important for cognition. Cytokines are proteins produced by the immune system.
Jennifer Donegan, graduate student, and David Morilak, PhD, professor of pharmacology in the School of Medicine, found that neutralizing the cytokine interleukin-6 in the brain impaired reversal learning in both stressed and nonstressed rats. Reversal learning is a form of cognitive flexibility that is diminished in psychiatric diseases such as depression, schizophrenia and post-traumatic stress disorder. Cognitive flexibility is the ability to change previously learned thoughts and behaviors in response to changes in the environment.
“When we started the project, we thought cognitive flexibility would be impaired by stress-induced inflammation in a region of the brain called the prefrontal cortex,” Donegan said. “We decided to block interleukin-6 during stress to prevent the cognitive deficit, and to our surprise this made things worse. This suggested that it may actually be beneficial to maintain a low level of this pro-inflammatory cytokine in the brain.”
As a key next step, the scientists were then able to fix the cognitive deficit caused by stress by restoring a low level of the cytokine specifically in the prefrontal cortex. Both scientists caution, however, that there is still much to learn about interleukin-6’s role in cognition and in diseases like depression. “We’ve replicated just one piece of a very complex disease so we can understand the biology,” Dr. Morilak said. “We found that, in one brain region, one cytokine facilitates cognitive flexibility and is beneficial after chronic stress. But we delivered the cytokine specifically into that brain region using a virus, which we cannot do in people. And its role in inflammation may be very different than in normal conditions. There’s still a lot of work to do.”
Source: University of Texas Health Science Center at San Antonio

Another presentation by Dean - Dementia prevention

I have fun at these, especially when I show them my abnormal brain scan as compared to normal ones. Gasps usually occur.
A Cafe Scientifique presentation.
http://www.lcc.edu/science/cafe_scientifique.aspx

Dementia Prevention - Why should you care and what to do about it.

Schuler Books - Eastwood Towne Center, Lansing,MI
Tuesday, February 18, 2014 - 7:00 p.m.
One in three seniors die with dementia or Alzheimer's.  Dean Reinke, our presenter, is a mainframe programmer, with no medical training.  He learned about the brain, because 7 years ago he had a massive stroke.  Strokies have a 33% chance of getting dementia/Alzheimers and he was determined that that was not going to happen to him.  He writes the Deans' Stroke Musings blog, which is the most popular stroke blog on the net.  Everything he will talk about is documented on the blog, with links to the relevant research articles.  He has written 107 posts on Alzheimers and 65 on dementia.


I will be comparing and contrasting my ideas with Harvard Medical School and generic prevention ideas.

Environmental enrichment extends ocular dominance plasticity into adulthood and protects from stroke-induced impairments of plasticity

This sounds exactly like what Dr. Dale Corbett was proposing in 2011. Maybe now stroke hospitals will do something about it if YOU tell them about this type of research.

Environmental enrichment extends ocular dominance plasticity into adulthood and protects from stroke-induced impairments of plasticity

1. Franziska Greifzu^a,
2. Justyna Pielecka-Fortuna^a,
3. Evgenia Kalogeraki^a,
4. Katja Krempler^b,¹,
5. Plinio D. Favaro^c,
6. Oliver M. Schlüter^c, and
7. Siegrid Löwel^a,²

Author Affiliations

1. Edited* by Michael P. Stryker, University of California, San Francisco, CA, and approved November 27, 2013 (received for review July 18, 2013)

Abstract

Ocular dominance (OD) plasticity in mouse primary visual cortex (V1) declines during postnatal development and is absent beyond postnatal day 110 if mice are raised in standard cages (SCs). An enriched environment (EE) promotes OD plasticity in adult rats. Here, we explored cellular mechanisms of EE in mouse V1 and the therapeutic potential of EE to prevent impairments of plasticity after a cortical stroke. Using in vivo optical imaging, we observed that monocular deprivation in adult EE mice (i) caused a very strong OD plasticity previously only observed in 4-wk-old animals, (ii) restored already lost OD plasticity in adult SC-raised mice, and (iii) preserved OD plasticity after a stroke in the primary somatosensory cortex. Using patch-clamp electrophysiology in vitro, we also show that (iv) local inhibition was significantly reduced in V1 slices of adult EE mice and (v) the GABA/AMPA ratio was like that in 4-wk-old SC-raised animals. These observations were corroborated by in vivo analyses showing that diazepam treatment significantly reduced the OD shift of EE mice after monocular deprivation. Taken together, EE extended the sensitive phase for OD plasticity into late adulthood, rejuvenated V1 after 4 mo of SC-rearing, and protected adult mice from stroke-induced impairments of cortical plasticity. The EE effect was mediated most likely by preserving low juvenile levels of inhibition into adulthood, which potentially promoted adaptive changes in cortical circuits.

Ocular dominance (OD) plasticity induced by monocular deprivation (MD) is one of the best studied models of experience-dependent plasticity in the mammalian cortex (1, 2). OD plasticity in primary visual cortex (V1) of C57BL/6J mice is maximal at 4 wk of age, declines after 2–3 mo, and is absent beyond postnatal day 110 (PD110) if animals are raised in standard cages (SCs) (3⇓⇓–6). In 4-wk-old mice, 4 d of MD are sufficient to induce an OD shift to the open eye; therefore, neurons in the binocular V1, which are usually dominated by the contralateral eye in rodents (3, 7), become activated more equally by both eyes (5, 8). This juvenile OD shift is predominantly mediated by a decrease in the visual cortical responses to the deprived eye (1, 9⇓–11), whereas significant OD shifts in older animals up to PD110 need 7 d of MD and are mediated primarily by increased open-eye responses in V1. Raising animals in an enriched environment (EE) gives them the opportunity of enhanced physical, social, and cognitive stimulation and influences brain physiology and behavior in many ways (12, 13). It has been shown previously that EE enhances visual system development in rats (14) and mice (15⇓–17), increases levels of the brain-derived neurotrophic factor and serotonin (18), reduces both extracellular GABA levels (18, 19) and the density of ECM perineuronal nets (PNNs) (19), and promotes OD plasticity in adult and aging rats (18⇓⇓–21). Here, we explored cellular mechanisms of EE in V1 of mice and the therapeutic potential of EE to prevent impairments of plasticity after a cortical stroke. Furthermore, we studied whether EE would prolong the sensitive phase for OD plasticity into adulthood and also restore this form of plasticity in mice that were raised in SC until PD110 (i.e., in animals that were already beyond their sensitive phase for OD plasticity). Despite pharmacological detection of in vivo GABA levels, suggesting that EE reduces intracortical inhibition, direct electrophysiological evidence is still missing. We therefore recorded GABA, AMPA, and NMDA currents in slices from EE- and SC-raised mice and also tested the efficacy of diazepam injections to abolish OD plasticity of EE mice in vivo. Finally, we studied whether raising mice in EE would protect them from lesion-induced impairments of OD plasticity. Our results show that raising mice in EE preserved OD plasticity into late adulthood rejuvenated the brain after 3 mo of SC-rearing, and protected adult mice from stroke-induced impairments of cortical plasticity. Our electrophysiological measurements and diazepam treatment indicate that the plasticity-promoting effect of EE was primarily mediated by reduced intracortical inhibition compared with SC-raised mice. These results suggest EE as a preventive intervention to enhance and preserve plasticity in adulthood and after a cortical lesion.

What Dr. Richard Harvey of RIC should have said to Julia

I put this together since this is all readily available for anyone with a modicum of stroke knowledge and smarts.  If the RIC were anything close to the #1 stroke rehabilitation hospital out there, this would be the minimum I would expect from them.  With a team of 5 people and a couple of years Dr. Harvey could have accomplished this, or just me in a couple of hours. Why didn't he?

The RIC episode fiasco as explained in a letter to them here;
http://mycerebellarstrokerecovery.com/2014/01/26/julia/
RIC failed miserably in point #2 from here. My opinion only since I'm not seeing any facts proving their competency.

How to tell you have an incompetent stroke doctor or hospital

-----------------------------------------------------------------------------

Pedro Bach-y-Rita had a stroke in 1958, it destroyed a large portion of his brain stem and yet over the last 7 years of his life he recovered most of his faculties. We have the methods he used, we should be able to modify them to help you.
http://oc1dean.blogspot.com/2011/05/brainstem-stroke-recovery.html

 If you have spasticity in your hand the only way I think its possible to stop spasticity is to exercise the spastic muscles, thus telling the brain that it has control and stop listening to those contract messages from the spinal cord. As Peter Levine talks about here;
http://physical-therapy.advanceweb.com/Article/The-Magic-Cure-for-Spasticity-Reduction.aspx
That does require the ability to grasp and close your hand

Since your control area for your fingers is probably dead, the next step is to find a new location for that control area, this is where the Good, the Bad and the Ugly come in. We really have no idea on how to accomplish that yet.

The Good, the Bad and the Ugly - neurons

The area that controlled your hand is probably dead, this means none of the standard therapies will work, but since we are #1 we have studied possibilities that show promise in bringing back those functions.
1. Mirror therapy
Mirror Therapy for Improving Motor Function After Stroke
Systematic Review on the Effectiveness of Mirror Therapy in Training Upper Limb Hemiparesis after Stroke
Regardless we have come up with some protocols to follow.

2. Action observation
From action representation to action execution: exploring the links between cognitive and biomechanical levels of motor control

Modulating the motor system by action observation: Implications for stroke rehabilitation

We have thousands of animated gifs and videos of hundreds of muscle movements.

3. Mental imagery
Motor Imagery As A Tool For Stroke Rehabilitation Improvement
 We believe this works even though some research suggests it doesn't.
4. Passive movement
Exoskeleton hand gives you robo-powered fingers
We are working on getting a prototype of this in RIC.

5. Thermal stimulation
Facilitation of Sensory and Motor Recovery by Thermal Intervention for the Hemiplegic Upper Limb in Acute Stroke Patients
Basically 15 seconds warm 30 seconds cool.

6. Lucid dreaming
Lucidity Research, Past And Future - dreaming

7. Extra sensation
According to Margaret Yekutiel  in the book, Sensory Re-Education of the Hand After Stroke in 2001 sensation is a great precursor to movement.


You have to hope that your executive control areas are strong enough to resist being taken over.

We have been studying the hundreds of neurogenesis research papers and while there is no defined standard of care for this yet we have some ideas worth trying. This is fairly far out there so we don't even have any reported successes yet.

Stem cells are not even close to any brain application.
We have the ability to get you closer to where you want to be.

Contact me RIC if you want even more innovative ideas to keep your #1 ranking.  Its obvious Dr. Harvey is not.

Stroke research at the NIH - Project Listing by Category

If we had a decent stroke association each one of these would be reported on on a monthly basis and we'd be able to instantly identify where the next proposed research dollars should go to. But alas we have craptastic stroke associations that do very little other than issue press releases. We need that SuperStroke survivor working at that great stroke association in order to accomplish that.
This is from 2009 and I couldn't figure out how to get 2013 or 2014 data.
http://report.nih.gov/categorical_spending_project_listing.aspx?FY=2009&ARRA=N&DCat=Stroke
2012 data is here;
http://report.nih.gov/categorical_spending_project_listing.aspx?FY=2012&ARRA=N&DCat=Stroke

Inactivity Can Remodel Your Brain: A Sedentary Lifestyle Changes The Shape Of Your Neurons

So is your doctor going to change all the lying around in the hospital not doing therapy?
Article here;
http://www.medicaldaily.com/inactivity-can-remodel-your-brain-sedentary-lifestyle-changes-shape-your-neurons-267797
Abstract here; 
Physical (in)activity-dependent structural plasticity in bulbospinal catecholaminergic neurons of rat rostral ventrolateral medulla.

Mischel NA, Llewellyn-Smith IJ, Mueller PJ.

Author information

• Department of Physiology, Wayne State University School of Medicine, Detroit, Michigan, 48201.

Abstract

Increased activity of the sympathetic nervous system is thought to play a role in the development and progression of cardiovascular disease. Recent work has shown that physical inactivity versus activity alters neuronal structure in brain regions associated with cardiovascular regulation. Our physiological studies suggest that neurons in the rostral ventrolateral medulla (RVLM) are more responsive to excitation in sedentary versus physically active animals. We hypothesized that enhanced functional responses in the RVLM may be due, in part, to changes in the structure of RVLM neurons that control sympathetic activity. We used retrograde tracing and immunohistochemistry for tyrosine hydroxylase (TH) to identify bulbospinal catecholaminergic (C1) neurons in sedentary and active rats after chronic voluntary wheel-running exercise. We then digitally reconstructed their cell bodies and dendrites at different rostrocaudal levels. The dendritic arbors of spinally projecting TH neurons from sedentary rats were more branched than those of physically active rats (P < 0.05). In sedentary rats, dendritic branching was greater in more rostral versus more caudal bulbospinal C1 neurons, whereas, in physically active rats, dendritic branching was consistent throughout the RVLM. In contrast, cell body size and the number of primary dendrites did not differ between active and inactive animals. We suggest that these structural changes provide an anatomical underpinning for the functional differences observed in our in vivo studies. These inactivity-related structural and functional changes may enhance the overall sensitivity of RVLM neurons to excitatory stimuli and contribute to an increased risk of cardiovascular disease in sedentary individuals. J. Comp. Neurol. 522:499-513, 2014. © 2013 Wiley Periodicals, Inc.

Benefits of an E-learning Intervention for Implementing Stroke Rehabilitation Best Practices

It takes a graduate student thesis to describe the complete stupidity of lack of transmission of stroke knowledge and protocols. An obvious failing of our stroke associations. Its only 200 pages. Hell this is precisely the reason most survivors start blogs and stroke forums.
http://scholar.google.com/scholar_url?hl=en&q=https://tspace.library.utoronto.ca/bitstream/1807/43666/1/Menon_Anita_201311_PhD_thesis.pdf&sa=X&scisig=AAGBfm1cqX4IKvjU5UKuCDoSDfZqiomLdA&oi=scholaralrt

Is stroke rehabilitation a metabolic problem?

Well I don't know so ask your doctor that question. And an email is provided for your doctors ease in contacting the researcher.

Is stroke rehabilitation a metabolic problem?

2014, Vol. 28, No. 2 , Pages 161-173 (doi:10.3109/02699052.2013.860470)

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Roberto Aquilani¹, Mirella Boselli², Baiardi Paola³, Evasio Pasini⁴, Paolo Iadarola⁵, Manuela Verri⁶, Simona Viglio⁷, Annamaria Condino⁸, & Federica Boschi⁸

¹Servizio di Fisiopatologia Metabolico-Nutrizionale e Nutrizione Clinica,

²Unità di Riabilitazione Neuromotoria, Unità Gravi Cerebrolesioni Acquisite, Fondazione S. Maugeri, IRCCS, Istituto Scientifico di Montescano,

Montescano, Pavia

, Italy,

³Consorzio Valutazioni Biologiche e Farmacologiche, Fondazione S. Maugeri e Università degli Studi di Pavia,

Pavia

, Italy,

⁴Fondazione S. Maugeri, IRCCS, Istituto Scientifico di Lumezzane,

Lumezzane, Brescia

, Italy,

⁵Dipartimento di Biologia e Biotecnologie, Università degli Studi di Pavia,

Pavia

, Italy,

⁶Dipartimento di Medicina Legale, Scienze Forensi e Farmaco-Tossicologiche ‘A. Fornari’, Sezione di Scienze Farmacologiche e Tossicologiche, Università degli Studi di Pavia,

Pavia

, Italy,

⁷Dipartimento di Medicina Molecolare, and

⁸Dipartimento di Scienze del Farmaco, Università degli Studi di Pavia,

Viale Taramelli, Pavia

, Italy

Correspondence:

Dr Federica Boschi

, Dipartimento di Scienze del Farmaco, Università degli Studi di Pavia,

Viale Taramelli, 12, 27100 Pavia

, Italy. Tel: 39-0382-987398. Fax: 39-0382-987405. Email: federica.boschi@unipv.it

Abstract

Background: This study looks at the impact of inflammation during the rehabilitation stage of strokes and its effect on neuro-functional recovery.
Methods: This study investigated 94 patients suffering from strokes and admitted to rehabilitation. Anthropometric characteristics, serum proteins and inflammatory markers, plasma amino acids and neurofunction were all assessed.
Results: 55.3% patients had an inflammatory status (Interleukin-6 = 19.24 ± 23.01 pg ml⁻¹ vs. 4.1 ± 1.6 pg ml⁻¹ for non-inflamed subjects (p < 0.001). Inflammation was positively linked to positive proteins (alpha-1 globulin, p < 0.02) and negatively linked to negative proteins (albumin, p < 0.02; prealbumin, p < 0.01; transferrin, p  < 0.05) of the acute-phase response. Inflammation was associated with low plasma concentrations of total amino acids. For the multiple logistic regression analysis, albumin (p < 0.001) and body weight maintenance (p  < 0.001) were independent predictors of patient functional independence. Inflammation in dysphagic stroke (31.9%) patients was associated with more accentuated disability compared to non-inflamed dysphagics. The serum positive reactant alpha 1 globulin was the most powerful predictor of dysphagia severity (p < 0.001). At discharge, dysphagia improvement was associated with improved acute-phase negative proteins.

Conclusions: An inflammatory status may persist for most patients with strokes during the rehabiliation stage of the disease, its prevalence being higher in dysphagic compared to non-dysphagic subjects. The improvement in circulating albumin(how is that done?) and body weight maintenance are predictors of neuro-function, even in dysphagic subjects.

Read More: http://informahealthcare.com/doi/abs/10.3109/02699052.2013.860470

Arteriosclerosis and Atherosclerosis - Treatment with Homeopathy, Schuessler salts and Accupressure

Wow, just wow, a whole book on treatment with nothing, homeopathy is just that - nothing.
But if you'd rather believe their explanations, go ahead, just be prepared for the upcoming stroke or heart attack.
http://books.google.com/books?hl=en&lr=&id=nb6jAgAAQBAJ&oi=fnd&pg=PT2&ots=ltdUzQZFua&sig=suJZG_baI7igpu7ZqIIG5X7mbog#v=onepage&q&f=false

The Role of G-Protein-Coupled Receptors in Adult Neurogenesis

And just what is your doctor going to do with this knowledge? Assuming that your doctors reads any research at all. I've written 256 posts on neurogenesis Has your doctor known about any of them?
http://link.springer.com/protocol/10.1007/978-1-62703-779-2_21

• Katie M. Collette,
• Van A. Doze,
• Dianne M. Perez

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Abstract

Adult neurogenesis is the process of creating new brain cells during adulthood. This involves several stages including proliferation, migration, differentiation, integration, and survival. G-protein-coupled receptors (GPCRs) regulate this process in both neurogenic regions of the brain: the subgranular and subventricular zones. The regulation of adult neurogenesis by GPCRs holds therapeutic promise for many neuropathologies. Several GPCRs activated by the neurotransmitters dopamine, glutamate, norepinephrine, and serotonin were shown to regulate adult neurogenesis. Melatonin, a neurohormone, and inflammatory molecules such as chemokines and prostaglandins modulate different stages of neurogenesis through GPCRs as well. The methods for studying the adult neurogenic stages depend upon labeling of dividing cells using the synthetic thymidine analog, nucleoside 5-bromo-2′-deoxyuridine (BrdU). BrdU incorporates into the DNA, is transferred to daughter cells, and is labeled using antibodies. The length of time after injection determines which stage of neurogenesis is being examined. Additional methods include culture of neonatal or adult neurospheres isolated from the subventricular zone, monolayer cultures of isolated neural stem cells, as well as transgenic manipulations via standard or viral-mediated techniques. In recent years, the use of Cre-inducible transgenic animals has developed and led to the creation of double- and triple-transgenic animals with specific activation of receptors in selected cell types. Future work in GPCR regulation of adult neurogenesis will likely include the use of opsin-receptor chimeras allowing precise spatial and temporal activation of GPCRs in neural stem/progenitor cells via optogenetics. This chapter summarizes the roles of various GPCRs involved in the regulation of adult neural stem cells and their progenitors and the current methods used to examine the actions of GPCRs in adult neurogenesis.

Effect of vitamin E and memantine on functional decline in Alzheimer disease: the TEAM-AD VA cooperative randomized trial

Prevention would probably be better.
This is what I'm doing for prevention.
This is what the Harvard Medical School suggests.
Generic dementia prevention here. 
Alpha tocopherol is not standard vitamin E. You know the drill, ask your doctor.
http://www.ncbi.nlm.nih.gov/pubmed/24381967

Dysken MW¹, Sano M², Asthana S³, Vertrees JE⁴, Pallaki M⁵, Llorente M⁶, Love S¹, Schellenberg GD⁷, McCarten JR¹, Malphurs J⁸, Prieto S⁸, Chen P⁵, Loreck DJ⁹, Trapp G¹⁰, Bakshi RS¹⁰, Mintzer JE¹¹, Heidebrink JL¹², Vidal-Cardona A¹³, Arroyo LM¹³, Cruz AR¹⁴, Zachariah S¹⁴, Kowall NW¹⁵, Chopra MP¹⁵, Craft S¹⁶, Thielke S¹⁶, Turvey CL¹⁷, Woodman C¹⁷, Monnell KA¹⁸, Gordon K¹⁸, Tomaska J¹, Segal Y¹, Peduzzi PN¹⁹, Guarino PD¹⁹.

Author information

• ¹Minneapolis VA Health Care System, Minneapolis, Minnesota.
• ²James J. Peters VA Medical Research Center, New York, New York.
• ³William S. Middleton Memorial Veterans Hospital, Madison, Wisconsin.
• ⁴Cooperative Studies Program Clinical Research Pharmacy Coordinating Center, Albuquerque, New Mexico.
• ⁵Louis Stokes Cleveland VA Medical Center, Cleveland, Ohio6Case Western Reserve University School of Medicine, Cleveland, Ohio.
• ⁶Washington DC VA Medical Center, Washington, DC.
• ⁷University of Pennsylvania School of Medicine, Philadelphia.
• ⁸Miami VA Healthcare System, Miami, Florida.
• ⁹VA Maryland Healthcare System, Baltimore11University of Maryland Medical School, Department of Psychiatry, Baltimore.
• ¹⁰VA North Texas Health Care System, Dallas.
• ¹¹Ralph H. Johnson VA Medical Center, Charleston, South Carolina14Department of Health Studies, Medical University of South Carolina, Charleston15Roper St Francis Healthcare, Charleston, South Carolina.
• ¹²VA Ann Arbor Healthcare System, Ann Arbor, Michigan.
• ¹³VA Caribbean Healthcare System, San Juan, Puerto Rico.
• ¹⁴Bay Pines VA Healthcare System, Bay Pines, Florida.
• ¹⁵VA Boston Healthcare System, Boston, Massachusetts.
• ¹⁶VA Puget Sound Health Care System, Seattle, Washington21Department of Psychiatry and Behavioral Sciences, University of Washington, Seattle.
• ¹⁷Iowa City VA Medical Center, Iowa City, Iowa23University of Iowa, Iowa City.
• ¹⁸W. G. (Bill) Hefner VA Medical Center, Salisbury, North Carolina.
• ¹⁹Cooperative Studies Program Coordinating Center, VA Connecticut Healthcare System, West Haven26Yale University School of Public Health, New Haven, Connecticut.

Abstract

IMPORTANCE:

Although vitamin E and memantine have been shown to have beneficial effects in moderately severe Alzheimer disease (AD), evidence is limited in mild to moderate AD.

OBJECTIVE:

To determine if vitamin E (alpha tocopherol), memantine, or both slow progression of mild to moderate AD in patients taking an acetylcholinesterase inhibitor.

DESIGN, SETTING, AND PARTICIPANTS:

Double-blind, placebo-controlled, parallel-group, randomized clinical trial involving 613 patients with mild to moderate AD initiated in August 2007 and concluded in September 2012 at 14 Veterans Affairs medical centers.

INTERVENTIONS:

Participants received either 2000 IU/d of alpha tocopherol (n = 152), 20 mg/d of memantine (n = 155), the combination (n = 154), or placebo (n = 152).

MAIN OUTCOMES AND MEASURES:

Alzheimer's Disease Cooperative Study/Activities of Daily Living (ADCS-ADL) Inventory score (range, 0-78). Secondary outcomes included cognitive, neuropsychiatric, functional, and caregiver measures.

RESULTS:

Data from 561 participants were analyzed (alpha tocopherol = 140, memantine = 142, combination = 139, placebo = 140), with 52 excluded because of a lack of any follow-up data. Over the mean (SD) follow-up of 2.27 (1.22) years, ADCS-ADL Inventory scores declined by 3.15 units (95% CI, 0.92 to 5.39; adjusted P = .03) less in the alpha tocopherol group compared with the placebo group. In the memantine group, these scores declined 1.98 units less (95% CI, -0.24 to 4.20; adjusted P = .40) than the placebo group's decline. This change in the alpha tocopherol group translates into a delay in clinical progression of 19% per year compared with placebo or a delay of approximately 6.2 months over the follow-up period. Caregiver time increased least in the alpha tocopherol group. All-cause mortality and safety analyses showed a difference only on the serious adverse event of "infections or infestations," with greater frequencies in the memantine (31 events in 23 participants) and combination groups (44 events in 31 participants) compared with placebo (13 events in 11 participants).

CONCLUSIONS AND RELEVANCE:

Among patients with mild to moderate AD, 2000 IU/d of alpha tocopherol compared with placebo resulted in slower functional decline. There were no significant differences in the groups receiving memantine alone or memantine plus alpha tocopherol. These findings suggest benefit of alpha tocopherol in mild to moderate AD by slowing functional decline and decreasing caregiver burden.

TRIAL REGISTRATION:

clinicaltrials.gov Identifier: NCT00235716.

Strengthening Human Adaptive Reasoning and Problem-Solving (SHARP) Program

This is exactly what survivors need as specified by -  Dr. Steven Wolfs contention, 'Stroke patients need to rely more on their own problem solving to regain mobility'. So do you really think your doctor will do anything like this?
http://www.iarpa.gov/Programs/sc/SHARP/sharp.html

HOT TOPICS 2014: Stroke

F*cking appalling that none of these supposed experts mention anything about stopping the neuronal cascade of death, only prevention.  Do they even know about the cascade of death? Once again showing how little research is read.
That's the question we asked Larry Goldstein, MD, director of the Duke Stroke Center in Durham, N.C., Jay Mohr, MD, professor of neurology at Columbia University Medical Center in New York City, and Patrick Lyden, MD, chair of the department of neurology at Cedars-Sinai Medical Center in Los Angeles.
http://www.medpagetoday.com/HOTTOPICS2014/special-reports/SpecialReports-Videos/359

Walking and an aha moment

Finally figured out one of my problems with walking today. I was quite literally swinging my left leg like a log - very little knee bend.  It seems I was never getting weight on my left leg to the point where the knee would start to bend. Maybe this was compensation after I left therapy but my PT ex should have been able to point that out if we ever went walking together.  Now I'll have to work even more at my dorsiflexion since the toe will be needed to lift even more sooner.
I never got to late flatfoot. And toe off most assuredly does not occur.
From this site come the phases of walking, looking at foot placement.

 http://www.footeducation.com/biomechanics-of-walking-gait