Deans' stroke musings

Changing stroke rehab and research worldwide now.Time is Brain!Just think of all the trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 438 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It's quite disgusting that this information is not available from every stroke association and doctors group.
My back ground story is here:http://oc1dean.blogspot.com/2010/11/my-background-story_8.html

Wednesday, December 17, 2014

SPINAL CORD INJURY Sprouting Neurological Function

Would this be useful after our strokes?
http://stm.sciencemag.org/content/6/267/267ec216.full?utm_source=eloqua
  1. Daniel K. Nishijima
+ Author Affiliations
  1. Department of Emergency Medicine, UC Davis School of Medicine, Sacramento, CA 95817, USA. E-mail: daniel.nishijima@ucdmc.ucdavis.edu
Injury to the spinal cord, the main information highway up and down the body, triggers upregulation of highly glycosylated proteins at the site of injury. This acts as a barrier to nerve regeneration and “traps” nerves’ growing tips, preventing neurological recovery. Lang et al. developed an inhibitor that interferes with proteoglycan binding to its receptor [protein tyrosine phosphatase σ (PTPσ)] and is able to reverse the nerve regrowth blockage after spinal cord injury and improve the animals’ functional recovery.
Rats with spinal cord injury were injected with the PTPσ-binding drug subcutaneously daily for several weeks. At the end of treatment, urinary function and walking were improved compared with control animals, with higher doses producing better urinary function. Unexpectedly, the researchers did not observe regeneration of corticospinal tract fibers through the injury in the treated rats. Rather, below the lesion, they saw significant sprouting of dense territories of serotonergic neurons. Treatment with a serotonin antagonist reduced locomotor and urinary function in the treatment group but not the control group. This result indicated that the neurological improvement was a result of increased serotonin production from sprouting and regrowth of nerves that survived the injury rather than of reconnections of injured nerve fibers.
The practical advantage of delivering the drug systemically and the positive results of this study suggest that this approach holds great potential as a treatment for patients with spinal cord injury.
B. T. Lang et al., Modulation of the proteoglycan receptor PTPσ promotes recovery after spinal cord injury. Nature 10.1038/nature13974 (2014). [Abstract]

The Global Fight Against Dementia

You are probably completely on your own as how to prevent dementia/Alzheimers. We would need something like this if we ever are going to solve stroke problems.
http://stm.sciencemag.org/content/6/267/267ed22.full
  1. Yves Joanette is the Scientific Director, Institute of Aging, Canadian Institute of Health Research, Ottawa, Canada. E-mail: yves.joanette@umontreal.ca
  2. Etienne C. Hirsch is the Director of the Institute for neurosciences, cognitive sciences, neurology and psychiatry, Aviesan, Paris, France.
  3. Michel Goldman is Past-Executive Director, Innovative Medicines Initiative, Brussels, Belgium.
Michel Goldman
CREDITS: PHILIPPE ATHLAN (Y.J.); Jean-Philippe Pariente (E.C.H.); ARNAUD GHYS (M.G.)
Very few of those reading this editorial will have had no contact with the devastating consequences of dementia. Dementia, caused by a variety of neurodegenerative conditions, including Alzheimer’s disease, occurs in 35% of individuals over 80 years of age (1). The disease ravages cognitive abilities, affecting not only the person with dementia but also the lives of family members acting as their caregivers. Despite decades of research aimed at identifying the mechanisms underpinning the neurodegenerative processes causing dementia, and despite the fact that the cascade of events characterizing neurodegeneration is now known to occur decades before any clinical manifestations, there are still no therapies that can prevent or modify the course of dementia. The current health and welfare systems of the developed world are not adapted to deal with the huge health and social pressures wrought by dementia. Because of the aging of the populations in the developed world, the number of individuals with dementia is calculated to double by 2050 in Group of Eight (G8) countries (2). Furthermore, in low- and middle-income countries, the number of those affected by dementia is set to quadruple by 2050 as people live longer due to a decline in infectious diseases (2). The scale of this impending health disaster requires a concerted global effort to tackle dementia at all levels. The World Health Organization (WHO) is set to sponsor the First Ministerial Conference on Global Action Against Dementia in March 2015 in Geneva, Switzerland. The principal goal is to develop a global action plan to address the challenges of dementia using as a basis the discussions that have taken place in a series of events in the past year.
In 2012, WHO recognized dementia as a global public health priority (1). Until then, multiple actions were launched by national governments (such as those of France, UK, USA, and Canada) and by the European Union (for example, the Joint Programming Initiative on Neurodegenerative Diseases and the Innovative Medicines Initiative). Although some progress has been made, it is now clear that a coordinated global effort is needed. The first step toward a concerted global effort was taken by the UK’s Prime Minister David Cameron in 2013, who as president of the G8 at that time, called for a G8 Summit on Dementia in December 2013 in London. It was at this summit that Global Action Against Dementia (GAAD) was launched (http://bit.ly/12Fre3T). Dennis Gillings, a consultant to the pharmaceutical industry, was appointed as the Global Dementia Envoy to coordinate the international efforts of GAAD. A World Dementia Council was appointed to support the Envoy and to oversee GAAD, with concurrent support from WHO and the Organisation for Economic Cooperation and Development (OECD). Composed of 18 members from nine countries representing funding agencies, governments, international organizations, industry, academia, and patients’ associations, the Council met three times in 2014 with support from the UK government. Specifically, the Council is focusing on five priority areas: (1) integrated development (addressing the global regulatory barriers to drug development, encouraging innovative collaborative research, ensuring effective public policy-making governance), (2) financial innovations and incentives, (3) open science and data, (4) care of patients with dementia, and (5) dementia risk reduction (http://bit.ly/12FsdRR). 

More at link.

Melatonin May Help Prevent Alzheimer’s Disease

This one you'll have to read and decide with your doctors help. I do take melatonin but it is mainly for helping me sleep.
http://www.life-enhancement.com/magazine/article/1738-melatonin-may-help-prevent-alzheimers-disease?
A few paragraphs;

A Melatonin “Laundry List”
Let’s outline some documented scientific facts and expert opinions regarding melatonin and Alzheimer’s disease (AD) and then see what they add up to. Most of the information that follows is from two recent review papers, one by scientists in China2 and the other by a team from Malaysia, the United States, Argentina, and Germany.3
  • In our forties or fifties, typically, our nightly melatonin output begins a steep decline from its youthful levels—a decline that correlates with physical deterioration of the pineal gland itself. By our late seventies, melatonin output has dropped to very low levels.
  • Accounting for age, abnormally low levels of melatonin in the blood and cerebrospinal fluid are observed even in the early, preclinical stages of AD, suggesting that this hormone may be a useful early marker for the disease. As AD progresses, the levels decline further—dramatically—in correlation with the severity of the patients’ cognitive impairment.

    Sundown(ing)
  • Melatonin output in AD can also be highly irregular, resulting in severe disruptions of normal circadian rhythms, including the sleep/wake cycle. This often manifests as sundowning, a decrease in cognitive functions and an increase in bizarre behaviors during the evening and nighttime hours. Melatonin has been successful in treating AD-related sleep disorders, the severity of which correlates with the severity of the patients’ cognitive impairment.
  • Oxidative stress—the damage done to molecular and cellular entities by reactive oxygen species, including free radicals—is very strongly implicated in AD, as both a causative factor and an exacerbating factor. The brain is exceptionally vulnerable to oxidative stress, owing to its high rate of chemical energy generation (through cellular respiration, the primary source of free radicals) and its high content of polyunsaturated fatty acids, which are easily damaged by free radicals.
  • Melatonin is a powerful antioxidant. Its actions occur not only through the scavenging of free radicals but also through a variety of other, less direct chemical mechanisms that reduce oxidative stress, including the upregulation of antioxidant enzymes and the downregulation of prooxidant enzymes. This makes melatonin more versatile and potent than conventional antioxidants. It also makes it extremely difficult for researchers to distinguish, where melatonin is concerned, between causal connections and mere correlations that may or may not mean anything.
  • Melatonin’s antioxidative protection may also be related to its chronobiological role as a regulator of circadian rhythms, the disruption of which promotes abnormal levels of oxidative stress. This suggests the value of melatonin supplementation in the elderly, in whom the normal daily fluctuations in melatonin levels are greatly reduced, and especially in AD patients, in whom the daily fluctuations may, in addition, be highly irregular, as noted above.
  • A significant advantage of melatonin over most other antioxidants is that its molecular structure allows it to cross the blood-brain barrier and to enter any component of the neurons (brain cells), including the mitochondria. These organelles, where the brain’s chemical energy is generated, are the chief source of free radicals—and they are its chief victims. Oxidative damage to the mitochondria is thought to be a centrally important factor in aging and dementia.
  • Melatonin is neuroprotective, i.e., it helps protect brain neurons from damage or death caused by a variety of factors, notably oxidative stress. This protective effect is most pronounced in the mitochondria and is believed to be melatonin’s most important benefit.
  • Melatonin is protective against neuritic plaques and neurofibrillary tangles, the two dominant neuropathological features of Alzheimer’s brains. Specifically, melatonin protects against the destructive effects of two dangerous proteins: amyloid-beta (the principal constituent of neuritic plaques) and hyperphosphorylated tau (of which neurofibrillary tangles are composed). Amyloid-beta attacks and destroys neurons, resulting in the substantial loss of brain matter seen in Alzheimer’s victims at autopsy. Hyperphosphorylated tau (rhymes with wow) is also destructive; it’s the result of a chemical modification of a benign (and vital) protein called simply tau.
  • Melatonin is believed to promote neurogenesis (the formation of new neurons) by playing a role in the construction of the cytoskeleton, the neuron’s structural framework. One of the key constituents of the cytoskeleton is tau, which, when it becomes damaged through hyperphosphorylation, forms neurofibrillary tangles. Melatonin inhibits that process.
  • Rats in which melatonin biosynthesis was inhibited (by means of the antipsychotic drug haloperidol) suffered impaired spatial memory. Administration of melatonin before and during the haloperidol treatment, however, significantly prevented memory loss. It also inhibited the hyperphosphorylation of tau, and it reduced oxidative stress. Those two benefits are probably related, because the former phenomenon is influenced by the latter.

    Typical fluctuations of core body temperature over a 24-hour period. This circadian rhythm is regulated by melatonin.
  • Oxidative stress is also implicated in the formation of amyloid-beta from its precursor, amyloid precursor protein (APP), and amyloid-beta itself promotes further oxidative stress, playing a role in the promotion of tau hyperphosphorylation and the death of brain neurons. Melatonin regulates APP metabolism and prevents amyloid-beta pathology and neuronal death—but only, apparently, if given before the deposition of neuritic plaques (which are also called senile plaques) begins; after that, it’s too late.
  • Amyloid-beta also has proinflammatory effects on brain tissue, mainly through its stimulation of molecules called cytokines and chemokines. Melatonin inhibits this activity and thus has an anti-inflammatory effect.
  • Melatonin has some protective effect on the brain’s cholinergic nervous system, i.e., those parts of the neural circuitry that depend on acetylcholine as the neurotransmitter. A marked decline in cholinergic activity is primarily responsible for the memory loss and other cognitive deficits seen in Alzheimer’s patients.
  • Melatonin is known to enhance immune-system function by promoting the production of T lymphocytes, a type of white blood cell that enhances the production of antibodies.
  • Melatonin promotes regular, healthy sleep, which is considered to be neuroprotective through its fostering of improved neuronal metabolism. That’s especially important in preventing age-related neurodegenerative diseases or attenuating their progression.
  • Melatonin has very low toxicity and can be taken by most people in large amounts (many milligrams daily) with no serious side effects. (As with many supplements, however, one must beware of possible interactions with prescription drugs; consult your doctor.) In the elderly, a common side effect of relatively large doses (3 mg or more) is reduced body temperature, the result of sudden alterations in melatonin’s circadian thermoregulatory function.

New Technology Advances Eye Tracking As Biomarker for Brain Function and Recovery from Brain Injury

Maybe an objective determination if you had a stroke, rather than sitting in an ER for hours waiting for visible motor deficits to occur. How many years before your hospital and ambulance crews get something like this?
http://communications.med.nyu.edu/media-relations/news/new-technology-advances-eye-tracking-biomarker-brain-function-and-recovery-brai

Unique Research Led by NYU Langone Medical Center Utilizes Music Videos to Study Eye Movements

Researchers at NYU Langone Medical Center have developed  new technology that can assess the location and impact of a brain injury merely by tracking the eye movements of patients as they watch music videos for less than four minutes, according to a study published Friday on-line in the Journal of Neurosurgery.
 The study suggests that the use of eye tracking technology may be a potential biological marker for assessing brain function and monitoring recovery for patients with brain injuries.
 Led by Uzma Samadani, MD, PhD, chief of neurosurgery at New York Harbor Health Care System and co-director of the Steven & Alexandra Cohen Veterans Center for the Study of Post-Traumatic Stress and Traumatic Brain Injury at NYU Langone, the study looked at 169 veterans; 157 of whom were neurologically healthy and 12 who either had known weaknesses in the nerves that move the eyes, or brain swelling adjacent to those nerves. These nerves affect how the eye moves up and down and side to side.
 Using a technology developed at NYU Langone, the investigators had the participants watch a music video or television content for 220 seconds while they measured the ratio of horizontal to vertical eye movements.  They discovered that in the neurologically healthy subjects, the ratios were close to one-to-one, with horizontal movements equaling vertical movements. But the 12 participants with nerve damage or swelling in the brain pressing on nerves all showed abnormal eye movement ratios correlating to the nerve that was affected. In every case where the abnormal eye movement was due to swelling in the brain, surgery to fix the brain problem also restored the eye movements to normal range.  
 “We are very excited about the findings because it offers a proof of concept that this technology can detect brain injury and suggest its location,” says Dr. Samadani. “One of the reasons that clinical trials for treatment of brain injury have failed in the past is that brain injury is hard to classify and quantitate with existing technologies. This invention suggests a potential new method for classifying and quantitating the extent of injury. Once validated, it will both accelerate diagnosis and aid in the development of better treatments.”
 Commenting on the study, Charles Marmar, MD, the Lucius Littauer professor and chairman of Psychiatry at NYU Langone, and executive director of NYU Langone’s Steven & Alexandra Cohen Veterans Center (which helps fund Dr. Samadani’s research), says:  “These results are extremely exciting because the technology is not overly complicated and, as a result, can move from the bench to the battlefield and other places where it will be easily accessible to all.”
 Dr. Marmar added that because of its easy usability, it can be applied, for example, to study hundreds of subjects in a relatively short period of time.  He pointed in particular to recent eye-tracking work led by Dr. Samadani of over 600 active military at Fort Campbell in Kentucky, who were assessed with this technology in the first week after they returned home from their deployment. “These studies will help further evaluate the technology’s effectiveness as a screening tool,” he adds.
 Brain injury is the number one cause of death and disability in Americans under age 35,   According to the U.S. Centers for Disease Control and Prevention. Every year, 1.4 million people suffer from a traumatic brain injury in the United States. Of those, 50,000 die and 235,000 require hospital admission.
 While the paper describes patients with brain problems that are apparent on imaging, Dr. Samadani says the technology will likely be most useful for the assessment of concussion and blast injury – which can be difficult to detect with standard imaging studies, and which is highly prevalent among returning veterans from the long Middle East wars. “Because eye tracking measures how well the brain functions rather than assesses what it looks like, it provides very different information than imaging studies” she says.
 It may also be helpful for triage. “When a person falls and hits their head, it can be difficult to determine whether the injury is life-threatening,” Dr. Samadani says. “Eye tracking is potentially a simple, non-invasive and cost-effective way to determine quickly which patients need immediate attention.”
 In addition to Dr. Samadani, co-authors of this study include Sameer Farooq;  Robert Ritlop, MEng.; Floyd Warren, MD; Marleen Reyes, BA; Elizabeth Lamm, BA; Anastasia Alex, BS; Elena Nehrbass, BS; Radek Kolecki, BS; Michael Jureller, BS; Julia Schneider; Agnes Chen, BA; Chen Shi, BS; Neil Mendhiratta, BA; Jason H. Huang, MD; Meng Qian, PhD; Roy Kwak, MD; Artem Mikheev, MS; Henry Rusinek, PhD; Ajax Goerge, MD; Robert Fergus, PhD; Douglas Kondziolka, MD; Paul P. Huang, MD; and Theodore Smith, Md, PhD.
 Dr. Samadani’s research is supported in part by the U.S. Department of Veterans Affairs (VA), Veterans Health Administration, Office of Research and Development, Rehabilitation and Research and Development Service via a VA Merit Award (1I01RX000319-01); a Career Development Award from the American College of Surgeons/Neurosurgery Research Education Foundation of the AANS; the Steven & Alexandra Cohen Veterans Center for the Study of Post-Traumatic Stress and Traumatic Brain Injury; The Thrasher Research  Fund; and Research to Prevent Blindness.
 Media Inquiries:
 Stacey Harris
(917) 697-7746
Stacey@harrishealth1.com
 Jim Mandler
(212) 404-3525
jim.mandler@nyumc.org

Effects of beta-hydroxybutyrate on cognition in memory-impaired adults - coconut oil

MCTs are found in coconut oil. Do not do anything here without your doctors ok.
http://www.ncbi.nlm.nih.gov/pubmed/15123336

Abstract

Glucose is the brain's principal energy substrate. In Alzheimer's disease (AD), there appears to be a pathological decrease in the brain's ability to use glucose. Neurobiological evidence suggests that ketone bodies are an effective alternative energy substrate for the brain. Elevation of plasma ketone body levels through an oral dose of medium chain triglycerides (MCTs) may improve cognitive functioning in older adults with memory disorders. On separate days, 20 subjects with AD or mild cognitive impairment consumed a drink containing emulsified MCTs or placebo. Significant increases in levels of the ketone body beta-hydroxybutyrate (beta-OHB) were observed 90 min after treatment (P=0.007) when cognitive tests were administered. beta-OHB elevations were moderated by apolipoprotein E (APOE) genotype (P=0.036). For 4+ subjects, beta-OHB levels continued to rise between the 90 and 120 min blood draws in the treatment condition, while the beta-OHB levels of 4- subjects held constant (P<0.009). On cognitive testing, MCT treatment facilitated performance on the Alzheimer's Disease Assessment Scale-Cognitive Subscale (ADAS-cog) for 4- subjects, but not for 4+ subjects (P=0.04). Higher ketone values were associated with greater improvement in paragraph recall with MCT treatment relative to placebo across all subjects (P=0.02). Additional research is warranted to determine the therapeutic benefits of MCTs for patients with AD and how APOE-4 status may mediate beta-OHB efficacy.

Anti-inflammatory, analgesic, and antipyretic activities of virgin coconut oil

I'm mainly using it for dementia prevention. But would this help prevent the initial start of inflammation that is the beginning of atherosclerorsis? Not to be done unless your doctor prescribes this.
http://www.ncbi.nlm.nih.gov/pubmed/20645831

Abstract

This study investigated some pharmacological properties of virgin coconut oil (VCO), the natural pure oil from coconut [Cocos nucifera Linn (Palmae)] milk, which was prepared without using chemical or high-heat treatment. The anti-inflammatory, analgesic, and antipyretic effects of VCO were assessed. In acute inflammatory models, VCO showed moderate anti-inflammatory effects on ethyl phenylpropiolate-induced ear edema in rats, and carrageenin- and arachidonic acid-induced paw edema. VCO exhibited an inhibitory effect on chronic inflammation by reducing the transudative weight, granuloma formation, and serum alkaline phosphatase activity. VCO also showed a moderate analgesic effect on the acetic acid-induced writhing response as well as an antipyretic effect in yeast-induced hyperthermia. The results obtained suggest anti-inflammatory, analgesic, and antipyretic properties of VCO.

Lack of Sleep During Critical Period of Night Linked to Dementia Risk

Are you getting this type of sleep while in the hospital? Does taking sleeping pills still allow for this type of sleep?
http://www.spring.org.uk/2014/12/lack-of-sleep-during-critical-period-of-night-linked-to-dementia-risk.php?

Alzheimer's disease

From the front page of Yahoo news. Alzheimers has obviously hit the tipping point. But if you look at the figures, stroke will have more people affected by 2050. Why hasn't stroke been more visible?
http://news.yahoo.com/video/alzheimer-39-disease-084835094.html
36 million people suffer from Alzheimer's around the world. According to a World Health Organisation estimate, this figure could reach 115 million by 2050 in the absence of a cure. With a new case diagnosed every 4 seconds, the disease remains one of medicine's greatest challenges as it robs ever more people of their memory and independence.VIDEOGRAPHIC
At 10 million survivors a year stroke will have 350 million survivors by 2050 and 175 million dead.
Sounds like a major catastrophe to me.

Neurons listen to glia cells

See what your doctor will do with this to update your stroke protocols. Your doctor is constantly updating your protocols? Right?
http://www.sciencedaily.com/releases/2014/12/141215101649.htm
Scientists at Johannes Gutenberg University Mainz (JGU) have discovered a new signal pathway in the brain that plays an important role in learning and the processing of sensory input. It was already known that distinct glial cells receive information from neurons. However, it was unknown that these same glial cells also transmit information to neurons. The glia release a specific protein fragment that influences neuronal cross-talk, most likely by binding to the synaptic contacts that neurons use for communication. Disruption of this information flow from the glia results in changes in the neural network, for example during learning processes. The team composed of Dr. Dominik Sakry, Dr. Angela Neitz, Professor Jacqueline Trotter, and Professor Thomas Mittmann unravelled the underlying mechanism, from the molecular and cellular level to the network and finally the resulting behavioral consequences. Their findings constitute major progress in understanding complex pathways of signal transmission in the brain.

In mammalian brains glial cells outnumber nerve cells, but their functions are still largely unelucidated. A group of glial cells, so-called oligodendrocyte precursor cells (OPC), develop into the oligodendrocytes which ensheathe neuronal axons with a protective myelin layer thus promoting the rapid transmission of signals along the axon. Interestingly, these OPCs are present as a stable proportion -- some five to eight percent of all cells in all brain regions, including adult brains. The Mainz-based researchers decided to take a closer look at these OPCs.
In 2000 it was discovered that OPCs receive signals from the neural network via synaptic contacts that they make with neurons. "We have now discovered that the precursor cells do not only receive information via the synapses, but in their turn use these to transmit signals to adjacent nerve cells. They are thus an essential component of the network," explained Professor Jacqueline Trotter from the Institute of Molecular Cell Biology at Mainz University. Classically, neurons have been considered as the major players in the brain. Over the past few years, however, increasing evidence has come to light that glial cells may play an equally important role. "Glial cells are enormously important for our brains and we have now elucidated in detail a novel important role for glia in signal transmission," explained Professor Thomas Mittmann of the Institute of Physiology of the Mainz University Medical Center.
The chain of communication starts with signals traveling from the neurons to the OPCs across the synaptic cleft via the neurotransmitter glutamate. This results in a stimulation of the activity of a specific protease, the alpha-secretase ADAM 10 in OPCs, which acts on the NG2 protein expressed by the precursor cells releasing a NG2 fragment into the extracellular space, where it influences neighboring neuronal synapses. The neurons react to this in the form of altered electrical activity. "We can use patch-clamp techniques to hear, as it were, how the cells talk to one another," said Mittmann.
"The process starts with the reception of signals coming from the neurons by the OPCs. This means that the feedback to the neurons cannot be seen as separated from the signal reception," explained Dr. Dominik Sakry, joint first author of the study, describing the cascade of events. The role of NG2 in this process became apparent when the researchers removed the protein: neuronal synaptic function is altered, modifying learning and disrupting the processing of sensory input that manifests in the form of behavioral changes in test animals.
The evidence that the communication between the two cell types in the brain is not a one-way system but a complex mechanism involving feedback loops was obtained in a collaborative project involving physiologists and molecular biologists. Participating in the project at Mainz University were the Faculties of Biology and Medicine and the Focus Program Translational Neurosciences (FTN) in the form of platform technology provided by the Mouse Behavioral Unit (MBU). The project was additionally supported by two Mainz Collaborative Research Centers (CRC 1080 and CRC-TR 128) and involved participation of the Leibniz Institute for Neurobiology in Magdeburg. Scientists from seven countries participated in the study.

Tuesday, December 16, 2014

Stroke Rounds: Memory Complaints Linked to Risk

Come come now, don't you think it is more likely that little strokes caused the memory problems? Does not anyone understand how cause and effect works?
http://www.medpagetoday.com/Cardiology/Strokes/49148?

An early marker for stroke risk among the well-educated?

Comparing Vegans’ Arteries to Runners’

Which way is your doctor pushing you to clean up your arteries?
http://nutritionfacts.org/2014/12/16/comparing-vegans-arteries-to-runners/?

What is rehabilitation potential? Development of a theoretical model through the accounts of healthcare professionals working in stroke rehabilitation services

I bet none of this is objectively looking at the brain scans and seeing what is just damaged so rehab can focus on those parts. The dead areas are pretty much a lost cause until more research is proven that tells us how to move functionality with any sense of being repeatable.
http://informahealthcare.com/doi/abs/10.3109/09638288.2014.991454
, , , , and
1School of Healthcare Sciences, Bangor University,
Bangor, Gwynedd
, UK,
2Faculty of Health Studies, School of Nursing, Bradford University,
Bradford
, UK,
3Stroke & Vascular Research, School of Nursing, Midwifery and Social Work, University of Manchester MAHSC,
Manchester
, UK, and
4Stroke & Vascular Research, University of Manchester MAHSC, Salford Royal NHS Foundation Trust,
Salford
, UK
Address for correspondence:
Christopher R. Burton
, Senior Research Fellow, School of Healthcare Sciences, Bangor University,
Bangor, Gwynedd LL57 2EF
, UK. Tel: 01248 382556. E-mail:

Abstract

Introduction: Multi-disciplinary team members predict each patient’s rehabilitation potential to maximise best use of resources. A lack of underpinning theory about rehabilitation potential makes it difficult to apply this concept in clinical practice. This study theorises about rehabilitation potential drawing on everyday decision-making by Health Care Professionals (HCPs) working in stroke rehabilitation services. Methods: A clinical scenario, checked for face validity, was used in two focus groups to explore meaning and practice around rehabilitation potential. Participants were 12 HCPs working across the stroke pathway. Groups were co-facilitated, audio-recorded and fully transcribed. Analysis paid attention to data grounded in first-hand experience, convergence within and across groups and constructed a conceptual overview of HCPs’ judgements about rehabilitation potential. Results: Rehabilitation potential is predicted by observations of “carry-over” and functional gain and managed differently across recovery trajectories. HCPs’ responses to rehabilitation potential judgements include prioritising workload, working around the system and balancing optimism and realism. Impacts for patients are streaming of rehabilitation intensity, rationing access to rehabilitation and a shifting emphasis between management and active rehabilitation. For staff, the emotional burden of judging rehabilitation potential is significant. Current service organisation restricts opportunities for feedback on the accuracy of previous judgements. Conclusion: Patients should have the opportunity to demonstrate rehabilitation potential by participation in therapy. As therapy resources are limited and responses to therapy may be context-dependent, early decisions about a lack of potential should not limit longer-term opportunities for rehabilitation. Services should develop strategies to enhance the quality of judgements through feedback to HCPs of longer-term patient outcomes.Implications for Rehabilitation
  • Rehabilitation potential is judged at the level of individual patients (rather than population-based predictive models of rehabilitation outcome), draws on different sources of often experiential knowledge, and may be less than reliable.
  • Decisions about rehabilitation potential may have far reaching consequences for individual patients, including the withdrawal of active rehabilitation in hospital or in the community and eventual care placement.
  • A better understanding of what people mean by rehabilitation potential by all team members, and by patients and carers, may improve the quality of joint decision making and communication.



Read More: http://informahealthcare.com/doi/abs/10.3109/09638288.2014.991454

Monday, December 15, 2014

Researchers tackle one of the biggest questions in dementia research

We have nothing like this for stroke because obviously all the biggest questions in stroke are too f*cking hard for anyone to solve. 'Run along Bobby and play and let the adults do nothing for stroke'.
http://medicalxpress.com/news/2014-12-tackle-biggest-dementia.html
Researchers in Southampton are tackling one of the biggest questions in dementia research; why might current approaches in Alzheimer's trials be failing? The new study is published in the Journal of Pathology and funded by Alzheimer's Research UK and the Medical Research Council.

More at link.

Matt Lopez Q & A, President - National Stroke Association

Basic Stationery Top - Redesign 2010
Dear Friend,
Like so many other stroke survivors, my stroke was unexpected and very personal. It has been a humbling experience to join National Stroke Association and be given the opportunity to give back to the stroke community.
I’d like to meet you and answer your questions. Join me on Dec. 17 at 10 a.m. MST for a video chat.
Your voice matters to me and I want to know what your needs are, how National Stroke Association can serve you better, and share with you my long-term vision to meet the growing needs of the stroke community.
I hope you’ll register for this exciting opportunity to chat live with me on Wednesday.
Photo of Matt Lopez
Sincerely,
signed by Matt Lopez, CEO
Matt Lopez
CEO

P.S. - The video chat will be hosted on YouTube LIVE. You do not need a YouTube account or video equipment to participate.
 -------------------------------------------------------------------------------------------------------------
My comments in the question box. As author of Deans' Stroke Musings I have thousands of questions that need answering. But we'll stick with the major problems in stroke.
What are you/NSA doing to solve these?
0. There is no fast, easy and objective w
ay to diagnose a stroke. Will the tricorder xPrize solve this?
1. tPA may save your life but with tPA having a 88% failure rate for full recovery, it's pretty lousy to depend on that.
2. Your neurologist doesn't have any concrete stroke protocols to save all the neurons that are dying in the first week. Neuronal cascade of death(5 causes).
3. Your neurologist or physiatrist doesn't have any clue about how to get you to full recovery. (Ask them exactly how to do it), you'll get excuses.
4. Only 10% get to full recovery..
5. No protocols to prevent your 33% dementia chance post-stroke from an Australian study.
6. Nothing to alleviate your fatigue.
7. Nothing that will cure your spasticity.
8. Nothing on cognitive training unless you find this yourself.
9. No published stroke protocols.
10. No way to compare your stroke hospital results vs. other stroke hospitals.
11. Excuses abound, the main one being the stupidity of 'All strokes are different, all stroke recoveries are different'.


Even if you can't go, sign up and pepper him with questions.
If you have a question you would like to ask Matt, please email it to events@stroke.org.

Anti-TNF drugs used in psoriatic arthritis trials - Etanercept

With this as an example Dr. Edward Tobinick could easily create clinical trials for his use of etanercept for stroke rehab and definitively prove whether this really works or not. But without a great stroke association pushing researchers to prove efficacy this will not get done.
http://www.uhnres.utoronto.ca/studies/cpsrd/psa/Psoriatic_Arthritis_Newsletter_August_18_2011.pdf

Recalling Nana's Face: Does Your Brain Store Memories?

Just read this, your brain doesn't store memories so obviously a stroke can't impair your memory
http://www.evolutionnews.org/2014/12/recalling_nanas091821.html
The last couple of paragraphs.
To assert that memories are stored in the brain is gibberish. And don't fall for the materialist invocation of promissory materialism -- "It's just a limitation of our current scientific knowledge, and we promise that science will solve the problem in due time." The assertion that the brain stores memories is logical nonsense that doesn't even rise to the level of empirical testability.
How then, you reasonably ask, can we explain the obvious dependence of memory on brain structure and function? While it is obvious that the memories aren't stored, it does seem that some parts of the brain are necessary ordinarily for memory. And that's certainly true. But necessary does not mean sufficient. There is a rough correspondence between activity in certain regions of the brain and the exercise of certain mental powers. That is what cognitive neuroscientists properly study. In some cases the correspondence between brain and memory is one of tight necessity -- the brain must have a specific activity for memory to be exercised. But the brain activity is not the same thing as the memory nor does it make any sense at all to say the brain activity codes for the memory or that the brain stores the memory.
What this all implies is that only some kind of dualism can provide a coherent understanding of the mind. But dualism is a many-headed hydra, and I don't think that Cartesian dualism or property dualism or epiphenomenalism or computational theories of the mind (which are inherently dualistic) explain things well either.
I hew to Thomistic dualism, which is a coherent view of the mind that takes an Aristotelian perspective and for which the participation of the brain in memory is not problematic at all.
Have fun.
PZ Myers take on this;

Ready to lose a few brain cells? You won’t need them, apparently

By pure reason alone, if we can call his argument a product of reason at all, he deduces that the brain could not possibly have any way of storing memories.

His first argument is by cock-eyed definition.

 

Sunday, December 14, 2014

Donating health data to PatientsLikeMe

Your choice. If we had a decent stroke association they would be gathering the statistics from the 800,000 strokes every year in the US and mine that data to find the commonalities and address them.
http://view.email.patientslikeme.com/?j=fec313757066027e&m=fe851271726d037476&ls=fe261777706004757c1673&l=fefe1575766701&s=fe5b15707d62007e7c11&jb=ffcf14&ju=fe6315767d640c7d7410&utm_medium=email&utm_source=newsletter&utm_campaign=general_20141214

High fat diet leads to brain inflammation and obesity

Has your hospital diet been scrubbed of the offending fats? You wouldn't want to make your damaged brain any worse. This research is in mice but is your hospital going to wait 30 years before it is replicated in humans before doing something about their food?
http://loonylabs.org/2014/12/13/food-inflammation-fat/

Increasing Rigor in Huntington’s Disease Research

And if we had anything approaching a minimally acceptable stroke association this would be a standard enforced practice for all stroke research.
http://blogs.discovermagazine.com/neuroskeptic/2014/12/14/increasing-rigor-huntingtons-disease-research/#.VI4gg2PYt8A

The Machine That Tried To Scan The Brain — In 1882

Yet 132 years later we still don't know how much more blood is needed when thinking hard. As survivors we are probably thinking hard 90% of the time while awake. Could that be causing our fatigue?
http://www.northcountrypublicradio.org/news/npr/340906546/the-machine-that-tried-to-scan-the-brain-in-1882
Angelo Mosso's "human circulation balance" machine worked like a seesaw to measure blood flow changes to the brain.

All generalizations are false, including this one.

Mark Twain.  I do tend to generalize a lot, but for some unknown reason not a single stroke medical person has written to me to complain. I wish they would, it would make for an interesting discussion as to why their profession has such a horrible record on getting survivors to recovery.
I'm unrepentant on thinking that my ideas are worth exploring in depth.
ASA - Dr. Mariell Jessup

NSA - Mr. Matt Lopez, 

WSO - Dr. Stephen Davis



I challenge you to tell me exactly where I'm wrong, with research backing you up. It will only take you 351 days to read my whole blog. Or you can have your minions read and critique it.

Saturday, December 13, 2014

Alanna Shaikh: How I'm preparing to get Alzheimer's

If your doctor isn't giving you any dementia prevention protocols is s/he at least providing you with something like this?
http://www.ted.com/talks/alanna_shaikh_how_i_m_preparing_to_get_alzheimer_s?

Putting stroke rehab technology through its paces

This joins the other rehab possibility by Jintronix . Which one does your doctor think is useful?

Smart Glove May Help Recover from Stroke

 

http://www.pulseitmagazine.com.au/index.php?option=com_content&view=article&id=2205:putting-stroke-rehab-technology-through-its-paces& 

The University of Tasmania is running a new study on the use of Canadian-designed software called Jintronix, which uses the Microsoft Kinect for Windows and virtual games to help people recovering from stroke to complete – and enjoy – their physiotherapy.
Led by UTAS lecturer and physiotherapist Marie-Louise Bird in association with Launceston General Hospital and the Tasmanian Health Organisation – North (THO-North), the randomised controlled trial will involve up to 70 patients using the Jintronix system and individualised therapy compared to traditional group therapy classes.
It will measure physical outcomes such as limb function and general physical activity on the ward using activity monitors, but also how much the client enjoys the therapy and how much time they spend in the program. Initially, the trial will look at outcomes while the patients are still in hospital, but the idea is to extend it to studying the technology when used at home.
While there are a number of other trials taking place around the country into providing stroke rehab at home through video conferencing, such as the University of Queensland's eHab program and Flinders University's Telehealth in the Home project, this trial will use the popular consumer device Kinect along with the Jintronix system, which has been designed specifically for stroke rehabilitation, Dr Bird said.
“The difference with our trial is the commercially available hardware – you can just go down to any retailer and just get a Kinect and a computer,” she said.
“At the moment we are trialling it in the hospital but the next part of the roll-out, and we are hoping to get more funding to make that happen, is to actually to do it in people’s homes.”
Five video game units have been set up in the physiotherapy area of the Launceston Hospital and another two in the THO-North public rehabilitation centre in Launceston. Dr Bird herself is based on the Newnham campus in Launceston but the technology allows for remote monitoring and the quick adjustment of the difficulty level of the exercises.
“For example, some of the software activities are for two minutes and some of them are for five repetitions,” she said. “At the beginning of their therapy, five repetitions might fatigue them and it will take them two or three minutes to do five repetitions. Whereas after they have practiced it for a while, they might do that in 20 seconds.
“I can then go in to the client management part of the system and have a look at the time they are spending in each program, and as well as that it will rate the accuracy.”
The software is able to calibrate the tasks every time they use the program depending on the range they have in their affected arm, using the Kinect motion sensor device. The Kinect also allows the unaffected arm to be used to switch to a new game, meaning they don't have to use a mouse.
The games also use audio and visual cues such as music and colour changes on the screen to tell the client when they have successfully completed the exercise.
Jintronix has a suite of 12 games, and Dr Bird has been working with the Canadian developers to add more levels of difficulty to provide more targeted levels of activity for that individual.
“It actually calibrates every day that they go into the program, how much range of movement they’ve got in their affected arm,” she said. “If I say I want to just have an easy program, it will be easy for the range they’ve got. If I say I want a hard program, it will be hard for the range they’ve got.
“Over the last year we’ve been working with the developers as originally it was just low, medium, hard. Now there’s not only 10 levels of difficulty, but I can actually say, for example with a squatting activity, I want this person to squat 5cm or 10cm. And even within the game, I can just click on a little spanner and instantly change the settings. It’s amazingly configurable.”
The trial currently involves a clinician working with the client to set up the program, but once it is up and running and the parameters are all set, therapy assistants can take over. With the remote monitoring capability, allowing the clinician to see whether the game is too hard or the client is fatigued, it quite easily allows for the program to be used in the client's home.
Dr Bird said the trial was a pragmatic one: the evidence is emerging that high levels of repetition in early physical rehabilitation results is important for good functional outcomes from stroke, and it also helps with concentration when used in association with occupational therapy. Evidence for the use of technology and gamification for rehab is also mounting, as is the need for therapy to be enjoyable.
Physiotherapists use physical activity enjoyment scales, known as PACES or PAE, to measure this factor, and Dr Bird and her team are using research by University of Melbourne physiotherapist Kelly Bower to measure enjoyment. Ms Bower has published extensively on the use of consumer devices such as Nintendo Wii for post-stroke rehabilitation.
“We are using a visual scale that was recently developed and published by Kelly Bower that looked at enjoyability, and with another paper that I’m working on, we've looked at technology with older adults and how they enjoy it,” Dr Bird said.
“We know that, if people enjoy physical activity, they are more likely to take it up and keep going in the longer term.”
The next stage is to recruit clients to use the system at home, such as those discharged into a transition care program, where clients receive therapy support at home for a certain amount of time. This will consist of providing the client with a computer, camera and a WiFi dongle, but does require a bit of IT configuration so the settings are correct.
One of the other trial leaders is Stuart Smith, director of the Healthy Eating, Active Living TecHnologY (HEALTHY) Research Centre, who is working with Dr Bird on extending it to rural communities.
“One of the things we would like to do is have a set-up in a community centre or a community gym,” Dr Bird said. “This could be supported by a health care worker or community champion who has a basic amount of training, and people could just go into the centre to participate in activities remote from their clinician. That way they get a little bit of socialisation, but they don’t have to then travel the 90 minutes to the hospital and 90 minutes back for their therapy.
“For stroke clients, fatigue is a huge thing, but as well for our rural clients you’ve got the other option of do you put the physio or OT in the car and they travel three or four hours. It’s just not a good use of people's time.”
There is also a lot of interest in the technology for children with disabilities but this software itself is not yet designed with children in mind. However, Dr Bird said the back-end technology is just the same.
“There’s a huge amount of applications,” she said. “We are using it for motor control with stroke but I think for just improving physical activity to prevent cardiovascular disease, or for wheelchair-bound children, there’s a huge potential there as well. There’s lots of stuff going on.”
The trial is being funded by the National Stroke Foundation with a $20,000 seeding grant added to financial and in-kind support from the University and the Department of Health and Human Services.

 

Study confirms controversial nitrite hypothesis

So are our doctors ever going to create a stroke protocol on how to get NO(nitric oxide) and how much? Or are we going to have to wing it like everything else in stroke rehab?
http://phys.org/news/2014-12-controversial-nitrite-hypothesis.html
Understanding how nitrite can improve conditions such as hypertension, heart attack and stroke has been the object of worldwide research studies. New research from Wake Forest University has potentially moved the science one step closer to this goal.

More at link.

Nasal Release Technique for Traumatic Brain Injury

Wow, just wow. I would never allow either this or Cranial Sacral Therapy. But you will probably  need to research this on your own. Nothing found in Google Scholar so you will need to ask for documented peer-reviewed research before going down this route.
https://www.youtube.com/watch?v=hQcZT3l7my8

Impaired Ipsilateral Upper Extremity Dexterity and Its Relationship with Disability in Post-Stroke Right Hemiparesis

I have no clue as to the point of this research. You may as well ask if water is wet.
http://jrsr.sums.ac.ir/index.php/jrsr/article/view/20
Maryam Parsaee, Shohreh Noorizadeh Dehkordi, Mehdi Dadgoo, Malahat Akbarfahimi

Abstract


Background: The objectives of this study were to compare manual dexterity (gross and fine) and coordination performance of the ipsilateral upper extremity of the right hemisphere stroke patients with the same side of a healthy group, and to determine the relationship of ipsilateral upper extremity dexterity and disability.
Methods: In a non-randomized analytical study, 30 individuals with a unilateral first-ever stroke from outpatient rehabilitation clinics and 30 age and sex-matched adults without history of neurological disorders were enrolled. Purdue Pegboard, Box and Block, and Finger to Nose tests were used to measure dexterity (fine and gross) and coordination performance of the stroke group compared with the same hand of the healthy group. The Barthel index was also used to assess disability or dependency of stroke patients in basic activities of daily living.
Results: Results showed that stroke individuals with involvement of ipsilateral hand had less coordination and dexterity when compared to the same hand of normal subjects (P=0.001). In addition, the relationship of gross and fine manual dexterity performance of the ipsilateral upper extremity with disability, including dependence in basic activities of daily living, were significant respectively (r=0.376, r= 0.391).
Conclusion: People with right stroke had significant ipsilateral upper extremity impairments (manual dexterity and coordination tasks), and this hand dexterity deterioration had an impact on their dependence in basic activities of daily living.

Methodology of the Stroke Self-Management Rehabilitation Trial: An International, Multisite Pilot Trial

Well, well, look at that, stroke researchers giving up on solving how to get better rehabilitation results. They want to throw all the responsibility for your rehabilitation on you. As Dr. Steven Wolf writes, a rehabilitation stroke expert and professor at Emory University School of Medicine in Atlanta.  "Stroke patients need to rely more on their own problem solving to regain mobility".
If we had anything resembling a decent stroke association, that president would be reading the riot act to anyone who throws up their hands like this and gives up on doing their job because it is too hard. F*cking hey, try rehabbing from a stroke with NO help from your doctor.

What a bunch of bullcrap, 'You've had this major brain attack and we know nothing about how to get you better.  So deal with this yourself, you will recover just as well without our help.'
But it will save a lot of money and our doctors will never need to read research again, washing their hands of their responsibility to help us get better. 


http://www.strokejournal.org/article/S1052-3057%2814%2900433-9/abstract 
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Annemarei Ranta, FRACP, MD, PG Cert Sci (Public Health)
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Emmanuel Sanya, FWACP, MSc, PhD
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on behalf of the
1SMART Study Group members (additional to the article coauthors): Yogini Ratnasabapathy, Denise Taylor, Elizabeth Kendall, Carolyn Ehrlich, Steven Wolf, Dominique Cadilhac, Marilyn MacKay-Lyons, Man Mohan Mehndiratta, Jeyaraj Durai Pandian, Deepti Arora, Peter Langhorn, Gustavo Saposnik, Narayanaswamy Venketasubramanian, Bo Norrving, Akshay Anand, Dheeraj Kurana, Michael Brainin, Natan Bornstein, Richard Lindley, Foad Abd-Allah, Reginald Obiako, Emmanuel Sanya, Maree O'Connor, Rene Stolwyk, and Peter New.
Publication stage: In Press Corrected Proof

Rationale

Stroke is a major cause of long-term adult disability with many survivors living in the community relying on family members for on-going support. However, reports of inadequate understanding of rehabilitation techniques are common. A self-management DVD-based observational learning tool may help improve functional outcomes for survivors of stroke and reduce caregivers' burden.

Aims

This article describes the methodology of the stroke self-management rehabilitation trial. The overall aim of this pilot trial is to assess the feasibility and preliminary efficacy of a DVD-based intervention for improving functional outcomes of survivors of stroke 2 months postrandomization to inform the design of a full-scale randomized clinical trial.

Design

Recruitment of a minimum of 20 survivors of stroke and their informal caregivers (where available) in each of the participating centers will occur across multiple international sites. After baseline assessments, participants will be randomly assigned to an intervention or standard care group. The intervention comprises a structured DVD observation and practice schedule over 8 weeks. All participants will complete follow-up assessments.

Study outcomes

The outcome measures will include a global shift in the Rankin Scale scores and dichotomized scores, changes in quality of life, general health, depression, and caregiver burden at 2 months postrandomization. A qualitative analysis of the effects of the intervention will also be undertaken.

Discussion

The results of the pilot study will provide knowledge of whether observational learning techniques delivered via DVD can effectively improve recovery after stroke and reduce caregiver burden.
 

Friday, December 12, 2014

Coffee and Artery Function

Fascinating look at all the research behind coffee and tea, but with no transcript it is almost impossible to look up this research yourself and see what you should do. I will keep drinking coffee to handle my fatigue and delay/prevent dementia. This is a perfect question for your doctor who should have absorbed all this information and be able to present you with answers on how to deal with this.
http://nutritionfacts.org/video/coffee-and-artery-function/?utm_source=rss&utm_medium=rss&utm_campaign=coffee-and-artery-function

Further Confirmation that AGE-Breaker Alagebrium Has No Significant Effect in Humans

Well, maybe this earlier post is no longer valid, but did your doctor know that?

Stiff arteries relax like younger blood vessels after taking alagebrium


https://www.fightaging.org/archives/2014/01/further-confirmation-that-age-breaker-alagebrium-has-no-significant-effect-in-humans.php

Strategy Training Shows Promise for Addressing Disability in the First 6 Months After Stroke

This is all well and good but I bet we wouldn't need as much after the fact rehabilitation if our stroke medical teams would stop all the death and destruction during the neuronal cascade of death in the first week. Would music listening produce the same results? Send your doctor after the strategy training protocols.
http://nnr.sagepub.com/content/early/2014/11/21/1545968314562113?papetoc
  1. Elizabeth R. Skidmore, PhD1
  2. Deirdre R. Dawson, PhD2,3
  3. Meryl A. Butters, PhD1,4
  4. Emily S. Grattan, MS1
  5. Shannon B. Juengst, PhD1
  6. Ellen M. Whyte, MD1,4
  7. Amy Begley, MA1,4
  8. Margo B. Holm, PhD1
  9. James T. Becker, PhD1
  1. 1University of Pittsburgh, Pittsburgh, PA, USA
  2. 2Rotman Research Institute at Baycrest, Toronto, Ontario, Canada
  3. 3University of Toronto, Toronto, Ontario, Canada
  4. 4Western Psychiatric Institute & Clinic, Pittsburgh, PA, USA
  1. Elizabeth Skidmore, Department of Occupational Therapy, University of Pittsburgh, 5012 Forbes Tower, Pittsburgh, PA 15260, USA. Email: skidmore@pitt.edu

Abstract

Background. Cognitive impairments occur frequently after stroke and contribute to significant disability. Strategy training shows promise but has not been examined in the acute phase of recovery. Objective. We conducted a single-blind randomized pilot study estimating the effect of strategy training, relative to reflective listening (attention control), for reducing disability and executive cognitive impairments. Methods. Thirty participants with acute stroke who were enrolled in inpatient rehabilitation and had cognitive impairments were randomized to receive strategy training (n = 15, 10 sessions as adjunct to usual inpatient rehabilitation) or reflective listening (n = 15, same dose). The Functional Independence Measure assessed disability at baseline, rehabilitation discharge, 3, and 6 months. The Color Word Interference Test of the Delis–Kaplan Executive Function System assessed selected executive cognitive impairments (inhibition, flexibility) at baseline, 3, and 6 months. Results. Changes in Functional Independence Measure scores for the 2 groups over 6 months showed significant effects of group (F1,27 = 9.25, P = .005), time (F3,74 = 96.00, P < .001), and group * time interactions (F3,74 = 4.37, P < .007) after controlling for baseline differences in stroke severity (F1,27 = 6.74, P = .015). Color Word Interference Inhibition scores showed significant effects of group (F1,26 = 6.50, P = .017) and time (F2,34 = 4.74, P = .015), but the group * time interaction was not significant (F2,34 = 2.55, P = .093). Color Word Interference Cognitive Flexibility scores showed significant effects of group (F1,26 = 23.41, P < .001), time (F2,34 = 12.77, P < .001), and group * time interactions (F2,34 = 7.83, P < .002). Interaction effects suggested greater improvements were associated with strategy training. Conclusions. Strategy training shows promise for addressing disability in the first 6 months after stroke. Lessons from this pilot study may inform future clinical trials.

Generalizability of the Proportional Recovery Model for the Upper Extremity After an Ischemic Stroke

No clue on what the usefulness of this is for your recovery. Once again proving that stroke medical personnel have no clue that looking at external manifestations of problems as seen by the Fugl-Meyer scores is rather stupid because you should look at the source of the problem, namely the dead and damaged neurons in the brain.
http://nnr.sagepub.com/content/early/2014/11/21/1545968314562115?papetoc
  1. Caroline Winters, MSc1
  2. Erwin E. H. van Wegen, PhD1
  3. Andreas Daffertshofer, PhD2
  4. Gert Kwakkel, PhD1,3
  1. 1Department of Rehabilitation Medicine, MOVE Research Institute Amsterdam, VU University Medical Center, Amsterdam, The Netherlands
  2. 2MOVE Research Institute Amsterdam, Faculty of Human Movement Sciences, VU University, Amsterdam, The Netherlands
  3. 3Department of Neurorehabilitation, Reade Centre for Rehabilitation and Rheumatology, Amsterdam, The Netherlands
  1. Erwin E. H. van Wegen, PhD, Department of Rehabilitation Medicine, MOVE Research Institute Amsterdam, VU University Medical Center; PO Box 7057, 1007 MB, Amsterdam, Netherlands. Email: e.vanwegen@vumc.nl

Abstract

Background and objective. Spontaneous neurological recovery after stroke is a poorly understood process. The aim of the present article was to test the proportional recovery model for the upper extremity poststroke and to identify clinical characteristics of patients who do not fit this model. Methods. A change in the Fugl-Meyer Assessment Upper Extremity score (FMA-UE) measured within 72 hours and at 6 months poststroke served to define motor recovery. Recovery on FMA-UE was predicted using the proportional recovery model: ΔFMA-UEpredicted = 0.7·(66 − FMA-UEinitial) + 0.4. Hierarchical cluster analysis on 211 patients was used to separate nonfitters (outliers) from fitters, and differences between these groups were studied using clinical determinants measured within 72 hours poststroke. Subsequent logistic regression analysis served to predict patients who may not fit the model. Results. The majority of patients (~70%; n = 146) showed a fixed proportional upper extremity motor recovery of about 78%; 65 patients had substantially less improvement than predicted. These nonfitters had more severe neurological impairments within 72 hours poststroke (P values <.01). Logistic regression analysis revealed that absence of finger extension, presence of facial palsy, more severe lower extremity paresis, and more severe type of stroke as defined by the Bamford classification were significant predictors of not fitting the proportional recovery model. Conclusions. These results confirm in an independent sample that stroke patients with mild to moderate initial impairments show an almost fixed proportional upper extremity motor recovery. Patients who will most likely not achieve the predicted amount of recovery were identified using clinical determinants measured within 72 hours poststroke.

A Systematic Review of the Effect of Mirror Visual Feedback on the Brain

Al these research articles and they still don't mention where to find the stroke protocols on how to use this to recover. You could try asking your doctor but I bet that will be useless.
http://nnr.sagepub.com/content/early/2014/08/22/1545968314546134.short?rss=1&ssource=mfr
  1. Frederik J. A. Deconinck, PhD1,2
  2. Ana R. P. Smorenburg, PhD3
  3. Alex Benham, PhD4
  4. Annick Ledebt, PhD5
  5. Max G. Feltham, PhD6
  6. Geert J. P. Savelsbergh, PhD5
  1. 1Ghent University, Ghent, Belgium
  2. 2Manchester Metropolitan University, Manchester, UK
  3. 3Burke-Cornell Medical Research Institute, White Plains, NY, USA
  4. 4Bradford Institute for Health Research, Bradford, UK
  5. 5VU University, Amsterdam, Netherlands
  6. 6University of Birmingham, Birmingham, UK
  1. Frederik J. A. Deconinck, Ghent University, Faculty of Medicine and Health Sciences, Department of Movement and Sports Sciences, Watersportlaan 2, Gent 9000, Belgium. Email: Frederik.Deconinck@UGent.be

Abstract

Background. Mirror visual feedback (MVF), a phenomenon where movement of one limb is perceived as movement of the other limb, has the capacity to alleviate phantom limb pain or promote motor recovery of the upper limbs after stroke. The tool has received great interest from health professionals; however, a clear understanding of the mechanisms underlying the neural recovery owing to MVF is lacking. Objective. We performed a systematic review to assess the effect of MVF on brain activation during a motor task. Methods. We searched PubMed, CINAHL, and EMBASE databases for neuroimaging studies investigating the effect of MVF on the brain. Key details for each study regarding participants, imaging methods, and results were extracted. Results. The database search yielded 347 article, of which we identified 33 suitable for inclusion. Compared with a control condition, MVF increases neural activity in areas involved with allocation of attention and cognitive control (dorsolateral prefrontal cortex, posterior cingulate cortex, S1 and S2, precuneus). Apart from activation in the superior temporal gyrus and premotor cortex, there is little evidence that MVF activates the mirror neuron system. MVF increases the excitability of the ipsilateral primary motor cortex (M1) that projects to the “untrained” hand/arm. There is also evidence for ipsilateral projections from the contralateral M1 to the untrained/affected hand as a consequence of training with MVF. Conclusion. MVF can exert a strong influence on the motor network, mainly through increased cognitive penetration in action control, though the variance in methodology and the lack of studies that shed light on the functional connectivity between areas still limit insight into the actual underlying mechanisms.