Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 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. Did your doctor somehow miss the recovery protocol that Pedro Bach-y-Rita used to recover fully back in 1958 with only a partial brain?

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. 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 lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Monday, February 23, 2015

VIDEO: "Too good to treat" stroke patients may benefit from tPA

This is f*cking appalling. Because the stroke medical world has put all their eggs in one basket - tPA, these people are totally screwed. Maybe if your doctor would look at   these 31 hyperacute possibilities I'm going to insist my doctor give me the first week. 
Or these 177 hyperacute therapies that need more research.
Damn it all, have your doctor do something useful, solve some of the problems in stroke.
Does this contradict this earlier research?

Outcomes mostly favorable for ‘too good to treat’ stroke patients



http://www.healio.com/cardiology/stroke/news/online/%7B87954125-bb0e-4c90-920d-f0faa8ad2c76%7D/video-too-good-to-treat-stroke-patients-may-benefit-from-tpa 
 Khwaja Siddiqui, MD, clinical research fellow in the department of neurology at the Massachusetts General Hospital Institute for Heart, Vascular and Stroke Care, outlines his study on predictors of poor outcomes among patients with stroke considered "too good to treat."
Patients with stroke who present within the window for treatment with IV tPA but have mild or rapidly improving symptoms are not usually treated, Siddiqui said at the International Stroke Conference. However, prior research has indicated that patients who do not receive treatment at presentation for this reason experience poor outcomes.
In this trial, researchers evaluated 238 patients with evaluable baseline and infarct characteristics who did not receive treatment on presentation due to mild or improving symptoms. A good outcome was defined as discharge home from the hospital, while negative outcomes included discharge elsewhere or death. Multivariate analysis indicated that advanced age, Hispanic ethnicity, bihemispheric infarcts and higher score on the NIH Stroke Scale were independent predictors of poor outcomes without treatment.
Siddiqui said this study provides a basis for recognizing patients with stroke who present with symptoms that would normally be considered "too good to treat," but may benefit from TPA.

Peptides used to protect stroke victims from brain damage

Totally worthless article. It doesn't reference the name of the peptide or the research name. Bruno Meloni doesn't show up with this in google scholar.  What a waste of print.
This other news source does identify the peptides;
Peptides May Reduce Brain Injury After Stroke
Using in vitro neuronal cell culture stroke models we soon discovered that poly-arginine and arginine-rich peptides on their own possessed potent neuroprotective properties.  Furthermore, we showed that as the length of the poly-arginine peptide increased so did the peptides neuroprotective properties.  Excitingly, the poly-arginine peptides were even more potent than the ”neuroprotective peptides” we had been working with and peptides developed by other overseas researchers.
We have now confirmed using a laboratory animal stroke model that poly-arginine peptides could reduce brain damage when administered up to 1-hour after the stroke. 

The news source that is worthless: 

Peptides used to protect stroke victims from brain damage


West Australian researchers have discovered a way to use peptides to protect stroke victims from brain damage, and say the breakthrough may reduce the risk of sustaining a serious disability from a stroke, especially for people living in remote Australia.
Professor David Blacker, the medical director of the West Australian Neuroscience Research Institute, said it was an important development in stroke research.
"In the rats that were given experimental peptides the volume of stroke damage was substantially smaller," he said.
"If we can apply that to human models, the hope would be that critical bits of the brain will be less affected."
The discovery is a big deal, especially for the 50,000 people who will have a stroke this year.
"It's devastating and there have been surveys that reveal older people will fear surviving a stroke with a substantial disability; they will fear that more than actually dying," Professor Blacker said.
Professor Blacker, who is also a neurologist at Perth's Sir Charles Gairdner Hospital, said most researchers had given up trying to find such a treatment.
"At these stroke conferences just recently, people have been standing and applauding the speakers ... because we're so used to trials that have had no result or been negative," he said.

It is hoped that giving victims peptides within an hour of a stroke will buy them more time before brain damage starts.
"It's all well and good if you're in a major metro centre and you collapse in the middle of the day and get brought to a hospital where you've got the team that can do the techniques to remove the clot," Professor Blacker said.
"But it's no good if you're rural and remote [in] Western Australia or Queensland or the Northern Territory where you're hours and hours away.
"If we could actually; the patient has a stroke and gets some of these drugs that slow down the clotting cascade, it'll buy you some extra time.
"Then the patient could be transported for more definitive treatment."

Research 'a game changer', second breakthrough this month

Professor Bruno Meloni led the research team and said the discovery was a potential game-changer.
"It could [mean] from a person who is paralysed to a person who has no paralysis, so it will definitely improve their standard of living and their outcomes," he said.
This is the second major breakthrough in the field this month.
Last week, Melbourne researchers revealed details of a new treatment that almost doubles stroke victims' chances of walking out of hospital without a disability.
It involves identifying which parts of the brain are salvageable after a stroke before removing the blood clot and giving the patient clot-busting drugs.
Professor Meloni said the two discoveries complement each other.
"The research that came out of Melbourne showed that if you can improve blood flow to the brain, this can limit brain injury and improve patient outcomes," he said.
"However, despite that treatment, the brain can still be vulnerable to the effects of stroke, and our peptides particularly target vulnerable tissue that may eventually become damage.
"So the peptides aim to further inhibit or suppress the brain damage that occurs after stroke."
This trial was done on rats and it is expected to be some years before the peptides are tested on humans in a clinical trial.
But Professor Blacker said time is always of the essence when it comes to stroke research.
"One in six people in the world will have a stroke," he said.
"Moving our studies on, moving the development of new drugs along quickly, is imperative."
The team also hopes to secure funding to explore how the peptides could help people suffering from other conditions, including cardiac arrest and spinal injury.

Sunday, February 22, 2015

Portable Neuromodulation Stimulator (PoNS) device

One of the chapters in Norman Doidges new book discusses this with respect to Parkinsons, stroke, and multiple sclerosis. You'll have to see what your doctor thinks on this and what protocols have been designed with its use in mind. More than likely your doctor has not heard of it.  Good luck.

Portable Neuromodulation Stimulator (PoNS) device

About The PoNS
The Portable Neuromodulation Stimulator (PoNS) device is an investigational medical device being studied for the treatment of neurological symptoms caused by disease or trauma. The PoNS is currently being studied in the United States for the treatment of balance disorder related to mild to moderate Traumatic Brain Injury (mTBI), and in Canada for the treatment of gait and balance disorder for patients with Multiple Sclerosis (MS). It represents the first in a series of non-invasive devices – based on the patented PoNS platform – designed to amplify the brain’s powerful ability to heal itself. This is part of a new approach being studied for symptom treatment for the rising number of patients who have experienced loss of function as a result of neurological disease or trauma.

Saturday, February 21, 2015

Growth cones carve a path through tissues

We need this for our neurons that are trying to reconnect. What is your doctor doing to facilitate this research? Does your hospital have goals and objectives for each of its' neurologists to produce viable stroke research each year? If not, you need to call your hospital president and ask why their stroke department is so f*cking incompetent.
http://www.sciencemag.org/content/347/6224/837.5.full?utm_campaign=email-sci-ec&
Figure
Neural growth cones use invadopodia-like fingers to push through tissues
PHOTO: TIMOTHY GOMEZ
A growth cone leading a neuron's development needs more than muscle to push its way through tissues and across boundaries. Santiago-Medina et al. found features on neuronal growth cones that are like the invadosomes of immune and metastatic cancer cells, which themselves have a knack for squeezing through existing tissues. These invadosomes, fingers that poke out into the surrounding tissue, are packed with cytoskeleton and exude proteases that degrade the extracellular matrix. The invadosomes were key for Xenopus motoneurons trying to find a path out of the spinal cord and into the developing musculature.
Development 10.1242/dev.108266 (2015).

How robotics might work for stroke

If we had ANYTHING approaching a decent stroke association they would be in contact with Boston Dynamics to explore the vast market of 10 million stroke survivors a year to see what robotics could do for survivors. But no, they will just sit on their asses because survivor rehabilitation is again somebody elses' problem to solve. No one is going to help us but ourselves.

http://www.bostondynamics.com/index.html

EFFING HEY

Friday, February 20, 2015

Can Parkinson’s disease be cured by stimulating neurogenesis?

Same question for stroke. Whom is researching the answer?
http://www.jci.org/articles/view/80822
Thomas Foltynie
Sobell Department of Motor Neuroscience, UCL Institute of Neurology, National Hospital for Neurology and Neurosurgery, London, United Kingdom.
Address correspondence to: Thomas Foltynie, Sobell Department of Motor Neuroscience, UCL Institute of Neurology, Box 146, National Hospital for Neurology and Neurosurgery, Queen Square, London, WC1N 3BG. Phone: 44.203.448.8726; E-mail: T.Foltynie@ucl.ac.uk.
Published February 17, 2015
There have been many attempts at slowing down or even reversing the neurodegenerative process of Parkinson’s disease (PD). To date, there are no treatments of proven value in this regard. One underexplored route to slow the neurodegenerative process is the use of agents that may stimulate neurogenesis in the subventricular zone. In animal models of PD, PDGF-BB has been shown to restore/protect against dopaminergic deficits caused by neurotoxins via increased neurogenesis in the subventricular zone. Previous work suggests that these new cells are not themselves dopaminergic but have trophic effects on residual dopaminergic cells in the substantia nigra. In this issue of the JCI, Paul et al. evaluate this agent in individuals with PD and show that i.c.v. administration of PDGF-BB is safe and well tolerated. This study lays the foundation for formal dose-finding studies and clinical trials to assess the efficacy of this agent as a potential neuroprotective treatment for PD.

Therapy-induced brain reorganization patterns in aphasia

You'll have to see what your doctor and speech therapist can use from this to make a stroke protocol.
http://brain.oxfordjournals.org/content/early/2015/02/14/brain.awv022.abstract

, , , ,
DOI: http://dx.doi.org/10.1093/brain/awv022 First published online: 16 February 2015

Summary

Both hemispheres are engaged in recovery from word production deficits in aphasia. Lexical therapy has been shown to induce brain reorganization even in patients with chronic aphasia. However, the interplay of factors influencing reorganization patterns still remains unresolved. We were especially interested in the relation between lesion site, therapy-induced recovery, and beneficial reorganization patterns. Thus, we applied intensive lexical therapy, which was evaluated with functional magnetic resonance imaging, to 14 chronic patients with aphasic word retrieval deficits. In a group study, we aimed to illuminate brain reorganization of the naming network in comparison with healthy controls. Moreover, we intended to analyse the data with joint independent component analysis to relate lesion sites to therapy-induced brain reorganization, and to correlate resulting components with therapy gain. As a result, we found peri-lesional and contralateral activations basically overlapping with premorbid naming networks observed in healthy subjects. Reduced activation patterns for patients compared to controls before training comprised damaged left hemisphere language areas, right precentral and superior temporal gyrus, as well as left caudate and anterior cingulate cortex. There were decreasing activations of bilateral visuo-cognitive, articulatory, attention, and language areas due to therapy, with stronger decreases for patients in right middle temporal gyrus/superior temporal sulcus, bilateral precuneus as well as left anterior cingulate cortex and caudate. The joint independent component analysis revealed three components indexing lesion subtypes that were associated with patient-specific recovery patterns. Activation decreases (i) of an extended frontal lesion disconnecting language pathways occurred in left inferior frontal gyrus; (ii) of a small frontal lesion were found in bilateral inferior frontal gyrus; and (iii) of a large temporo-parietal lesion occurred in bilateral inferior frontal gyrus and contralateral superior temporal gyrus. All components revealed increases in prefrontal areas. One component was negatively correlated with therapy gain. Therapy was associated exclusively with activation decreases, which could mainly be attributed to higher processing efficiency within the naming network. In our joint independent component analysis, all three lesion patterns disclosed involved deactivation of left inferior frontal gyrus. Moreover, we found evidence for increased demands on control processes. As expected, we saw partly differential reorganization profiles depending on lesion patterns. There was no compensatory deactivation for the large left inferior frontal lesion, with its less advantageous outcome probably being related to its disconnection from crucial language processing pathways.

Safety and life-saving efficacy of statins have been exaggerated, says USF scientist

Who to believe?

Safety and life-saving efficacy of statins have been exaggerated, says USF scientist


 

 

This Is Your Brain on a Motorcycle

I'm sure your doctor will prescribe motorcycle riding in order to improve your cognitive functions post-stroke. Do NOT do this without a doctors prescription.
https://web.archive.org/web/20120921011709/http://www.motorcycleinsurance.com/this-is-your-brain-on-a-motorcycle/
Riding a motorcycle every day might actually keep your brain functioning at peak condition, or so says a study conducted by the University of Tokyo. The study demonstrated that riders between the age of 40 and 50 were shown to improve their levels of cognitive functioning, compared to a control group, after riding their motorcycles  daily to their workplace for a mere two months.

Scientists believe that the extra concentration needed to successfully operate a motorcycle can contribute to higher general levels of brain function, and it’s that increase in activity that’s surely a contributing factor to the appeal of the motorcycles as transportation. It’s the way a ride on a bike turns the simplest journey into a challenge to the senses that sets the motorcyclist apart from the everyday commuter. While the typical car-owning motorist is just transporting him or her self from point A to point B, the motorcyclist is actually transported into an entirely different state of consciousness .
Riding a motorcycle is all about entrance into an exclusive club where the journey actually is the destination.
Dr Ryuta Kawashima, author of Dr Kawashima’s Brain Training: How Old Is Your Brain, reported the outcome of his study of “The relationship between motorcycle riding and the human mind.”
Kawashima’s experiments involved current riders who currently rode motorcycles on a regular basis (the average age of the riders was 45) and  ex-riders who once rode regularly but had not taken a ride for 10 years or more. Kawashima asked the participants to ride on courses in different conditions while he recorded their brain activities. The eight courses included a series of curves, poor road conditions, steep hills, hair-pin turns and a variety of other challenges.
What did he find? After an analysis of the data, Kawashima found that the current riders and ex-riders used their brain in radically different ways. When the current riders rode motorcycles, specific segments of their brains (the right hemisphere of the prefrontal lobe) was activated and riders demonstrated a higher level of concentration.
His next experiment was a test of how making a habit of riding a motorcycle affects the brain.
Trial subjects were otherwise healthy people who had not ridden for 10 years or more. Over the course of a couple of months, those riders used a  motorcycle for their daily commute and in other everyday situations while Dr Kawashima and his team studied how their brains and mental health changed.
The upshot was that the use of motorcycles in everyday life improved cognitive faculties, particularly those that relate to memory and spatial reasoning capacity. An added benefit? Participants revealed on questionnaires they filled out at the end of the study that their stress levels had been reduced and their mental state changed for the better.
So why motorcycles? Shouldn’t driving a car should have the same effect as riding a motorcycle?
“There were many studies done on driving cars in the past,” Kawashima said. “A car is a comfortable machine which does not activate our brains. It only happens when going across a railway crossing or when a person jumps in front of us. By using motorcycles more in our life, we can have positive effects on our brains and minds”.
Yamaha participated in a second joint research project on the subject of the relationship between motorcycle riding and brain stimulation with Kawashima Laboratory at the Department of Functional Brain Imaging, Institute of Development, Aging and Cancer at Tohoku University.
The project began in September 2009 and ran until December 2010, and the focus of the research was on measurement and analysis of the cause and effect relationship involved in the operation of various types of vehicles and brain stimulation. The study measured changes in such stimulation over time by means of data gathered from a long-term mass survey.
The reason for Yamaha Motor’s participation in this project is pretty obvious and not a little self-serving, but further research into the relationship between motorcycle riding and brain stimulation as it relates to the “Smart Aging Society” will certainly provide some interesting results.
The second research project was divided into two time periods throughout 2009 and 2010 compared differences in the conditions of brain stimulation as they related to the type of vehicle and driving conditions. A second set of tests measuring the changes in brain stimulation over time involved a larger subject group.
Yamaha Motors provided vehicles for the research and made its test tracks and courses available for the study. What the study revealed is that what you’re thinking about while you’re riding – and your experience on the bike -  changes the physical structure of your brain.
Author Sharon Begley concurs with Kawashima’s findings. In her tome, Train Your Mind – Change Your Brain, Begley found much the same outcomes.
“The brain devotes more cortical real estate to functions that its owner uses more frequently and shrinks the space devoted to activities rarely performed,” Begley wrote. “That’s why the brains of violinists devote more space to the region that controls the digits of the fingering hand.”
And you may also get some mental and physical benefits from just thinking about going for a ride on your machine.
A 1996 experiment at Harvard Medical School by neuroscientist Alvaro Pascual-Leone had volunteers practice a simple five finger exercise on the piano over five days for a couple of hours each day. Pascual-Leone found that the brain space devoted to these finger movements grew and pushed aside areas less used.  A separate group of volunteers were asked to simply think about doing the piano exercises during that week as well, and they dedicated the same amount of “practice time.”
Pascual-Leone was somewhat take aback to discover that the region of the brain which controls piano playing finger movement expanded in the same way for volunteers who merely imagined playing the piano.
Along with the obvious benefits of riding motorcycles; like saving money (motorcycle insurance is relatively inexpensive), motorcycles take the edge off the grind of the daily commute, and that appears to make your brain a better place to be…

Hot tub stroke rehabilitation

Last night was our monthly potluck and wine party based upon this wine school article;
Your Next Lesson: Langhe Nebbiolo
Between the 9 of us we polished off 5 bottles. Reasons here;

Red Wine Prevents Memory Loss

After most people left 4 of us entered the hot tub. This became a never ending rehab exercise. In order not to slip off the bench I had to force my spastic left leg to stay connected to the floor, while still holding the wine glass above the water. It was not a good idea to let my leg start wandering into other peoples spaces. The thermal stimulation was great for sensation. Even after two hours in the tub my bicep refused to relax and straighten out. Spasticity sucks big time.

New brain mapping reveals unknown cell types

No wonder we have a hell of a time getting competently rehabbed. We don't even know yet what types of brain cells we have or what they do. I wonder where the 65 billion number came from, it used to be assumed that we had 100 billion until someone a couple of years ago determined there was no basis for it and came up with 80 billion. 

New brain mapping reveals unknown cell types


Using a process known as single cell sequencing, scientists at Karolinska Institutet have produced a detailed map of cortical cell types and the genes active within them. The study, which is published in the journal Science, marks the first time this method of analysis has been used on such a large scale on such complex tissue. The team studied over three thousand cells, one at a time, and even managed to identify a number of hitherto unknown types.
“If you compare the brain to a fruit salad, you could say that previous methods were like running the fruit through a blender and seeing what colour juice you got from different parts of the brain,” says Sten Linnarsson, senior researcher at the Department of Medical Biochemistry and Biophysics. “But in recent years we’ve developed much more sensitive methods of analysis that allow us to see which genes are active in individual cells. This is like taking pieces of the fruit salad, examining them one by one and then sorting them into piles to see how many different kinds of fruit it contains, what they’re made up of and how they interrelate.”
The knowledge that all living organisms are built up of cells is almost 200 years old. Since the discovery was made by a group of 19th century German scientists, we have also learnt that the nature of a particular body tissue is determined by its constituent cells, which are, in turn, determined by which genes are active in their DNA. However, little is still known about how this happens in detail, especially as regards the brain, the body’s most complex organ.
In the present study, the scientists used large-scale single-cell analysis to answer some of these questions. By studying over three thousand cells from the cerebral cortex in mice, one at a time and in detail, and comparing which of the 20,000 genes were active in each one, they were able to sort the cells into virtual piles. They identified 47 different kinds of cell, including a large proportion of specialised neurons, some blood vessel cells and glial cells, which take care of waste products, protect against infection and supply nerve cells with nutrients.
With the help of this detailed map, the scientists were able to identify hitherto unknown cell types, including a nerve cell in the most superficial cortical layer, and six different types of oligodendrocyte, which are cells that form the electrically insulating myelin sheath around the nerve cells. The new knowledge the project has generated can shed more light on diseases that affect the myelin, such as multiple sclerosis (MS).
 “We could also confirm previous findings, such as that the pyramidal cells of the cerebral cortex are functionally organised in layers,” says Jens Hjerling-Leffler, who co-led the study with Dr Linnarsson. “But above all, we have created a much more detailed map of the cells of the brain that describes each cell type in detail and shows which genes are active in it. This gives science a new tool for studying these cell types in disease models and helps us to understand better how brain cell respond to disease and injury.”
There are estimated to be 100 million cells in a mouse brain, and 65 billion in a human brain. Nerve cells are approximately 20 micrometres in diameter, glial cells about 10 micrometres. A micrometre is equivalent to a thousandth of a millimetre.
The study was carried out by Sten Linnarsson’s and Jens Hjerling-Leffler’s research groups at the department of medical biochemistry and biophysics, in particular by Amit Zeisel and Ana Muños Manchado. It also involved researchers from Karolinska Institutet’s Department of Oncology-Pathology, and Uppsala University.
 The study was financed with grants from several bodies, including the European Research Council, the Swedish Research Council, the Swedish Cancer Society, the EU’s Seventh Framework Programme, the Swedish Society of Medicine, the Swedish Brain Fund, Karolinska Institutet’s strategic programme for neuroscience (StratNeuro), the Human Frontier Science Program, the Åke Wiberg Foundation and the Clas Groschinsky Memorial Fund.
Karolinska Institutet - a medical university: ki.se/english
http://ki.se/pressroom

HypeWatch: Researcher Claims Pot-Stroke Link on Limited Data - Conclusion based on analysis of 64 cases, no controls.

This is an awful study, the three comments explain exactly why it is so bad.
http://www.medpagetoday.com/Cardiology/Strokes/50109?xid=nl_mpt_DHE_2015-02-20&
Worse Than No Study At All
We need valid studies with control groups, and the influence of possible mitigating factors, to identify whether their really is an association with stroke, instead of these worthless attempts to inject personal prejudices into a complicated discussion. The article did not even make the first distinction necessary to discuss stroke, i. e. hemorrhagic vs atherosclerotic strokes, which have completely different etiologies. For example, if we know the risk rises due to sclerotic disease, can we mitigate those patients through the standard ASA / statin / beta blocker combo that we use for heart disease? 50 or 60 case histories of stroke, people who just happen to use cannabis, tells us nothing. Weed is here to stay. It's time to grow up and try to help this significant population through pragmatic study and harm reduction if possible. [Ed.: All the cases involved ischemic stroke.].
larry katz
This type of medical incompetence is applied to Cannabis research over and over again. The lack of proper research protocols is clearly an example of the intentional injection of bogus information meant to cloud the public's perception of the potential value of the drug. A little real research will undoubtedly prove this scare tactic is borne of a connection to big pharma that has little use for pot as a profit source. This "researcher" should be ashamed to publish such garbage on the level of "Reefer Madness".
Steve Edelman, MSN/FNP-BC
If this was another drug being "investigated" we would laugh at this researcher and, from that point on we would ignore him. Still sounds like a good plan to me!.

Thursday, February 19, 2015

Changes in chronotype after stroke: a pilot study

I have absolutely no idea what possible use this could be for survivors and their rehab, so punt it to your doctor. 

Changes in chronotype after stroke: a pilot study

Thomas Kantermann1,2*, imageAndreas Meisel3,4, imageKatharina Fitzthum3,4, imageThomas Penzel5, imageIngo Fietze5 and imageLena Ulm3,4,6
  • 1Chronobiology Unit, Groningen Institute for Evolutionary Life Sciences, University of Groningen, Groningen, The Netherlands
  • 2Clinical Centre, Institute for Occupational, Social and Environmental Medicine, Ludwig-Maximilians University Munich, Munich, Germany
  • 3NeuroCure Clinical Research Center, Charité – Universitätsmedizin Berlin, Berlin, Germany
  • 4Department of Neurology, Center for Stroke Research Berlin, Charité – Universitätsmedizin Berlin, Berlin, Germany
  • 5Center of Sleep Medicine, Charité – Universitätsmedizin Berlin, Berlin, Germany
  • 6Centre for Clinical Research, The University of Queensland, Herston, QLD, Australia
This study aimed to elucidate associations between stroke onset and severity as well as chronotype (phase of entrainment) and internal time of stroke. Fifty-six first-ever ischemic stroke patients participated in a cross-sectional study assessing chronotype (mid-sleep on work-free days corrected for sleep deficit on workdays; MSFsc) by applying the Munich ChronoType Questionnaire (MCTQ). The MCTQ was completed twice, on average 68 ± 24 (SD) days post stroke and retrospectively for the time before stroke. To assess the impact of stroke in relation to internal time, InTstroke was calculated as MSFsc minus local time of stroke. Stroke severity was assessed via the standard clinical National Institute Health Stroke Scale (NIHSS) and modified Ranking Scale (mRS), both at hospital admission and discharge. Overall, most strokes occurred between noon and midnight. There was no significant association between MSFsc and stroke onset. MSFsc changed significantly after stroke, especially in patients with more severe strokes. Changes in MSFsc varied with InTstroke – the earlier the internal time of a stroke relative to MSFsc-before-stroke, the more MSFsc advanced after stroke. In addition, we provide first evidence that MSFsc changes varied between stroke locations. Larger trials are needed to confirm these findings.

Introduction

The onset of vascular events exhibits a circadian (about 24-h) pattern, with a prominent peak in the morning hours and a second, smaller peak in the early evening (1–4). This phenomenon is thought being caused by diurnal variations in underlying pathophysiological mechanisms, e.g., platelet aggregation, blood pressure, and catecholamine concentrations (3, 5). Several animal studies demonstrated that cerebrovascular events, in turn, also impact circadian rhythms and sleep architecture (6–9). Longer latencies to fall asleep, fragmented sleep, NREM sleep instability, and hypersomnia have also been described in stroke patients, indicating changes in sleep homeostasis and circadian rhythmicity after stroke (10, 11). Two studies with small sample sizes provided some evidence of altered timing in urinary melatonin as a marker of disturbed circadian rhythms in stroke patients (12, 13). However, knowledge on the interplay between sleep homeostasis, the circadian timing of sleep, and vascular events is still incomplete.
The circadian timing of sleep is regulated by an internal clock, which is synchronized (entrained) by light to the 24-h day (14, 15). The relation between external (local) and internal (circadian) time is called phase of entrainment (16) and people that differ in this trait are referred to as different chronotypes. Chronotype can easily be assessed with the Munich ChronoType Questionnaire [MCTQ; (16)] as the mid-point of sleep on work-free days (MSF), corrected for sleep deficit accumulated across the workweek (MSF sleep corrected; MSFsc). MSFsc as a measure for internal time allows calculating the internal time point of a physiological event (17, 18). Social jetlag (the difference between MSF and mid-sleep on workdays, MSW) is a surrogate measure for circadian rhythm disruption and has been linked to elevated heart rate in shift-workers (19), smoking (20), and depression (21). To date, no study has assessed phase of entrainment (chronotype) and social jetlag before and after stroke to compare the impact of stroke in relation to internal time.
The current study was the first to investigate associations between stroke onset and severity and internal time before and after stroke. We hypothesized that (a) there is a correlation between chronotype (MSFsc) and stroke onset, (b) experiencing a stroke results in chronotype changes, and (c) the impact of stroke varies with the internal time point a stroke happened.

The U.S. government is poised to withdraw longstanding warnings about cholesterol

Maybe we will eventually focus on the correct problem with atheroscelrosis. Stopping the original inflammation that starts the process of plaque formation. But don't count on that for 50-100 years. The stain industry is too well entrenched and profitable. 25% of the cholesterol in your body is found in your brain
With that knowledge why is your doctor recommending statin therapy?  Don't listen to me, I know nothing. You'll have to probe your doctors thinking on this subject, I doubt it is anything more than reciting facts from medical school.

The U.S. government is poised to withdraw longstanding warnings about cholesterol



Nutrition Panel Calls for Less Sugar and Eases Cholesterol and Fat Restrictions

Wednesday, February 18, 2015

Study clarifies link between dieting, exercise and reduced inflammation

This might explain why intermittent fasting is good for dementia prevention.

The latest here:
Study clarifies link between dieting, exercise and reduced inflammation

If you’ve ever wondered how dieting and exercise reduce inflammation, read on. According to new research, a compound that our bodies crank out when energy supplies are low could be the link between diet and exercise, and reduced swelling in the body.
When diet, fasting and exercise starve the body for calories, the body increases production of a compound called beta hydroxybutyrate (BHB). This compound has long been known as an alternate source of energy; the new research suggests that BHB can also block the inflammatory response.
In their study, published this week in Nature Medicine online (subscription required), a team of scientists co-led by Yun-Hee Youm and Kim Yen Nguyen at the Yale School of Medicine, discovered that the compound BHB reduces swelling in the body by inactivating a group of proteins, called the inflammasome, that drive the inflammatory response.
The research team used human immune cells and mice to explore the effects of BHB in the body. They found that mice given BHB directly, and mice fed a low-carbohydrate diet (that prompted their bodies to synthesize their own BHB), both benefited from reduced inflammation.
These results are noteworthy because a better understanding of the mechanism that links diet, exercise and inflammation could help scientists develop more effective treatments for inflammatory disorders such as Type 2 diabetes, atherosclerosis and Alzheimer’s disease.
Previously: Newly identified type-2 diabetes gene’s odds of being a false finding equal one in 1 followed by 19 zeroes, Improving your health using herbs and spices, Exercise may alleviate symptoms of arthritis regardless of weight loss, Study points to inflammation as cause of plaque buildup in heart vessels and Examining the role of exercise in managing and preventing diabetes
Via ScienceDaily
- See more at: http://scopeblog.stanford.edu/2015/02/18/study-clarifies-link-between-dieting-exercise-and-reduced-inflammation/#sthash.THkxszJI.dpuf  If you’ve ever wondered how dieting and exercise reduce inflammation, read on. According to new research, a compound that our bodies crank out when energy supplies are low could be the link between diet and exercise, and reduced swelling in the body.

When diet, fasting and exercise starve the body for calories, the body increases production of a compound called beta hydroxybutyrate (BHB). This compound has long been known as an alternate source of energy; the new research suggests that BHB can also block the inflammatory response.
In their study, published this week in Nature Medicine online (subscription required), a team of scientists co-led by Yun-Hee Youm and Kim Yen Nguyen at the Yale School of Medicine, discovered that the compound BHB reduces swelling in the body by inactivating a group of proteins, called the inflammasome, that drive the inflammatory response.

The research team used human immune cells and mice to explore the effects of BHB in the body. They found that mice given BHB directly, and mice fed a low-carbohydrate diet (that prompted their bodies to synthesize their own BHB), both benefited from reduced inflammation.

These results are noteworthy because a better understanding of the mechanism that links diet, exercise and inflammation could help scientists develop more effective treatments for inflammatory disorders such as Type 2 diabetes, atherosclerosis and Alzheimer’s disease.

Previously: Newly identified type-2 diabetes gene’s odds of being a false finding equal one in 1 followed by 19 zeroes, Improving your health using herbs and spices, Exercise may alleviate symptoms of arthritis regardless of weight loss, Study points to inflammation as cause of plaque buildup in heart vessels and Examining the role of exercise in managing and preventing diabetes
Via ScienceDaily
- See more at: http://scopeblog.stanford.edu/2015/02/18/study-clarifies-link-between-dieting-exercise-and-reduced-inflammation/#sthash.THkxszJI.dpuf
If you’ve ever wondered how dieting and exercise reduce inflammation, read on. According to new research, a compound that our bodies crank out when energy supplies are low could be the link between diet and exercise, and reduced swelling in the body.
When diet, fasting and exercise starve the body for calories, the body increases production of a compound called beta hydroxybutyrate (BHB). This compound has long been known as an alternate source of energy; the new research suggests that BHB can also block the inflammatory response.
In their study, published this week in Nature Medicine online (subscription required), a team of scientists co-led by Yun-Hee Youm and Kim Yen Nguyen at the Yale School of Medicine, discovered that the compound BHB reduces swelling in the body by inactivating a group of proteins, called the inflammasome, that drive the inflammatory response.
The research team used human immune cells and mice to explore the effects of BHB in the body. They found that mice given BHB directly, and mice fed a low-carbohydrate diet (that prompted their bodies to synthesize their own BHB), both benefited from reduced inflammation.
These results are noteworthy because a better understanding of the mechanism that links diet, exercise and inflammation could help scientists develop more effective treatments for inflammatory disorders such as Type 2 diabetes, atherosclerosis and Alzheimer’s disease.
Previously: Newly identified type-2 diabetes gene’s odds of being a false finding equal one in 1 followed by 19 zeroes, Improving your health using herbs and spices, Exercise may alleviate symptoms of arthritis regardless of weight loss, Study points to inflammation as cause of plaque buildup in heart vessels and Examining the role of exercise in managing and preventing diabetes
Via ScienceDaily
- See more at: http://scopeblog.stanford.edu/2015/02/18/study-clarifies-link-between-dieting-exercise-and-reduced-inflammation/#sthash.THkxszJI.dpuf

Turbo training can help recovery for stroke victims, finds study

I would think it is far more likely that the ones that can do this have lesser damage to begin with. It is extremely simple to prove, you do objective 3d scans with CT/MRI. Please learn about cause and effect. 

Turbo training can help recovery for stroke victims, finds study 


Cycling on a turbo trainer, albeit a motorised bike, can help a stroke patients’ brain and motor skills recovery.
A small study of 17 stroke survivors by the Cleveland Clinic, Ohio, showed how those who completed cycling exercises made greater improvement in the recovery of motor skills.
Research has frequently found that aerobic exercise helps the brains to learn new information and similar studies have noted how stationary cycling has helped Parkinson’s disease recovery.
The authors of this particular study believe that cycling helps enhance the brain’s ability to reorganize itself and create new connections.
The study involved the 17 participants, aged between 23 and 84 and who had suffered a stroke in the past six to twelve months, being randomly assigned to one of three groups: exercise on a motorised stationary bike; a stationary bike without a motor; or no aerobic exercise but twice as much upper body repetitive task therapy.
>>> Turbo training sessions: Get the most out of your indoor training
The cycling sessions were a duration of 45 minutes and were completed before the repetitive task therapy which aimed to help patients regain the use of their arms.
Over eight weeks all three groups did 24 exercise sessions with those in the motorised stationary bike group showing a 34 per cent improvement in motor skills. This bettered the 16 per cent improvement figure of the non-motorised stationary bike group and 17 per cent shown by the third no aerobic exercise group.
A motored bike helps patients with reduced mobility to pedal, researchers said. It also allows them to achieve and maintain the intensity of training that is believed to be required to affect brain function.
Susan Linder, a physical therapist at the Cleveland Clinic who presented the research to the American Stroke Association’s International Stroke Conference 2015, said: “We’re improving cardiovascular health and stroke patients often have cardiovascular (problems). If we can improve motor recovery and cardiovascular health simultaneously, patients can regain lost motor function and improve their quality of life.”

Stroke rehab costs mount for Canadian patients, families

The solution is not more therapy, the solution is to prevent the damage that occurs during the first week with the neuronal cascade of death.
Is there not a single person in the whole stroke medical world that understands cause and effect? Yes this is going to be difficult but leaders accept challenges.
http://www.cbc.ca/news/canada/ottawa/stroke-rehab-costs-mount-for-canadian-patients-families-1.2691484 

Dietary and lifestyle guidelines for the prevention of Alzheimer's disease

The abstract does not contain them;
http://www.ncbi.nlm.nih.gov/pubmed/24913896
But this writeup does;
http://brainposts.blogspot.com/2015/02/exercise-guidelines-in-prevention-of.html
Here is the list of all 7 prevention recommendations from the manuscript. Readers can access the free full-text manuscript by clicking on the PMID link below.
Prevention Recommendations for Alzheimer's Disease
  1. Minimize dietary saturated and trans fats
  2. Increase intake of vegetables, fruits, legumes and grains
  3. Daily vitamin E intake from foods of 15 mg
  4. Daily vitamin B12 in diet or supplement with blood B12 level monitoring
  5. Daily multivitamins not recommended but if used avoid those with iron and copper
  6. Aluminum link to AD is controversial but avoid antacids and baking soda that contains aluminum
  7. Aerobic exercise of 40 minutes at least 3 times per week
Ask your doctor for a definitive dementia prevention protocol. Not just the unusable generalities  from Mayo clinic, or the generic crap from Harvard. 

My complete list here: Don't listen to me, your doctor obviously knows more than I do. Have him/her prove that knowledge or fire them.
Dementia prevention 19 ways

Efficacy of Mechano-Acoustic Vibration on Strength, Pain, and Function in Poststroke Rehabilitation: A Pilot Study

It has only been out for 6  months, what protocol has your doctor setup about this? Does your doctor even read research at all?
http://www.maneyonline.com/doi/abs/10.1310/tsr2105-391
Background: Vibration therapy may be used to help cortical reorganization after stroke as it can cause different adaptive metabolic and mechanical effects. Objective: This study examined whether the application of mechano-acoustic vibration on upper limb muscles could induce changes in range of motion (ROM), function, pain, and grip strength in individuals with chronic stroke. Methods: Out of 52 individuals post stroke with upper limb spasticity who were eligible,16 received mechano-acoustic vibration therapy (ViSS device) 3 times weekly for 12 sessions. The frequency of vibration was set to 300 Hz for 30 minutes. The treated muscles were the extensor carpi radialis longus and brevis and triceps brachii during voluntary contraction. All participants were evaluated in both upper limbs before (T0) and at the end (T1) of treatment with a dynamometer (hand grip strength), Modified Ashworth Scale, QuickDASH, FIM score, Fugl-Meyer scale, Verbal Numerical Rating Scale of pain, and Jebsen-Taylor Hand Function Test. Results: After 4 weeks, hand grip power had improved and pain and spasticity had decreased. Improvements were recorded for all parameters and were considered statistically significant. Conclusions: Application of vibratory stimuli to a muscle can increase the motor-evoked potential recorded from the muscle, suggesting an enhancement of corticospinal excitability. Low amplitude, high-frequency vibration treatment (300 Hz) can significantly decrease tone and pain and improve strength in upper limb of hemiplegic individuals, when applied for 30 minutes, 3 times a week over 4 weeks.

Hip protector saves you when you slip

Considering the various times I've already fallen directly on my affected hip this might be useful. I'm sure I haven't broken my hip yet because I'm fairly young and must have built up bone strength over the years.And each one of those falls probably strengthens those bones, similar to the stresses boxers put their hands through so they don't break bones when fighting.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=149836&CultureCode=en
Are you well used to wearing studded shoes in winter? If so, you're probably ready for yet another step towards tackling the eternally icy winter streets.

Last week it was extremely cold in Oslo. On average, every day in January 50 people have to report to A&E clinics after slipping and falling on the icy streets. This greatly increases the risk of hip fractures.
According to Norwegian state broadcaster NRK, almost 10,000 people suffer hip fractures every year. And according to figures from Norwegian Health Informatics, a little more than half of these accidents involve fractures of the upper femur.
Very expensive falls
"The costs of treatment, rehabilitation and nursing home services amount to between 1.5 and 2.5 billion a year", says Tore Christian Storholmen, a researcher and product designer at SINTEF.
He and his colleagues want everyone to know about these figures. Fractures of the upper femur have major consequences both for the sufferer and society as a whole. Together with Protex, a company from Ålen, they are now launching a brand new product – the HiP hip protector.
Sporty hip protector
The protector is soft and flexible, and features a sporty design. However, on impact the material becomes firmer and distributes the pressure over a larger area. This is due to the use of an advanced polyurethane foam which can absorb as much as 90 per cent of the impact of a fall.
"The problem of hip fractures is even greater than it might seem at first glance", says Storholmen. "As many as about 25 per cent of elderly people who suffer hip fractures die within a year of their injury. In other words, this recently developed belt which protects its wearers when they fall may make a contribution towards vastly reducing what has become a major health issue for society", he says.
The protector looks surprisingly stylish – just like a sporty bum-bag. And this is no accident. Elderly people today won't wear just anything!
"Our aim has been to design a hip protector that people really want to wear", smiles Storholmen. "It may save society enormous sums of money. There is also the benefit of increased quality of life, with the best outcome being a longer life for some", he says.
"We've been working very closely with users, physiotherapists and ergotherapists, involving many workshops and a lot of testing. There have been a few 'reality checks' along the way when it comes to design and user-friendliness, and Trondheim municipality has assisted us with testing the prototype", says Storholmen.
Protex drowned with calls
The icy streets have meant a busy period for manufacturers Protex in Ålen.
"We've been almost drowned in calls from people who've heard about the protector and want to have one", says General Manager Margrethe Engan Gjære. "They include doctors, physio- and other therapists working to rehabilitate people who want HiP for sporting activities or for personal use. So we're fairly sure we've manufactured a product that people will want ", she says.
"We're now working as fast as we can to get a distribution contract so that anyone can ask for the HiP belt in the shops. In the meantime we've decided to sell it via our website", says Gjære.
Design and function top priority
The level of demand doesn't surprise researcher Tore Christian Storholmen at SINTEF.
"The only thing available previously is this", he says, showing me a pair of bulky, shapeless pants fitted with two large foam pads in pockets at the sides, designed to protect the hips. This is meant to do the same job as the researchers' brand new innovation.
"The problem is that no-one wants to wear these because they're associated with sickness and non-activity", he says. "A key success criterion has been to give the protector a sporty design and prevent it from looking like a surgical support", says Storholmen.
Feedback from the "test pilots" is proof that Storholmen and Protex have succeeded. According to Storholmen people say that they feel safer. They feel they can be more active and move around without supports. They are more relaxed and their movements less strained and awkward. The hip protector also satisfies users' aesthetic tastes. They like the fabric and the way it looks.
It's thinner than the old pants, and more user-friendly, consisting of an adjustable belt which can be worn outside everyday clothes. The belt is covered with a breathable material that wicks moisture away from the body.
"We want the protector to be used by people in our target group as soon as possible – availability is key", says Storholmen.  "It will be exciting to see if the product takes off when it becomes widely available on the market soon", he says.
For in spite of their modern lifestyles and youthful outlook, statistics on the elderly speak for themselves. The risk of a fall increases after the age of 65, and every year 30% of all over 65's experience a fall.
http://www.gemini.no/en