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 493 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:

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.My back ground story is here:

Wednesday, December 31, 2014

Stroke falls one place to fifth leading cause of death in US

And if we would ever figure out how to stop the neuronal cascade of death this could probably be lowered much further.
All this is going to do is allow the existing stroke associations to assert that their focus on prevention is what caused the decline and not focus on solving all the existing problems in stroke.
Damn will they be lazy? Or not?  The tsunami of stroke is coming and nobody is prepared.

Stroke at 20: Like having a three sandbags attached to you

Interview with stroke blogger Elizabeth Ashmore who writes - Training for a marathon

SUP - Stand Up Paddleboarding

This is on my list of things to accomplish. I was reminded of this when I was back in Minnesota and driving over the Minnesota River there were two paddleboarders going downriver. Maybe 20F at the time. A friend has an inflatable one I can borrow, this past summer it never got consistently hot enough to try it.  I figure the inflatable one is much safer since I will fall off and the bounces with be softer than with a hard board.  I have no idea how I will get back on the board after falling off. It will be much easier to get this into a car and down to the waters edge than the canoeing I used to do. Someday I'll find in my storage locker my drysuit.

Effects of Robot-Assisted Therapy on Upper Limb Recovery After Stroke: A Systematic Review

My god, this was written in 2007. Where is the written protocol explaining exactly how this should be used for your recovery? Demand an answer from your doctor. More failures from our stroke organizations that should be doing something as simple as monitoring research and applying it to help survivors.
  1. Gert Kwakkel, PhD
    1. Department Rehabilitation Medicine and Research Institute MOVE, VU University Medical Center Amsterdam, The Netherlands, Department Rehabilitation Medicine, Rudolf Magnus Institute of NeuroScience, University Medical Center Utrecht, The Netherlands,
  1. Boudewijn J. Kollen, PhD
    1. Research Bureau, Isala Klinieken Zwolle, The Netherlands
  1. Hermano I. Krebs, PhD
    1. Mechanical Engineering Department, Massachusetts Institute of Technology, Cambridge, Massachusetts, Department of Neurology and Neuroscience, Burke Institute of Medical Research, Weill Medical College, Cornell University, White Plains, New York, Department of Neurology, University of Maryland, School of Medicine, Baltimore, Maryland


Objective. The aim of the study was to present a systematic review of studies that investigate the effects of robot-assisted therapy on motor and functional recovery in patients with stroke. Methods. A database of articles published up to October 2006 was compiled using the following Medline key words: cerebral vascular accident, cerebral vascular disorders, stroke, paresis, hemiplegia, upper extremity, arm, and robot. References listed in relevant publications were also screened. Studies that satisfied the following selection criteria were included: (1) patients were diagnosed with cerebral vascular accident; (2) effects of robot-assisted therapy for the upper limb were investigated; (3) the outcome was measured in terms of motor and/or functional recovery of the upper paretic limb; and (4) the study was a randomized clinical trial (RCT). For each outcome measure, the estimated effect size (ES) and the summary effect size (SES) expressed in standard deviation units (SDU) were calculated for motor recovery and functional ability (activities of daily living [ADLs]) using fixed and random effect models. Ten studies, involving 218 patients, were included in the synthesis. Their methodological quality ranged from 4 to 8 on a (maximum) 10-point scale. Results. Meta-analysis showed a nonsignificant heterogeneous SES in terms of upper limb motor recovery. Sensitivity analysis of studies involving only shoulder-elbow robotics subsequently demonstrated a significant homogeneous SES for motor recovery of the upper paretic limb. No significant SES was observed for functional ability (ADL). Conclusion. As a result of marked heterogeneity in studies between distal and proximal arm robotics, no overall significant effect in favor of robot-assisted therapy was found in the present meta-analysis. However, subsequent sensitivity analysis showed a significant improvement in upper limb motor function after stroke for upper arm robotics. No significant improvement was found in ADL function. However, the administered ADL scales in the reviewed studies fail to adequately reflect recovery of the paretic upper limb, whereas valid instruments that measure outcome of dexterity of the paretic arm and hand are mostly absent in selected studies. Future research into the effects of robot-assisted therapy should therefore distinguish between upper and lower robotics arm training and concentrate on kinematical analysis to differentiate between genuine upper limb motor recovery and functional recovery due to compensation strategies by proximal control of the trunk and upper limb.

Bradford Hill criteria for causation

Have your doctor explain using this why s/he believes that stroke risk factors actually cause stroke.
Or why dementia prevention ideas from Mayo and Cleveland Clinics are correct.

The Bradford Hill considerations on causality: a counterfactual perspective

The actual paper here: 

The Environment and Disease: Association or Causation?



Tuesday, December 30, 2014

cross-education after stroke

What does your doctor have to say about only training your good side and letting cross-education transfer it to your bad side?

Cross-Education of Strength Depends on Limb Dominance: Implications for Theory and Application

High-intensity unilateral dorsiflexor resistance training results in bilateral neuromuscular plasticity after stroke

Cross education and the human central nervous system



A Novel Study on Natural Robotic Rehabilitation Exergames using the unaffected Arm of Stroke Patients

It is only 7 pages.With any decent stroke association at all they could write up this idea into a stroke protocol and include these other similar ipsilateral ideas.

Magnetic therapy on the good side of the brain.

Immediate Effects of Unaffected Arm Exercise in Poststroke Patients with Spastic Upper Limb Hemiparesis

Mirror Training The Mirror as the Element Connecting Both Hands to One Hemisphere

Magic for Stroke Patients: The One-Sided Workout

 Cortical Reorganization After Stroke How Much and How Functional?

New model of how brain functions are organized may revolutionize stroke rehab

New Rehabilitation Institute of Chicago Brain Stimulation Study Reveals Breakthrough in Stroke Recovery
Abstract—It is well known that home exercise is as good as
rehab center. However, people with severe stroke typically lack
the ability to move their affected arm, and hence they need
a very special rehabilitation program that usually available in
hospitals or professional centers. Therapists train the affected
hand of those patients by using robotic-assisted therapy devices,
or sometimes by holding the affected arms of the patients
and stretching it for them. However, such robotic devices and
professional therapists are not available at home. In this study,
we design and implement a low-cost rehabilitation glove to
meet the needs of those patients who have paralysis in their
affect hand. The novelty of this glove is that it is to be worn
on the unaffected hand which acts as a natural robotic arm
during the rehabilitation session. The glove is equipped with FSR
sensors that measure the forces exerted by the affected hand
on the unaffected hand. A virtual reality rehabilitation game
is developed using Microsoft Kinect to facilitate the exercises
and motivate the patients. The system is tested on three patients
for six weeks. Objective measurements showed that patients
have significantly improved over the study period. Moreover, the
patients themselves gave a positive feedback about the whole
system; wearing the glove on the unaffected hand made their life
easier and let them enjoyed the rehabilitation sessions.

Noninvasive intranasal stem cells bypass the blood-brain barrier to target the brain to treat Parkinson's disease, stroke, MS, brain tumors, cerebral ischemia, Alzheimer's and other CNS disorders

What clinical trial is your doctor proposing to see if this would help survivors?[]=23&path[]=98

William H. Frey II

Center for Memory & Aging (Alzheimer's Research Center), Regions Hospital, 640 Jackson St., St. Paul, MN 55101, Department of Pharmaceutics, Neurology and Neuroscience, University of Minnesota, USA.

Together with my collaborators in Germany, especially Lusine Danielyan M.D., we discovered and patented (1) that therapeutic cells, including adult stem cells and genetically-engineered cells, can be non-invasively delivered to the CNS using the noninvasive intranasal delivery method that I developed (2). The first of our scientific papers on this new discovery describes this successful method of delivery and proprietary formulations that enhance delivery (3).  The second of our papers describes the successful treatment of Parkinson's disease in an animal model with intranasal adult bone marrow derived mesenchymal stem cells (4).
Intranasal stem cells bypass the blood-brain barrier to target the brain by traveling extracellularly along the olfactory neural pathway with minimal delivery to other organs.  Once in the brain, adult stem cells target the damaged areas of the brain specifically to treat the underlying disease (4).  Researchers at University Medical Center Utrecht in the Netherlands have demonstrated the effectiveness of intranasal stem cell treatment technology in an animal model of neonatal cerebral ischemia (5) and also in animals with neonatal brain damage (6) and subarachnoid hemorrhage (6a).  
Researchers at Emory University have used our intranasal stem cell treatment successfully in an animal model of stroke (7), and researchers at Uppsala University in Sweden have demonstrated that intranasal T regulatory cell therapy delivered and targeted the cells to the brain and efficiently suppressed ongoing inflammation in an EAE model of multiple sclerosis leading to reduced disease symptoms (8).  Intranasal adult neural stem cells have also been shown to improve the EAE model of MS (9) as have intranasal mesenchymal stromal cells (10).  
Other researchers have reported that intranasal stem cells target and treat brain tumors (11, 12).  This intranasal delivery, targeting and treatment technology can make stem cell treatments practical for CNS disorders by eliminating the need for invasive neurosurgical implantation of cells and by eliminating the need for intravenous delivery that disperses cells throughout the body resulting in unwanted systemic exposure.  This delivery and treatment method can facilitate the development of stem cell and genetically-engineered cell therapies for Parkinson's, PSP, Huntington's, Alzheimer's, MS, epilepsy, stroke, neonatal ischemia, brain tumors, traumatic brain injury (TBI), spinal cord (SCI) injury, etc.
In humans, GnRH neurons or Gonadotropin-releasing hormone expressing neurons are known to reach the brain by using this same olfactory neural pathway during development.  In addition, pathologic cells, such as the amoeba Naegleria fowleri, are known to enter the brains of humans by this same pathway and cause amoebic infection of the brain.  We have discovered how to use this pathway to delivery therapeutic cells, including stem cells, to the brain to treat disorders of the central nervous system.  This intranasal therapeutic cell delivery, targeting and treatment technology is available for licensing.

Reliability of the measures of weight-bearing distribution obtained during quiet stance by digital scales in subjects with and without hemiparesis

You'll have to ask your therapist what is the point of this test and the protocols that can be used to pass the test.
I assume that weight bearing while walking is much more useful to accomplish.
Measuring weight-bearing distribution by your socks;

Sensor embedded socks

Measuring weight-bearing distribution by your insoles;

Rapid Rehab Smart Insole Will Train Athletes and Assist Rehab Patients 
Address correspondence to
Emerson Fachin-Martins
, Faculty of Ceilandia, University of Brasilia,
, Brazil. E-mail:


Described as an alternative way of assessing weight-bearing asymmetries, the measures obtained from digital scales have been used as an index to classify weight-bearing distribution. This study aimed to describe the intra-test and the test/retest reliability of measures in subjects with and without hemiparesis during quiet stance. The percentage of body weight borne by one limb was calculated for a sample of subjects with hemiparesis and for a control group that was matched by gender and age. A two-way analysis of variance was used to verify the intra-test reliability. This analysis was calculated using the differences between the averages of the measures obtained during single, double or triple trials. The intra-class correlation coefficient (ICC) was utilized and data plotted using the Bland–Altman method. The intra-test analysis showed significant differences, only observed in the hemiparesis group, between the measures obtained by single and triple trials. Excellent and moderate ICC values (0.69–0.84) between test and retest were observed in the hemiparesis group, while for control groups ICC values (0.41–0.74) were classified as moderate, progressing from almost poor for measures obtained by a single trial to almost excellent for those obtained by triple trials. In conclusion, good reliability ranging from moderate to excellent classifications was found for participants with and without hemiparesis. Moreover, an improvement of the repeatability was observed with fewer trials for participants with hemiparesis, and with more trials for participants without hemiparesis.

Read More:


Glutamate Excitotoxicity and Neurodegeneration

Your doctor should be able to use this understanding to figure out if two of the processes involved in the neuronal cascade of death are the reason for your 33% dementia chance post-stroke from an Australian study?
What exactly is your doctor doing to stop those two neuronal death processes and maybe prevent your dementia?
Ezza HSA1* and Khadrawyb YA2
1Zoology Department, Faculty of Science, Cairo University, Giza, Egypt
2Medical Physiology Department, Medical Division, National Research Center, Giza, Egypt
*Corresponding author: Ezza HSA, Zoology Department, Faculty of Science, Cairo University, Giza, Egypt, Tel: 20237753565; Fax: +202 33387758; E-mail:
Rec Date: May 20, 2014; Acc date: October 06, 2014; Pub date: October 08, 2014
Copyright: © 2014 Ezza HSA. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use,
distribution, and reproduction in any medium, provided the original author and source are credited.

Glutamate plays crucial roles in the physiology of the central nervous system as it can control many functions such as memory, learning, cognitive, emotional, endocrine and other visceral functions. In addition, glutamate is the major excitatory neurotransmitter in the mammalian central nervous system. It has the potential to be involved in the pathogenesis of many CNS diseases either due to excessive release, reduced uptake or alteration of receptor functions. Growing evidence links glutamate excitotoxicity to various neurodegenerative diseases as cerebral ischemia, epilepsy, Alzheimer's disease, Parkinsons' disease and multiple sclerosis. In addition, several
environmental pollutants result in excessive glutamatergic neurotransmission and may eventually lead to neurodegenerative diseases.

Running exercise delays neurodegeneration in amygdala and hippocampus of Alzheimer’s disease (APP/PS1) transgenic mice

Is your doctor going to figure out a way for you to get some kind of running exercise to counteract your 33% chance of getting dementia post-stroke?
Even though this is just in mice what is the downside of doing this for stroke survivors? Keep demanding answers from your doctors, they are supposed to be helping you recover. 
Choose an option to locate/access this article:
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Neurodegeneration occurs in the hippocampus and amygdala of young transgenic mice.
Neurodegeneration in the amygdala is more severe than that in the hippocampus.
Exercise counteracts the transgene-induced neurodegeneration.
Exercise enhances the BDNF signaling pathways and Aβ clearance.


Alzheimer’s disease (AD) is an age-related neurodegenerative disease. Post-mortem examination and brain imaging studies indicate that neurodegeneration is evident in the hippocampus and amygdala of very early stage AD patients. Exercise training is known to enhance hippocampus- and amygdala-associated neuronal function. Here, we investigated the effects of exercise (running) on the neuronal structure and function of the hippocampus and amygdala in APP/PS1 transgenic (Tg) mice. At 4-months-old, an age before amyloid deposition, the amygdala-associated, but not the hippocampus-associated, long-term memory was impaired in the Tg mice. The dendritic complexities of the amygdalar basolateral neurons, but not those in the hippocampal CA1 and CA3 neurons, were reduced. Furthermore, the levels of BDNF-TrkB signaling molecules (i.e. p-TrkB, p-Akt and p-PKC) were reduced in the amygdala, but not in the hippocampus of the 4-month-old Tg mice. The concentrations of Aβ40 and Aβ42 in the amygdala were higher than those in the hippocampus. Ten weeks of treadmill training (from 1.5- to 4-month-old) increased the hippocampus-associated memory and dendritic arbor of the CA1 and CA3 neurons, and also restored the amygdala-associated memory and the dendritic arbor of amygdalar basolateral neurons in the Tg mice. Similarly, exercise training also increased the levels of p-TrkB, p-Akt and p-PKC in the hippocampus and amygdala. Furthermore, exercise training reduced the levels of soluble Aβ in the amygdala and hippocampus. Exercise training did not change the levels of APP or RAGE, but significantly increased the levels of LRP-1 in both brain regions of the Tg mice. In conclusion, our results suggest that tests of amygdala function should be incorporated into subject selection for early prevention trials. Long-term exercise protects neurons in the amygdala and hippocampus against AD-related degeneration, probably via enhancements of BDNF signaling pathways and Aβ clearance. Physical exercise may serve as a means to delay the onset of AD.

Monday, December 29, 2014

Why you can live a normal life with half a brain

An entertaining blog post. Why can't you just live with the damage you have?

Statin use linked to risk for cataracts

This was written up in 2012. Does it take dozens of years before important information like this gets down to the patients? Has your doctor warned you about these side effects?

Statins linked with development of cataracts  August 2012

Statins linked with development of cataracts  September, 2012

The latest here;
Patients treated with statins for CVD prevention were more likely than nonusers to develop cataracts requiring surgical treatment, researchers reported in the Canadian Journal of Cardiology.

Researchers evaluated data from two cohorts selected from the British Columbia Ministry of Health databases (2000-2007) and the IMS LifeLink database (2001-2011) to identify patients who were diagnosed with and underwent surgery for cataracts. The British Columbia cohort comprised 162,501 men and women and 650,004 matched controls and the IMS LifeLink cohort comprised 45,065 men and 450,650 matched controls.
Within the British Columbia cohort, the adjusted rate ratio for cataracts requiring surgery with any statin use was 1.27 (95% CI, 1.24-1.3). The risk increase was observed in new users (adjusted RR=1.36; 95% CI, 1.3-1.42) and prior users (adjusted RR=1.24; 95% CI, 1.2-1.27). Long-term regular use of each individual statin evaluated was associated with greater risk for cataracts requiring surgical intervention, with RRs ranging from 1.14 (95% CI, 1.04-1.26) for lovastatin to 1.42 (95% CI, 1.27-1.59) for rosuvastatin (Crestor, AstraZeneca).
Within the IMS LifeLink cohort, the adjusted RR for cataracts requiring surgery among with any statin use was 1.07 (95% CI, 1.04-1.1). Analysis of individual statins indicated significantly greater risk with use of simvastatin (RR=1.05; 95% CI, 1-1.11), atorvastatin (RR=1.07; 95% CI, 1.02-1.12) and lovastatin (RR=1.14, 95% CI, 1.04-1.26). The same association was not observed with fluvastatin, rosuvastatin or pravastatin.
Researchers calculated an age-adjusted absolute risk for cataracts requiring surgery among statin users in the British Columbia cohort of 20 cases per 1,000 person-years compared with 15 per 1,000 person-years among nonusers. The age-adjusted absolute risk in the IMS LifeLink cohort was 24 per 1,000 person-years among statin users compared with 20 per 1,000 person-years among nonusers.
“This study found statin use to be significantly associated with increased risk for cataract leading to surgical intervention,” the researchers concluded. “… Further assessment of the clinical effect of this relationship is recommended, especially in light of increased statin use for primary prevention of CVD and the importance of acceptable vision in old age, when CVD is common.” However, due to the low RR and high efficacy and safety of cataract surgery, the link between statins and cataract development should be disclosed to patients, but not considered a deterrent to statin use for CVD prevention, they wrote.
In a related editorial, Steven E. Gryn, MD, FRCPC, and Robert A. Hegele, MD, FRCPC, from the Schulich School of Medicine and Dentistry, Western University, London, Ontario, Canada, noted that these results contribute to “previously hazy” literature on the link between cataracts and statins, but that the issue has yet to be clearly resolved.
“For those of us who have prescribed high doses of statins for almost 3 decades, there is certainly no epidemic of cataracts among our longtime lipid clinic patients,” they wrote. “Nevertheless, if the findings of Wise et al are confirmed, physicians might need to factor in this potential risk when discussing statin use with patients.”

The Buffalo Theory of neurons

From Cheers.

The Buffalo Theory as told by Cliff Clavin: No one can explain this as well as Cliff Clavin, on Cheers. One afternoon at Cheers, Cliff Clavin was explaining the Buffalo Theory to his buddy Norm. and here's how it went:
"Well ya see, Norm, it's like this... A herd of buffalo can only move as fast as the slowest buffalo. And when the herd is hunted, it is the slowest and weakest ones at the back that are killed first. This natural selection is good for the herd as a whole, because the general speed and health of the whole group keeps improving by the regular killing of the weakest members.
"In much the same way, the human brain can only operate as fast as the slowest brain cells. Excessive intake of alcohol, as we know, kills brain cells. But naturally it attacks the slowest and weakest brain cells first.
In this way, regular consumption of beer eliminates the weaker brain cells, making the brain a faster and more efficient machine. That's why you always feel smarter after a few beers."
There is this actual research;
Dark beer is good for you, in moderation
Can alcohol make men smarter? Study suggests yes

driving failures

In the 12-13 hour drive back to Minnesota I tried and failed once again. Normally  I sit on my left hand thumb with it under either the right or the left leg. I tried putting my left hand around the left steering wheel spoke as I was going down the long entrance ramp from a rest area. The bicep spasticity screamed in horror before I even made it to the freeway and overpowered my finger spasticity to pull the hand from the steering wheel. Later I tried resting my left elbow on the gel pad I attached to the arm rest in the door and placed my hand in the seven o'clock position. This time the elbow would not stay the 6 inches out from my side, the hand manged to stay on the wheel but the elbow forced its way next to my side.

In search of arrogance - Seth Godin

A great Seth Godin blog. I have arrogance in spades.

Training finger individuation with a mechatronic-virtual reality system leads to improved fine motor control post-stroke

If I had any individual finger movement at all I might try this. But you can demand that your therapist set up a stroke protocol for individual fingers.
Kelly O Thielbar, Thomas J Lord, Heidi C Fischer, Emily C Lazzaro, Kristin C Barth, Mary E Stoykov, Kristen M Triandafilou and Derek G Kamper
Journal of NeuroEngineering and Rehabilitation 2014, 11:171  doi:10.1186/1743-0003-11-171
Published: 26 December 2014

Abstract (provisional)


Dexterous manipulation of the hand, one of the features of human motor control, is often compromised after stroke, to the detriment of basic functions. Despite the importance of independent movement of the digits to activities of daily living, relatively few studies have assessed the impact of specifically targeting individuated movements of the digits on hand rehabilitation. The purpose of this study was to investigate the impact of such finger individuation training, by means of a novel mechatronic-virtual reality system, on fine motor control after stroke.


An actuated virtual keypad (AVK) system was developed in which the impaired hand controls a virtual hand playing a set of keys. Creation of individuated digit movements is assisted by a pneumatically actuated glove, the PneuGlove. A study examining efficacy of the AVK system was subsequently performed. Participants had chronic, moderate hand impairment resulting from a single stroke incurred at least 6 months prior. Each subject underwent 18 hour-long sessions of extensive therapy (3x per week for 6 weeks) targeted at finger individuation. Subjects were randomly divided into two groups: the first group (Keypad: N = 7) utilized the AVK system while the other group (OT: N = 7) received a similarly intensive dose of occupational therapy; both groups worked directly with a licensed occupational therapist. Outcome measures such as the Jebsen-Taylor Hand Function Test (JTHFT), Action research Arm Test (ARAT), Fugl-Meyer Upper Extremity Motor Assessment/Hand subcomponent (FMUE/FMH), grip and pinch strengths were collected at baseline, post-treatment and one-month post-treatment.


While both groups exhibited some signs of change after the training sessions, only the Keypad group displayed statistically significant improvement both for measures of impairment (FMH: p = 0.048) and measures of task performance (JTHFT: p = 0.021). Additionally, the finger individuation index - a measure of finger independence - improved only for the Keypad group after training (p = 0.05) in the subset (Keypad: N = 4; OT: N = 5) of these participants for which it was measured.


Actively assisted individuation therapy comprised of non task-specific modalities, such as can be achieved with virtual platforms like the AVK described here, may prove to be valuable clinical tools for increasing the effectiveness and efficiency of therapy following stroke.

The complete article is available as a provisional PDF. The fully formatted PDF and HTML versions are in production.

Sunday, December 28, 2014

Walking on ice

Over Christmas I was at home with my parents and two blocks away is a lake that I've spent a lot of time on fishing, ice skating, swimming. It was frozen at least 4-5 inches and on my walk to get to 10,000 steps for the day I decided to walk a couple hundred yards on the lake with 1/8 inch of fresh snow over the slick ice. With a fair amount of hubris I decide that this would be no problem at all. Forty yards in I crashed on my affected left hip, cap and glasses flying off. Stood up and with little diminished hubris set off walking again. Made it 30 yards before again crashing to the ice the exact same way. Finally learned my lesson and made my way to the shore and walked along the frozen sand. Don't do this, I really push myself and no one should follow my example. Ended up with a stiff neck from preventing my head from slamming into the ice. I guess I won't be trying ice skating anytime soon.

This Brain Disease Will Affect Nearly Every Family. Now Nanotechnology Can Detect It Early

Will your doctor be using a test like this to identify your 33% chance of getting dementia post-stroke early while something can still be done about it? 
Does your doctor have anything better than my ideas with research to back them up?
My complete list here:
Dementia prevention 19 ways 
A new type of brain scan which can detect the toxins which cause Alzheimer’s disease has been developed by scientists at Northwestern University.
The test, which uses nanotechnology, identifies the early signs of dementia and could be used to both monitor and combat the disease.
The areas of the brain which contain the amyloid beta toxins are seen on the brain scan as large dark patches.
The new test is a breakthrough because previously it was only possible to detect the amyloid plaques — once these have developed it is probably too late for any effective therapy.

More at link.

Saturday, December 27, 2014

NeuroGrid: recording action potentials from the surface of the brain

And with this our doctors could determine what problems exist and match stroke protocols to correct those problems.
Nature Neuroscience
Published online


Recording from neural networks at the resolution of action potentials is critical for understanding how information is processed in the brain. Here, we address this challenge by developing an organic material–based, ultraconformable, biocompatible and scalable neural interface array (the ‘NeuroGrid’) that can record both local field potentials(LFPs) and action potentials from superficial cortical neurons without penetrating the brain surface. Spikes with features of interneurons and pyramidal cells were simultaneously acquired by multiple neighboring electrodes of the NeuroGrid, allowing for the isolation of putative single neurons in rats. Spiking activity demonstrated consistent phase modulation by ongoing brain oscillations and was stable in recordings exceeding 1 week's duration. We also recorded LFP-modulated spiking activity intraoperatively in patients undergoing epilepsy surgery. The NeuroGrid constitutes an effective method for large-scale, stable recording of neuronal spikes in concert with local population synaptic activity, enhancing comprehension of neural processes across spatiotemporal scales and potentially facilitating diagnosis and therapy for brain disorders.

Brain–Machine Interfaces:Past, Present and Future

What is your doctor using of these to help your recovery?
S.Senthilkumar1, T.Shanmugapriya2
Assistant Professor, Department of Electronics and Instrumentation, Bharath University, Chennai, Tamil Nadu, India1
Assistant Professor, Department of Information Technology, SSN Engineering College, Chennai, Tamil Nadu, India2
ABSTRACT: Since the original demonstration that electrical activity generated by ensembles of cortical neurons can be employed directly to control a robotic manipulator, research on brain-machine interfaces (BMIs) has experienced an impressive growth. Today BMIs designed for both
experimental and clinical studies can translate raw neuronal signals into motor commands that
reproduce arm reaching and hand grasping movements in artificial actuators. Clearly, these
developments hold promise for the restoration of limb mobility in paralyzed subjects. However, as
we review here, before this goal can be reached several bottlenecks have to be passed. These
include designing a fully implantable biocompatible recording device, further developing real-time
computa- tional algorithms, introducing a method for providing the brain with sensory feedback
from the actuators, and designing and building artificial prostheses that can be controlled directly by
brain-derived signals. By reaching these milestones, future BMIs will be able to drive and control
revolutionary prostheses that feel and act like the human arm.

The Use of Cuff Weights for Aquatic Gait Training in People Post-Stroke with Hemiparesis

I wish these people would write this up as a stroke protocol so critiques could be made for and against it. My suspicion is that the extra weight calms down the spasticity allowing for a much more normal walk.;jsessionid=0B7BF36BE28C2C3D60B56BB7051316E5.f01t02?
  1. Ryota Nishiyori1,
  2. Byron Lai2,
  3. Do Kyeong Lee3,
  4. Konstantinos Vrongistinos2 and
  5. Taeyou Jung2,*
Article first published online: 22 DEC 2014
DOI: 10.1002/pri.1617


  • stroke;
  • exercise;
  • physiotheraphy


Background and Purpose

This study aimed to examine how spatiotemporal and kinematic gait variables are influenced by the application of a cuff weight during aquatic walking in people post-stroke. The secondary purpose was to compare the differences in gait responses between the placements of cuff weights on the proximal (knee weight) and distal end (ankle weight) of the shank.


Twenty-one participants post-stroke with hemiparesis aged 66.3 ± 11.3 years participated in a cross-sectional comparative study. Participants completed two aquatic walking trials at their self-selected maximum walking speed across an 8-m walkway under each of the three conditions: 1) walking with a knee weight; 2) walking with an ankle weight; and 3) walking with no weight. Cuff weights were worn on the paretic leg of each participant. Gait speed, cadence, step width and joint kinematics of the hip, knee and ankle joints were recorded by a customized three-dimensional underwater motion analysis system.


Mean aquatic walking speeds significantly increased with the use of cuff weights when compared to walking with no weight. Changes in gait variables were found in the non-paretic leg with the addition of weight, while no significant changes were found in the paretic leg.


The results suggest that the use of additional weight can be helpful if the goal of gait training is to improve walking speed of people post-stroke during pool floor walking. However, it is interesting to note that changes in gait variables were not found in the paretic limb where favourable responses were expected to occur.

Feeding the Brain’s Curiosity Helps Delay Alzheimer’s, Study Says

I feed my brain with hundreds of stroke research studies each year. Something your doctor should be doing for you  but obviously is figuring that your need to keep up to date on research is more important for preventing your dementia than solving your problems with stroke recovery.
People genetically prone to Alzheimer’s who went to college, worked in complex fields and stayed engaged intellectually held off the disease almost a decade longer than others, a study found.
Lifelong intellectual activities such as playing music or reading kept the mind fit as people aged and also delayed Alzheimer’s by years for those at risk of the disease who weren’t college educated or worked at challenging jobs, the researchers said in the study published today in JAMA Neurology.
More than 5 million Americans have Alzheimer’s disease, the most common form of dementia, and the number is expected to triple by 2050, according to the Alzheimer’s Association. Today’s findings show that intellectual enrichment pursued over a lifetime may help reduce the number of people who will develop the disease, the authors said.
“Keeping your brain mentally stimulated is a lifelong enterprise,” David Knopman, a study author and a professor of neurology at the Mayo Clinic in Rochester, Minnesota, said in a telephone interview. “If one can remain intellectually active and stimulated throughout one’s lifespan, that’s protective against late-life dementia. Staying mentally active is definitely good for your brain.”
Currently there are no effective treatments for Alzheimer’s. A report by the Alzheimer’s Association projected that any treatment that could delay the onset of Alzheimer’s by five years would reduce the expected number of patients with the disease in the U.S. by about 43 percent by 2050.

Reducing Dementia

Knopman said providing mid-to late-life cognitive activities across the population may not be as beneficial as an actual treatment for Alzheimer’s and dementia. Still if new cases of dementia were reduced even by a fraction it would be a “great success.”
Researchers studied 1,995 people ages 70 to 89 without dementia who lived in Minnesota. They looked at their education and occupation and their mid-to late-life cognitive activity.

More at link.

Baycrest memory experts launch 'thermometer' for the mind

I haven't had time yet to do this test to see if I am well or not.
If you are in the 50 to 79 age bracket, worried about your memory changes and whether you need to see a doctor, there is a free online brain health test developed by the memory experts at Baycrest Health Sciences that will help you with that decision.
The test – co-developed by the brain health solutions company Cogniciti Inc. (owned by Baycrest and partner MaRS Discovery District) – takes about 20 minutes to complete and is available to the public at
The game-like tests tap into functions such as memory and attention, which are affected by aging and brain disease. You can take the test on a desktop or laptop computer at home (with internet access), and receive an overall score of your cognitive health immediately after you finish.
According to the test's creators, the majority of people will score in the normal, healthy range for their age – which will help reassure the "worried well".  For the small percentage (approximately 2 - 3%) that scores below average for their age and education, those adults will be encouraged to re-test after a week. If their score again falls below the normal threshold for their age, they will be provided with a personalized report to help them start the conversation about their brain health with a doctor.
Designed by a team of clinical neuropsychologists and cognitive scientists at Baycrest Health Sciences and its world-renowned Rotman Research Institute – and lab tested with 300 adults aged 50 to 79 recruited from various sources including CARP Canada's subscriber base – the brain health assessment hammers a stake in the ground in an increasingly crowded field of online brain fitness products.
"Our aim with the brain health test is to reassure the worried well and nudge that small percentage of people who do have serious memory issues to discuss their concerns with a doctor," said Dr. Angela Troyer, program director of Neuropsychology and Cognitive Health at Baycrest, and a lead member of the research team that developed the test. 
"Given the growing consumer demand for quality brain health self-assessments, this new online test can help address the concerns of millions among the worried well," said Alvaro Fernandez, CEO and co-founder of, an inde­pen­dent mar­ket research firm tracking health and performance applications of neuroscience. SharpBrains has 100,000 monthly readers for its popular brain blog and 45,000 eNewsletter subscribers.

Good luck, more at link

Using ultrasound to treat stroke: Cerevast Therapeutics raises $10M

But isn't this just likely to push the broken up clot farther downstream?  It is the same reason that blowing up an asteroid heading for earth collison will not work unless it is pulverized enough that the pieces burn up on reentry. I wouldn't trust breaking up a clot into small enough pieces that they don't cause downstream problems. But ask your doctor about this as you are being treated if you are conscious enough to understand questions.
Good luck.
They say that with a stroke, “time lost is brain lost” – so when a stroke happens, each second counts to stave off further brain damage. Seattle-area startup Cerevast Therapeutics is developing a device that emits ultrasound waves meant to quickly dislodge stroke-causing blood clots in the brain.
And company just raised $10 million, according to a regulatory filing.
The company’s head-worn device, called the ClotBust ER, is made up of a number of ultrasound transducers that are placed in regions where the majority of vessel occlusions in the brain are known to occur, Cerevast says.
Screen Shot 2014-12-24 at 8.18.48 PM
This fall, Cerevast announced the first interim results of its ongoing Phase 3 trial. This initial bit analyzed the 90-day functional recovery of 250 randomized patients.
The study’s being conducted at 60 stroke centers in 14 countries.
The company’s Clotbust ER trial is currently enrolling patrients.

Friday, December 26, 2014

Effects of Physical Exercise on Neuroinflammation, Neuroplasticity, Neurodegeneration, and Behavior

Exercise has been proven multiple times to be helpful in recovery. Who the hell is going to write up a stroke protocol for this? Or are you as a survivor going to have to figure this out on your own?
  1. Martina Svensson, MSc1
  2. Jan Lexell, MD, PhD2,3
  3. Tomas Deierborg, PhD1
  1. 1Department of Experimental Medical Sciences, Experimental Neuroinflammation Laboratory, Lund University, Lund, Sweden
  2. 2Department of Health Sciences, Rehabilitation Medicine Research Group, Lund University, Lund, Sweden
  3. 3Department of Neurology and Rehabilitation Medicine, Skane University Hospital, Lund, Sweden
  1. Tomas Deierborg, Experimental Neuroinflammation Laboratory, Department of Experimental Medical Science, Lund University, BMC B11, Lund 221 84, Sweden. Email:


Physical exercise is a cornerstone in the management of many neurodegenerative disorders, such as Parkinson’s disease, dementia, and stroke. However, much of its beneficial effects on improving motor functions and cognition as well as decreasing neurodegeneration and neuroinflammation are not yet well understood. The obvious limitations of studying the protective mechanisms behind exercise, for example, brain plasticity and neurodegeneration, could be overcome by generating novel animal models of neurodegenerative disorders. In this narrative review, we discuss the beneficial effects of exercise performed in animal models of neurodegenerative disorders and how the results from animal studies can be used in clinical settings. From preclinical studies, the positive effects of exercise have been related to increased levels of neurotrophic factors, elevated expression of anti-inflammatory cytokines, and reduced levels of pro-inflammatory cytokines and activated microglia. It is clear that parameters influencing the effect of exercise, such as intensity, still remain to be investigated in animal studies in order to find the optimal program that can be translated into exercise interventions for patients with neurodegenerative diseases.

Evaluating the Quality of Medical Care

Whom is doing this for stroke? Because if we don't know about the problems in stroke and the current disastrous results we will never be able to make them better.
A medical blogger arguing against using this for pay for performance.

The problem with “measuring quality” – as Donabedian told us

I forcibly disagree, we have to start evaluating stroke results or we will never fix the problems. Once again proving that our stroke doctors have their heads so far up their asses they will never see any helpful research.

Hugh Herr: The new bionics that let us run, climb and dance

Creating something from this to help stroke survivors should be a piece of cake. If only we had a great stroke association willing to dream and pursue impossible dreams.
Hugh Herr is building the next generation of bionic limbs, robotic prosthetics inspired by nature's own designs. Herr lost both legs in a climbing accident 30 years ago; now, as the head of the MIT Media Lab’s Biomechatronics group, he shows his incredible technology in a talk that's both technical and deeply personal — with the help of ballroom dancer Adrianne Haslet-Davis, who lost her left leg in the 2013 Boston Marathon bombing, and performs again for the first time on the TED stage.

Fatal gastrointestinal hemorrhage after a single dose of dabigatran.

Be careful out there on those Warfarin replacements. Has your doctor told you all the side effects of Warfarin vs. Pradaxa?  Don't listen to me, if your doctor doesn't tell you about these problems s/he must not consider them worthwhile or even worse does not know about the problems.
A good friend of mine refused to go on Pradaxa because of the lack of a reversal agent.

How To Grow Muscles Without Lifting Weights

Your doctor should be jumping all over this to prevent your muscles from atrophying. But you won't get a stroke protocol from them because it wasn't taught in medical school. You don't want to do this on your own because of the extreme dangers of mental imagery.

Wednesday, December 24, 2014

Over-The-Counter Drug Used To Cure Cold And Fever Could Hold Key To A Longer Life - Ibuprofen

I sure you don't really want to trust that the effect in worms translates to humans without a bunch of testing.
These other uses of ibuprofen make for interesting consideration by your doctor.

Nasal NSAIDs for Alzheimer's Disease

FDA revisits heart risks with NSAIDs

High-Dose NSAIDs Hike Risk of Heart Attack and Stroke

Common Medicine Helps Repair Brain After Stroke, Study in Rats Suggests


 Over-The-Counter Drug Used To Cure Cold And Fever Could Hold Key To A Longer Life - Ibuprofen



Main Stroke Protocol - Use for all suspected stroke-TIA patients - NHS England

Still missing anything at all for stopping the neuronal cascade of death. Who is working on solving that problem? ANYONE AT ALL?
It has  - Do not start statins before 72 hours from onset.
What about this?
Don't listen to anything I have to say, I'm not medically trained and am obviously stupid in my stroke-addled brain.

The International Common Data Elements Project for TBI – Getting Further, Faster

This is precisely what we need for stroke, because if we can't even competently and accurately describe the problems we will never be able to solve them. I don't expect either the the NSA, ASA or WSO to take on this challenging task because that would entail hard work. Prove me wrong!
The brain is the most complex organ of the body and repairing it after injury is challenging. To address this challenge, research scientists are working to increase our understanding of brain function and to develop better diagnostic tools and treatments for the millions of people worldwide living with traumatic brain injury (TBI). The National Institute of Neurological Disorders and Stroke (NINDS) is the lead institute at the National Institutes of Health (NIH) for TBI research and supports a range of high quality research on this topic.
Understanding reasons for good and poor recoveries after TBI is an important step toward developing better treatments, and several years ago NINDS supported a study to address this question. The study was unusual in that it evaluated thousands of cases of severe TBI by combining data retrospectively from several clinical trials. Such large data sets were previously unavailable, and the study successfully identified several major factors associated with recovery. However, some research questions could not be fully addressed because the original studies did not include the data needed to answer them. It became clear that many important questions about recovery after TBI would need to be addressed in new studies. Moreover, investigators also discovered that retrospectively comparing data from multiple studies was excruciatingly difficult and time consuming because the same types of information were coded in different ways. For example, some studies reported a subject’s educational status as “none, grade school, high school, college, or graduate school” while other studies reported “total years of school.” Hundreds of these types of examples existed, and investigators spent years figuring out ways to make the studies comparable and then reformatting the data. There had to be a better way to combine information from multiple studies!
The better way is the International TBI Common Data Elements Project, a collaboration among the NIH, Department of Defense (DOD), National Institute on Disability and Rehabilitation Research, Department of Veterans Affairs, and Centers for Disease Control and Prevention to standardize definitions and protocols for TBI research. Rather than retrospectively reformatting and harmonizing data after a study ends, the goal of the International TBI Common Data Elements Project is to standardize data collection at the beginning. The project includes hundreds of scientific experts from around the world who serve on working groups and steering committees to develop recommendations for collecting data in a uniform manner. The standardized data recommendations are referred to as common data elements (CDEs).
Currently, more than 900 CDEs for TBI research (Hicks et al., 2013) exist, and are available on multiple websites, including the NINDS Common Data Elements website. A small number of the CDEs are so commonly used that they are called “CORE CDEs” and recommended for use in virtually all TBI research studies. Other CDEs are recommended for use depending on the type of study, such as epidemiology, acute-hospital, rehabilitation, or mild TBI/concussion. Some of the CDEs are relevant to subjects of all ages, and others are specific to children or adults.  
Following the development of the TBI CDEs, the next major step was to try them out to see if they could actually work in a research study conducted across multiple centers on a wide range of subjects. To give them a test-run, four TBI hospitals collaborated to collect data on more than 650 subjects with TBI, with injuries ranging from mild to severe, in a study called TRACK-TBI. The TRACK-TBI study revealed that the TBI CDEs had a few minor issues, but overall they were useable. In addition, the CDEs accelerated the research as the data were collected in just two years. Most of the data are still being analyzed; one early publication demonstrated that an MRI of the brain was more predictive of recovery outcomes at 3 months than a conventional CT scan (Yuh et al., 2013). Although previous smaller studies had shown similar findings, the large number of subjects in the TRACK-TBI study greatly increased the clinical significance and impact. 
Lastly, there is the question of how to put the TBI CDEs into practice. It’s one thing to develop CDEs and another thing to actually use them. Fortunately, there are two major activities underway to promote the use of the TBI CDEs and data sharing. One is the NIH and DOD collaboration to provide a Federal Interagency TBI Research (FITBIR) Informatics System. FITBIR provides a database for TBI research at no cost to the research scientists, as well as an electronic data capture tool, and a platform for collaboration and data sharing. FITBIR uses the TBI CDEs for its data dictionary. The second major activity is the International TBI Research (InTBIR) Initiative (Tosetti et al., 2013). InTBIR is a collaboration among the NIH, European Union Research Directorate and Canadian Institutes of Health Research to support international team science to study 10,000 children and adults with TBI. InTBIR researchers will use the TBI CDEs in their studies to facilitate data sharing and analysis toward the development of better diagnostic tools and more effective treatments.
In summary, the International TBI Common Data Elements Project built a foundation for the FITBIR Informatics System and the InTBIR Initiative, and together all of these projects will help us to get further, faster on understanding TBI and identifying ways to promote recovery.