Deans' stroke musings

Changing stroke rehab and research worldwide now.Time is Brain!Just think of all the trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 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:

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

Saturday, November 30, 2013

Trail clearing rehab

My battery powered chainsaw is a problem. When cutting thru thicker wood the chain loosens up and comes off the bar after 5 minutes. I thought 4 weeks ago that I had just 2 trees to clear. 2 weeks ago a storm came through and I had another 4 trees to clear. This afternoon I finally got through one of the problem trees and got to walk the back loop. Another 4 more trees to clear yet. As long as the snow holds off for a couple more weekends I can get this accomplished and xc ski the trails this winter. In carrying the branches off the trails I managed to heavily fall on my left butt twice, luckily not into brambles or rose bushes.  I'm walking with a heavy limp tonight because of that and using vitamin I.  I am using gumshoe boots to walk the trails now. An excellent stroke rehab  boot because it has  no ankle support. 2 hours of walking is great for my ankle muscles and balance.

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

I know vibration doesn't really have that much research behind it but I'm following what Margaret Yekutiel wrote in the book, Sensory Re-Education of the Hand After Stroke in 2001. 
7-speed Secret Love Finger Fun Vibator Vibration Massager with Sexy Dice 
I am not going to get the Chinese characters on the dice translated.
I looked at vibrating gloves. 

But I knew I would not be able to get it on unassisted. 

And wrong hand.

Fukuoku Black Right Hand Five Finger Vibrating Massage Glove - (fits Medium To Large Hand)

Buying this would never have been possible while married. It will be an interesting conversation if I ever get a lady friend. The silicone loops for the fingers seem to be sized for womens hands but I'll make do. I just went straight to the 7th speed. And no you are not going to get a picture of the box it came in. And by placing the third finger against the finger pads I can cover three fingers at once.


'If You Want to Gather Honey, Don't Kick Over the Beehive'

Chapter 1 of Dale Carnegie How to Win Friends and Influence People.
I'm doing everything wrong according to  this chapter, I criticize every person involved in stroke. Which will just make them dig in their heels and not listen.
Chapter 2 - How to determine what people want/need.
That's simple for our doctors and therapists, they want standardized protocols that they can just work through. Somebody has to create them and its not any of our fucking failures of stroke associations.

Plasticity beyond peri-infarct cortex: Spinal up regulation of structural plasticity, neurotrophins, and inflammatory cytokines during recovery from cortical stroke

I'm sure your wonderful up-to-date doctor can explain all this and how it is already incorporated into your 100% recovery protocol. You don't have a 100% recovery protocol? Why not? Is your doctor not any good?
  • a Centre for Neuroscience, University of Alberta, Edmonton, Alberta, Canada T6G 2R3
  • b Faculty of Rehabilitative Medicine, University of Alberta, Edmonton, Alberta, Canada T6G 2R3
  • c Department of Psychiatry, University of Alberta, Edmonton, Alberta, Canada T6G 2R3
  • d Neurochemical Research Unit, University of Alberta, Edmonton, Alberta, Canada T6G 2R3


Cortical stroke induces heightened expression of GAP-43 in the spinal cord
Plasticity in the spinal cord after cortical stroke has a finite temporal window
TNF-α, IL-6, and NT-3 protein levels in spinal cord correlate with GAP-43 levels
BDNF increases transiently in spinal cord prior to heightened GAP-43 expression


Stroke induces pathophysiological and adaptive processes in regions proximal and distal to the infarct. Recent studies suggest that plasticity at the level of the spinal cord may contribute to sensorimotor recovery after cortical stroke. Here, we compare the time course of heightened structural plasticity in the spinal cord against the temporal profile of cortical plasticity and spontaneous behavioural recovery. To examine the relation between trophic and inflammatory effectors and spinal structural plasticity, spinal expression of brain derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) were measured. Growth-associated protein 43 (GAP-43), measured at 3, 7, 14, or 28 days after photothrombotic stroke of the forelimb sensorimotor cortex (FL-SMC) to provide an index of periods of heightened structural plasticity, varied as a function of lesion size and time after stroke in the cortical hemispheres and the spinal cord. Notably, GAP-43 levels in the cervical spinal cord were significantly increased after FL-SMC lesion, but the temporal window of elevated structural plasticity was more finite in spinal cord relative to ipsilesional cortical expression (returning to baseline levels by 28 post-stroke). Peak GAP-43 expression in spinal cord occurred during periods of accelerated spontaneous recovery, as measured on the Montoya Staircase reaching task, and returned to baseline as recovery plateaued. Interestingly, spinal GAP-43 levels were significantly correlated with spinal levels of the inflammatory cytokines TNF-α and IL-6 as well as the neurotrophin NT-3, while a transient increase in BDNF levels preceded elevated GAP-43 expression. These data identify a significant but time-limited window of heightened structural plasticity in the spinal cord following stroke that correlates with spontaneous recovery and the spinal expression of inflammatory cytokines and neurotrophic factors.


  • IC, ipsilesional cortex;
  • CC, contralesional cortex;
  • CSC, cervical spinal cord;
  • LSC, lumbar spinal cord;
  • FL-SMC, forelimb sensorimotor cortex;
  • GAP-43, growth associated protein-43;
  • TNF-α, tumor necrosis factor - alpha;
  • IL-6, interleukin 6;
  • BDNF, brain derived neurotrophic factor;
  • NT-3, neurotrophin-3


  • Ischemia;
  • Sensorimotor cortex;
  • Plasticity;
  • Spinal cord;
  • Inflammation;
  • Neurotrophins;
  • GAP-43;
  • TNF-alpha;
  • IL-6;
  • BDNF;
  • NT-3

Brain Power: McCallie teen awarded patent for revolutionary stroke treatment design

Great idea. But once again proving that stroke medical personnel  don't even know that a ton of neurons  keep dying after circulation is restored. Its almost as if they have never heard of the neuronal cascade of death. From 2009. Would you see any other doctor that is 4 years out-of-date? 
Christian's device prototype also uses a catheter-into-artery approach, but instead aims to drill through the clot before any attempt to remove it is made. Once through, it can supply the barren, neglected side of the artery with direly needed blood flow in as little as five minutes.

But is this just showering the downstream arteries and capillaries with debris? 

Falls, Fractures, and Osteoporosis After Stroke

This must not have affected me too much considering  my epic failure at bike stroke therapy  My doctor had 4 years to read about this and never told me to watch out for this.

Time to Think About Protection?

  1. Elizabeth A. Warburton, MA, DM, MRCP
+ Author Affiliations
  1. From the Department of Stroke Medicine (K.E.S.P., E.A.W.) and Medical Research Council Bone Research Group (J.R.), Addenbrooke’s Hospital, Cambridge, UK.
  1. Correspondence to Dr Elizabeth A. Warburton, Department of Stroke Medicine, Department of Medicine, University of Cambridge, Addenbrooke’s Hospital, Box 83, Cambridge CB2 2QQ, UK. E-mail


Background Osteoporosis is a significant complication of stroke. The clinical course of hemiplegic stroke predisposes patients to disturbed bone physiology. Sudden immobility and unilateral loss of function unload the skeleton at key areas such as the affected hip. This is manifest by an early reduction in bone density at this site. Stroke patients may also have motor, sensory, and visual/perceptual deficits that predispose them to falls. These factors result in an early but sustained increase in hip fractures after stroke.
Summary of Comment Potential bone loss is often overlooked in stroke treatment. Morbidity and mortality from hip fractures might be reduced by preventing bone loss at an early stage. In the crucial first year after stroke, bone loss seems to be due to accelerated resorption. Bisphosphonates are the drugs of choice in preventing osteoclastic bone resorption, but oral administration soon after stroke may be impractical. Potent new intravenous bisphosphonates have been used in postmenopausal women with osteoporosis with good preliminary results. Effective dosing regimens for osteoporosis have included a single annual or semiannual injection of bisphosphonate as well as weekly oral dosing. This article reviews the current literature on osteoporosis and hip fractures after stroke, making a case for a trial of intravenous bisphosphonates early after stroke.
Conclusions Hip fracture after stroke is an increasingly recognized problem. Measures to prevent bone loss and preserve bone architecture have not been part of stroke management thus far. Because rapid bone loss is a risk factor for fracture, we believe that a randomized, placebo-controlled trial of intravenous bisphosphonates given in the early phase of stroke rehabilitation is indicated.

Stroke: Know when to act, and act quickly

From Harvard Medical School Healthbeat newsletter.
I absolutely hate these public service announcements because they make it sound as if all you have to do to recover from a stroke is get to a stroke hospital fast enough. If people knew how little can be done and how ineffective stroke treatments are, they would be screaming at the absurdity of this.  Until it is acknowledged that stroke treatments are a complete failure will better treatments be found. But that will require smart arrogant medical persons to acknowledge that they have failed stroke patients for the last 30 years.

And I thought people from Harvard were smart.

When stroke symptoms occur, quick action is vital. If you think you or someone with you is having a stroke call 911. Ideally the person affected should be taken to a hospital emergency room that has expertise and experience in treating stroke as it occurs (called acute stroke). If you or someone you love is at high risk for having a stroke, you should know the name and location of the nearest hospital that specializes in treating acute stroke. Ask your doctor for help in finding out which facilities fit that bill.
The goal of stroke treatment is to restore blood circulation before brain tissue dies. To prevent brain cell death that is significant enough to cause disability, treatment is most effective if it starts within 60 minutes of the onset of symptoms.
An important goal of ongoing stroke research is to find treatments that can buy time by protecting the person’s brain until blood circulation is restored, which can increase the chances of survival and decrease the chances of disability. (This is what is wrong, they don't even know that a ton of neurons  keep dying after circulation is restored. Its almost as if they have never heard of the neuronal cascade of death. Damn them all.)
For more information on ways to prevent and treat strokes, buy Stroke: Preventing and treating “brain attack,” a Special Health Report from Harvard Medical School.

A Key Role for TRPM7 Channels in Anoxic Neuronal Death

Maybe #1 in my list of neuronal cascade of death items is not really a problem. Or at least not an easy problem to solve.
1.  Excitotoxicity
2.  Glutamate poisoning
3.  Capillaries that don't open due to pericytes
4.  Inflammatory action leaking through the blood brain barrier
5. Lysosomal Membrane Permeabilization as a Key Player in Brain Ischemic Cell Death.
6.   Reperfusion injury
Cell, Volume 115, Issue 7, 863-877, 26 December 2003
Copyright © 2003 Cell Press All rights reserved.



Excitotoxicity in brain ischemia triggers neuronal death and neurological disability, and yet these are not prevented by antiexcitotoxic therapy (AET) in humans. Here, we show that in neurons subjected to prolonged oxygen glucose deprivation (OGD), AET unmasks a dominant death mechanism perpetuated by a Ca2+-permeable nonselective cation conductance (IOGD). IOGD was activated by reactive oxygen/nitrogen species (ROS), and permitted neuronal Ca2+ overload and further ROS production despite AET. IOGD currents corresponded to those evoked in HEK-293 cells expressing the nonselective cation conductance TRPM7. In cortical neurons, blocking IOGD or suppressing TRPM7 expression blocked TRPM7 currents, anoxic 45Ca2+ uptake, ROS production, and anoxic death. TRPM7 suppression eliminated the need for AET to rescue anoxic neurons and permitted the survival of neurons previously destined to die from prolonged anoxia. Thus, excitotoxicity is a subset of a greater overall anoxic cell death mechanism, in which TRPM7 channels play a key role.

Friday, November 29, 2013

How to Open a Spastic Hand: Video tip

From Jan Davis at International Clinical Educators, Inc. (ICE)
This may be good for those with carers but I really need one that can be done alone.

Stroke survivors celebrating their recovery - Newcastle Australia

You'll have to ask your therapist to find Bernadette Matthias PhD research into the impact of choral singing on stroke recovery.
A group of Hunter stroke survivors have united to celebrate their recovery through song.
Two stroke rehabilitation study groups will join forces for a combined concert on Sunday as part of the renowned BrainWaves choir.
Conducted by Hunter Medical Research Institute researcher and East Maitland woman Bernadette Matthias, BrainWaves will join other community vocal ensembles in the Making Waves: A Celebration of Song.
Ms Matthias formed the original BrainWaves choir in 2012 as part of her PhD research into the impact of choral singing on stroke recovery.
A second group was recruited in February this year, undergoing a
12-week singing course before making their public debut in June.
The choir recently gained national prominence on the SBS Insight program.
While the results of the study are yet to be published, choir members have reported benefits in their communication skills and well-being.
“There appears to be a rich interconnection between the processes involved in singing and speech,” Ms Matthias said. “So in addition to the benefits for well-being and depression, stimulating the brain by singing might help the
language centre recover as well. “
BrainWaves will perform at the Harold Lobb Concert Hall, at the Newcastle Conservatorium of Music, on Sunday at noon.

Rhythm in disguise: why singing may not hold the key to recovery from aphasia

What does your speech therapist think of this? Its only 2 years old. Sept. 2011.
  1. Stefan Geyer
+ Author Affiliations
  1. Max Planck Institute for Human Cognitive and Brain Sciences, 04103 Leipzig, Germany
  1. Correspondence to: Benjamin Stahl, Max Planck Institute for Human Cognitive and Brain Sciences, Stephanstraße 1A, 04103 Leipzig, Germany E-mail:
  • Received June 23, 2011.
  • Revision received August 11, 2011.
  • Accepted August 15, 2011.


The question of whether singing may be helpful for stroke patients with non-fluent aphasia has been debated for many years. However, the role of rhythm in speech recovery appears to have been neglected. In the current lesion study, we aimed to assess the relative importance of melody and rhythm for speech production in 17 non-fluent aphasics. Furthermore, we systematically alternated the lyrics to test for the influence of long-term memory and preserved motor automaticity in formulaic expressions. We controlled for vocal frequency variability, pitch accuracy, rhythmicity, syllable duration, phonetic complexity and other relevant factors, such as learning effects or the acoustic setting. Contrary to some opinion, our data suggest that singing may not be decisive for speech production in non-fluent aphasics. Instead, our results indicate that rhythm may be crucial, particularly for patients with lesions including the basal ganglia. Among the patients we studied, basal ganglia lesions accounted for more than 50% of the variance related to rhythmicity. Our findings therefore suggest that benefits typically attributed to melodic intoning in the past could actually have their roots in rhythm. Moreover, our data indicate that lyric production in non-fluent aphasics may be strongly mediated by long-term memory and motor automaticity, irrespective of whether lyrics are sung or spoken.

Researchers identify stem cell population responsible for heart regeneration

Where the hell are our stroke researchers coming up with similar breakthroughs?
The readable blogger discussing it here;

The abstract this breakthrough came from:

Bilateral representation of language: A critical review and analysis of some unusual cases

I'm sure your speech therapist and neurologist have already noticed this in their patients.
  • a Department of Radiology/Research Institute, Miami Children's Hospital, Miami, FL, USA
  • b Department of Communication Sciences and Disorders, Florida International University, Miami, FL, USA


Language is usually and mostly associated with the left hemisphere activity.
There is diverse evidence of potential bilateral representation of language.
Two classifications of language lateralization patterns can be suggested.


It is well known that for right-handed individuals, language is usually and mostly associated with the left hemisphere activity. The question of the potential bilateral representation of language, however, has been barely approached. The evidence regarding the bilateral representation of language taken from Wada test, PET, fMRI, tractography, and magneto-encephalography is examined. Departing from the modularity concept and data flow computing models, two classifications – topographic and functional – of potential language lateralization patterns are proposed; it is pointed out that language can be bilaterally represented in different patterns, accordingly with the distribution of the main domains (expressive vs. receptive) and their subfunctions; and with respect to different modalities of data flow. Five illustrative cases of bilateral representation of language are presented. It is concluded that language dominance is mostly a matter of hemispheric advantage for a specific cognitive function.

Graph at link.

636,120 Ways to Have Posttraumatic Stress Disorder

And stroke is one of them. Is your doctor diagnosing you with this? Does your doctor even know about this?
1.  PTSD May Be Barrier to Stroke Recovery
2.  Prevalence of PTSD in Survivors of Stroke and Transient Ischemic Attack: A Meta-Analytic Review 
 Check out yourself here;
1.  Screening for Posttraumatic Stress Disorder (PTSD)

636,120 Ways to Have Posttraumatic Stress Disorder
  1. Isaac R. Galatzer-Levy1
  2. Richard A. Bryant2
  1. 1New York University School of Medicine
  2. 2University of New South Wales, Kensington, New South Wales, Australia
  1. Isaac R. Galatzer-Levy, New York University School of Medicine, 1 Park Ave, New York, NY 10016 E-mail:


In an attempt to capture the variety of symptoms that emerge following traumatic stress, the revision of posttraumatic stress disorder (PTSD) criteria in the 5th edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM–5) has expanded to include additional symptom presentations. One consequence of this expansion is that it increases the amorphous nature of the classification. Using a binomial equation to elucidate possible symptom combinations, we demonstrate that the DSM–IV criteria listed for PTSD have a high level of symptom profile heterogeneity (79,794 combinations); the changes result in an eightfold expansion in the DSM–5, to 636,120 combinations. In this article, we use the example of PTSD to discuss the limitations of DSM-based diagnostic entities for classification in research by elucidating inherent flaws that are either specific artifacts from the history of the DSM or intrinsic to the underlying logic of the DSM’s method of classification. We discuss new directions in research that can provide better information regarding both clinical and nonclinical behavioral heterogeneity in response to potentially traumatic and common stressful life events. These empirical alternatives to an a priori classification system hold promise for answering questions about why diversity occurs in response to stressors.

Combined arm stretch positioning and neuromuscular electrical stimulation during rehabilitation does not improve range of motion, shoulder pain or function in patients after stroke: a randomised trial

I'm beginning to know that our therapists have absolutely no clue as to whether any of their interventions work at all. We are just on an extended guinea pig research trial with no reality behind it.
  • 1 School of Physiotherapy, Hanze University of Applied Sciences, Groningen
  • 2 Department of Rehabilitation Medicine, University of Groningen, University Medical Center Groningen, Groningen
  • 3 Department of Oral and Maxillofacial Surgery, University of Groningen, University Medical Center, Groningen
  • 4 ViaReva, Center for Rehabilitation, Apeldoorn, The Netherlands
  • 5 Department of Rehabilitation, Radboud University Nijmegen Medical Center, Nijmegen, The Netherlands


Does static stretch positioning combined with simultaneous neuromuscular electrical stimulation (NMES) in the subacute phase after stroke have beneficial effects on basic arm body functions and activities?


Multicentre randomised trial with concealed allocation, assessor blinding, and intention-to-treat analysis.


Forty-six people in the subacute phase after stroke with severe arm motor deficits (initial Fugl-Meyer Assessment arm score ≤ 18).


In addition to conventional stroke rehabilitation, participants in the experimental group received arm stretch positioning combined with motor amplitude NMES for two 45-minute sessions a day, five days a week, for eight weeks. Control participants received sham arm positioning (ie, no stretch) and sham NMES (ie, transcutaneous electrical nerve stimulation with no motor effect) to the forearm only, at a similar frequency and duration.

Outcome measures

The primary outcome measures were passive range of arm motion and the presence of pain in the hemiplegic shoulder. Secondary outcome measures were severity of shoulder pain, restrictions in performance of activities of daily living, hypertonia, spasticity, motor control and shoulder subluxation. Outcomes were assessed at baseline, mid-treatment, at the end of the treatment period (8 weeks) and at follow-up (20 weeks).


Multilevel regression analysis showed no significant group effects nor significant time × group interactions on any of the passive range of arm motions. The relative risk of shoulder pain in the experimental group was non-significant at 1.44 (95% CI 0.80 to 2.62).


In people with poor arm motor control in the subacute phase after stroke, static stretch positioning combined with simultaneous NMES has no statistically significant effects on range of motion, shoulder pain, basic arm function, or activities of daily living.

Trial registration


Barriers and facilitators to engagement in rehabilitation for people with stroke: a review of the literature

I'm impressed with this as an undergraduate project.
Grace A MacDonald
BHSc (Physiotherapy), NZRP
Physiotherapist (Shore Physiotherapy)
Nicola M Kayes
MSc(Hons), PhD
Senior Lecturer, Person Centred Research Centre, Health and Rehabilitation Research Institute, AUT University
Felicity Bright
BSLT (Hons), MHSc (Hons), MNZSTA
Speech Language Therapist, School of Rehabilitation and Occupation Studies
PhD Candidate, Person Centred Research Centre, Health and Rehabilitation Research Institute, AUT University
While there is a growing acknowledgement of the significant role that engagement plays in rehabilitation, there is limited knowledge
of the factors that may help or hinder engagement in stroke rehabilitation. This review drew on systematic principles and aimed
to explore what is currently known about the perceived barriers and facilitators to engagement in stroke rehabilitation. EBSCO,
SCOPUS and Google Scholar databases and reference lists were searched for papers that provided insight into the process of
engagement or disengagement in stroke rehabilitation.
Data were extracted and synthesised thematically from 17 papers. Themes
included goal setting, therapeutic connection, personalised rehabilitation, paternalism versus independence, patient centered practice,
knowledge is power, and feedback and achievement. None of the papers identified however, explicitly sought to investigate the
complexities of engagement in rehabilitation specifically within the stroke population. Future research is needed to explore this topic
in more depth from the perspective of all the key stakeholders. A more comprehensive understanding of engagement in stroke
rehabilitation may inform the development of interventions to better equip rehabilitation providers with the clinical skills to facilitate
engagement and effectively deliver rehabilitation modalities.
MacDonald GA, Kayes NM, Bright F (2013) Barriers and facilitators to engagement in rehabilitation for people with
stroke: a review of the literature New Zealand Journal of Physiotherapy 41(3): 112-121

Full 10 page paper at the link.

Cervical artery dissection: a biomechanical perspective

Complete and total apologist for the chiropractic profession. I will never get my neck adjusted. These guys will say anything to not take responsibility.
I won't have this done for these reasons;
1. Call for age limit after chiropractor breaks baby's neck
2. 'My chiropractor gave me locked-in syndrome, but I survived': Astonishing recovery of woman, 46, who beat the odds to walk and talk  again
3. Woman claims stroke stems from spinal manipulation by chiropractor
4. Comparing chiropractic neck adjustment to hanging
5.  Mitchell, SD chiropractor denies causing Gunkel's stroke
6.  Cerebrospinal fluid leak secondary to chiropractic manipulation
7.  Chiropractor forged consent form after patient's stroke
8.  Letting a chiropractor 'crack' your neck to ease pain could trigger stroke
9.  Deaths after chiropractic: a review of published cases.
10.  Chiropractic stroke

The  apologist here:
Cervical artery dissection: a biomechanical perspective
J Can Chiropr
Assoc 2013; 57(4)
Although there has been a putative ??? link between cervical
spinal manipulative treatment (cSMT) and cervical artery
dissection (CAD) ever since Thornton’s report in the literature in 19341
, recent evidence suggests that this is an association rather than a causal relationship. Since 2008, several studies published by Cassidy and co-workers2-4
have attributed the association between cSMT and CAD
to patients seeking chiropractic care for neck pain and
headaches during the prodrome ??? of a stroke.
Most reviews in the literature now generally report
that there are no convincing data, either to prove or disprove, any causality between cSMT and CAD5. (really?)

However, case reports and case series still accumulate that identify
chiropractic as the sole cause of CAD6-7.

Furthermore, Tuchin8 recently tested the causality between CAD and SMT using Hill’s criteria, and concluded that there is no evidence that SMT is causally related to stroke. Nevertheless, some authors continue to claim that cSMT causes CAD.
Rather than using an epidemiologic approach to assess
the risk of whether cSMT can cause CAD, another approach is to investigate the mechanism(s) of how cSMT can cause CAD. Since 20029, our laboratory has focused on the latter strategy. Using cadaveric vertebral arteries (VAs) as a model for the in vivo neck, we have measured
the strains experienced by VAs using ultrasonography to dynamically measure the changes in VA segment lengths during manipulative procedures. The details of the experimental procedures have been described elsewhere9-11.
We have now replicated these experiments on a total of 16 VAs obtained from 10 cadavers9-11 in 3 different papers. 
You can read the rest of the blathering at the link.

Thursday, November 28, 2013

Preliminary medical testing results have shown that aspirin may prevent dementia and intestinal cancers

Give me this, marijuana,  some beer, some more dark beer,  and a volume of Shakespeare and I'll delay dementia until I die. And have a chat with these nuns.
Challenge your doctor to give you something better to prevent dementia. Something better than this from Harvard Medical School. Or this generic stuff.
The study of 15,000 healthy Australians aged over 70 was the largest ever clinical trial on the use of aspirin to prevent disease in the elderly.
Professor Mark Nelson from Hobart's Menzies Research Institute says the clinical trials could lead to cheap and simple treatment procedures.

Dementia Prevention – What Can Be Done?

Fairly generic prescriptions mainly because they really don't know much about this yet.
1.  Hypertension/High Blood Pressure: 
2.  Smoking: 
3.  Keep Your Body and Mind Active:
4.  Maintain a Healthy Diet: 
5.  Brush Your Teeth. 
6.  Treatment of Atrial Fibrillation is Important. 

Watching Sports Can Make You Fitter

And will your doctor research whether this applies to strokies?

Published in:

Frontiers in Autonomic Neuroscience

Study Further:

Researchers have reported that watching other people exercise usually increases heart rate of the person along with some other physiological parameters as the person himself is doing exercise.

Lots more at link.

OTC painkiller may blunt memory loss from puffing pot

And look at that, marijuana may reduce the effect of Alzheimers. When the hell is your doctor going to influence the FDA and Congress to allow marijuana to be legalized?
A great post from Neurorexia 

3 paragraphs, rest at link.

Pot’s not the best thing for your memory. Yes, I know there are functional potheads who enjoy their greens and get also their work done. Still, it’s hard to ignore the legions of studies that show Δ9-THC consumption impairs spatial learning and working memory – that is, the ability to hold several pieces of information in mind and manipulate them to reach a mental goal.
Welcome to downtown BC and BC Bud! Source:
Yet paradoxically, THC may benefit those with Alzheimer’s disease. Previous research in rats show that the compound breaks down clumps of disease-causing proteins (called β-amyloid plagues) by upregulating a “scissor” enzyme that chops them up. Sweeping out these junk protein plagues decreased the number of dying neurons in the hippocampus, a brain area crucial for learning and memory. THC also has powerful anti-oxidant effects and may protect the integrity of mitochondria – the “power plants” of our cells.
So here’s the dilemma: THC may potentially battle dementia, yet it also naturally impairs memory. In an unexpected turn of events, scientists from Louisiana State University discovered a key protein that mediates THC-caused memory loss, and show in mice that you can have your edibles and eat it too.


Does visual feedback during walking result in similar improvements in trunk control for young and older healthy adults?

God, this is so damned simple. Run the same research for unhealthy stroke afflicted adults. Even your doctor might be able to manage that, no thinking involved, just repeat exactly the same conditions for strokies. A great stroke association would do it if we had one. But alas, we have the ASA, NSA and WSO.
Eric Anson, Russell Rosenberg, Peter Agada, Tim Kiemel and John Jeka
For all author emails, please log on.
Journal of NeuroEngineering and Rehabilitation 2013, 10:110  doi:10.1186/1743-0003-10-110
Published: 26 November 2013

Abstract (provisional)


Most current applications of visual feedback to improve postural control are limited to a fixed base of support and produce mixed results regarding improved postural control and transfer to functional tasks. Currently there are few options available to provide visual feedback regarding trunk motion while walking. We have developed a low cost platform to provide visual feedback of trunk motion during walking. Here we investigated whether augmented visual position feedback would reduce trunk movement variability in both young and older healthy adults.


The subjects who participated were 10 young and 10 older adults. Subjects walked on a treadmill under conditions of visual position feedback and no feedback. The visual feedback consisted of anterior-posterior (AP) and medial-lateral (ML) position of the subject's trunk during treadmill walking. Fourier transforms of the AP and ML trunk kinematics were used to calculate power spectral densities which were integrated as frequency bins "below the gait cycle" and "gait cycle and above" for analysis purposes.


Visual feedback reduced movement power at very low frequencies for lumbar and neck translation but not trunk angle in both age groups. At very low frequencies of body movement, older adults had equivalent levels of movement variability with feedback as young adults without feedback. Lower variability was specific to translational (not angular) trunk movement. Visual feedback did not affect any of the measured lower extremity gait pattern characteristics of either group, suggesting that changes were not invoked by a different gait pattern.


Reduced translational variability while walking on the treadmill reflects more precise control maintaining a central position on the treadmill. Such feedback may provide an important technique to augment rehabilitation to minimize body translation while walking. Individuals with poor balance during walking may benefit from this type of training to enhance path consistency during over-ground locomotion.

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

Key protein responsible for controlling communication between brain cells identified

You will have to ask someone else to tell how to put this into a stroke protocol. A great stroke association would do it if we had one.
A writeup on it here:
The abstract here:
Chun Guo1, Keri L Hildick1, Jia Luo1, Laura Dearden1, Kevin A Wilkinson1 and Jeremy M Henley1
  1. School of Biochemistry, University of Bristol, University Walk, Bristol, UK
Correspondence to:
Jeremy M Henley, School of Biochemistry, University of Bristol, University Walk, Medical Sciences Building, Bristol BS8 1TD, UK. Tel.:+44 (0)117 331 1945; Fax:+44 (0)117 331 2168; E-mail:
Received 9 January 2013; Accepted 27 February 2013
Global increases in small ubiquitin-like modifier (SUMO)-2/3 conjugation are a neuroprotective response to severe stress but the mechanisms and specific target proteins that determine cell survival have not been identified. Here, we demonstrate that the SUMO-2/3-specific protease SENP3 is degraded during oxygen/glucose deprivation (OGD), an in vitro model of ischaemia, via a pathway involving the unfolded protein response (UPR) kinase PERK and the lysosomal enzyme cathepsin B. A key target for SENP3-mediated deSUMOylation is the GTPase Drp1, which plays a major role in regulating mitochondrial fission. We show that depletion of SENP3 prolongs Drp1 SUMOylation, which suppresses Drp1-mediated cytochrome c release and caspase-mediated cell death. SENP3 levels recover following reoxygenation after OGD allowing deSUMOylation of Drp1, which facilitates Drp1 localization at mitochondria and promotes fragmentation and cytochrome c release. RNAi knockdown of SENP3 protects cells from reoxygenation-induced cell death via a mechanism that requires Drp1 SUMOylation. Thus, we identify a novel adaptive pathway to extreme cell stress in which dynamic changes in SENP3 stability and regulation of Drp1 SUMOylation are crucial determinants of cell fate.

Wednesday, November 27, 2013

Prolyl isomerase Pin1 and protein kinase HIPK2 cooperate to promote cortical neurogenesis by suppressing Groucho/TLE:Hes1-mediated inhibition of neuronal differentiation

Yes, lets suppress Groucho so I can have neurogenesis. Your doctor needs to follow up on this for your protocol.
R Ciarapica, L Methot, Y Tang, R Lo, R Dali, M Buscarlet, F Locatelli, G del Sal, R Rota and S Stifani
The Groucho/transducin-like Enhancer of split 1 (Gro/TLE1):Hes1 transcriptional repression complex acts in cerebral cortical neural progenitor cells to inhibit neuronal differentiation. The molecular mechanisms that regulate the anti-neurogenic function of the Gro/TLE1:Hes1 complex during cortical neurogenesis remain to be defined. Here we show that prolyl isomerase Pin1 (peptidyl-prolyl cis-trans isomerase NIMA-interacting 1) and homeodomain-interacting protein kinase 2 (HIPK2) are expressed in cortical neural progenitor cells and form a complex that interacts with the Gro/TLE1:Hes1 complex. This association depends on the enzymatic activities of both HIPK2 and Pin1, as well as on the association of Gro/TLE1 with Hes1, but is independent of the previously described Hes1-activated phosphorylation of Gro/TLE1. Interaction with the Pin1:HIPK2 complex results in Gro/TLE1 hyperphosphorylation and weakens both the transcriptional repression activity and the anti-neurogenic function of the Gro/TLE1:Hes1 complex. 

These results provide evidence that HIPK2 and Pin1 work together to promote cortical neurogenesis, at least in part, by suppressing Gro/TLE1:Hes1-mediated inhibition of neuronal differentiation.

The Cytokine Network of Wallerian Degeneration: Tumor Necrosis Factor-α, Interleukin-1α, and Interleukin-1β

This is the best I can do Elizabeth, your doctor should know whom to ask to explain it.
Full 9 pages at the link.


Wallerian degeneration (WD) is the inflammatory response of the nervous system to axonal injury, primarily attributable to the production of cytokines, the mediator molecules of inflammation. We presently document the involvement of the inflammatory cytokines TNFα, interleukin (IL)-1α, and IL-1β in peripheral nerve (PNS) injury in C57/BL/6NHSD (C57/BL) mice that display the normal rapid progression of WD (rapid-WD) and C57/BL/6-WLD/OLA/NHSD mice that display abnormal slow progression of WD (slow-WD). TNFα and IL-1α mRNAs were expressed, whereas TNFα but not IL-1α protein was synthesized in intact PNS of C57/BL mice. TNFα and IL-1α protein synthesis and secretion were rapidly upregulated during rapid-WD in Schwann cells. IL-1β mRNA expression and protein synthesis and secretion were induced sequentially in Schwann cells with a delay after injury. Thereafter, recruited macrophages contributed to the production of TNFα, IL-1α, and IL-1β, which in turn augmented myelin phagocytosis by macrophages. Observations suggest that TNFα and IL-1α are the first cytokines with protein production that is upregulated during rapid-WD. TNFα and IL-1α may initiate, therefore, molecular and cellular events in rapid-WD (e.g., the production of additional cytokines and NGF). TNFα, IL-1α, and IL-1β may further regulate, indirectly, macrophage recruitment, myelin removal, regeneration, and neuropathic pain. In contrast to rapid-WD, the production of TNFα, IL-1α, and IL-1β protein was deficient in slow-WD, although their mRNAs were expressed. mRNA expression and protein production of TNFα, IL-1α, and IL-1β were differentially regulated during rapid-WD and slow-WD, suggesting that mRNA expression, by itself, is no indication of the functional involvement of cytokines in WD.

Hypoxia Limits Inhibitory Effects of Zn2+ on Spreading Depolarizations

This sounds like something your doctor and researchers should be working on to generate a protocol.

Isamu Aiba, C. William Shuttleworth
Department of Neurosciences, University of New Mexico, Albuquerque, New Mexico, United States of America

Corresponding Author


Competing Interests

The authors have declared that no competing interests exist.

Author Contributions

Conceived and designed the experiments: IA CWS. Performed the experiments: IA. Analyzed the data: IA. Wrote the manuscript: IA CWS.


Spreading depolarizations (SDs) are coordinated depolarizations of brain tissue that have been well-characterized in animal models and more recently implicated in the progression of stroke injury. We previously showed that extracellular Zn2+ accumulation can inhibit the propagation of SD events. In that prior work, Zn2+ was tested in normoxic conditions, where SD was generated by localized KCl pulses in oxygenated tissue. The current study examined the extent to which Zn2+ effects are modified by hypoxia, to assess potential implications for stroke studies. The present studies examined SD generated in brain slices acutely prepared from mice, and recordings were made from the hippocampal CA1 region. SDs were generated by either local potassium injection (K-SD), exposure to the Na+/K+-ATPase inhibitor ouabain (ouabain-SD) or superfusion with modified ACSF with reduced oxygen and glucose concentrations (oxygen glucose deprivation: OGD-SD). Extracellular Zn2+ exposures (100 µM ZnCl2) effectively decreased SD propagation rates and significantly increased the initiation threshold for K-SD generated in oxygenated ACSF (95% O2). In contrast, ZnCl2 did not inhibit propagation of OGD-SD or ouabain-SD generated in hypoxic conditions. Zn2+ sensitivity in 0% O2 was restored by exposure to the protein oxidizer DTNB, suggesting that redox modulation may contribute to resistance to Zn2+ in hypoxic conditions. DTNB pretreatment also significantly potentiated the inhibitory effects of competitive (D-AP5) or allosteric (Ro25-6981) NMDA receptor antagonists on OGD-SD. Finally, Zn2+ inhibition of isolated NMDAR currents was potentiated by DTNB.

 Together, these results suggest that hypoxia-induced redox modulation can influence the sensitivity of SD to Zn2+ as well as to other NMDAR antagonists. Such a mechanism may limit inhibitory effects of endogenous Zn2+ accumulation in hypoxic regions close to ischemic infarcts.

Targeting Perciytes for Angiogenic Therapies

Since pericytes clamp down on small capillaries in the immediate aftermath of a stroke and don't release. Your doctor should be able to use the knowledge gained here to fix one of the neuronal cascade of death problems.


In pathological scenarios, such as tumor growth and diabetic retinopathy, blocking angiogenesis would be beneficial. In others, such as myocardial infarction and hypertension, promoting angiogenesis might be desirable. Due to their putative influence on endothelial cells, vascular pericytes have become a topic of growing interest and are increasingly being evaluated as a potential target for angioregulatory therapies. For example, the strategy of manipulating pericyte recruitment to capillaries could result in anti- or pro-angiogenic effects. However, our current understanding of pericytes is limited by knowledge gaps regarding pericyte identity and lineage. To use a music analogy, this review is a “mash-up” that attempts to integrate what we know about pericyte functionality and expression with what is beginning to be elucidated regarding their regenerative potential. We explore the lingering questions regarding pericyte phenotypic identity and lineage. The expression of different pericyte markers (e.g., SMA, Desmin, NG2 and PDGFR-β) varies for different subpopulations and tissues. Previous use of these markers to identify pericytes has suggested potential phenotypic overlaps and plasticity toward other cell phenotypes. Our review chronicles the state of the literature, identifies critical unanswered questions, and motivates future research aimed at understanding this intriguing cell type and harnessing its therapeutic potential.

Guelph gets dedicated stroke care unit - Ontario Canada

Good for the area. But are they doing anything other than the standard protocols that barely work?
1. Any objective way to diagnose a stroke between bleeder and clot?
2. Use of tPA at better than 12% efficacy?
3. Any therapy/drugs that stop the neuronal cascade of death?
4. Better than 10% full recovery?
 You will have to ask these difficult questions because the medical teams are too busy patting themselves on the back to even know that standard treatment is a failure. Its better than nothing but still a failure.