Deans' stroke musings

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

What this blog is for:

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

Thursday, April 16, 2015

Frozen shoulder

If you are running out of PT sessions you might be able to claim this and get more sessions. This is not an admonition to study the symptoms so you know how to respond to any questions. I was once asked by one of my insurance staff if I wanted to try to claim frozen shoulder to get more sessions. I declined, I didn't know enough about it to sound factual.
http://www.mayoclinic.org/diseases-conditions/frozen-shoulder/basics/definition/con-20022510/?

Consortium aims to boost patient involvement in drug development

A great stroke association would be partnering with this and have contact with hundreds of thousands of survivors. I bet I have more contact with survivors than the ASA and NSA combined.
http://www.biocentury.com/biotech-pharma-news/regulation/2015-04-13/how-fda-industry-and-patient-community-can-increase-number-and-quality-of-pros-a01

Use It Or Lose It:

No it's not about stroke recovery, I have to put in a light hearted post once a year or so.
http://www.medicaldaily.com/use-it-or-lose-it-how-age-hormones-and-masturbation-predict-sexual-health-329366

Getting Distracted Can Be A Good Thing: How And When Interruptions Help You

How is your doctor using this to help your recovery?
http://www.medicaldaily.com/getting-distracted-can-be-good-thing-how-and-when-interruptions-help-you-329434

National Stroke Awareness Month - May

Big f*cking whoopee.
The only way this should be celebrated is by pointing out all the f*cking failures and problems in stroke.
What you need to tell the world;
If you just had a stroke, You are F*cking screwed
 
First you have to at least acknowledge that stroke is hopelessly lost and needs to be on the 'Sky is falling' press releases.

OR you can read the pablum from the National Stroke Association;
May is National Stroke Awareness Month
Spread the Word About Stroke 
Be aware and share this May for National Stroke Awareness Month. Download Facebook cover photos, e-cards, a stroke symptoms poster, and more. Share with family and friends. It’s all available at our Stroke Awareness Resource Center.
Get Started Arrow


Science Connect: The Translational Approach

We need this if we ever expect to get stroke research put into stroke protocols than can help us recover. But don't expect anything from our stroke associations, this will just sit on their asses like usual.
http://www.rdmag.com/videos/2015/04/science-connect-translational-approach?
Translational research is a paradigm for research designed to enable innovative thinking by leveraging the benefits of collaboration. First emerging in the mid-1990s in reference to cancer studies spanning basic science, over the past two decades the definition has broadened and evolved. When most think of translational research, they default to a bench-to-bedside concept, but ideas about interaction and collaboration generated by early clinical translational models have grown to include a broad spectrum of new ideas that have influenced lab design, research methods, implementation and scientific education. The tenets of translational research can be, and have been, applied to many fields of research beyond the original bench research to clinical research connections, including engineering technologies, community, education and more. For more information on translational research, please visit www.labdesignnews.com.

The Number One Cause Of Depression — Everywhere - relation to stroke recovery

Does this mean that those survivors with limited gene function implied in both BDNF and serotonin transmission will have a harder time recovering because of the usefulness of BDNF? Ask your doctor for an answer and a stroke protocol to overcome that BDNF deficiency. I've got 73 posts written on BDNF if your doctor wants to try to know more than you about it.

Brain-derived neurotrophic factor: a bridge between inflammation and neuroplasticity

BDNF Induced by Treadmill Training Contributes to the Suppression of Spasticity and Allodynia After Spinal Cord Injury via Upregulation of KCC2

Brain Derived Neurotrophic Factor Key Element in Recovery from Stroke

Scorpion Venom Heat-Resistant Peptide (SVHRP) Enhances Neurogenesis and Neurite Outgrowth of Immature Neurons in Adult Mice by Up-Regulating Brain-Derived Neurotrophic Factor (BDNF) 

The depression article here:

 The Number One Cause Of Depression — Everywhere

 

 

 

 

Rehabilitation Hand Robot for Stroke Patient Hemiparesis

Have your doctor see which of the 108 hand posts and 26 fingers posts I've done to see which method is best for your hand recovery.
http://scholarworks.boisestate.edu/eng_15/16/

Document Type

Student Presentation

Presentation Date

2015

Faculty Sponsor

Lynn Catlin

Abstract

An exoskeleton device was created to rehabilitate stroke patients with hemiparesis, a muscle weakness or paralysis on one side of the body. Hemiparesis affects approximately 500,000 people within the United States every year. The current standard of care utilizes systems that are bulky and expensive. Development of an effective and affordable technology that can be utilized with minimal assistance from medical professionals is needed. A device was created to promote the recovery of fine motor function in the hand by improving range of motion through flexion and extension of the fingers. This device utilizes a feedback system controlled by amplified electromyography (EMG) signals generated by the forearm muscles that control the hand. When the EMG sensors detect the patient’s muscle activation, an electromechanical system assists in the desired movement of the phalanges. This system uses linear actuators and a 3D-printed exoskeleton on each finger to create the kinematic motion. This system promotes active involvement by the patient while performing grasping exercises, which are a key component of fine motor control rehabilitation. The device has been tested to ensure it can assist a patient in completing a full range of motion of the phalangeal joints.

Moving Stem Cells to the Clinic: Potential and Limitations for Brain Repair

Have your doctor get this article and see how many decades it will be before stem cells are useful for us.
http://www.sciencedirect.com/science/article/pii/S0896627315001981
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Stem cell-based therapies hold considerable promise for many currently devastating neurological disorders. Substantial progress has been made in the derivation of disease-relevant human donor cell populations. Behavioral data in relevant animal models of disease have demonstrated therapeutic efficacy for several cell-based approaches. Consequently, cGMP grade cell products are currently being developed for first in human clinical trials in select disorders. Despite the therapeutic promise, the presumed mechanism of action of donor cell populations often remains insufficiently validated. It depends greatly on the properties of the transplanted cell type and the underlying host pathology. Several new technologies have become available to probe mechanisms of action in real time and to manipulate in vivo cell function and integration to enhance therapeutic efficacy. Results from such studies generate crucial insight into the nature of brain repair that can be achieved today and push the boundaries of what may be possible in the future.

Cardioprotective effect of virgin coconut oil in heated palm oil diet-induced hypertensive rats

But what about for humans? Doctor?
http://informahealthcare.com/doi/abs/10.3109/13880209.2014.971383
 
Posted online on April 8, 2015. (doi:10.3109/13880209.2014.971383)
, , , , , , , , , , and
1Department of Pharmacology, Faculty of Medicine, UKMMC, Universiti Kebangsaan Malaysia,
Kuala Lumpur
, Malaysia,
2Faculty of Dentistry, Universiti Sains Islam Malaysia,
Kuala Lumpur
, Malaysia, and
3Department of Anatomy, Faculty of Medicine, UKMMC, Universiti Kebangsaan Malaysia,
Kuala Lumpur
, Malaysia
*These authors contributed equally to the study.
Correspondence:
Yusof Kamisah, PhD
, Department of Pharmacology, Faculty of Medicine, UKMMC, Universiti Kebangsaan Malaysia,
Jalan Yaacob Latif, 56000 Kuala Lumpur
, Malaysia. Tel: +60 3 91459575. Fax: +60 3 2693 8205. E-mail:


Abstract

Context: Virgin coconut oil (VCO) contains high antioxidant activity which may have protective effects on the heart in hypertensive rats.
Objectives: The study investigated the effects of VCO on blood pressure and cardiac tissue by measuring angiotensin-converting enzyme (ACE) activity and its histomorphometry in rats fed with a heated palm oil (HPO) diet.
Materials and methods: Thirty-two male Sprague–Dawley rats were randomly divided into four groups: (i) control, (ii) orally given VCO (1.42 ml/kg), (iii) fed with a HPO (15%) diet, and (iv) fed with a HPO diet and supplemented with VCO (1.42 ml/kg, po) (HPO+VCO) for 16 weeks. Blood pressure was measured monthly. After 16 weeks, rat hearts were dissected for lipid peroxidation (TBARS) and ACE activity measurement and histomorphometric study.
Results: Systolic blood pressure was significantly increased in the HPO group compared with the control starting at week eight (112.91 ± 1.32 versus 98.08 ± 3.61 mmHg, p < 0.05) which was prevented by VCO supplementation (91.73 ± 3.42 mmHg). The consumption of HPO increased TBARS and ACE activity in heart, which were inhibited by VCO supplementation. The increases in the myofiber width and area as well as nuclear size reduction in the HPO group were significantly prevented by VCO supplementation.
Conclusion: These results suggested that VCO supplementation possesses a cardioprotective effect by preventing the increase in blood pressure via an antioxidant mechanism and remodeling in rats fed repeatedly with a HPO diet


3D mapping of neuronal migration in the embryonic mouse brain with magnetic resonance microimaging

I do think that knowing how neurons migrate just might be useful to know in helping us recover. So DEMAND your doctor and hospital create a clinical trial to figure this out in humans.
http://www.sciencedirect.com/science/article/pii/S105381191500289X
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Highlights

Ultrasound-guided injection of micron-sized particles of iron-oxide (MPIO) in the embryonic mouse brain
In situ magnetic labeling of embryonic neural progenitor cells
Automated threshold detection and segmentation of MPIO-labeled cells
3D micro-MRI analysis of neural cell migration patterns


Abstract

A prominent feature of the developing mammalian brain is the widespread migration of neural progenitor (NP) cells during embryogenesis. A striking example is provided by NP cells born in the ventral forebrain of mid-gestation stage mice, which subsequently migrate long distances to their final positions in the cortex and olfactory bulb. Previous studies have used two-dimensional histological methods, making it difficult to analyze three-dimensional (3D) migration patterns. Unlike histology, magnetic resonance microimaging (micro-MRI) is a non-destructive, quantitative and inherently 3D imaging method for analyzing mouse embryos. To allow mapping of migrating NP cells with micro-MRI, cells were labeled in situ in the medial (MGE) and lateral (LGE) ganglionic eminences, using targeted in utero ultrasound-guided injection of micron-sized particles of iron-oxide (MPIO). Ex vivo micro-MRI and histology were then performed 5–6 days after injection, demonstrating that the MPIO had magnetically labeled the migrating NP populations, which enabled 3D visualization and automated segmentation of the labeled cells. This approach was used to analyze the distinct patterns of migration from the MGE and LGE, and to construct rostral–caudal migration maps from each progenitor region. Furthermore, abnormal migratory phenotypes were observed in Nkx2.1−/− embryos, most notably a significant increase in cortical neurons derived from the Nkx2.1−/− LGE. Taken together, these results demonstrate that MPIO labeling and micro-MRI provide an efficient and powerful approach for analyzing 3D cell migration patterns in the normal and mutant mouse embryonic brain.

Dose-related effects of chronic resveratrol administration on neurogenesis, angiogenesis, and corticosterone secretion are associated with improved spatial memory retention following global cerebral ischemia

You'll have to ask your doctor to figure out the resveratrol dose needed when converting from rat size to human size and then into how many glasses of wine you need each day. Type of wine would be good to know. Cabernet Sauvignon, Chianti, Malbec, Merlot, Nebbiolo, Pinot Noir, Syrah, Tempranillo, Zinfandel?
Don't do this on your own, your doctor has to prescribe the red wine for you. You do want most of it paid for from your insurance, don't you?
http://www.maneyonline.com/doi/abs/10.1179/1476830515Y.0000000020




The polyphenol resveratrol has shown regulatory effects on hippocampal neurogenesis, which according to the neurovascular niche hypothesis, likely to involve stimulation of angiogenesis. In rodents, global cerebral ischemia leads to selective CA1 neuronal damage, spatial memory impairments, lasting changes in corticosterone (CORT) secretion, and increased neurogenesis. This study examined dose-related effects of 21-day RSV treatment on markers associated with neurogenesis (DCX, PSA-NCAM) and angiogenesis (CD31) in the hippocampus at short (7-day) and long-term (85-day) intervals following global ischemia. In parallel, post-ischemic and stress-induced CORT levels and spatial memory in the Morris water maze were determined.
Five groups of male Wistar rats were included: sham/saline, ischemia/saline, ischemia/1 mg/kg RSV, ischemia/10 mg/kg RSV, and sham/10 mg/kg RSV. Changes in expression of plasticity markers were paralleled by assessment of basal- and stress-induced CORT secretions, and spatial memory performance.
Our findings revealed a significant attenuation of ischemia-induced DCX/PSA-NCAM expression in RSV-treated rats, whereas RSV treatment increased angiogenesis in the injured CA1 region. RSV attenuated CORT levels 3 days post-ischemia and a trend toward attenuating CORT secretion in response to 15 minutes restraint stress. Increased swimming latencies in the target quadrant during the MWM probe trial in RSV-treated ischemic rats support beneficial effects of on spatial memory retention.
Our findings uncover time- and dose-related effects of RSV and global ischemia on the regulation of hippocampal plasticity. Changes in neuro- and angiogenesis are consistent with RSV neuroprotective effects, but appear independent of RSV regulatory effects on corticosterone secretion.

Wednesday, April 15, 2015

Adult neurogenesis 20 years later: physiological function vs. brain repair

In these 20 years what changes to your stroke protocols from your doctor have occurred?
ANY AT ALL?
http://journal.frontiersin.org/article/10.3389/fnins.2015.00071/full?

Adult neurogenesis 20 years later: physiological function vs. brain repair

  • 1Neuroscience Institute Cavalieri Ottolenghi, Orbassano, Italy
  • 2Life Sciences and Systems Biology, University of Turin, Torino, Italy
  • 3Department of Veterinary Sciences, University of Turin, Torino, Italy
Two decades of intense investigation in the field of adult neurogenesis (AN) provided us with a fully renewed vision of brain plasticity, involving stem/progenitor cells capable of generating new neurons and glial cells throughout life. We know for sure that new neurons produced within canonical stem cell niches do play a significant role in cognitive tasks (learning/memory) operated by specific neural systems (Lepousez et al., 2013; Aimone et al., 2014). The fact that neural stem/progenitor cells (NSC) produce new elements that can integrate within some regions of the mature brain, replacing lost neurons/glial cells or adding to pre-existent neural circuits, appears extremely fascinating in the perspective of regenerative therapeutic approaches. Since the burst of investigations in AN/NSC field in the nineties, many neurobiologists addressed their studies on brain plasticity in the hope of brain repair, often discussing their results in a translational context. Nevertheless, in spite of striking efforts to clarify mechanisms/factors regulating AN and its physiological function, the question whether it can be exploited for healing neurologic diseases remains unsolved.(This is precisely why we need a strategy) More recent findings revealed additional examples of “non-canonical” neurogenesis and gliogenesis in various regions of the mammalian central nervous system (CNS; reviewed in Bonfanti and Peretto, 2011). These discoveries also open new hopes for brain repair, since the occurrence of spontaneous neuro-gliogenesis within the parenchyma does represent an endogenous source of progenitor cells even outside the restricted environment of canonical neurogenic sites. Nevertheless, parenchymal cell genesis remains substantially obscure as to its functional meaning(s) and outcome(s), and not yet exploitable for brain repair. Such an impasse largely resides on evolutionary discrepancies: most vertebrates use AN for brain repair as a byproduct of evolution, in addition to its physiological functions; mammals have lost such capacity, mainly because of unfavorable environments for repair/regeneration in their mature CNS (Bonfanti, 2011). A scarce perception of these facts might have produced misconceptions among scientists, sometimes leading to attitudes of unconditional optimism.
This Editorial is part of a Frontiers' research topic (and related e-book), gathering 18 articles which were intended to explore the relationships between actual existence of NCSs in mammals (playing homeostatic roles in AN and responding to pathological conditions) and lack of effective reparative outcome in terms of regenerative neurology.

Much more at link.

A perspective on neural and cognitive mechanisms of error commission - stroke recovery

And if we had a genius stroke person out there she could apply this to stroke recovery  and make our errors useful for correcting the stroke problems.  I'm sure your doctor has no clue how to relate this to your problems in recovery.
http://journal.frontiersin.org/article/10.3389/fnbeh.2015.00050/full?utm_source=newsletter&

A perspective on neural and cognitive mechanisms of error commission

  • 1Performance Psychology, Institute of Psychology, German Sport University Cologne, Cologne, Germany
  • 2Cognitive Neurophysiology, Department of Child and Adolescent Psychiatry, Faculty of Medicine of the TU Dresden, University Hospital Carl Gustav Carus, Dresden, Germany
Behavioral adaptation and cognitive control are crucial for goal-reaching behaviors. Every creature is ubiquitously faced with choices between behavioral alternatives. Common sense suggests that errors are an important source of information in the regulation of such processes. Several theories exist regarding cognitive control and the processing of undesired outcomes. However, most of these models focus on the consequences of an error, and less attention has been paid to the mechanisms that underlie the commissioning of an error. In this article, we present an integrative review of neuro-cognitive models that detail the determinants of the occurrence of response errors. The factors that may determine the likelihood of committing errors are likely related to the stability of task-representations in prefrontal networks, attentional selection mechanisms and mechanisms of action selection in basal ganglia circuits. An important conclusion is that the likelihood of committing an error is not stable over time but rather changes depending on the interplay of different functional neuro-anatomical and neuro-biological systems. We describe factors that might determine the time-course of cognitive control and the need to adapt behavior following response errors. Finally, we outline the mechanisms that may proof useful for predicting the outcomes of cognitive control and the emergence of response errors in future research.

Introduction

Errare humanum est, sed in errare perseverare diabolicum (Seneca). In other words: “who commits an error and does not correct it, commits a second one” (Confucius). Similar notions can be found in texts by Seneca, Horaz, Cicero and Aristotle. Already these philosophical notions stipulate the relevance and importance of the detection and compensation of errors. However, obviously there exist several types of errors. Basically, one can commit “mistakes” (e.g., not knowing the correct decision) or “slips” (the selected action is not what has been intended). The latter is what is this manuscript is about: a situation leading to an inappropriate action selection, likely making you think: “Upps.”

Retinoic acid-loaded polymeric nanoparticles induce neuroprotection in a mouse model for Parkinson's disease

Inquiring minds demand to know. Would this help survivors during the first week?  We have no one to ask this of because our stroke associations are not the repository of any stroke strategy. We are F*cking screwed because we have no one to follow up on any promising leads from research.  A great stroke association would do translational research and create stroke protocols for promising ideas. In a perfect world it would do that, but not here.
http://journal.frontiersin.org/article/10.3389/fnagi.2015.00020/full?
Marta Esteves1, Ana C. Cristóvão1, Tatiana Saraiva1, Sandra M. Rocha1, Graça Baltazar1, Lino Ferreira2,3 and Liliana Bernardino1*
  • 1Faculty of Health Sciences, Health Sciences Research Centre, University of Beira Interior, Covilhã, Portugal
  • 2Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal
  • 3Biocant – Center of Innovation in Biotechnology, Cantanhede, Portugal
Retinoic acid (RA) plays an important role in the commitment, maturation and survival of neural cells. Recently, RA was pointed as a therapeutic option for some neurodegenerative diseases, including Parkinson's disease (PD). The administration of RA has been defying, and in this sense we have previously developed novel RA-loaded polymeric nanoparticles (RA-NPs) that ensure the efficient intracellular transport and controlled release of RA. Herein, we show that nanoformulation as an efficient neuroprotective effect on dopaminergic (DA) neurons in the 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP) induced mouse model for PD. The results showed that the RA-NPs administration induced a significant reduction of DA neuron loss in the substantia nigra (SN) as well as their neuronal fiber/axonal innervations in the striatum. Furthermore, we observed an increase in the expression levels of the transcription factors Pitx3 and Nurr1 induced by RA-NPs, showing its supportive effect on the development and functional maintenance of DA neurons in PD. This is the first study showing that RA-NPs can be an innovative strategy to halt the progression of PD pathogenesis, suggesting that this nanoformulation could be of particular interest for the development of new approaches for PD therapeutics.

This Supplement May Stop Sadness Becoming Depression - Probiotics

But you will need to validate with your doctor the benefits of taking an anti-depressant anyway.
Do we not have consensus that all survivors should get anti-depression drugs because they lead to a better recovery?
Antidepressants may help people recover from stroke even if they are not depressed

 This Supplement May Stop Sadness Becoming Depression

Influence of piperine on the pharmacokinetics of curcumin in animals and human volunteers - black pepper

In case you were thinking of taking curcumin. Piperine is the compound that gives black pepper its pungency and has long been recognized for its restorative properties. See what your doctor says.

Adding 'spice' to curcumin’s health-promoting benefits

Influence of piperine on the pharmacokinetics of curcumin in animals and human volunteers 


Abstract

The medicinal properties of curcumin obtained from Curcuma longa L. cannot be utilised because of poor bioavailability due to its rapid metabolism in the liver and intestinal wall. In this study, the effect of combining piperine, a known inhibitor of hepatic and intestinal glucuronidation, was evaluated on the bioavailability of curcumin in rats and healthy human volunteers. When curcumin was given alone, in the dose 2 g/kg to rats, moderate serum concentrations were achieved over a period of 4 h. Concomitant administration of piperine 20 mg/kg increased the serum concentration of curcumin for a short period of 1-2 h post drug. Time to maximum was significantly increased (P < 0.02) while elimination half life and clearance significantly decreased (P < 0.02), and the bioavailability was increased by 154%. On the other hand in humans after a dose of 2 g curcumin alone, serum levels were either undetectable or very low. Concomitant administration of piperine 20 mg produced much higher concentrations from 0.25 to 1 h post drug (P < 0.01 at 0.25 and 0.5 h; P < 0.001 at 1 h), the increase in bioavailability was 2000%. The study shows that in the dosages used, piperine enhances the serum concentration, extent of absorption and bioavailability of curcumin in both rats and humans with no adverse effects.

Study: More Divorces, More Heart Troubles

Well this will be easy for me to avoid. Don't get married again, that way I won't get divorced the 2nd or 3rd time and increasing my stroke risk substantially. I hate these simplistic statements, divorce is not the direct cause, stress probably is which causes high blood pressure and that is directly related to stroke. Send these researchers back to school for remedial training. We deserve better knowledge than this.
http://www.medpagetoday.com/Cardiology/MyocardialInfarction/50998?
For women who had ever been married, the risk was 24% elevated with one divorce and 77% elevated with two or more divorces versus none in competing-risks models.
For men, the multivariate-adjusted risk was only significant with two or more divorces (hazard ratio 1.30 versus none, 95% CI 1.02-1.66).

More at link.

COGNITIVE AGING An Action Guide for Individuals and Families - From the Institute of Medicine

Have your doctor compare this to his/her protocol on preventing cognitive decline to mine. I know mine should not be listened to because there is no clinical proof that any of it works.
You can compare these to mine.
Dementia prevention 19 ways
http://www.iom.edu/~/media/Files/Report%20Files/2015/Cognitive_aging/Action%20Guide%20for%20Individuals%20and%20Families_V3.pdf 
 The top 3 actions you can take to help
protect your cognitive health as you age

1.  Be physically active.
 Staying physically active can promote
cognitive health in middle-aged and older adults.
2.  Reduce your cardiovascular risk factors (including hypertension,
diabetes, and smoking).  Maintaining cardiovascular health
supports cognitive health.
3.  Manage your medications.
A number of medications can have a
negative effect on cognitive function when used alone or in
combination with other medications. The effects can be temporary
or long-term. It’s important to review all of your medications with a
health care professional and learn about their effects on cognitive
health.
Other actions that may promote cognitive health
• Be socially and intellectually active, and continually seek
opportunities to learn.
• Get adequate sleep and seek professional treatment for sleep
disorders, if needed.
• Talk to your health care provider to learn more about preventing
delirium (a decline in cognitive function that can be associated with
some medications and hospitalization)

Tuesday, April 14, 2015

Money spent on dementia and stroke too low, say researchers - UK

And the only way I see to fix this is to have our stroke associations go directly for grant money and use that for stroke research. Bypass the government.  We can't let our stroke researchers come up with their own research ideas. We need to be following a strategy if we ever expect to solve stroke.  Swinging for the fences like with stem cells is not the way to do this.
http://www.yorkshirepost.co.uk/news/main-topics/general-news/money-spent-on-dementia-and-stroke-too-low-say-researchers-1-7207621

AMOUNTS OF money spent on research into dementia and stroke in the UK are still far too low, experts warn today.

Analysis of funding for research into the four main causes of death and disability in the UK - cancer, heart disease, dementia and stroke - found just 10 per cent was allocated to dementia and seven per cent to stroke research.
The study, led by researchers at Oxford University, said this was despite these conditions having huge economic and personal impact, with the social care costs of dementia outweighing that of the other three conditions combined.
The combined amount of research funding allocated by the Government and charities to all four conditions came to £855 million in 2012, almost two-thirds of which (64 per cent or £546m) was spent on cancer.
Around one fifth (19 per cent or £165m) was devoted to heart disease, with £85m on dementia and £58m on stroke research.
That same year, there were around 2.3m cases of cancer, the same number of coronary heart disease cases, 800,000 cases of dementia and 1.2m of stroke, the study said.
The costs of healthcare were highest for cancer (£4.4 billion) and lowest for dementia, at £1.4bn, while stroke was £1.8bn.
But researchers found that the social care costs of dementia outweighed the social care costs of the other three conditions combined.

Massive IBM deal gives Watson purpose and puts it in pole position to transform healthcare - What about stroke?

And if our stroke associations don't partner with Watson to solve all the problems in stroke they are complete f*cking idiots.  You don't have to worry, this will never occur since the boards of directors seem to have no iniative to do anything useful about solving stroke. If they truly wanted to solve stroke I would have heard from them by now, not because of my suggested solutions but to sue me for disparaging them.
http://medcitynews.com/2015/04/massive-ibm-deal-gives-watson-purpose-pole-position-transform-healthcare/?

Auto detection and segmentation of physical activities during a Timed-Up-and-Go (TUG) task in healthy older adults using multiple inertial sensors

This would be so f*cking easy for our stroke associations to duplicate for stroke survivors. No thinking involved. It would provide vast amounts of information to figure out how to help us walk better.  But it won't occur.
http://www.jneuroengrehab.com/content/12/1/36/abstract
Hung P Nguyen1, Fouaz Ayachi1, Catherine Lavigne–Pelletier1, Margaux Blamoutier2, Fariborz Rahimi3, Patrick Boissy4, Mandar Jog5 and Christian Duval1*
For all author emails, please log on.
Journal of NeuroEngineering and Rehabilitation 2015, 12:36  doi:10.1186/s12984-015-0026-4
Published: 11 April 2015

Abstract (provisional)

Background Recently, much attention has been given to the use of inertial sensors for remote monitoring of individuals with limited mobility. However, the focus has been mostly on the detection of symptoms, not specific activities. The objective of the present study was to develop an automated recognition and segmentation algorithm based on inertial sensor data to identify common gross motor patterns during activity of daily living. 
Method A modified Time-Up-And-Go (TUG) task was used since it is comprised of four common daily living activities; Standing, Walking, Turning, and Sitting, all performed in a continuous fashion resulting in six different segments during the task. Sixteen healthy older adults performed two trials of a 5 and 10 meter TUG task. They were outfitted with 17 inertial motion sensors covering each body segment. Data from the 10 meter TUG were used to identify pertinent sensors on the trunk, head, hip, knee, and thigh that provided suitable data for detecting and segmenting activities associated with the TUG. Raw data from sensors were detrended to remove sensor drift, normalized, and band pass filtered with optimal frequencies to reveal kinematic peaks that corresponded to different activities. Segmentation was accomplished by identifying the time stamps of the first minimum or maximum to the right and the left of these peaks. Segmentation time stamps were compared to results from two examiners visually segmenting the activities of the TUG.  
Results We were able to detect these activities in a TUG with 100% sensitivity and specificity (n = 192) during the 10 meter TUG. The rate of success was subsequently confirmed in the 5 meter TUG (n = 192) without altering the parameters of the algorithm. When applying the segmentation algorithms to the 10 meter TUG, we were able to parse 100% of the transition points (n = 224) between different segments that were as reliable and less variable than visual segmentation performed by two independent examiners. 
Conclusions The present study lays the foundation for the development of a comprehensive algorithm to detect and segment naturalistic activities using inertial sensors, in hope of evaluating automatically motor performance within the detected tasks.

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

New Compound Could Offer Therapy for Alzheimer’s, Parkinson’s

Why don't we ever get any breathless articles like this on stroke? I blame our stroke associations for not  carrying out a strategy to solve all the problems in stroke
http://www.biosciencetechnology.com/articles/2015/04/new-compound-could-offer-therapy-alzheimers-parkinsons?
.

Getting Bigger Brains Through Exercise

Why isn't your doctor giving you an exercise protocol to increase your brain size?
http://www.biosciencetechnology.com/articles/2015/04/getting-bigger-brains-through-exercise?

Statins linked to coronary atheroma calcification

One more statin side effect to consult with your doctor on. Hopefully s/he already knows about the 43 blog posts I've written about statin side effects.

http://www.healio.com/cardiology/chd-prevention/news/online/%7B7dfd86ce-5265-4402-b583-4d20a68721bd%7D/statins-linked-to-coronary-atheroma-calcification
Definition of atheroma, it does not sound good;
http://medical-dictionary.thefreedictionary.com/atheroma

MTfp-­siRNA reduces blood vessel infarct, improves overall brain activity in ischemic stroke model

How many decades is this going to take to get it proven in humans? I'm betting 100 years because we have shit for brains in our stroke associations with no strategy and no way to solve any of the problems in stroke.
http://www.news-medical.net/news/20150319/MTfp-c2adsiRNA-reduces-blood-vessel-infarct-improves-overall-brain-activity-in-ischemic-stroke-model.aspx
BIOASIS TECHNOLOGIES INC. (OTCQX:BIOAF; TSX.V:BTI), a pioneering biopharmaceutical company focused on overcoming the limitations of therapeutic drug delivery across the blood-­‐brain barrier (BBB), announces the results from an animal ischemic stroke model performed at the National Research Council Canada with the biOasis Transcend carrier peptide, MTfp and siRNA (MTfp-­‐siRNA). Two key therapeutic effects were shown with MTfp-­‐siRNA; A high degree of reduction of the area of blood vessel infarct and improvement of overall brain activity as determined by neurological scoring.
On July 25th, 2014, biOasis announced that its newly discovered carrier peptide (MTfp), part of the biOasis Transcend family of carrier technologies, effectively delivered siRNA across the BBB and into brain cells. The company also announced that it achieved the goal of silencing the expression of a selected target gene in the brain by approximately 50%. This study prompted the company to move to a model of disease where therapeutic effects could be measured.
Ischemic stroke is the most common type of stroke in humans and an animal model that mimics stroke was chosen to establish the effectiveness of MTfp-­‐siRNA treatment administered immediately prior to induction of ischemic stroke.
Key Findings of Ischemic Stroke Model Treated with MTfp-­‐siRNA:
(1) The area of infarct (damage) was highly reduced in the animals treated with MTfp-­‐siRNA. Brain images revealed significantly less stroke damage in brain sections from animals treated with the MTfp-­‐siRNA when compared to the same brain regions in the control animals. The brain section images may be viewed below. The images show that there is more stroke damage (white areas) in the five sections from control animals (Left Panel) when compared to the same brain regions in the animals with stroke treated with the MTfp-­‐siRNA (Right Panel).
(2) Thirty-­‐minutes after induction of stroke, the neurological scores of the animals treated with the MTfp-­‐siRNA were significantly better than those of control animals. At 24 hours, controls animals demonstrated a slight improvement in neurological scores while MTfp-­‐siRNA treated animals showed a vast improvement and exhibited nearly normal neurological scores.
“The results clearly demonstrate that in an established animal model of stroke, therapeutic levels of siRNA that down-­‐regulate the expression of a key pathogenic gene were successfully delivered by MTfp to the brain, resulting in a significant reduction of infarct damage and improvement of neurological scores associated with healthy brain function,” said Dr. Wilfred Jefferies, biOasis Founding Scientist.

Stroke patients can benefit from clot-busting drug, shows brain scan study

You'll have to not so politely ask your stroke hospital to resolve the difference between these two articles. You brain is at risk if they don't do this correctly. Or maybe you'd rather die and have your heirs sue for malpractice. Up to you how you want to respond.

REVEALED: Most commonly prescribed stroke drug linked to fatal brain bleeds and death - Alteplase UK NHS

 Stroke patients can benefit from clot-busting drug, shows brain scan study

Monday, April 13, 2015

Rocking chair stroke rehabilitation at the Charlotte NC airport

It's amazing how friendly toward survivors this is.  You could spend hours doing your hamstring exercises. I was passing thru on my way to Tampa for work. Doesn't your doctor have a stroke protocol for this with a specified number of repetitions?

Sunday, April 12, 2015

Mobile van offers stroke care on the go - Cleveland Clinic

Even the vaunted Cleveland Clinic can't seem to read news about stroke. This is going to be an expensive short term test.  Do they not know that the Qualcomm Xprize for the tricorder has selected 10 finalists? How long before this comes to fruition and makes the expensive and time-consuming MRI and CT scans obsolete? We also shouldn't need neurologists on call to interpret those scans.
But do you really think your hospital will recommend this when it goes to production? It's a neurologist job killer and I doubt the stroke department head will recommend reducing head count unless you call the hospital president and make the case.
 http://www.king5.com/story/news/health/2015/04/09/stroke-tpa-mobile-unit-cleveland-cinic/25539693/

Stroke Drug May Also Help Alzheimer's Patients - edaravone

You'll have to ask your doctor why the hell edaravone is approved in Asia but not the US.
http://www.psychiatryadvisor.com/stroke-drug-may-also-help-alzheimers-patients/article/408376/

REVEALED: Most commonly prescribed stroke drug linked to fatal brain bleeds and death - Alteplase UK NHS

This really should lead to nanoparticles of the drug with magnetic delivery. That could mean a much smaller bolus. But that is not where this will lead unless YOU tell them what the research points to. I have absolutely no confidence that they will look at this correctly.

Magnetic nanoparticles could stop blood clot-caused strokes

 Most commonly prescribed stroke drug linked to fatal brain bleeds and death - Alteplase UK NHS

 

Saturday, April 11, 2015

Angiogenesis - Good or bad for for stroke rehabilitation?

Send this directly to your doctor to come up with an answer. Do not allow deflection and 'I don't know' for an answer. This is your brain needing help, your doctor needs to figure out how to help it. If no answer is forthcoming call the hospital president and ask why the stroke department knows nothing helpful.
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Poststroke Angiogenesis, Con: Dark Side of Angiogenesis
  • Joanna Adamczak and
  • Mathias Hoehn
Stroke. 2015; published online before print March 26 2015, doi:10.1161/STROKEAHA.114.007642
2015 American Heart Association, Inc. 2015 other Basic Science Controversy Poststroke Angiogenesis, ConDark Side of Angiogenesis Joanna Adamczak PhD Mathias Hoehn PhD Correspondence to Mathias Hoehn...
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Poststroke Angiogenesis, Pro: Making the Desert Bloom
  • David A. Greenberg
Stroke. 2015; published online before print March 26 2015, doi:10.1161/STROKEAHA.114.007641
2015 American Heart Association, Inc. 2015 other Basic Science Controversy Poststroke Angiogenesis, ProMaking the Desert Bloom David A. Greenberg MD, PhD Correspondence to David A. Greenberg, MD...
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Poststroke Angiogenesis: Blood, Bloom, or Brood?
  • Jialing Liu
Stroke. 2015; published online before print March 26 2015, doi:10.1161/STROKEAHA.115.007643
2015 American Heart Association, Inc. 2015 other Basic Science Controversy Poststroke AngiogenesisBlood, Bloom, or Brood? Jialing Liu PhD Correspondence to Jialing Liu, PhD, Department of Neurological...

Neurogenesis: What Can I Do To Stimulate Brain Recovery And Regrowth?

What does your doctor think of these ideas?
https://drnibber.com/neurogenesis-what-can-i-do-to-stimulate-brain-recovery-and-regrowth/
Details at the link.
DHA

A working memory training to decrease rumination in depressed and anxious individuals: A double-blind randomized controlled trial

So it doesn't work, what precisely is your doctor doing to address your depression and rumination problems?
http://www.jad-journal.com/article/S0165-0327%2814%2900813-1/abstract?rss=yes
, ,
Institute of Psychology, Erasmus University Rotterdam, The Netherlands

Abstract

Background

Rumination is one of the hallmark characteristics of both anxiety disorders and depression, and has been linked to deficient executive functioning, particularly working memory (WM). Previous findings show that working memory capacity can be increased through training.

Methods

The current study explored whether an adaptive stand-alone WM training could increase WMC and consequently reduce rumination, anxiety and depression by means of a double-blind randomized controlled trial in a sample of 98 patients with symptoms of anxiety and/or depression.

Results

No positive effect of training on WMC was found. In addition, the results show that a WM training was not associated with a reduction of rumination, depression, nor anxiety.

Limitations

The high drop-out rate in both groups (20.11% from pre- to post-training) and the overrepresentation of men and use of anti-depressants in the placebo group might have influenced the results. Furthermore, expectations and perceptions about the training might have interacted with performance on WM tasks.

Conclusions

Overall, results show that a stand-alone WM training in patients with symptoms of anxiety and/or depression does not result in reduced rumination nor in reduced symptoms of depression and anxiety. We discuss potential explanations for these findings.

Friday, April 10, 2015

Thursday, April 9, 2015

Stroke rehabilitation: What to expect as you recover - From Mayo Clinic

What a load of whitewashed shit.
http://www.mayoclinic.org/stroke-rehabilitation/art-20045172/?linkId=13382418&pg=1
The truth from a survivor, that's me:
If you just had a stroke, You are F*cking screwed

A neuromechanics-based powered ankle exoskeleton to assist walking post-stroke: a feasibility study

Will your doctor use this or stick to static AFOs?
http://www.jneuroengrehab.com/content/12/1/23/abstract
Kota Z Takahashi1*, Michael D Lewek2 and Gregory S Sawicki1*
For all author emails, please log on.
Journal of NeuroEngineering and Rehabilitation 2015, 12:23  doi:10.1186/s12984-015-0015-7
Published: 25 February 2015

Abstract

Background

In persons post-stroke, diminished ankle joint function can contribute to inadequate gait propulsion. To target paretic ankle impairments, we developed a neuromechanics-based powered ankle exoskeleton. Specifically, this exoskeleton supplies plantarflexion assistance that is proportional to the user’s paretic soleus electromyography (EMG) amplitude only during a phase of gait when the stance limb is subjected to an anteriorly directed ground reaction force (GRF). The purpose of this feasibility study was to examine the short-term effects of the powered ankle exoskeleton on the mechanics and energetics of gait.

Methods

Five subjects with stroke walked with a powered ankle exoskeleton on the paretic limb for three 5 minute sessions. We analyzed the peak paretic ankle plantarflexion moment, paretic ankle positive work, symmetry of GRF propulsion impulse, and net metabolic power.

Results

The exoskeleton increased the paretic plantarflexion moment by 16% during the powered walking trials relative to unassisted walking condition (p < .05). Despite this enhanced paretic ankle moment, there was no significant increase in paretic ankle positive work, or changes in any other mechanical variables with the powered assistance. The exoskeleton assistance appeared to reduce the net metabolic power gradually with each 5 minute repetition, though no statistical significance was found. In three of the subjects, the paretic soleus activation during the propulsion phase of stance was reduced during the powered assistance compared to unassisted walking (35% reduction in the integrated EMG amplitude during the third powered session).

Conclusions

This feasibility study demonstrated that the exoskeleton can enhance paretic ankle moment. Future studies with greater sample size and prolonged sessions are warranted to evaluate the effects of the powered ankle exoskeleton on overall gait outcomes in persons post-stroke.