Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 493 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.My back ground story is here:

Wednesday, April 30, 2014

One Night Cough Syrup

We need to find the maker of this.


Pictures from here:
and here:
Alcohol for these 12 reasons;
Cannabis for these reasons:
I'm going to be using it after my next stroke for all these 13 reasons.
I have nothing for chloroform or morphia.

Don't do this.

The Sports Concussion Conference

I bet not a single report in here will talk about fish oil. Proving once again that medical persons don't read research, or can't even be bothered to hire someone to summarize research for them.

Maybe by rubbing two functioning neurons together they might look at these.  What's the downside? Fish breath?
Looking at pretreatment with fish oil or post-treatment with fish oil

After the fact here;
Aspirin plus fish oil for a hyperacute treatment

July 11-13, 2014, in Chicago.

Brain Salt

I bet this is at least as good as what our doctors don't give us.
Send your doctor in search of it.

Stress May Naturally Make Stem Cells of Mature Cells

Check it out, even if the acid bath proposal went downhill, this seems to have more support.
Stress or injury may naturally prompt mammals to make “extraordinary” stem cells out of certain “ordinary” mature cells via dedifferentiation.
Three strong papers suggesting this were quietly published within weeks of the controversial Nature “acid bath” work, where a team from Japan’s Riken Institute, and the US’s Harvard University, reported dedifferentiating neonatal mouse spleen cells into stem cells by stressing them, artificially in a dish, with coffee-mild acid.
Confidence in the “acid” work has hit a new low. It has not been repeated. A Riken investigation found lead author Haruko Obokata committed two acts of falsification and fabrication that may have crippled the papers—and may prompt retraction. (See Bioscience Technology stories on “acid bath” developments.)
But the other three studies – conducted by unrelated teams on mammalian stomach, trachea, and kidney—have generated no controversy. Two drew raves from the Faculty of 1000.

More at link.  What does your doctor think?

Stem Cells from Teeth Can Make Brain-like Cells

This can join the other 19 possibilities here: Which possibility is your doctor working on?
Scientists Create Stem Cells From a Drop of Blood 

 Stem Cells from Teeth Can Make Brain-like Cells
University of Adelaide researchers have discovered that stem cells taken from teeth can grow to resemble brain cells, suggesting they could one day be used in the brain as a therapy for stroke.
In the University's Center for Stem Cell Research, laboratory studies have shown that stem cells from teeth can develop and form complex networks of brain-like cells. Although these cells haven't developed into fully fledged neurons, researchers believe it's just a matter of time and the right conditions for it to happen.
"Stem cells from teeth have great potential to grow into new brain or nerve cells, and this could potentially assist with treatments of brain disorders, such as stroke," said Dr. Kylie Ellis, commercial development manager with the University's commercial arm, Adelaide Research & Innovation (ARI).
Ellis conducted this research as part of her Physiology Ph.D. studies at the University, before making the step into commercialization. The results of her work have been published in the journal Stem Cell Research & Therapy.
"The reality is, treatment options available to the thousands of stroke patients every year are limited," Ellis said. "The primary drug treatment available must be administered within hours of a stroke and many people don't have access within that timeframe, because they often can't seek help for some time after the attack.
"Ultimately, we want to be able to use a patient's own stem cells for tailor-made brain therapy that doesn't have the host rejection issues commonly associated with cell-based therapies. Another advantage is that dental pulp stem cell therapy may provide a treatment option available months or even years after the stroke has occurred," she said.
Ellis and her colleagues, Professors Simon Koblar, David O'Carroll and Stan Gronthos, have been working on a laboratory-based model for actual treatment in humans. As part of this research Ellis found that stem cells derived from teeth developed into cells that closely resembled neurons.
"We can do this by providing an environment for the cells that is as close to a normal brain environment as possible, so that instead of becoming cells for teeth they become brain cells," Ellis said. "What we developed wasn't identical to normal neurons, but the new cells shared very similar properties to neurons. They also formed complex networks and communicated through simple electrical activity, like you might see between cells in the developing brain."
This work with dental pulp stem cells opens up the potential for modelling many more common brain disorders in the laboratory, which could help in developing new treatments and techniques for patients.

Treating Post-Traumatic Stress: Public Briefing

Since PTSD can be an aftereffect of stroke I would fully expect every stroke hospital to be sending a person to this, along with the ASA and NSA. You don't really believe that will occur, Do you?
Prevalence of PTSD in Survivors of Stroke and Transient Ischemic Attack: A Meta-Analytic Review 
And look at this, an actual treatment:
Medical Marijuana – A Magic Bullet for Treating PTSD?
 Send those emails to your hospital, Only you can change how stroke is treated. I bet your hospital will prove their failures once again.

The briefing:
Through the support of the Dana Foundation, the American Association for the Advancement of Science (AAAS) is hosting a public luncheon briefing on treating post-traumatic stress.
Post-traumatic stress (PTS) or post-traumatic stress disorder can afflict individuals after a trauma or life-threatening event. It affects more than five million adults per year and is a particular concern for the military. Come hear about how PTS affects service members and veterans and how researchers are treating PTS through different styles of therapy:
Friday, May 9, 2014
12:00-1:30 p.m.
2168 Rayburn House Office Building
The Honorable Chaka Fattah, D-PA
General Peter Chiarelli, U.S. Army (Retired), CEO, One Mind
Kathleen Chard, PhD, Professor of Psychiatry and Behavioral Neuroscience, University of Cincinnati
JoAnn Difede, PhD, Professor of Psychology in Psychiatry, Weill Cornell Medical College
Moderator Alan Leshner, PhD, CEO of AAAS
For questions, please contact Sara Spizzirri at 202-326-6789 or by email at

Plasma phospholipids identify antecedent memory impairment in older adults

This may be years down the road but I'd like to know so I can fasttrack my dementia prevention program. What does your doctor think and what is their dementia prevention program? Does your doctor remember your  33% chance of getting dementia/Alzheimers post stroke.
My program here:
1. Fish Oil Might Guard Against Loss of Brain Cells
2. Shakespeare and Wordsworth boost the brain, new research reveals
3. Physical activity is beneficial for late-life cognition
4. Omega 3 fatty acid for the prevention of cognitive decline and dementia
5. To keep sharp, retirees need to find a purpose
6.  Keep Working to Keep Dementia at Bay.
7. Preliminary medical testing results have shown that aspirin may prevent dementia and intestinal cancers
8.   THC(marijuana) may benefit those with Alzheimer’s disease.
9.  Common BP Drugs Tied to Lower Risk of Alzheimer's
10.  Study: Fruits and veggies may prevent dementia 
11.  Coffee May Lower Your Risk of Dementia
12.  Light-to-moderate alcohol consumption, in comparison with abstinence, was associated with approximately 35-45% lower risk of cognitive decline or dementia.
13.  Activation of neuronal nicotinic acetylcholine receptors (nAChRs) has been shown to maintain cognitive function following aging or the development of dementia.
14.  Overeating is associated with an increased risk of mild cognitive impairment (MCI) in people 70 or older
15.  To Stave off Alzheimer’s, Stay Hungry?
16.  Calorie Restriction Prevents Neurodegeneration
17.  Researchers: Mini-Fast Prevents Alzheimer's
18. Evidence-Based Medicinal Properties of Coconut Oil - brain boosting

19.  Dementia Prevention – What Can Be Done? The generic medical version
     I bet your doctor gives you this.

I however am not going to wait for doctors and researchers to come up with a solution. You are going to have to read and decide for yourself how you want to approach dementia prevention. I doubt your doctor will be any help.

The possible test here:
Nature Medicine
Published online

Alzheimer's disease causes a progressive dementia that currently affects over 35 million individuals worldwide and is expected to affect 115 million by 2050 (ref. 1). There are no cures or disease-modifying therapies, and this may be due to our inability to detect the disease before it has progressed to produce evident memory loss and functional decline. Biomarkers of preclinical disease will be critical to the development of disease-modifying or even preventative therapies2. Unfortunately, current biomarkers for early disease, including cerebrospinal fluid tau and amyloid-β levels3, structural and functional magnetic resonance imaging4 and the recent use of brain amyloid imaging5 or inflammaging6, are limited because they are either invasive, time-consuming or expensive. Blood-based biomarkers may be a more attractive option, but none can currently detect preclinical Alzheimer's disease with the required sensitivity and specificity7. Herein, we describe our lipidomic approach to detecting preclinical Alzheimer's disease in a group of cognitively normal older adults. We discovered and validated a set of ten lipids from peripheral blood that predicted phenoconversion to either amnestic mild cognitive impairment or Alzheimer's disease within a 2–3 year timeframe with over 90% accuracy. This biomarker panel, reflecting cell membrane integrity, may be sensitive to early neurodegeneration of preclinical Alzheimer's disease.

Thermal Processing Enhances the Nutritional Value of Tomatoes by Increasing Total Antioxidant Activity

So the lycopene content I'm getting from tomatoes should be in a cooked format. I've been trying to eat two medium tomatoes at every dinner. This is why I'm going for tomatoes. But don't listen to me, I know nuthin, that's what your doctor is for.
Tomatoes Linked to Lower Stroke Risk

Heating them here:
Department of Food Science and Institute of Comparative and Environmental Toxicology, Stocking Hall, Cornell University, Ithaca, New York 14853
J. Agric. Food Chem., 2002, 50 (10), pp 3010–3014
DOI: 10.1021/jf0115589
Publication Date (Web): April 17, 2002
Copyright © 2002 American Chemical Society


Processed fruits and vegetables have been long considered to have lower nutritional value than their fresh commodities due to the loss of vitamin C during processing. This research group found vitamin C in apples contributed <0.4% of total antioxidant activity, indicating most of the activity comes from the natural combination of phytochemicals. This suggests that processed fruits and vegetables may retain their antioxidant activity despite the loss of vitamin C. Here it is shown that thermal processing elevated total antioxidant activity and bioaccessible lycopene content in tomatoes and produced no significant changes in the total phenolics and total flavonoids content, although loss of vitamin C was observed. The raw tomato had 0.76 ± 0.03 μmol of vitamin C/g of tomato. After 2, 15, and 30 min of heating at 88 °C, the vitamin C content significantly dropped to 0.68 ± 0.02, 0.64 ± 0.01, and 0.54 ± 0.02 μmol of vitamin C/g of tomato, respectively (p < 0.01). The raw tomato had 2.01 ± 0.04 mg of trans-lycopene/g of tomato. After 2, 15, and 30 min of heating at 88 °C, the trans-lycopene content had increased to 3.11± 0.04, 5.45 ± 0.02, and 5.32 ± 0.05 mg of trans-lycopene/g of tomato (p < 0.01). The antioxidant activity of raw tomatoes was 4.13 ± 0.36 μmol of vitamin C equiv/g of tomato. With heat treatment at 88 °C for 2, 15, and 30 min, the total antioxidant activity significantly increased to 5.29 ± 0.26, 5.53 ± 0.24, and 6.70 ± 0.25 μmol of vitamin C equiv/g of tomato, respectively (p < 0.01). There were no significant changes in either total phenolics or total flavonoids. These findings indicate thermal processing enhanced the nutritional value of tomatoes by increasing the bioaccessible lycopene content and total antioxidant activity and are against the notion that processed fruits and vegetables have lower nutritional value than fresh produce. This information may have a significant impact on consumers' food selection by increasing their consumption of fruits and vegetables to reduce the risks of chronic diseases.

Depression is detectable in the blood

Finally we may have an objective test and put away the questionaires that throw almost every stroke survivor into a depression diagnosis because they so heavily weight fatigue.  Secondly why do we even need a depression test for survivors? Isn't there enough proof that anti-depressants are quite helpful in recovery?
Antidepressants may help people recover from stroke even if they are not depressed

Depression is detectable in the blood
Researchers at the MedUni Vienna have demonstrated the possibility of using a blood test to detect depression. While blood tests for mental illnesses have until recently been regarded as impossible, a recent study clearly indicates that, in principle, depression can in fact be diagnosed in this way and this could become reality in the not too distant future.
Serotonin transporter (SERT) is a protein in the cell membrane that facilitates the transport of the neurotransmitter serotonin (popularly known as the "happiness hormone") into the cell. In the brain, serotonin transporter regulates neural depression networks. Depressive conditions can frequently be caused by a lack of serotonin. As a result, the serotonin transporter is also the point of action for the major antidepressant drugs.
The serotonin transporter, however, also occurs in large quantities in numerous other organs such as the intestines or blood. Recent studies have shown that the serotonin transporter in the blood works in exactly the same way as in the brain. In the blood, it ensures that blood platelets maintain the appropriate concentration of serotonin in the blood plasma.
Researchers at the MedUni Vienna have now used functional magnetic resonance imaging of the brain and pharmacological investigations to demonstrate that there is a close relationship between the speed of the serotonin uptake in blood platelets and the function of a depression network in the brain.

More at link.

Tuesday, April 29, 2014

Male Scent May Compromise Biomedical Research

Another problem in rodents to watch out for. Goes along with rodent inflammation is not the same as human inflammation. 

Melatonin plus treadmill exercise synergistically promotes neurogenesis and reduce apoptosis in focal cerebral ischemic rats (877.17)

This would be so simple to construct a human clinical trial on this. Why hasn't your doctor started it up yet? Melatonin is easily available. However, don't do this, you know how dangerous doing anything without your doctors ok is. Side effects here:
And treadmills are dammed dangerous.
  1. Yonggeun Hong2,1
+ Author Affiliations
  1. 1Cardiovascular & Metabolic Disease Center, College of Biomedical Science & Engineering, Inje University Gimhae Korea, Republic of
  2. 2Department of Rehabilitation Science in Interdisciplinary PhD Program Graduate School of Inje University Gimhae Korea, Republic of


Ischemic stroke results from sudden decrease or loss of blood flow to the brain, resulting in damage to neurological function and neuronal networks, cognition. The purpose of this study, we determined whether melatonin and/or treadmill exercise could induce neurogenesis, thereby promoting functional recovery in ischemic brain. Following the MCAo, Sprague-Dawley (SD) rats were randomly divided into control (Con), MCAo, MCAo+Exercise (MCAo+Ex), MCAo+Melatonin (MCAo+MT), Melatonin combined Exercise in MCAo (MCAo+MT+Ex). The 8 week old SD rats were treated twice daily with melatonin (10 mg/kg) at 17:00 and 19:00, and trained twice daily with treadmill exercise (20 m/min, 6 days/week) at 17:00 and 22:00. At the Golgi-cox staining, dendrite density in the MCAo+MT+Ex group was higher than in MCAo group. We confirmed that MCAo+MT+ME group was significantly recovered the neurological symptom in behavioral assessment (p<.01). Moreover, MCAo+MT and MCAo+MT+Ex were significantly increased both DCx and GFAP mRNA expression. In conclusion, we suggest that melatonin with and without treadmill exercise intervention enhanced neurogenesis and neuronal cell reconstruction in damaged brain lesions, thereby induced improvement of neurological dysfunction in animal model. Key words: Melatonin, Treadmill exercise, Neurogenesis, Apoptosis, Focal cerebral ischemia

Physical rehabilitation approaches for the recovery of function and mobility following stroke

You didn't search enough if you didn't find that therapy post stroke may help but with only 10% almost full recovery has to be considered a total failure. Which should have led you to preventing neuronal death in the first place by stopping the neuronal cascade of death.  There must not be anyone with a modicum of brains working in the stroke field.
  1. Alex Pollock1,*,
  2. Gillian Baer2,
  3. Pauline Campbell1,
  4. Pei Ling Choo3,
  5. Anne Forster4,
  6. Jacqui Morris5,
  7. Valerie M Pomeroy6,
  8. Peter Langhorne7
Editorial Group: Cochrane Stroke Group
Published Online: 22 APR 2014
Assessed as up-to-date: 6 FEB 2014
DOI: 10.1002/14651858.CD001920.pub3



Various approaches to physical rehabilitation may be used after stroke, and considerable controversy and debate surround the effectiveness of relative approaches. Some physiotherapists base their treatments on a single approach; others use a mixture of components from several different approaches.


To determine whether physical rehabilitation approaches are effective in recovery of function and mobility in people with stroke, and to assess if any one physical rehabilitation approach is more effective than any other approach.
For the previous versions of this review, the objective was to explore the effect of 'physiotherapy treatment approaches' based on historical classifications of orthopaedic, neurophysiological or motor learning principles, or on a mixture of these treatment principles. For this update of the review, the objective was to explore the effects of approaches that incorporate individual treatment components, categorised as functional task training, musculoskeletal intervention (active), musculoskeletal intervention (passive), neurophysiological intervention, cardiopulmonary intervention, assistive device or modality.
In addition, we sought to explore the impact of time after stroke, geographical location of the study, dose of the intervention, provider of the intervention and treatment components included within an intervention.

Search methods

We searched the Cochrane Stroke Group Trials Register (last searched December 2012), the Cochrane Central Register of Controlled Trials (CENTRAL) (The Cochrane Library Issue 12, 2012), MEDLINE (1966 to December 2012), EMBASE (1980 to December 2012), AMED (1985 to December 2012) and CINAHL (1982 to December 2012). We searched reference lists and contacted experts and researchers who have an interest in stroke rehabilitation.

Selection criteria

Randomised controlled trials (RCTs) of physical rehabilitation approaches aimed at promoting the recovery of function or mobility in adult participants with a clinical diagnosis of stroke. Outcomes included measures of independence in activities of daily living (ADL), motor function, balance, gait velocity and length of stay. We included trials comparing physical rehabilitation approaches versus no treatment, usual care or attention control and those comparing different physical rehabilitation approaches.

Data collection and analysis

Two review authors independently categorised identified trials according to the selection criteria, documented their methodological quality and extracted the data.

Main results

We included a total of 96 studies (10,401 participants) in this review. More than half of the studies (50/96) were carried out in China. Generally the studies were heterogeneous, and many were poorly reported.
Physical rehabilitation was found to have a beneficial effect, as compared with no treatment, on functional recovery after stroke (27 studies, 3423 participants; standardised mean difference (SMD) 0.78, 95% confidence interval (CI) 0.58 to 0.97, for Independence in ADL scales), and this effect was noted to persist beyond the length of the intervention period (nine studies, 540 participants; SMD 0.58, 95% CI 0.11 to 1.04). Subgroup analysis revealed a significant difference based on dose of intervention (P value < 0.0001, for independence in ADL), indicating that a dose of 30 to 60 minutes per day delivered five to seven days per week is effective. This evidence principally arises from studies carried out in China. Subgroup analyses also suggest significant benefit associated with a shorter time since stroke (P value 0.003, for independence in ADL).
We found physical rehabilitation to be more effective than usual care or attention control in improving motor function (12 studies, 887 participants; SMD 0.37, 95% CI 0.20 to 0.55), balance (five studies, 246 participants; SMD 0.31, 95% CI 0.05 to 0.56) and gait velocity (14 studies, 1126 participants; SMD 0.46, 95% CI 0.32 to 0.60). Subgroup analysis demonstrated a significant difference based on dose of intervention (P value 0.02 for motor function), indicating that a dose of 30 to 60 minutes delivered five to seven days a week provides significant benefit. Subgroup analyses also suggest significant benefit associated with a shorter time since stroke (P value 0.05, for independence in ADL).
No one physical rehabilitation approach was more (or less) effective than any other approach in improving independence in ADL (eight studies, 491 participants; test for subgroup differences: P value 0.71) or motor function (nine studies, 546 participants; test for subgroup differences: P value 0.41). These findings are supported by subgroup analyses carried out for comparisons of intervention versus no treatment or usual care, which identified no significant effects of different treatment components or categories of interventions.

Authors' conclusions

Physical rehabilitation, comprising a selection of components from different approaches, is effective for recovery of function and mobility after stroke.(Bullshit!!! 10% full recovery is not effective) Evidence related to dose of physical therapy is limited by substantial heterogeneity and does not support robust conclusions. No one approach to physical rehabilitation is any more (or less) effective in promoting recovery of function and mobility after stroke. Therefore, evidence indicates that physical rehabilitation should not be limited to compartmentalised, named approaches, but rather should comprise clearly defined, well-described, evidenced-based physical treatments, regardless of historical or philosophical origin.

Changes in Serum Growth Factors in Stroke Rehabilitation Patients and Their Relation to Hemiparesis Improvement

Your doctor could use this but this doesn't explain why the effects occur or how to increase/decrease those effects.  Someone will need to translate this into a stroke protocol.
Received 31 October 2013; received in revised form 9 January 2014; accepted 16 January 2014. published online 25 April 2014.
Corrected Proof
Predicting recovery from hemiparesis after stroke is important for rehabilitation. A few recent studies reported that the levels of some growth factors shortly after stroke were positively correlated with the clinical outcomes during the chronic phase. The aim of this study was to examine the relationships between the serum levels of growth factors (vascular endothelial growth factor [VEGF], insulin-like growth factor-I [IGF-I], and hepatocyte growth factor [HGF]) and improvement in hemiparesis in stroke patients who received rehabilitation in a postacute rehabilitation hospital. Subjects were 32 stroke patients (cerebral infarction: 21 and intracerebral hemorrhage [ICH]: 11). We measured serum levels of VEGF, IGF-I, and HGF and 5 items of the Stroke Impairment Assessment Set (SIAS) for hemiparesis on admission and at discharge. Age-matched healthy subjects (n = 15) served as controls. Serum levels of VEGF and HGF in cerebral infarct patients on admission were higher than those in control subjects, and the serum levels of IGF-I in stroke patients were lower than those in controls. The level of HGF in ICH patients on admission was negatively correlated with gains in SIAS, and higher outliers in HGF concentration were correlated with lower gains in SIAS. Focusing on the extremely high levels of these factors may be a predictor of the low recovery from hemiparesis after stroke.

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Pomegranate ameliorates Alzheimer’s disease-type neurodegeneration in tg 2576 mouse model (846.1)

Somewhat suspect because it references pomegranates grown in Oman and was a research grant from Oman. but have your doctor check it out to prevent your  33% chance of getting dementia/Alzheimers post stroke.
  1. Gilles Guillemin2
+ Author Affiliations
  1. 1Ageing and Dementia Research Group Muscat Oman
  2. 2Macqaurie Unviersity North Ryde Australia
  3. 3Behavioral Medicine Sultan Qaboos University Muscat Oman
  4. 4Food Science and Nutrition Sultan Qaboos University Muscat Oman
  5. 5Neurology - Department of Medicine Sultan Qaboos University Muscat Oman
  6. 6Old age Psychiatry University of New South Wales Sydney Australia


Alzheimer disease (AD) is a neurodegenerative disease which is characterized by the presence of extracellular senile plaques mainly composed of amyloid-β peptide (Aβ), intracellular neurofibrillary tangles, and selective synaptic and neuronal loss. AD brains revealed elevated levels of oxidative stress markers which have been implicated in Aβ-induced toxicity. Multiple components present in pomegranate and various pomegranate preparations are known to exert pleiotropic protective effects as demonstrated in various in vitro and in vivo model systems. The present study was designed to investigate the dietary supplementation of 4% pomegranate fruit grown in Oman on oxidative stress in the hippocampus, and hippocampal neuron injury in Tg2576 mice. The Tg 2576 mice were treated with 4% pomegranate by dietary supplementation for 15 months. After 15 months, the mice were sacrificed for measuring non-enzymatic [4-hydroxynonenal, TBARS, hydrogen peroxide, reduced glutathione (GSH), vitamin A, E, C and enzymatic antioxidants activity in the hippocampus, and expression of choline acetyltransferase (ChAT) positive neuron. The non-enzymatic and enzymatic antioxidants were significantly reduced along with elevated oxidative stress markers. Loss of ChAT positive neuron and severe damage to hippocampal neurons in Tg 2576 were also found. These abnormalities were significantly improved by 4% pomegranate treatment. In contrast, administration of 4% pomegranate diet to mice strongly suggested a putative delay in the formation of plaques, as indicated by a decreasing tendency of soluble and fibrillar Aβ levels in hippocampus which correlated with a decrease in Aβ (1-40, 1-42) plasma content. The study suggests that pomegranate could offer protection against neuronal injury and oxidative stress, and may be used as a potential agent in treatment of neurodegenerative diseases such as AD. This project was supported by a research grant from The Research Council, Oman (RC/AGR/FOOD/11/01).

AAN: Beyond MS, Cannabis Unproven in Neurology

Of course nothing is proven because our stupid legislators haven't removed the Schedule I classification in order to test it out. I'm going to be using it after my next stroke for all these 13 reasons.
You'll have to ask your doctor exactly how to get some, Michigan is stupid that way, you have to grow your own and stroke is not one of the approved uses, although you can probably shoehorn it into the spasticity one.  I will do the 17 hour 10 minute drive to Denver. Although considering it took me two years to drive after the last stroke, the therapeutic time period has probably long passed. More reasons we need that great stroke association that actually advocates for survivors.  You'll have to contact Dr. Mariel L. Jessup, ASA president and Mr. James Baranski, NSA CEO directly to see what their organizations are doing about marijuana.

Beyond MS, Cannabis Unproven in Neurology

Monday, April 28, 2014

Optical Bedside Monitoring of Cerebral Blood Flow in Acute Ischemic Stroke Patients During Head-of-Bed Manipulation

This was first written about in Nov. 2011 and I bet not one single hospital in the world tried to implement this. Prove me wrong.
  1. John A. Detre, MD
+ Author Affiliations
  1. From the Departments of Neurology (C.G.F., M.M., X.L., S.E.K., J.H.G., J.A.D.), Physics and Astronomy (R.C.M., M.N.K., D.L.M., A.G.Y.), and Radiology (J.A.D.), University of Pennsylvania, Philadelphia, PA; Institute of Physics, University of Campinas, Campinas, Brazil (R.C.M.); and ICFO-Institut de Ciències Fotòniques, Castelldefels, Barcelona, Spain (T.D.).
  1. Correspondence to John A. Detre, MD, Department of Neurology, University of Pennsylvania, 3400 Spruce St, 3 West Gates, Philadelphia, PA 19104-4283. E-mail
  1. Guest Editor for this article was Markku Kaste, MD, PhD.
  2. * Drs Favilla and Mesquita are joint first authors and contributed equally.


Background and Purpose—A primary goal of acute ischemic stroke (AIS) management is to maximize perfusion in the affected region and surrounding ischemic penumbra. However, interventions to maximize perfusion, such as flat head-of-bed (HOB) positioning, are currently prescribed empirically. Bedside monitoring of cerebral blood flow (CBF) allows the effects of interventions such as flat HOB to be monitored and may ultimately be used to guide clinical management.
Methods—Cerebral perfusion was measured during HOB manipulations in 17 patients with unilateral AIS affecting large cortical territories in the anterior circulation. Simultaneous measurements of frontal CBF and arterial flow velocity were performed with diffuse correlation spectroscopy and transcranial Doppler ultrasound, respectively. Results were analyzed in the context of available clinical data and a previous study.
Results—Frontal CBF, averaged over the patient cohort, decreased by 17% (P=0.034) and 15% (P=0.011) in the ipsilesional and contralesional hemispheres, respectively, when HOB was changed from flat to 30°. Significant (cohort-averaged) changes in blood velocity were not observed. Individually, varying responses to HOB manipulation were observed, including paradoxical increases in CBF with increasing HOB angle. Clinical features, stroke volume, and distance to the optical probe could not explain this paradoxical response.
Conclusions—A lower HOB angle results in an increase in cortical CBF without a significant change in arterial flow velocity in AIS, but there is variability across patients in this response. Bedside CBF monitoring with diffuse correlation spectroscopy provides a potential means to individualize interventions designed to optimize CBF in AIS.

Putting It All Together for Best Stroke Practice, All the Time

Well  damn it all, more blather about reducing door to needle times for the appalling failure rate of 88% for tPA. I think I need to start sending out factual emails to these supposed experts.
  1. Edward C. Jauch, MD, MS
+ Author Affiliations
  1. From the Department of Neurosciences (S.D.O., E.C.J.), and Division of Emergency Medicine, Department of Medicine (E.C.J.), Medical University of South Carolina, Charleston.
  1. Correspondence to Edward C. Jauch, MD, MS, 169 Ashley Ave, MSC 300, Medical University of South Carolina, Charleston, SC 29425. E-mail
Key Words:
See related article, p 1387.
Each year nearly 800 000 people in the United States have a clinically evident stroke. Despite the availability of an effective and time-dependent treatment, intravenous recombinant tissue-type plasminogen activator (r-tPA), in 2011, only 33.8%1(That spells failure to me) of eligible ischemic stroke patients received treatment within 60 minutes from time of hospital arrival, as recommended by current acute stroke guidelines.2 This suboptimal expediency of treatment, nearly constant for a decade, represents lost opportunity for optimal neurological outcome and reduced mortality. The pooled analyses of the Alteplase Thrombolysis for Acute Noninterventional Therapy in Ischemic Stroke (ATLANTIS), European Cooperative Acute Stroke Study (ECASS), and National Institute of Neurological Disorders and Stroke r-tPA Stroke Study (NINDS) r-tPA trials by Hacke et al3 in 2004 showed a strong association between early treatment and improved outcomes in patients with ischemic stroke treated with r-tPA. A recent analysis of the Get With the Guidelines Stroke registry by Saver et al4 confirmed that earlier treatment yields better patient outcomes.
The American Heart Association/American Stroke Association Target Stroke initiative was created to provide a framework through which hospitals could reduce their door-to-needle (DTN) times. In the development of the Target Stroke program, best practice strategies were identified by a multidisciplinary work group after reviewing published literature and expert consensus. Strategies proven successful in reducing time to treatment of ST-segment–elevation myocardial infarction were identified as best practice strategies that could be easily and effectively adopted by acute care hospitals in the treatment of stroke. Eleven such strategies were promoted, including prehospital notification; the use of single-call stroke team activation; rapid triage, imaging, and laboratory testing; and the direct prehospital transport to the computed tomographic scanner, among others.5
In this issue, Xian et al6 provide an insightful analysis of the adoption and relative efficacy of these Target Stroke strategies. Baseline data about the use of these best practice strategies were obtained via a survey of 350 hospitals entering the Target Stroke program and later compared with postimplementation data. Hospitals were asked to rate their use of the best practice strategies on a scale of none of the time, some of the time, or all of the time. The frequency of use for each strategy was analyzed against the hospital reported DTN time to determine the impact of each strategy. Hospitals that always used a rapid triage protocol, single-call activation system, the presence of trainees, and those that stored r-tPA in the Emergency Department were those likely to have the shortest treatment times. The strategies with the greatest impact were also ones most infrequently used. The effects of implementation of these strategies were cumulative; hospitals using more of the strategies had shorter times to treatment, with each strategy saving ≈1.3 minutes off a hospital’s DTN time, for a total of 14 minutes if all strategies were used.
Although one of the central goals of the Target Stroke campaign was to identify strategies that could be universally adoptable, herein lies the study’s major criticism, one of selection bias. Hospitals surveyed were not representative of the overall hospital population; instead, they were more likely to be academic centers with larger patient volumes, greater procedural experience with r-tPA administration, and shorter DTN times—in short, they were not the limited-resource community hospitals most likely to benefit from the systemic overhaul that Target Stroke represented. There is, thus, a question of generalizability of these findings to hospitals dissimilar to those represented in the survey, such as rural lifeline hospitals with lower patient volumes. In a 2012 study of implementation of similar concurrent strategies in a Helsinki, Finland, hospital system where DTN times were reduced to 20 minutes, Meretoja et al7 faced similar criticism of generalizability,7 though the follow-up study of implementation of the Helsinki model in a Melbourne, Australia, hospital provided proof of concept that such systemic improvements could be transferable.8
The hospitals surveyed were a self-selected population enrolling in a quality improvement program. As such, they are hospitals already interested in actively improving the system of stroke care at their facility. (They have failed spectacularily) However, it is important to note that this selection bias is not a factor that reduces the study’s validity. Any intervention, medical or systematic, is likely to yield the greatest benefit in those willing to adhere to a prescription for improvement. Furthermore, the rise of regionalization of stroke care and mandated shunting of stroke patients to primary stroke centers legislated in multiple states suggest that the hospitals surveyed will be the ones most likely to receive stroke patients.9 Indeed, the idea that patient volume and quality of care are interrelated has been validated in a study by Bray et al,10 which showed that stroke centers that have experienced higher patient volumes often achieve faster DTN treatment times.
Despite its emphasis on producing an optimal process for rapid treatment at all hospitals, the current study also speaks to the need to individualize the approach to achieving rapid treatment on a case-by-case, hospital-by-hospital basis. By using multivariate analyses to account for differences in demographic and clinical features on a case-by-case basis, this study added additional value by identifying the highest yield targets for further study and development of strategies personalized to the needs of individual patients and the general patient base representative of a given hospital’s demographic and clinical cohort. Of concern, 10% of hospitals did not administer r-tPA during the entire study, and 1 hospital (volume unknown) reported no ischemic events during the study. Because stroke is a high-frequency condition, this suggests that even in hospitals eager to engage in quality improvement activities, acute strokes are being missed. Additional study is necessary to determine whether this is the case.
A key strategy in the Target Stroke Initiative is the use of a team-based approach,5 yet the authors succumb to the thought process that events in the chain of survival that happen outside the hospital are out of the hospital’s control. By stating that prehospital notification is a prehospital or emergency medical services factor rather than a hospital factor, the role of the hospital in promoting a culture of rapid effective care is unnecessarily limited. If we are to make inroads into the problem of patients not recognizing the time importance of stroke, all those who come in contact with the patient must be on message, embracing their individual roles in promoting quality stroke care. Outreach efforts to inform and reinforce the importance of prehospital notification, which is an effective means of priming the receiving facility with a sense of urgency that starts the evaluation and treatment process off right, is critical.
It would be easy for critics of this study to question its impact, given that the implementation of each strategy would only improve times to treatment by slightly more than a minute. Although each strategy could represent a mere 1.3 minutes, however, their value lies in the cumulative improvement in treatment times. The average DTN time nationally is ≈72 minutes; a reduction of 14 minutes would bring the average into the guideline recommended treatment within 60 minutes of arrival. On a patient level, 14 minutes saved through the implementation of all strategies represents 28 million neurons,11 a total that for the patient may mean a difference in functional independence and reduced time in a rehabilitation facility.
Despite being deemed best practices, this study illustrates that often time-saving strategies are not adopted in their entirety. Additional research is required to determine why hospitals fail in their adoption or implementation of seemingly simple best practice strategies. Incomplete (less than always) adoption of individual strategies for improving treatment times was a common theme among hospitals, despite the apparent efficacy of these strategies. Efforts to improve adherence to the prescribed strategies should be pursued. The greatest hurdle in achieving low DTN times does not appear in the implementation of a novel intervention. It is the same hurdle faced by nearly every public health initiative, turning use of a positive initiative from some of the time into all of the time.