Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

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.

Thursday, September 28, 2017

Simple, 15-Minute Test Can Differentiate Patients With MCI From Those With Alzheimer’s Disease

What is your doctor using to baseline your cognition? You need it.

1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.
2. Then this study came out and seems to have a range from 17-66%. December 2013.
3. A 20% chance in this research.   July 2013.

These earlier ones?

Artificial intelligence predicts dementia before onset of symptoms August 2017 

Researchers suggest dual gait testing as early predictor of dementia May 2017

The latest here:

Simple, 15-Minute Test Can Differentiate Patients With MCI From Those With Alzheimer’s Disease

September 23, 2017
By Denise Baez
KYOTO, Japan -- September 23, 2017 -- A simple bedside cognitive tool can identify patients with mild cognitive impairment (MCI), and can help detect progression to Alzheimer’s disease (AD), according to a study presented here at the 23rd World Congress of Neurology (WCN).
The Fifteen-Minute Assessment of Cognition Over the Telephone (FACT) can also help differentiate patients with MCI from those with AD.
“Our aim was to determine whether it was possible to diagnose dementia in just 15 minutes for people who were unable to visit hospitals,” explained Ratnavalli Ellajosyula, MD, Department of Neurology, Manipal Hospitals, Bangalore, India.
FACT consists of 27 items designed to test the interview subject’s orientation, memory, language, and executive functions domains over the phone.
The study included 22 patients with MCI, 20 patients with AD, and 23 healthy volunteers. The researchers administered the FACT screening test 1 week after presentation and neuropsychological testing at the clinic.
Performance on the Addenbrookes Cognitive Examination (ACE III) was used to correlate test performance on the FACT.
The Pearson correlation coefficient between the FACT and the ACE III was 0.82 (P = .00). Correlations on the subcomponents of the FACT and the counterpart domains of the ACE III indicated moderated to high correlations. The area under the ROC curve for FACT discriminating MCI from AD was 0.92 and MCI from healthy volunteers was 0.83.
“FACT proved to be a comparable and effective tool to the ACE III in detecting MCI and monitoring progression to AD,” the authors concluded. “It successfully differentiates patients with MCI from AD, which has clinical and research implications for early intervention and better monitoring of cognitive decline.”
[Presentation title: The Fifteen Minute Assessment of Cognition Over the Telephone (FACT): a Telephone Interview to Detect and Monitor Cognitive. Abstract FP05]

Cardioprotective Effects of Pomegranate (Punica granatum) Juice in Patients with Ischemic Heart Disease

Would this also help reperfusion injury after stroke? We'll never know with our fucking failures of stroke associations never following up possibly useful research. 
Or are you one of the lucky ones where your doctor is already prescribing pomegranate juice based on this research?

Pomegranate juice consumption for 3 years by patients with carotid artery stenosis reduces common carotid intima-media thickness, blood pressure and LDL oxidation  June 2004 

And this one from 2006:

Regular pomegranate juice administered to hypertensive patients caused a significant drop in blood pressure [26], a reduction in carotid plaque development [27]  Aug. 2006

 

Cardioprotective Effects of Pomegranate (Punica granatum) Juice in Patients with Ischemic Heart Disease

Abstract

Ischemic heart disease is the leading cause of mortality worldwide. The purpose of this study was to evaluate the cardioprotective effects of pomegranate juice in patients with ischemic heart disease. One hundred patients, diagnosed with unstable angina or myocardial infarction, were randomly assigned to the test and the control groups (n = 50, each). During 5 days of hospitalization, in addition to the conventional medical therapies, the test groups received 220 mL pomegranate juice, daily. During the hospitalization period, the blood pressure, heart rate, as well as the intensity, occurrence, and duration of the angina were evaluated on a regular basis. At the end of the hospitalization period, the serum levels of malondialdehyde, interleukin-6, and tumor necrosis factor alpha were measured in all patients. The levels of serum troponin and high-sensitive C-reactive protein levels were also assayed in patients diagnosed with myocardial infarction. Pomegranate juice caused significant reductions in the intensity, occurrence, and duration of angina pectoris in patients with unstable angina. Consistently, the test patients had significantly lower levels of serum troponin and malondialdehyde. Other studied parameters did not change significantly. The results of this study suggest protective effects of pomegranate juice against myocardial ischemia and reperfusion injury. Copyright © 2017 John Wiley & Sons, Ltd.

KEYWORDS:

Punica granatum; ischemic heart disease; myocardial ischemia and reperfusion; pomegranate; unstable angina
PMID:
28913846
DOI:
10.1002/ptr.5901

Role of transcranial Doppler ultrasonography in stroke

Only 10 years old. Is your stroke hospital using this to objectively evaluate the state of your cranial arteries? Or is it just by guess and by golly take aspirin or warfarin and hope that is enough?

Role of transcranial Doppler ultrasonography in stroke

Abstract

Transcranial Doppler sonongraphy is a non‐invasive, non‐ionising, inexpensive, portable and safe technique that uses a pulsed Doppler transducer for assessment of intracerebral blood flow. This article deals with the principles and technique of transcranial Doppler sonography. It gives a brief overview of its use in evaluation of intracranial steno‐occlusive disease, subarachnoid haemorrhage, and extracranial diseases (including carotid artery disease and subclavian steal syndrome). The role of transcranial Doppler in detection of microembolic signals and evaluation of right to left shunts is also dealt with. Finally, its use in acute stroke is briefly outlined.
Keywords: stroke, transcranial Doppler ultrasoound
Ultrasound has been used for the evaluation of cerebrovascular disease for over a decade (20 years old now, your doctors use of it?) and has made considerable progress. Transcranial Doppler sonography is a non‐invasive, non‐ionising, inexpensive, portable and safe technique that uses a pulsed Doppler transducer for assessment of intracerebral blood flow.
With the advent of thrombolytic treatment for acute ischaemic stroke, the internist would probably benefit from having a knowledge of transcranial Doppler ultrasound (TCD), which is a useful tool for the detection of occlusion of intracranial vasculature. In addition, success of thrombolytic treatment can also be assessed by TCD.
This review article aims to provide a basic understanding about the use of TCD in clinical practice. A brief outline is provided of the principles and techniques of TCD and its role in acute ischaemic stroke, including abnormalities affecting both intracranial and extracranial parts of vessels supplying the brain. We then explore the role of TCD in the detection of microembolic signals, which help in stratification of risk of recurrence of stroke or transient ischaemic attack (TIA), and its role of in the detection and quantification of right‐to‐left shunts. We also outline the possible role of TCD in subarachnoid haemorrhage and subclavian steal syndrome. Finally, the role of TCD during carotid endarterectomy is discussed (box 1).

Box 1: Use of transcranial Doppler ultrasound

  • Detection of site/degree of stenosis/occlusion of cerebral vasculature
  • Assessment of recanalisation following occlusion (with/without thrombolytic treatment)
  • Assessment of collateral flow in intracranial vasculature in cases of critical carotid artery stenosis (extracranial)
  • Detection of microemboli: stratification of risk of recurrence of stroke/TIA
  • Detection and quantification of right to left shunts
  • Detection of degree of vasospasm following subarachnoid haemorrhage
  • Complementary to duplex carotid scan in diagnosis of subclavian steal syndrome
  • Intraoperative monitoring of carotid endarterectomy

Association between subjective risk perception and objective risk estimation in patients with atrial fibrillation: A cross-sectional study

So you can discuss your risk perception vs. your doctors perception of atrial fibrillation risks. Good luck with that. And if your doctor is wrong about the risk coming true then you are the one having the disability, not your doctor. 

Association between subjective risk perception and objective risk estimation in patients with atrial fibrillation: A cross-sectional study


BMJ Open | September 28, 2017
Zweiker D, et al. - This study probed into the connection between subjective risk perception and objective risk estimation in patients with atrial fibrillation. The data shed light on eminent variations between patients’ perceptions and physicians’ analyses of the risks and benefits of oral anticoagulation (OAC). The findings recommended paying extra focus to evidence-based and useful communication strategies, with the intention of ensuring shared decision-making and informed consent.

Methods

  • This cross-sectional prevalence trial utilized the convenience sampling and telephone follow-up.
  • It was carried out at 8 hospital departments and one general practitioner in Austria.
  • Patients’ perception of stroke and bleeding risk was opposed to commonly used risk scoring.
  • The enrollment consisted of patients with newly diagnosed AF and indication for anticoagulation.
  • The main outcome included the comparison of subjective risk perception with CHA2DS2-VASc and HAS-BLED scores illustrating the probable discrepancies between subjective and objective risk estimation.
  • An association was noted between the patients’ judgement of their own knowledge on AF and education with the accuracy of subjective risk appraisal.

Results

  • 91 patients (age 73±11 years, 45% female) were enrolled.
  • There was no link between the subjective stroke and bleeding risk estimation with risk scores (ρ=0.08 and ρ=0.17).
  • Maximum patients (57%) underestimated the individual stroke risk.
  • Patients feared stroke more than bleeding (67% vs 10%).
  • No association was observed between accurate perception of stroke and bleeding risks and education level.
  • A connection, however, was determined between the patients’ judgement of their own knowledge of AF and correct assessment of individual stroke risk (ρ=0.24, p=0.02).
  • The patients experienced the following events: death (n=5), stroke (n=2), bleeding (n=1), during follow-up.
  • OAC discontinuation rate regradless of the indication was 3%.

New drug beats heart disease by reducing inflammation

How much would this help in preventing stroke?
Hopefully you can use this off-label.  They would rather pay for your heart attack or stroke. 

New drug beats heart disease by reducing inflammation 


By Dr. Manny Alvarez, Fox News

About every 40 seconds, an American has a heart attack, and almost 15 percent of those heart attacks are fatal. As the leading cause of death in the U.S., heart disease has been the subject of thousands of studies in the last several decades, and breakthroughs in the last 50 years have been significant.
First, diet, exercise, and smoking cessation were all proven to play an enormous role in heart health, helping physicians guide patients to less risky lifestyle choices.
Then, in the 1980s, the first commercial statin was approved by the FDA, ushering in an era in which medication could be used alongside lifestyle changes to lower cholesterol levels, potentially reducing heart attack risk by over a third for some high risk patients.
STDS HIT RECORD HIGH IN US, 2M CASES REPORTED IN 2016
Despite these gains and the fact that statins are one of the most frequently prescribed drugs, heart disease is still the number one killer of Americans, but researchers are excited about the results of a study published last month in the New England Journal of Medicine that investigates the impact of a new drug on cardiovascular risk.
The trial is the Canakinumab Anti-inflammatory Thrombosis Outcomes Study (CANTOS), and the drug, called Canakinumab, may be able to bring heart attack risk to an all-time low by targeting inflammation.
This study is the first in which a systemic anti-inflammatory, a drug that reduces inflammation throughout the body, has been shown to lower heart attack risk independent of cholesterol-lowering medications.
The purpose of the trial was to see whether reducing inflammation could reduce the risk of recurring cardiovascular events among people who had already had a heart attack and who had elevated levels of high sensitivity C-reactive protein (hsCRP), an indication of systemic inflammation.
The study was the culmination of more than 25 years of research. By treating all patients in the trial with standard care (high doses of statins) and then dividing them into groups that would receive either 50, 150, or 300 mg of Canakinumab (or a placebo), the researchers were able to accurately assess the impact of the new drug. More than 10,000 patients took part in the trial, some of whom were monitored for up to four years.

The results showed a 15 percent reduction in heart attacks and strokes for patients taking either 150 or 300 mg of the of Canakinumab, proving for the first time that inflammation plays a role in heart disease risk independent of cholesterol levels.
This discovery may change therapeutic practice for patients at high risk of heart attack or stroke. More studies are underway to establish the best strategies for using Canakinumab – which patients benefit most and how the drug can be used in combination with other therapies.
“These findings represent the end game of more than two decades of research, stemming from a critical observation: Half of heart attacks occur in people who do not have high cholesterol," Paul M. Ridker, M.D., the study's lead author, said. "For the first time, we’ve been able to definitively show that lowering inflammation independent of cholesterol reduces cardiovascular risk. This has far-reaching implications. It tells us that by leveraging an entirely new way to treat patients — targeting inflammation — we may be able to significantly improve outcomes for certain very high-risk populations.”
The need for invasive and expensive interventions, like bypass surgery and angioplasty, were reduced by more than 30 percent in patients taking Canakinumab, a far greater reduction than is usually found with the use of statins alone.

Wednesday, September 27, 2017

Immune cell-related proteins may speed healing after stroke

I don't know why people even bother to write hopeful articles like this. We have NO stroke leadership and NO stroke strategy that will do ANY followup to get this into translation science.
Now if we could just get some followup on this which LEADERS would accomplish. But we have none.  Ask your stroke hospital president whom the LEADERS are in stroke and what they are doing that makes them LEADERS. 

Immune cell-related proteins may speed healing after stroke


At a Glance

  • Two proteins associated with immune cells may play critical roles in helping the brain to heal after a stroke.
  • Additional studies are needed to find out whether these proteins could be used for treating stroke. 
Microscopic image of brain cell culture Brain nerve cells (green) and astrocytes (red), a type of support cell, in a rat cell culture after exposure to a mixture from red blood cells. The researchers used this as a model for the damage caused to the brain by intracerebral hemorrhagic stroke.Aronowski lab, University of Texas Health Science Center, Houston
Intracerebral hemorrhages are a form of stroke caused by ruptured blood vessels. The leaked blood causes swelling and increased pressure in the skull, which damage cells and tissues in the brain. Over time, additional damage may be caused by the buildup of toxic levels of blood products and infiltrating immune cells. Symptoms of a hemorrhagic stroke can include sudden weakness; paralysis or numbness of the face, arms, or legs; trouble speaking or understanding speech; and trouble seeing.
Decades of research suggest that neutrophils are some of the earliest immune cells to respond to a hemorrhage, and that they may have both harmful and healing effects in the brain. A team led by Dr. Jaroslaw Aronowski at the University of Texas Health Science Center at Houston set out to find out what role neutrophils may play in healing after hemorrhagic stroke. The study was funded by NIH’s National Institute of Neurological Disorders and Stroke (NINDS). Results appeared on September 19, 2017, in Nature Communications.
The team first measured interleukin-27 (IL-27), a protein that controls the activity of various immune cells, in the brain and blood of mice after a brain hemorrhage. They detected elevated IL-27 levels within an hour after hemorrhage. Levels peaked at 24 hours and remained high for 3 days. Further experiments suggested that brain cells called microglia produced IL-27 in response to the presence of red blood cells.
The team found that, once released, the IL-27 molecules appeared to travel to the bones of the mice and infiltrate the marrow, where neutrophils are born. When the researchers extracted neutrophils from the bones and treated them with IL-27, the chemical raised the activity of genes associated with healing. IL-27 may thus shift the role of neutrophils from harming to helping with recovery.
The researchers injected IL-27 into mice after a hemorrhage. Days after the stroke, the treated mice were better than untreated mice at walking, limb stretching, and navigating holes in a floor. The brains of the mice treated with IL-27 also showed less damage. They had less swelling around the hemorrhages and lower levels of two compounds that are toxic at high levels, iron and the blood protein hemoglobin. In contrast, injections of a compound that blocked natural IL-27 activity slowed recovery.
One notable gene for which IL-27 raised the level of activity in neutrophils was the gene for lactoferrin, a protein that neutralizes toxic iron. The team tested lactoferrin’s effect on stroke recovery. They injected mice and rats with lactoferrin 30 minutes after a brain hemorrhage. The treated animals recovered faster and had less brain damage than animals given placebos. Giving mice lactoferrin 24 hours after a stroke was also effective.
“Intracerebral hemorrhage is a damaging and often fatal form of stroke for which there are no effective medicines,” Aronowski says. “Our results are a hopeful first step towards developing a treatment for this devastating form of stroke.”

Related Links

References: Neutrophil polarization by IL-27 as a therapeutic target for intracerebral hemorrhage. Zhao X, Ting SM, Liu CH, Sun G, Kruzel M, Roy-O'Reilly M, Aronowski J. Nat Commun. 2017 Sep 19;8(1):602. doi: 10.1038/s41467-017-00770-7. PMID: 28928459.
Funding: NIH’s National Institute of Neurological Diseases and Stroke (NINDS).


Arm swing

Had a 4 mile walk - 8000 steps - this afternoon on sidewalks. 3 miles in my left arm actually started to swing a bit. The elbow is still bent so the hand catches on the left thigh coming and going.  I never get arm swing walking in the woods. I got to do this because I had a colonoscopy this morning and since you are sedated you aren't allowed to drive yourself back. I had to use one of those handicapped vans and had them drop me off at work. It was 4 miles from work to the clinic to pick up my car.  Drove myself back to work. Will also violate one other prohibition tonight.  Do not drink alcohol. Well that won't work. I'm visiting a friend to watch Project Runway and wine will be consumed.
It was good, no polyps.

Even Open-Label Placebos Work – if They Are Explained

Don't prescribe a placebo to yourself.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=179316&CultureCode=en
26 September 2017 Universität Basel
For some medical complaints, open-label placebos work just as well as deceptive ones. As psychologists from the University of Basel and Harvard Medical School report in the journal Pain, the accompanying rationale plays an important role when administering a placebo.
The successful treatment of certain physical and psychological complaints can be explained to a significant extent by the placebo effect. The crucial question in this matter is how this effect can be harnessed without deceiving the patients. Recent empirical studies have shown that placebos administered openly have clinically significant effects on physical complaints such as chronic back pain, irritable bowel syndrome, episodic migraine and rhinitis.
Cream for pain relief
For the first time, researchers from the University of Basel, along with colleagues from Harvard Medical School, have compared the effects of administering open-label and deceptive placebos. The team conducted an experimental study with 160 healthy volunteers who were exposed to increasing heat on their forearm via a heating plate. The participants were asked to manually stop the temperature rise as soon as they could no longer stand the heat. After that, they were given a cream to relieve the pain.
Some of the participants were deceived during the experiment: they were told that they were given a pain relief cream with the active ingredient lidocaine, although it was actually a placebo. Other participants received a cream that was clearly labeled as a placebo; they were also given fifteen minutes of explanations about the placebo effect, its occurrence and its effect mechanisms. A third group received an open-label placebo without any further explanation.
The subjects of the first two groups reported a significant decrease in pain intensity and unpleasantness after the experiment. “The previous assumption that placebos only work when they are administered by deception needs to be reconsidered,” says Dr. Cosima Locher, a member of the University of Basel’s Faculty of Psychology and first author of the study.
Stronger pain when no rationale is given

When detailed explanations of the placebo effect were absent – as in the third group – the subjects reported significantly more intense and unpleasant pain. This suggests the crucial role of the accompanying rationale and communication when administering a placebo; the researchers speak of a narrative. The ethically problematic aspect of placebos, the deception, thus does not appear all that different from a transparent and convincing narrative. “Openly administering a placebo offers new possibilities for using the placebo effect in an ethically justifiable way,” says co-author Professor Jens Gaab, Head of the Division of Clinical Psychology and Psychotherapy at the University of Basel.
https://www.unibas.ch/en/News-Events/News/Uni-Research/Even-Open-Label-Placebos-Work---if-They-Are-Explained.html

Anti-Inflammatory Effects of Vinpocetine in Atherosclerosis and Ischemic Stroke: A Review of the Literature

I'm sure no followup has occurred with NO stroke leadership.

Pros on using this:

Vinpocetine increases cerebral blood flow and oxygenation in stroke patients: a near infrared spectroscopy and transcranial Doppler study

 

Cons on using this:

 

Vinpocetine, for instance, has been observed to disrupt myelin repair, which could be especially problematic for MS patients.

 

Anti-Inflammatory Effects of Vinpocetine in Atherosclerosis and Ischemic Stroke: A Review of the Literature

Linjie Zhang and Li Yang *
Department of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, 154, Anshan Road, Heping District, Tianjin 300052, China
*
Author to whom correspondence should be addressed; Tel.: +86-22-6081-4536; Fax: +86-22-6081-7471.
Academic Editor: Derek J. McPhee
Received: 24 October 2014 / Accepted: 19 December 2014 / Published: 26 December 2014

Abstract

: Immune responses play an important role in the pathophysiology of atherosclerosis and ischemic stroke. Atherosclerosis is a common condition that increases the risk of stroke. Hyperlipidemia damages endothelial cells, thus initiating chemokine pathways and the release of inflammatory cytokines—this represents the first step in the inflammatory response to atherosclerosis. Blocking blood flow in the brain leads to ischemic stroke, and deprives neurons of oxygen and energy. Damaged neurons release danger-associated molecular patterns, which promote the activation of innate immune cells and the release of inflammatory cytokines. The nuclear factor κ-light-chain-enhancer of activated B cells κB (NF-κB) pathway plays a key role in the pathogenesis of atherosclerosis and ischemic stroke. Vinpocetine is believed to be a potent anti-inflammatory agent and has been used to treat cerebrovascular disorders. Vinpocetine improves neuronal plasticity and reduces the release of inflammatory cytokines and chemokines from endothelial cells, vascular smooth muscle cells, macrophages, and microglia, by inhibiting the inhibitor of the NF-κB pathway. This review clarifies the anti-inflammatory role of vinpocetine in atherosclerosis and ischemic stroke.

Study: Giving Oxygen No Help After Stroke

Well, well you fucking idiots you used the Rankin scale which has no objectivity and discriminatory power at all. If you truly wanted to know if it helped you would do PET scans to see if the extent of penumbra damage was less.
I bet they had no clue how much extra oxygen got to the brain because they didn't do this:

Brain Tissue Oxygen Monitoring and the Intersection of Brain and Lung: A Comprehensive Review

Hopefully this latest result doesn't stop further research since this 2005 pilot study showed promise:

 

A Pilot Study of Normobaric Oxygen Therapy in Acute Ischemic Stroke 2005

 

Or is it more important to increase the loading ability of red blood cells to carry more oxygen? 

Like this?

University of Glasgow Study Demonstrates the Ability of Oxycyte® to Supply Oxygen to Critical Penumbral Tissue in Acute Ischemic Stroke  August 2012

 

Or like this?

chronic cannabis users have higher cerebral blood flow and extract more oxygen from brain blood flow than nonusers.

 

Or maybe you want to starve your brain of oxygen, tested in mice;

This is a fascinating idea, treat your recently oxygen starved brain with more reduced oxygen supply.

 

 

The failed and bad research trial here.

Study: Giving Oxygen No Help After Stroke

Trial showed no effect on death, disability in non-hypoxic acute stroke

  • by Senior Associate Editor, MedPage Today
  • This article is a collaboration between MedPage Today® and:
    Medpage Today
Acute stroke patients with sufficient oxygenation levels didn't benefit from provision of low-dose supplemental oxygen, whether continuous or at night only, the SO2S trial showed.
Three days of oxygen therapy -- given at 3 L/min for a baseline oxygen saturation of 93% or less and at 2 L/min over that -- had no impact on death and disability at 3 months as measured by modified Rankin Scale score with ordinal logistic regression (common OR 0.97 for a one level improvement, 95% CI 0.89-1.05) compared with oxygen given only when clinically indicated.
Those pooled results held also for the two oxygen arms individually, with no significant difference between continuous administration and nighttime use only (OR 1.03, 95%CI 0.93-1.13), reported Christine Roffe, MD, of Keele University in Stoke-on-Trent, England, and colleagues in the Journal of the American Medical Association.
"No subgroup could be identified that benefited from oxygen," they wrote, concluding that "These findings do not support low-dose oxygen in this setting."
The findings from the pragmatic clinical trial of 8,003 patients with acute stroke randomized to the three treatment groups within 24 hours of admission came on the heels of another large trial negative for supplemental oxygen in a different setting -- acute MI.
DETO2X-AMI, reported at the European Society of Cardiology (ESC) meeting and online in the New England Journal of Medicine in August 2017, showed no impact on 1-year all-cause mortality, rehospitalization for MI, extent of myocardial injury, or other outcomes from routine use of 6 L/min oxygen supplementation versus room air for 6 to 12 hours.
While supplemental oxygen has been routine in the U.S. in acute MI, cardiologists at ESC agreed with an editorialist regarding patients without hypoxemia: "It is clearly time for clinical practice to change to reflect this definitive evidence."
In stroke, though, Roffe's group suggested their results might still leave a chance at benefit for one group.
Whether very early administration of high-dose oxygen might help at-risk brain tissue or broaden the the time window for neuroprotection or thrombolysis remains to be seen definitively in the PROOF trial. An underpowered subgroup analysis in SO2S showed no difference in the 101 participants enrolled within 3 hours of symptom onset as in those enrolled later.
For other subgroups though, the researchers wrote: "Because of the large overall size of this trial, these patient subgroups were each sufficiently large for the lack of observed benefit to be likely real and not a false negative."
They noted that low-dose oxygen supplementation as used in their trial probably wasn't enough to prevent severe desaturation, which occurred similarly with oxygen and without. But randomized trials of high-flow oxygen treatment in acute stroke haven't suggested higher doses are any better for outcomes.
The low-dose oxygen tested in SO2S wasn't associated with more treatment-related adverse events or a difference in serious adverse events overall.
The project was funded by the NIHR Health Technology Assessment Programme and the Research for Patient Benefit Programme.
Roffe disclosed support from the Research for Patient Benefit Programme and the Health Technology Assessment Programme of the National Institute for Health Research and relevant relationships with Air Liqude and the PROOF trial.

Tuesday, September 26, 2017

INCIDENCE AND MANAGEMENT OF SEIZURES AFTER ISCHEMIC STROKE: SYSTEMATIC REVIEW AND META-ANALYSIS

So every single stroke doctor in the world should take this course and the course expired 7 days ago. So you are out of luck if you need seizures managed post-stroke.  And since seizures occur in about 10% of stroke patients you may want your doctor to get educated on this.
https://cme.neurology.org/attendee/view_program.jsp?programCode=27864P2CEiHD

About this course

  • Released: 9/19/2017
  • Expires: 9/19/2020


INCIDENCE AND MANAGEMENT OF SEIZURES AFTER ISCHEMIC STROKE: SYSTEMATIC REVIEW AND META-ANALYSIS

LEARNING OBJECTIVES:

Upon completion of the article by Wang et al, the participant should be able to:
  • State the incidence of early poststroke seizures in this systematic review and meta-analysis
  • Discuss the results of studies described in this review comparing antiepileptic drugs in the treatment of poststroke epilepsy with regards to adverse effects and efficacy
  • Discuss the reasons for finding a lower poststroke seizure incidence proposed by the authors of this review
     

CORE COMPETENCIES:

The article by Wang et al covers the following core competency:
  • Medical Knowledge

Clinical Imaging Factors Associated With Infarct Progression in Patients With Ischemic Stroke During Transfer for Mechanical Thrombectomy

You better hope like hell that you have the correct stroke so your doctor actually has an intervention that can be used. Otherwise you are screwed, better start planning now and make sure you also have the classic signs so you are correctly diagnosed as having a stroke.

Clinical Imaging Factors Associated With Infarct Progression in Patients With Ischemic Stroke During Transfer for Mechanical Thrombectomy

JAMA Neurol. Published online September 25, 2017. doi:10.1001/jamaneurol.2017.2149
Key Points
Question  Among patients with ischemic stroke transferred for mechanical thrombectomy, what baseline clinical imaging factors portend an unfavorable evolution to a point at which the patient may not derive clinical benefit from mechanical thrombectomy at arrival?
Findings  This cohort study of prospectively collected data found that, along with initial clinical severity, poor collateral blood vessel status was the most determinant factor of evolution to an unfavorable imaging profile during transfer.
Meaning  In certain subgroups of patients with ischemic stroke, vascular imaging at the referring hospitals may play a critical role in determining the benefits of transfer for thrombectomy.
Abstract
Importance  When transferred from a referring hospital (RH) to a thrombectomy-capable stroke center (TCSC), patients with initially favorable imaging profiles (Alberta Stroke Program Early CT Score [ASPECTS] ≥6) often demonstrate infarct progression significant enough to make them ineligible for mechanical thrombectomy at arrival. In rapidly evolving stroke care networks, the question of the need for vascular imaging at the RHs remains unsolved, resulting in an important amount of futile transfers for thrombectomy.
Objective  To examine the clinical imaging factors associated with unfavorable imaging profile evolution for thrombectomy in patients with ischemic stroke initially transferred to non-TCSCs.
Design, Setting, and Participants  Data from patients transferred from 1 of 30 RHs in our regional stroke network and presenting at our TCSC from January 1, 2010, to January 1, 2016, were retrospectively analyzed. Consecutive patients with acute ischemic stroke initially admitted to a non–thrombectomy-capable RH and transferred to our center for which a RH computed tomography (CT) and a CT angiography (CTA) at arrival were available for review.
Main Outcomes and Measures  ASPECTS were evaluated. The adequacy of leptomeningeal collateral blood flow was rated as no or poor, decreased, adequate, or augmented per the adapted Maas scale. The main outcome was an ASPECTS decay, defined as an initial ASPECTS of 6 or higher worsening between RH and TCSC CTs to a score of less than 6 (making the patient less likely to derive clinical benefit from thrombectomy at arrival).
Results  A total of 316 patients were included in the analysis (mean [SD] age, 70.3 [14.2] years; 137 [43.4%] female). In multivariable models, higher National Institutes of Health Stroke Score, lower baseline ASPECTSs, and no or poor collateral blood vessel status were associated with ASPECTS decay, with collateral blood vessel status demonstrating the highest adjusted odds ratio of 5.14 (95% CI, 2.20-12.70; P < .001). Similar results were found after stratification by vessel occlusion level.
Conclusions and Relevance  In patients with ischemic stroke transferred for thrombectomy, poor collateral blood flow and stroke clinical severity are the main determinants of ASPECTS decay. Our findings suggest that in certain subgroups vascular imaging, including collateral assessment, can play a crucial role in determining the benefits of transfer for thrombectomy.

Influence of Penumbral Reperfusion on Clinical Outcome Depends on Baseline Ischemic Core Volume

If they wanted to objectively determine reperfusion they would use 3d scans and PET imaging and drop the Rankin scale as a measurement tool.  

Influence of Penumbral Reperfusion on Clinical Outcome Depends on Baseline Ischemic Core Volume

Chushuang Chen, Mark W. Parsons, Matthew Clapham, Christopher Oldmeadow, Christopher R. Levi, Longting Lin, Xin Cheng, Min Lou, Timothy J. Kleinig, Kenneth S. Butcher, Qiang Dong, Andrew Bivard
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Abstract

Background and Purpose—In alteplase-treated patients with acute ischemic stroke, we investigated the relationship between penumbral reperfusion at 24 hours and clinical outcomes, with and without adjustment for baseline ischemic core volume.
Methods—Data were collected from consecutive acute ischemic stroke patients with baseline and follow-up perfusion imaging presenting to hospital within 4.5 hours of symptom onset at 7 hospitals. Logistic regression models were used for predicting the effect of the reperfused penumbral volume on the dichotomized modified Rankin Scale (mRS) at 90 days and improvement of National Institutes of Health Stroke Scale at 24 hours, both adjusted for baseline ischemic core volume.
Results—This study included 1507 patients. Reperfused penumbral volume had moderate ability to predict 90-day mRS 0 to 1 (area under the curve, 0.77; R2, 0.28; P<0.0001). However, after adjusting for baseline ischemic core volume, the reperfused penumbral volume was a strong predictor of good functional outcome (area under the curve, 0.946; R2, 0.55; P<0.0001). For every 1% increase in penumbral reperfusion, the odds of achieving mRS 0 to 1 at day 90 increased by 7.4%. Improvement in acute 24-hour National Institutes of Health Stroke Scale was also significantly related to the degree of reperfused penumbra (R2, 0.31; P<0.0001). This association was again stronger after adjustment for baseline ischemic core volume (R2, 0.41; P<0.0001). For each 1% of penumbra that was reperfused, the 24-hour National Institutes of Health Stroke Scale decreased by 0.069 compared with baseline.
Conclusions—In patients treated with alteplase, the extent of the penumbra that is reperfused is a powerful predictor of early and late clinical outcomes, particularly when baseline ischemic core is taken into account.

Effects of Statin Intensity and Adherence on the Long-Term Prognosis After Acute Ischemic Stroke

But shouldn't statins already be a protocol that is given to all stroke patients? For your doctor to consider.

Simvastatin attenuates axonal injury after experimental traumatic brain injury and promotes neurite outgrowth of primary cortical neurons  Oct. 2012



Effects of Statin Intensity and Adherence on the Long-Term Prognosis After Acute Ischemic Stroke

Jinkwon Kim, Hye Sun Lee, Chung Mo Nam, Ji Hoe Heo
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Abstract

Background and Purpose—Statin is an established treatment for secondary prevention after ischemic stroke. However, the effects of statin intensity and adherence on the long-term prognosis after acute stroke are not well known.
Methods—This retrospective cohort study using a nationwide health insurance claim data in South Korea included patients admitted with acute ischemic stroke between 2002 and 2012. Statin adherence and intensity were determined from the prescription data for a period of 1 year after the index stroke. The primary outcome was a composite of recurrent stroke, myocardial infarction, and all-cause mortality. We performed multivariate Cox proportional regression analyses.
Results—We included 8001 patients with acute ischemic stroke. During the mean follow-up period of 4.69±2.72 years, 2284 patients developed a primary outcome. Compared with patients with no statin, adjusted hazard ratios (95% confidence interval) were 0.74 (0.64–0.84) for good adherence, 0.93 (0.79–1.09) for intermediate adherence, and 1.07 (0.95–1.20) for poor adherence to statin. Among the 1712 patients with good adherence, risk of adverse events was lower in patients with high-intensity statin (adjusted hazard ratio [95% confidence interval], 0.48 [0.24–0.96]) compared with those with low-intensity statin. Neither good adherence nor high intensity of statin was associated with an increased risk of hemorrhagic stroke.
Conclusions—After acute ischemic stroke, high-intensity statin therapy with good adherence was significantly associated with a lower risk of adverse events.

Assessment Model to Identify Patients With Stroke With a High Possibility of Discharge to Home

The goal should be 100% recovery and return to home. You wouldn't need discharge planning then. The problem is that stroke rehab is a total fucking failure. You solve that by not having to provide very much of it. And that is by researching and creating protocols that stop the neuronal cascade of death in the first week.

Assessment Model to Identify Patients With Stroke With a High Possibility of Discharge to Home

A Retrospective Cohort Study

Takahiro Itaya, Yusuke Murakami, Akiko Ota, Eiichi Nomura, Tomoko Fukushima, Masakazu Nishigaki
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Abstract

Background and Purpose—Discharge planning for inpatients with acute stroke can enhance reasonable use of healthcare resources, as well as improve clinical outcomes and decrease financial burden of patients. Especially, prediction for discharge destination is crucial for discharge planning. This study aimed to develop an assessment model to identify patients with a high possibility of discharge to home after an acute stroke.
Methods—We reviewed the electronic medical records of 3200 patients with acute stroke who were admitted to a stroke center in Japan between January 1, 2011, and December 31, 2015. The outcome variable was the discharge destination of postacute stroke patients. The predictive variables were identified through logistic regression analysis. Data were divided into 2 data sets: the learning data set (n=2240) for developing the instrument and the test data set (n=960) for evaluating the predictive capability of the model.
Results—In all, 1548 (48%) patients were discharged to their homes. Multiple logistic regression analysis identified 5 predictive variables for discharge to home: living situation, type of stroke, functional independence measure motor score on admission, functional independence measure cognitive score on admission, and paresis. The assessment model showed a sensitivity of 85.0% and a specificity of 75.3% with an area under the curve equal to 0.88 (95% confidence interval, 0.86–0.89) when the cutoff point was 10. On evaluating the predictive capabilities, the model showed a sensitivity of 88.0% and a specificity of 68.7% with an area under the curve equal to 0.87 (95% confidence interval, 0.85–0.89).
Conclusions—We have developed an assessment model for identifying patients with a high possibility of being discharged to their homes after an acute stroke. This model would be useful for health professionals to adequately plan patients’ discharge soon after their admission.

Pericytes Make Spinal Cord Breathless after Injury

We already know that pericytes cause problems post stroke so this should be immediately followed up to see if this inhibition of proteins would help in stroke.

Capillaries that don't open due to pericytes


Pericytes Make Spinal Cord Breathless after Injury

First Published September 21, 2017 Research Article


Traumatic spinal cord injury is a devastating condition that leads to significant neurological deficits and reduced quality of life. Therapeutic interventions after spinal cord lesions are designed to address multiple aspects of the secondary damage. However, the lack of detailed knowledge about the cellular and molecular changes that occur after spinal cord injury restricts the design of effective treatments. Li and colleagues using a rat model of spinal cord injury and in vivo microscopy reveal that pericytes play a key role in the regulation of capillary tone and blood flow in the spinal cord below the site of the lesion. Strikingly, inhibition of specific proteins expressed by pericytes after spinal cord injury diminished hypoxia and improved motor function and locomotion of the injured rats. This work highlights a novel central cellular population that might be pharmacologically targeted in patients with spinal cord trauma. The emerging knowledge from this research may provide new approaches for the treatment of spinal cord injury.

Practicing Evidence-Based Stroke Medicine

You will notice that there are no EBMs for stroke rehab, just the removal of the clot, nothing to treat anything about the neuronal cascade of death.
http://stroke.ahajournals.org/content/48/10/2647?etoc=

Marc Fisher, Karen Furie

The practice of evidence-based medicine depends on several steps: a basic science derived understanding of disease pathophysiology, epidemiological research, and the results of well-conducted and appropriately analyzed randomized clinical trials (RCTs). The approval of new therapies by regulatory agencies is also based largely on RCT determination of the safety and therapeutic efficacy of drugs and devices. Once a new therapy is approved for use in clinical practice, clinicians typically begin to use it in a manner which mirrors the clinical trial design, for example, in the population for who risk and benefit have been established. It must be acknowledged that in the United States and in other countries, clinicians have leeway in their therapeutic decision making and it is not uncommon for therapies to be used for situations not tested in the RCTs that led to approval, the so-called off-label use. The off-label use of stroke-related therapies is relatively common, and we will consider the appropriateness of doing this in 3 common clinical scenarios.

Performing Thrombectomy

The relatively recent demonstration of the efficacy of thrombectomy within 6 hours of stroke onset in 6 well-conducted RCTs provides convincing evidence that this treatment is highly effective in improving functional outcome.1,2 These RCTs carefully selected patients with small-to-moderate ischemic cores, primarily by assessing the pretreatment Alberta Stroke Program Early CT Score (ASPECTS) on a noncontrast head CT, but computerized tomography perfusion (CTP) and diffusion-weighted magnetic resonance imaging were also acquired in some patients. In these trials, the median baseline ASPECTS score was 9, indicating a very small ischemic core and in 3 of the trials a baseline score of ≤5 was an exclusion. Even in MR CLEAN (Multicenter Randomized Clinical Trial of Endovascular Treatment for Acute Ischemic Stroke in the Netherlands), a trial which did not specify an ASPECTS exclusion criterion, the median baseline score was 9. A minority of patients in the trials had scores of 6 to 7, and very few had scores of ≤5. The inclusion of patients with a proximal vessel occlusion proven by computerized tomographic angiography or magnetic resonance angiography and small/moderate ischemic core ensured that a large region of at risk ischemic tissue, the ischemic penumbra, was present before thrombectomy. This factor along with the very high rate of vessel recanalization achieved and rapidity of vessel opening led to the dramatic therapeutic success.3 The US Food and Drug Administration approval of the Solitaire device mentions that it should be used in ischemic patients with a smaller infarct core. In clinical practice, a wide range of strategies is being used to identify patients for thrombectomy within 6 hours of stroke onset. In some centers, after demonstration of a proximal vessel occlusion and a computerized tomography (CT) with no evidence of hemorrhage, almost all patients undergo thrombectomy with no attempt to identify the extent of the ischemic core by ASPECTS, CTP, or diffusion-weighted magnetic resonance imaging. Patients with a very large hypodense region qualitatively identified are presumably excluded. Proponents of this strategy would argue that thrombectomy is highly effective as we do not yet know how large an ischemic core at baseline identifies patients who will no longer respond to thrombectomy. In other centers, the ASPECTS score is used to identify thrombectomy candidates. Unfortunately, the ASPECTS score has low interobserver reliability, and conspicuity on head CT scanning is related to the amount of radiation used to acquire the scan.4,5 Most centers use a reduced dose of radiation to acquire their head CT scans so the literature supporting the use of ASPECTS may not reflect routine practice. An argument for using CT ASPECTS would be that even if the score is off by 1 to 2 points most treated patients would still be in the ≥6 range as in the RCTs. Some centers use CTP to either qualitatively or quantitatively identify the ischemic core. Using CTP is probably more precise than CT ASPECTS, but ischemic core identification is dependent on the parameter used to identify it and the threshold that is considered to represent the ischemic core. In the past, cerebral blood volume maps were widely used to identify the ischemic core, but these are notoriously inaccurate.6 Currently, cerebral blood flow (CBF) or mean transit maps are widely used to identify the ischemic core, and many studies support a threshold of CBF <30% of the contralateral hemisphere as a reasonable threshold for estimating the extent of the ischemic core.7
This approach was used in the recently reported diffusion-weighted magnetic resonance imaging and CTP Assessment in the DAWN trial (Triage of Wake-up and Late Presenting Strokes Undergoing Neurointervention) that demonstrated the remarkable therapeutic efficacy of thrombectomy with the Trevo device in the 6- to 24-hour time window in stroke patients with ischemic cores of <20 or 30 mL (depending on their age) with an National Institutes of Health Stroke Scale score between 10 and 20 and an ischemic core of ≤50 mL with an National Institutes of Health Stroke Scale score >20.8 The regulatory approval of the Trevo device for 6- to 24-hour patients will likely include a requirement for ischemic core volume measurement. For thrombectomy candidates in the <6-hour time window, we do not know the extent of CBF-derived ischemic core volume on CTP that is no longer responsive to therapy. Clinicians should at least attempt to identify the extent of the ischemic core before thrombectomy. If the ASPECTS score is used and centers are confident in their ability to derive the score accurately, patients with a score of ≤5 should not be treated. If CTP is used, then CBF maps using the threshold of ischemic tissue with a CBF of ≤30% should be used to identify the volume of ischemic tissue. Some centers may wish to exclude patients with a large ischemic core volume, perhaps >70 or even 100 mL. Other centers may treat patients irrespective of the CTP-derived core volume. We encourage centers to maintain an outcome registry that relates the pretreatment imaging and clinical characteristics to 90-day modified Rankin Scores so that data can be pooled for analysis and the volume of ischemic core not amenable to thrombectomy identified. For patients beyond 6 hours, the inclusion criteria used in the DAWN trial should be adhered to in most cases or it is likely that clinical practice outcomes will not recapitulate the trial results. For both early and late thrombectomy patients, the rapidity of the procedure and extent of vessel opening should be maximized because time is brain.

Combination Antithrombotic Therapy

A second area of concern on the practice of evidence-based stroke medicine is antithrombotic therapy. For secondary stroke prevention in patients with noncardioembolic ischemic stroke, 3 antiplatelet drugs, aspirin, clopidogrel, and aspirin plus dipyridamole, are approved in the United States for secondary stroke prevention.9 The use of combining aspirin and clopidogrel for enhancing secondary stroke prevention was tested in several RCTs with long-term follow-up, and any benefits on prevention of ischemic events were negated by major bleeding side effects. The SAMMPRIS trial (Stenting and Aggressive Medical Management for Preventing Recurrent Stroke in Intracranial Stenosis) did demonstrate that the combination of aspirin plus clopidogrel significantly reduced the 90-day rate of ischemic outcome events in patients with symptomatic high-grade intracranial stenosis and the CHANCE (Clopidogrel in High-Risk Patients With Acute Nondisabling Cerebrovascular Events) also demonstrated a reduction of 90-day ischemic events with this combination compared with aspirin alone in a more general Chinese mild stroke and transient ischemic attack population.10,11 In both trials, bleeding risk with combination therapy used for 90 days was reasonable. Therefore, the only RCT data currently available to support using the combination of aspirin and clopidogrel for ischemic stroke prevention are 90-day use, and it is currently unclear that this combination is efficacious in a non-Chinese patient without high-grade intracranial stenosis or beyond the 90-day time period. The ongoing POINT trial (Platelet-Oriented Inhibition in New TIA and Minor Ischemic Stroke Trial) will provide evidence concerning the 90-day efficacy and safety of the clopidogrel/aspirin combination in patients with a broader range of ethnic and racial backgrounds. Despite the lack of evidence, it is not uncommon for clinicians to use this combination in ischemic stroke or transient ischemic attack patients who have their event on aspirin or clopidogrel alone and then continue treatment indefinitely. Similarly, in patients with atrial fibrillation who have a stroke or transient ischemic attack while taking warfarin or one of the newer anticoagulants, some clinicians add an antiplatelet drug to the anticoagulant after the event. There is no evidence that this combination reduces the risk of subsequent ischemic events and clear evidence that the major bleeding risk is significantly increased.9 Both of these therapeutic practices should be avoided unless future RCT results demonstrate efficacy and safety.

Use of Statins After Ischemic Stroke

A third area of concern is the broad use of statins after ischemic stroke in patients who were not studied in RCTs and in whom statins are not recommended in practice guidelines. The primary RCT providing evidence about statin therapy reducing the risk for recurrent events was SPARCL (Stroke Prevention by Aggressive Reduction in Cholesterol Levels).12 In this study, atorvastatin significantly reduced the risk for recurrent stroke in patients with large artery and lacunar stroke, but patients with cardioembolic stroke were excluded. The most recent American Heart Association secondary stroke prevention guidelines recommend high-dose statin therapy in patients with atherothrombotic stroke, but no recommendation is correctly made for cardioembolic stroke unless they have another indication for statin therapy such as coronary artery disease,r an unfavorable lipid profile or a cardiovascular risk stratification score suggesting a substantial risk for cardiovascular events.9 Despite the RCT results and American Heart Association guideline recommendation, high-dose statins are routinely prescribed in cardioembolic stroke patients who have no other indication for them. A recent observational study from a large database evaluated the risk of recurrent stroke in patients with or without atrial fibrillation who took statins after their stroke.13 The risk of recurrent stroke was strongly related to adherence with the statin prescription and adherence in both groups, suggesting that statins may reduce recurrent stroke risk in stroke related to atrial fibrillation. Though intriguing, this study is not definitive, and the results may have been affected by bias and confounding. An RCT will be needed to provide evidence that statins reduce recurrent stroke risk in atrial fibrillation–related stroke.
The stroke field has seen an increasing number of positive RCTs that have led to remarkable, proven treatment advances for prevention and acute treatment. Clinicians need to carefully read the results of these RCTs and be aware how they were incorporated into the regulatory approval of these therapies. They can then decide how to use them in their clinical practices. In most situations to truly practice evidence-based medicine, clinicians should try to replicate how the therapies were evaluated in the RCTs and practice accordingly. Of course, clinical judgment allows for exceptions based on individual circumstances of the patient. This is the art of medicine. At Stroke, we will continue to provide our readers with expert evaluations of important RCTs that appear in other journals, so that clinicians can have help in how they interpret trial results and in their consideration as to how to use the results in daily practice.