MGH scientists develop software that provides automated support for diagnosing cause of stroke

It doesn't talk about crytogenic strokes only those already identified as ischemic. so this doesn't seem that useful.
http://www.news-medical.net/news/20170329/MGH-scientists-develop-software-that-provides-automated-support-for-diagnosing-cause-of-stroke.aspx
Determining the cause of an ischemic stroke - one caused by an interruption of blood supply - is critical to preventing a second stroke and is a primary focus in the evaluation of stroke patients. But despite that importance, physicians have long lacked a robust and objective means of doing so. Now a team of investigators at the Athinoula A. Martinos Center for Biomedical Imaging at the Massachusetts General Hospital (MGH) and the MGH Stroke Service have developed a software package that provides evidence-based, automated support for diagnosing the cause of stroke. Their study validating the package - called Causative Classification of Stroke (CCS) - was published online in JAMA Neurology.
"This was a much-needed study because, although stroke classifications systems are often used in research and clinical practice, these systems are not always able to produce subtypes with discrete pathophysiological, diagnostic and prognostic characteristics," says Hakan Ay, MD, a vascular neurologist, Martinos Center investigator and senior author of the JAMA Neurology paper. "We found that the CCS-based classifications provided better correlations between clinical and imaging stroke features and were better able to discriminate among stroke outcomes than were two conventional, non-automated classification methods."
There are more than 150 different possible causes - or etiologies - of ischemic stroke, and approximately half of patients exhibit features suggesting more than one possible cause. This leads to considerable complexity in determining the cause of a stroke and, in roughly one of two patients, can lead to disagreements among physicians about the cause. The CCS software helps to reduce this complexity by exploiting classification criteria that are well defined, replicable and based on evidence rather than subjective assessment.
The CCS software does this in several ways. First, it weights the possible etiologies by considering the relative potential of each to cause a stroke. Second, in the presence of multiple potential causes it incorporates the clinical and imaging features that make one mechanism more probable than others for an individual patient. Third, it determines the likelihood of that cause by taking into account the number of diagnostic tests that were performed. And finally, it ensures that data is entered in a consistent manner. The software can also serve as an important research tool, by providing investigators with both the ability to examine how stroke etiologies interact with one another and the flexibility to define new etiology subtypes according to the needs of the individual research project.

The MGH team previously showed that use of the CCS algorithm reduced the disagreement rate among physicians from 50 percent to approximately 20 percent. The recently published JAMA Neurology study further established the utility of the algorithm by demonstrating its ability to generate categories of etiologies with different clinical, imaging and prognostic characteristics for 1,816 ischemic stroke patients enrolled in two previous MGH-based studies. Based on patient data, CCS was able to assign etiologies to 20 to 40 percent of the patients for which two other systems were unable to determine a cause. It also was better at determining the likelihood of second stroke within 90 days.
"The validity data that have emerged from the current study add to the utility of the software-based approach and highlight once again that careful identification and accurate classification of the underlying etiology is paramount for every patient with stroke," says Ay, who is an associate professor of Radiology at Harvard Medical School. "The information the software provides not only is critical for effective stroke prevention but also could increase the chances for new discoveries by enhancing the statistical power in future studies of etiologic stroke subtypes. We estimate that, compared to conventional systems, the use of CCS in stroke prevention trials testing targeted treatments for a particular etiologic subtype could reduce the required sample size by as much as 30 percent."
The MGH-licensed CCS is available at https://ccs.mgh.harvard.edu/ and is free for academic use. The software was designed to be a "living algorithm" and can accommodate new information as it emerges. New etiology-specific biomarkers, genetic markers, imaging markers and clinical features that become available can be incorporated into the existing CCS algorithm to further enhance its ability to determine the underlying causes of stroke.

Source:

http://www.massgeneral.org/about/pressrelease.aspx?id=2080

Functional Recovery and Mobility After Inpatient Rehabilitation of Ischemic and Hemorrhagic Stroke

No clue if this has any use at all for survivors, but it is 47 pages long. Using Brunnstrom stages is pretty useless for discrimination of recovery successes.

Functional Recovery and Mobility After Inpatient Rehabilitation of Ischemic and Hemorrhagic Stroke

Aim: To compare the level of independence in daily activities and level of mobility between admission to inpatient rehabilitation and discharge of patients with history of intracerebral hemorrhage and cerebral infarction.

Methods: Patients with first-ever stroke admitted to inpatient rehabilitation program were included in this study. Patients were separated into 2 groups as ischemic and hemorrhagic based on neuroradiologic assessments. Level of independence in daily activities was evaluated by Barthel index, mobility status was evaluated by, Rivermead Mobility Index, motor performance was evaluated by Brunnstrom states of motor recovery during hospital admission and discharge.

Results: Two-hundred patients were included. 140 cases of cerebral infarct and 60 cases had cerebral hemorrhage. Mean age of the patients in hemorrhagic group was significantly lower than mean age of patients with ischemic lesions (p = 0.003).

Comparison of two groups did not reveal significant differences in Barthel and Rivermead Mobility Index scores on both admission and discharge. The most frequent risk factor in both groups was hypertension. The frequency of ischemic heart diseasewas significantly higher in ischemic group than hemorrhagic group (p < 0.001).

Conclusion: The etiology of stroke did not have major effect on the duration of rehabilitation or level of functional activity of pa­tients.

And in Turkish:

Amaç: İntraserebral kanama ve serebral infarkt hikayesi olan hastaların rehabilitasyon servisine yatış ve taburculuk arasındaki günlük aktivite sırasındaki bağımsızlık ve mobilite seviyelerinin karşılaştırılmasıdır.

Yöntem: Bu çalışmaya rehabilitasyon servisine yatırılmış olan ilk defa inme geçiren hastalar alınmıştır. Hastalar, nöroradyolojik değerlendirmeler baz alınarak iskemik ve hemorajik olmak üzere 2 gruba ayrılmıştır. Günlük aktiviteler sırasındaki bağımsızlık seviyesi Barthel indeksi ile, mobilite durumu Rivermead Mobilite indeksi ile, motor performans hastaneye yatış ve taburculukta bakılan Brunnstrom motor iyileşme evreleri ile değerlendirilmiştir.

Sonuçlar: Serebral infarkt olan 140 kişi ve serebral kanama olan 60 kişi olmak üzere toplam 200 hasta çalışmaya dahil edilmiştir.

Hemorajik gruptaki ortalama yaş, iskemik gruptaki ortalama yaşa göre belirgin ölçüde daha düşüktür (p=0.003). İki grup arasındaki karşılaştırma yatış ve taburculuk sırasında hesaplanan Barthel ve Rivermead Mobilte indeks skorları arasında önemli bir fark göstermemiştir. İki grupta da en sık risk faktörü hipertansiyondur. İskemik grupta, iskemik kalp hastalıkları sıklığı hemorajik gruba göre belirgin oranda yüksektir (p < 0.001).

Tartışma: Bu çalışmanın sonucuna göre, inmenin etiyolojisi, rehabilitasyon süresi veya hastaların fonksiyonel aktiviteleri üzerinde büyük bir etkiye sahip değildir.

Thrombectomy within 8 Hours after Symptom Onset in Ischemic Stroke

Does your hospital have the expertise to do this?

Thrombectomy within 8 Hours after Symptom Onset in Ischemic Stroke

Tudor G. Jovin, M.D., Angel Chamorro, M.D., Erik Cobo, Ph.D., María A. de Miquel, M.D., Carlos A. Molina, M.D., Alex Rovira, M.D., Luis San Román, M.D., Joaquín Serena, M.D., Sonia Abilleira, M.D., Ph.D., Marc Ribó, M.D., Mònica Millán, M.D., Xabier Urra, M.D., Pere Cardona, M.D., Elena López-Cancio, M.D., Alejandro Tomasello, M.D., Carlos Castaño, M.D., Jordi Blasco, M.D., Lucía Aja, M.D., Laura Dorado, M.D., Helena Quesada, M.D., Marta Rubiera, M.D., María Hernandez-Pérez, M.D., Mayank Goyal, M.D., Andrew M. Demchuk, M.D., Rüdiger von Kummer, M.D., Miquel Gallofré, M.D., and Antoni Dávalos, M.D. for the REVASCAT Trial Investigators

April 17, 2015DOI: 10.1056/NEJMoa1503780

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Abstract

Article

References

Citing Articles (2)

Background

We aimed to assess the safety and efficacy of thrombectomy for the treatment of stroke in a trial embedded within a population-based stroke reperfusion registry.

Full Text of Background...

Methods

During a 2-year period at four centers in Catalonia, Spain, we randomly assigned 206 patients who could be treated within 8 hours after the onset of symptoms of acute ischemic stroke to receive either medical therapy (including intravenous alteplase when eligible) and endovascular therapy with the Solitaire stent retriever (thrombectomy group) or medical therapy alone (control group). All patients had confirmed proximal anterior circulation occlusion and the absence of a large infarct on neuroimaging. In all study patients, the use of alteplase either did not achieve revascularization or was contraindicated. The primary outcome was the severity of global disability at 90 days, as measured on the modified Rankin scale (ranging from 0 [no symptoms] to 6 [death]). Although the maximum planned sample size was 690, enrollment was halted early because of loss of equipoise after positive results for thrombectomy were reported from other similar trials.

Full Text of Methods...

Results

Thrombectomy reduced the severity of disability over the range of the modified Rankin scale (adjusted odds ratio for improvement of 1 point, 1.7; 95% confidence interval [CI], 1.05 to 2.8) and led to higher rates of functional independence (a score of 0 to 2) at 90 days (43.7% vs. 28.2%; adjusted odds ratio, 2.1; 95% CI, 1.1 to 4.0). At 90 days, the rates of symptomatic intracranial hemorrhage were 1.9% in both the thrombectomy group and the control group (P=1.00), and rates of death were 18.4% and 15.5%, respectively (P=0.60). Registry data indicated that only eight patients who met the eligibility criteria were treated outside the trial at participating hospitals.

Full Text of Results...

Conclusions

Among patients with anterior circulation stroke who could be treated within 8 hours after symptom onset, stent retriever thrombectomy reduced the severity of post-stroke disability and increased the rate of functional independence. (Funded by Fundació Ictus Malaltia Vascular through an unrestricted grant from Covidien and others; REVASCAT ClinicalTrials.gov number, NCT01692379.)

Full Text of Discussion...

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Medscape Quiz: Do You Know the Complications, Proper Workup, and Best Treatment Practices for Ischemic Stroke?

This is a fucking appalling quiz. Not one item in there even mentions treating the neuronal cascade of death. I got all but one correct. I don't give a shit if  'There is no clinical research for any neuroprotective treatment in the first week'.  Damn it all there are neurons dying by the boatload and your doctor is just sitting by letting you become more disabled by the minute. My 177 hyperacute therapies that need more research. Or  these 31 hyperacute possibilities I'm going to insist my doctor give me the first week. 
Charge your doctor/hospital $1 for every neuron they fail to save($950,000 a minute). I'm sure you can find some lawyer willing to take on the case.
It should be fairly easy to get an app for your iPad or iPhone that keeps a running total of dead neurons that can be shown every time your doctor does rounds.

Medscape stroke quiz

Cite this article: Edward C. Jauch. Quiz: Do You Know the Complications, Proper Workup, and Best Treatment Practices for Ischemic Stroke? Medscape. Dec 29, 2014.

N-Terminal Pro–B-type Natriuretic Peptide and Stroke Risk

Does your doctor know how to test and evaluate your stroke risks with this? Or will you again have to tell them about new or even old research papers?
https://stroke.ahajournals.org/content/early/2014/04/22/STROKEAHA.114.004712.abstract?sid=d0b12f5a-d0a9-48f9-9bf9-6014959fd049

The Reasons for Geographic and Racial Differences in Stroke Cohort

1. Mary Cushman, MD, MSc,
2. Suzanne E. Judd, PhD,
3. Virginia J. Howard, PhD,
4. Brett Kissela, MD, MS,
5. Orlando M. Gutiérrez, MD, MMSc,
6. Nancy S. Jenny, PhD,
7. Ali Ahmed, MD, MPH,
8. Evan L. Thacker, PhD and
9. Neil A. Zakai, MD, MSc

+ Author Affiliations

1. From the Departments of Medicine and Pathology, University of Vermont, Colchester (M.C., N.S.J., N.A.Z.); Departments of Epidemiology and Medicine, University of Alabama at Birmingham (S.E.J., V.J.H., O.M.G., A.A., E.L.T.); Department of Neurology, University of Cincinnati, OH (B.K.); and Department of Medicine, Veterans Affairs Medical Center, Birmingham, AL (A.A.).

1. Correspondence to Mary Cushman, MD, MSc, Departments of Medicine and Pathology, University of Vermont, 208 S Park Dr, Colchester, VT 05446. E-mail mary.cushman@uvm.edu

Abstract

Background and Purpose—Improved identification of those at risk of stroke might improve prevention. We evaluated the association of the cardiac function biomarker N-terminal pro–B-type natriuretic peptide (NT-proBNP) with stroke risk in the 30 239 black and white participants of the Reasons for Geographic and Racial Differences in Stroke (REGARDS) cohort.

Methods—During 5.4 years of follow-up after enrollment in 2003 to 2007, NT-proBNP was measured in baseline blood samples of 546 subjects with incident ischemic stroke and 956 without stroke.

Results—NT-proBNP was higher with older age and in those with heart disease, kidney disease, atrial fibrillation, and lower low-density lipoprotein-cholesterol. Adjusting for age, race, sex, income, education, and traditional stroke risk factors, there was an increased risk of stroke across quartiles of NT-proBNP; participants with NT-proBNP in the top versus the bottom quartile had a hazard ratio of 2.9 (95% confidence interval, 1.9–4.5). There was no impact of added adjustment for kidney function and heart failure. Among pathogenetic stroke subtypes, the association was largest for cardioembolic stroke, with a hazard ratio of 9.1 (95% confidence interval, 2.9–29.2). Associations did not differ by age, sex, or race, or after excluding those with baseline heart failure or atrial fibrillation. Predicted stroke risk was more accurate in 27% of participants if NT-proBNP was considered after traditional stroke risk factors (P<0.001).

Conclusions—NT-proBNP was a major independent risk marker for stroke. Considering this and other data for stroke, coronary disease, and atrial fibrillation, the clinical use of NT-proBNP measurement in primary prevention settings should be considered. 

But what type of stroke? Ischemic? hemorrhagic?

Ischemic Stroke Brain Sends Indirect Cell Death Signals to the Heart

And if we had decent causes of death we wouldn't have the catchall of death caused by stroke. That is not detailed enough to be able to figure out how to stop these types of deaths if we don't autopsy them properly. Is your neurologist calling in a cardiac doctor to make sure your heart continues to function ok after your stroke? Damn there is going to be a lot to remember to tell my doctor about keeping me alive after my next stroke.
http://stroke.ahajournals.org/content/44/11/3175.abstract.html?etoc

1. Hiroto Ishikawa, MD, PhD;
2. Naoki Tajiri, PT, PhD;
3. Julie Vasconcellos, BS;
4. Yuji Kaneko, PhD;
5. Osamu Mimura, MD, PhD;
6. Mari Dezawa, MD, PhD;
7. Cesar V. Borlongan, PhD

+ Author Affiliations

1. From the Department of Neurosurgery and Brain Repair, University of South Florida College of Medicine, Tampa, FL (H.I., N.T., J.V., Y.K., C.V.B.); Department of Ophthalmology, Hyogo College of Medicine, Nishinomiya, Japan (H.I., O.M.); and Department of Stem Cell Biology and Histology and Department of Anatomy and Anthropology, Tohoku University Graduate School of Medicine, Sendai, Japan (M.D.).

1. Correspondence to Cesar V. Borlongan, PhD, Department of Neurosurgery and Brain Repair, University of South Florida, 12901 Bruce B. Downs Blvd MDC78, Tampa, FL 33612. E-mail cborlong@health.usf.edu

Abstract

Background and Purpose—Ischemic stroke is a leading cause of mortality and morbidity in the world and may be associated with cardiac myocyte vulnerability. However, it remains uncertain how an ischemic brain contributes to cardiac alternations. Here, we used experimental stroke models to reveal the pathological effects of the ischemic brain on the heart.

Methods—For the in vitro study, primary rat neuronal cells were subjected to 90-minute oxygen–glucose deprivation (OGD). Two hours after OGD, the supernatant was collected and cryopreserved until further biological assays. Primary rat cardiac myocytes were exposed to ischemic–reperfusion injury and subsequently to the supernatant derived from either the OGD or non–OGD-exposed primary rat neuronal cells for 2, 6, 24, or 48 hours. Thereafter, we measured cell viability and mitochondrial activity in rat cardiac myocytes. For the in vivo study, we subjected adult rats to transient middle cerebral artery occlusion, and their brains and hearts were harvested for immunohistochemical analyses at 3 months later.

Results—The supernatant from the OGD, but not the non–OGD-exposed primary rat neuronal cells, caused significant reduction in cell viability and mitochondrial activity in rat cardiac myocytes. Ischemic stroke animals displayed phenotypic expression of necrosis, apoptosis, and autophagy in their hearts, which paralleled the detection of these same cell death markers in their brains.

Conclusions—Ischemic stroke was accompanied by cardiac myocyte death, indicating a close pathological link between brain and heart. These results suggest a vigilant assessment of the heart condition in stroke patients, likely requiring the need to treat systemic cardiac symptoms after an ischemic brain episode.

Telestroke is Cost-effective for Hospitals, Mayo Clinic Researchers Show

This is a major problem, medical persons not recognizing when a newer process/procedure needs to be implemented. They were  way too focused on getting tPA to work and missed possibly better ways to tell the difference between hemorrhage and ischemic. See 11 possibilities here; Damn don't people ever think at all.
http://www.healthcanal.com/public-health-safety/34565-Telestroke-Cost-effective-for-Hospitals-Mayo-Clinic-Researchers-Show.html
In telestroke care, the use of a telestroke robot allows a patient with stroke to be examined in real time by a neurology specialist elsewhere who consults via computer with an emergency room physician in the rural site.
"Previous studies have demonstrated that a hub-and-spoke telestroke network is cost-effective from the societal perspective — we can assess medical services, like telemedicine, in terms of the net costs to society for each year of life gained," says neurologist Bart Demaerschalk, M.D., director of Mayo Clinic Telestroke Program, and co-author of the telestroke cost effectiveness study. "However, to date the costs and benefits from the perspectives of network hospitals have not been formally estimated."
Contrary to a common perception that a telestroke referral network poses a substantial financial burden on hospitals, the study revealed that it is likely to save hospitals money and also improve patient outcomes by enabling patients to be discharged sooner.
"The health economic results from an earlier study conducted from the societal perspective convincingly demonstrated that telestroke was cost effective compared to the usual model of care," says Dr. Demaerschalk. "It's a relatively small amount of money, comparatively, telestroke costs a couple thousand dollars more to save quality years of life — so it's a bargain really."
The Circulation study estimates that compared with no network, a telestroke system of a single hub and seven spoke hospitals may result in the use of more clot-busting drugs, procedures and other stroke therapies, more stroke patients discharged home independently, and despite upfront and maintenance expenses, a greater total cost savings for the entire network of hospitals.
Using data from Mayo Clinic and the Georgia Health Sciences University telestroke networks, the research model estimated that every year, compared to no telemedicine network, 45 more patients would be treated with intravenous thrombolysis and 20 more with endovascular stroke therapies — leading to 6.11 more independent patients discharged home. This represents more than $100,000 in cost savings for each of the participating rural hospitals each year, according to the study.
"If the costs associated with the technology are reduced or if reimbursement opportunities increase we will recognize that this treatment method may, in fact, save even more money," Dr. Demaerschalk says. "The upfront costs associated with setting up the telestroke technology and managing the network organization are quickly offset by the financial gains that result from a higher proportion of patients receiving clot busting drugs and the reduced stroke-related disability and subsequent reduced need for rehabilitation, nursing home care and assistance at home."
The results of this economic research have implications on the assignment of financial responsibility between hub and spoke hospital partners. For instance, in a network that is principally designed to aid spoke hospitals' capacity to effectively assess, treat, and admit more patients with stroke, it is the spoke hospitals which benefit economically — and it then makes sense that the spoke hospitals should contribute to financing the telestroke network system.
The study was conducted by researchers at Mayo Clinic, Georgia Health Sciences University, Analysis Group, and was funded by Genentech, Inc.
Mayo Clinic first used telemedicine technology with the stroke telemedicine program in 2007, when statistics revealed that 40 percent of residents in Arizona lacked local stroke experts.
Mayo Clinic was the first medical center in Arizona to do pioneering clinical research to study telemedicine as a means of serving patients with stroke in non-urban settings, and today serves as the "hub" in a network of 12 "spoke" centers. Since the telestroke program began more than 1,500 emergency consultations for stroke between Mayo stroke neurologists and physicians at the spoke centers in Arizona have taken place. Beyond Arizona, Mayo Clinic Telestroke is represented nationally, with hub and spoke networks already in existence in Florida and in a development phase in Minnesota and Mayo Clinic Health System.

City needs stroke unit says health campaigner - Worcester

Under the current system of hyperacute interventions for stroke using tPA this very expensive and time-consuming process needs to be setup. This just points out the imperative need to completely change the way ischemic vs. hemorrhagic strokes are identified. Numerous ways are listed here.
So rather than trying to shoehorn the existing broken system into a very expensive shoe maybe we should rethink exactly what truly needs to be done. Try using your thinking caps sometime.

 http://www.worcesternews.co.uk/news/10017943.City_needs_stroke_unit_says_health_campaigner/
A PATIENT leader says a hyper acute stroke service for Worcester is vital in the new-look NHS as a region-wide review of stroke services continues.
The NHS in the Midlands and East region, which includes Worcester, is reviewing care for those who suffer strokes or transient ischaemic attacks (TIAs) which are also called mini-strokes.
The review covers stroke care for adults from pre-hospital care through to rehabilitation/social care and end of life and aims to improve survival rates and reduce disability.
Hyper acute stroke services deal with emergency care within the first 72 hours of a stroke rather than later rehabilitation.
All stroke patients in Worcestershire are currently admitted to A&E and assessed for thrombolysis. If required, they are thrombolysed in A&E and then admitted to the acute stroke unit. If not required, they are admitted directly to the acute stroke unit. There were 718 confirmed stroke admissions in Worcestershire last year and 238 TIA admissions.

Hereford’s stroke services, which treats around 20 per cent of stroke patients from Powys, Wales, are also subject to the review.
Although no formal options have yet been announced, patient representative Brendan Young, of Powick, near Worcester, has been involved in discussions with health chiefs and has been pressing for hyper acute stroke services at the Worcestershire Royal Hospital, Worcester. “I made it clear that the centralised option for hyper acute stroke services at Worcestershire Royal Hospital was non-negotiable since we have gone through a rigorous, lengthy and sometimes painful process to arrive at that decision earlier this year,” said Mr Young.
“We could not have Worcester not having hyper acute stroke services. In an ideal world Hereford should have a hyper acute stroke service as well,” he said.

The Hereford and Worcester Cardiac and Stroke Network is in talks with local hospital leaders to identify what are the best options to move towards providing the best service possible for stroke patients, but this is still described as a work in progress.
The networks will submit their final recommended proposals to the external expert advisory group, an independent board of experts from a number of disciplines involved in stroke care including consultants, nurses and therapists, in January. Firm plans are scheduled to be submitted in March and by April members of the new NHS Commissioning Board will oversee the review through to its conclusion.

Safety results of intra-arterial stem cell clinical trial for stroke presented

I can't tell why they think this will help recovery(magical thinking maybe?)
Why only ischemic?
http://www.healthcanal.com/blood-heart-circulation/32893-Safety-results-intra-arterial-stem-cell-clinical-trial-for-stroke-presented.html
Early results of a Phase II intra-arterial stem cell trial for ischemic stroke showed no adverse events associated with the first 10 patients, allowing investigators to expand the study to a targeted total of 100 patients.
The results were presented today by Sean Savitz, M.D., professor of neurology and director of the Stroke Program at The University of Texas Health Science Center at Houston (UTHealth), at the 8^th World Stroke Congress in Brasilia, Brazil.
The trial is the only randomized, double-blind, placebo-controlled intra-arterial clinical trial in the world for ischemic stroke. It is studying the safety and efficacy of a regenerative therapy developed by Aldagen Inc., a wholly-owned subsidiary of Cytomedix, Inc., that uses a patient’s own bone marrow stem cells, which can be administered between 13 and 19 days post-stroke.
The therapy, called ALD-401, consists of stem cells that are identified using Aldagen’s proprietary technology to isolate cells that express high levels of an enzyme that serves as a marker of stem cells. Pre-clinical studies found that these cells enhance recovery after stroke in mice. The cells are administered into the carotid artery. Patients are followed for 12 months to monitor safety and to assess mental and physical function.
“We have been approved by the Data Safety Monitoring Board (DSMB) to move the study into the next phase, which will allow us to expand the number of sites in order to complete enrollment,” said Savitz, senior investigator for the multi-center study. As per the protocol for the trial, the Food and Drug Administration required a review by the DSMB prior to advancing to the next phase.
Preclinical research, including research at the UTHealth Medical School, has suggested that stem cells can promote the repair of the brain after an ischemic stroke, which is caused by a blood clot in the brain. Stroke is a leading cause of disability and the fourth-leading cause of death in the United States, according to 2008 statistics reported by the Centers for Disease Control and Prevention.
For patient information about the intra-arterial stem cell clinical trial for stroke, call 713-500-7183 or email jennifer.m.garrett@uth.tmc.edu

Vanderbilt Leading International THERAPY Trial to Study Benefits of Combined Drug and Interventional Therapy Approach for Stroke Victims

I hope the efficacy tested includes full recovery instead of just preventing death. I don't believe tPA was adequately tested since it doesn't always lead to full recovery. That should have led to more searches right after it was approved in 1996, rather than 16 years later.
http://www.newswise.com/articles/vanderbilt-leading-international-therapy-trial-to-study-benefits-of-combined-drug-and-interventional-therapy-approach-for-stroke-victims
Researchers at Vanderbilt University Medical Center are leading an international clinical trial to examine the functional benefits of a combined therapy to treat acute ischemic stroke, a type of stroke where a blood clot becomes lodged in an artery within the brain, reducing blood flow and depriving brain cells of oxygen. Eighty-seven percent of strokes are ischemic.

The THERAPY trial involves use of the standard-of-care, clot-busting intravenous drug tPA (tissue plasminogen activator) and an interventional device treatment, the Penumbra System, that gently suctions away blood clots to restore blood flow to the brain’s affected area.

The trial will evaluate a combined therapy using IV tPA and interventional clot removal with the Penumbra System, compared to IV tPA treatment alone.

During the minimally invasive procedure a catheter is threaded to the clot and the Penumbra System’s technology gently suctions away the mass to restore blood flow. The Penumbra System, which was FDA-approved in December 2007, has been used in approximately 15,000 stroke treatment procedures in the U.S.

Principal investigator J Mocco, M.D., associate professor of Neurological Surgery, said the trial hopes to involve 75 stroke treatment centers worldwide to participate, with a target enrollment of 692 patients.

“When patients come in with a stroke they are distressed,” Mocco said. “They can’t move half their body, they often can’t talk, and they can’t understand language. They are often headed toward permanent disability, or death.”

“The device evaluated in this trial works like a straw, it literally sucks the clot out. In our recent experience at Vanderbilt, almost half of the treated patients are completely independent afterwards. These are patients who otherwise would likely be devastated with severe disability.”

Stroke is the fourth leading cause of death in the U.S. and the leading cause of long-term adult disability, affecting 800,000 Americans every year. Common stroke symptoms include numbness, weakness or paralysis along one side of the body, slurred speech, and difficulty understanding speech and/or trouble walking.

The standard of care for acute ischemic stroke in most stroke centers involves administration of intravenous (IV) tPA within 3 to 4 1/2 hours of the onset of symptoms. However, most patients do not arrive in time, and the treatment may fail if a clot is too large or difficult to dissolve. If this occurs, alternative minimally invasive, inside-the-artery clot removal can be used up to eight hours after onset of symptoms.

The trial will also examine the use of certain patient selection criteria to determine if interventional therapy is appropriate. Recent advancements in CT scan imaging have helped physicians better assess the size and location of a patient’s clot and whether inside-the-artery clot removal will work.

“If successful, the THERAPY trial will help to identify a patient population most likely to benefit from interventional therapy, as well as reveal a treatment paradigm that may have a true impact on improving the standard of care for ischemic stroke patients,” Mocco said.

“Acute stroke intervention technology has grown by leaps and bounds. In fact, it has only been in the past decade that any technology has been available to mechanically remove clots causing stroke,” Mocco said.

Solitaire™ FR Revascularization Device

Cool video at the link, I do wonder if  this is better than tPA
http://www.ev3.net/neuro/intl/flow-restoration/solitaire-fr-revascularization-device.htm

Proteome Sciences Providing Biomarker Analysis for $14.6M Stroke Initiative

So I wonder which model of hypothermia they will use and if they will use the drug that stops the shivering.
http://www.genomeweb.com/proteomics/proteome-sciences-providing-biomarker-analysis-146m-stroke-initiative
Proteome Sciences today said that it will be performing biomarker analysis for a new European research initiative to study hypothermia as a treatment after stroke.

The research project, called EuroHyp-1, is a phase III clinical trial and today its leaders announced an €11 million ($14.6 million) grant from the European Commission under the Seventh Framework Programme to fund research involving 1,500 stroke victims to determine if cooling the brain within six hours of a stroke can effectively treat such patients. In pilot studies, the method has shown to be "remarkably effective," as a treatment, EuroHyp-1 said.

As part of the project, UK-based Proteome Sciences will use its mass spectrometry-based assays to perform biomarker analysis of patient samples in blood, the company said.

The trial funded by today's grant involves 60 universities and hospitals in 25 countries and seeks to recruit patients who have had an acute ischemic stroke. A particular focus will be on those without a "truly effective treatment or who exhibit limited response to the existing standard interventions," EuroHyp-1 said in a statement.

Cooling the brain after cardiac arrest and birth injuries is already used to reduce ischemic brain injury. It acts by inducing a form of hibernation of the brain, "minimizing the need for oxygen and preventing further damage," EuroHype-1 said, and added that the European Space Agency is interested in the method for its potential use in long distance space travel.

The two methods here:
http://oc1dean.blogspot.com/2011/10/hypothermia-supplies-for-strokes.html
http://oc1dean.blogspot.com/2011/06/brain-cooling-and-stroke-recovery.html
The drug for body temperature regulation here:
http://oc1dean.blogspot.com/2012/02/cool-aid-drug-that-lets-body.html

Athersys, University Hospitals partner for clinical trials of MultiStem for stroke

Earlier I posted about using this for TBI. I can't tell if this is for chronic or acute. I do wonder how they plan to get thru the blood-brain barrier. Everyone should clamor to get involved.
http://www.medcitynews.com/2011/09/athersys-reveals-plans-for-phase-2-stroke-clinical-trial/
Stem cell developer Athersys (NASDAQ:ATHX) has taken the next of many steps toward commercializing its MultiStem therapy for stroke, the most promising application for the therapy.

The Cleveland-based company detailed its plans for a phase 2 ischemic stroke clinical trial that’s estimated to involve about 140 patients, according to ClinicalTrials.gov, a website maintained by the National Institutes of Health.

The double-blind, randomized, placebo-controlled study is designed to evaluate the safety and effectiveness of treating stroke patients with MultiStem, an off-the-shelf stem cell treatment derived from the bone marrow of adults or other nonembryonic sources.

The trial is scheduled to start enrollment this month, with October 2013 estimated as the time frame for final data collection. The trial is expected to be completed by November 2014.

A company official declined comment.

The company believes MultiStem could represent a significant advancement in treating ischemic stroke patients. The technology has shown promise in reducing inflammation, protecting damaged tissue and forming new blood vessels.

Ischemic stroke is caused by a blood clot in the brain and accounts for 87 percent of all stroke cases.

As for the reason that stroke is the most promising application of MultiStem — which is also being investigated for the treatment of heart attack, inflammatory bowel disease, orthopedics and blood diseases — it’s simple: stroke represents the largest market.

CEO Gil Van Bokkelen has pegged the potential stroke market at $15 billion.

Still, the company faces a long, bumpy road to commercialization, with any application of MultiStem unlikely to hit the market for at least four or five years.

Thrombin Activity Associated with Neuronal Damage during Acute Stage of Ischemic Stroke

A new hyperacute damage finding.
http://www.eurekalert.org/pub_releases/2012-02/cmc-ais013112.php
After ischemic stroke – the type caused by a clogged artery but with no bleeding into the brain – a normal protein that plays a positive role in blood clotting escapes intact arteries and seriously damages healthy brain cells. Scientists previously knew that thrombin leaked out during hemorrhagic strokes, and large amounts of the protein killed neurons. In new studies, researchers found thrombin in the brain after ischemic stroke; injecting a drug to counter the effects of thrombin improved stroke symptoms. Patrick D. Lyden, MD, chair of the Department of Neurology, the Carmen and Louis Warschaw Chair in Neurology at Cedars-Sinai and senior author of the poster presentation abstract, is available for interviews.

Genetic variant increases risk of common type stroke

Since I had a large ischemic stroke I should be contacted for testing to see if my genetic makeup would prove the theory. But since there is no central place for stroke info to be consolidated this means we are all on our own. If survivors were in charge there wouldn't be these holes in information.
www.sciencecodex.com/genetic_variant_increases_risk_of_common_type_stroke-85446

A genetic variant that increases the risk of a common type of stroke has been identified by scientists in a study published online in Nature Genetics today. This is one of the few genetic variants to date to be associated with risk of stroke and the discovery opens up new possibilities for treatment.

Stroke is the second leading cause of death worldwide (more than one in 10 of all deaths, and over six million deaths annually), and also in developed countries is a major cause of chronic disability. As the world's populations age the impact of stroke on wellbeing is likely to increase further.

Several different mechanisms underlie strokes. One of the most common types is when blood flow is impaired because of a blockage to one or more of the large arteries supplying blood to the brain – large artery ischemic stroke. This accounts for over a third of all strokes.

Researchers from St George's, University of London and Oxford University, working with scientists from Europe, America and Australia, in one of the largest genetic studies of stroke to date, compared the genetic make-up of 10,000 people who had suffered from a stroke with 40,000 healthy individuals. The study was funded by the Wellcome Trust.

The researchers discovered an alteration in a gene called HDAC9 which affects a person's risk of large artery ischemic stroke. This variant occurs on about 10 per cent of human chromosomes. Those people who carry two copies of the variant (one inherited from each parent) have nearly twice the risk for this type of stroke compared to those with no copies of the variant.

The protein produced by HDAC9 is already known to play a role in the formation of muscle tissue and heart development. However, the exact mechanism by which the genetic variant increases the risk of stroke is not yet known. A better understanding of the mechanism could lead to new drugs to treat or prevent stroke; however, the researchers stress that this is still some way off.

Professor Hugh Markus, from St George's, University of London, who co-led the study says: "This discovery identifies a completely new mechanism for causing stroke. The next step is to determine in more detail the relationship between HDAC9 and stroke and see whether we can develop new treatments that reduce the risk of stroke. Interestingly, there are already drugs available which inhibit the HDAC9 protein. However, it is important that we understand the mechanism involved before trialling the effects of these drugs on stroke."

The researchers went on to show that the new variant does not have the same effect on the risk of other types of stroke which include bleeding in the brain (haemorrhagic stroke).

Professor Peter Donnelly, Director of the Wellcome Trust Centre for Human Genetics in the University of Oxford, who co-led the study, says: "Our study shows that the different subtypes of stroke could involve quite different genetic mechanisms. This is really fascinating, and if it holds up more generally, will move us closer to personalised medicine, where treatments and preventions can be tailored more precisely to individual patients."

Dr Peter Coleman, Deputy Director of Research at The Stroke Association, who funded collection of some of the samples used in this study, said:

"Over a third of strokes are caused by a blockage in one of the large blood vessels supplying blood to the brain (large artery stroke). Findings from this ground breaking study appear to show a genetic link which may affect a person's risk of large vessel stroke. Further study is needed, but this research could potentially lead to new methods of screening and prevention for large vessel stroke, and ultimately, new methods of treatment."

Biomarker for acute ischemic stroke shows promise

This one takes 24 hours to determine you had an ischemic strokewhat about a bleeder?
And detecting acrolein can be done in 30 minutes in an earlier post of mine.
Or measure levels of a brain chemical called glutamate within an hour in an earlier post of mine.
Acrolin:
http://oc1dean.blogspot.com/2011/07/detecting-possible-stroke-biomarker-in.html
Glutamate:
http://www.webmd.com/stroke/news/20110929/blood-test-may-help-spot-stroke

Biomarker here: http://www.theheart.org/article/1294591.do
Increased NR2 peptide levels accurately identify patients with acute ischemic stroke within 24 hours of symptom onset and correlate with neuroimaging findings, results of a pilot study suggest [1].

The NR2 peptide may improve the diagnosis and management of patients presenting with acute stroke symptoms, the researchers conclude.

"I think this can be a very meaningful test," said Dr Kerstin Bettermann (Penn State College of Medicine, Hershey), who reported the results here at the American Neurological Association 2011 Annual Meeting.

The NR2 peptide, a proteolytic breakdown product of the brain-specific NMDA receptor, is an indicator of damage to the blood-brain barrier that follows an acute cerebral ischemic event. The peptide is rapidly released into the bloodstream during acute brain ischemia.

The pilot study involved 50 adults with acute ischemic stroke confirmed by either head CT or brain MRI within 24 hours of symptom onset and 102 age- and gender-matched controls. The control group consisted of 26 healthy adults, 48 adults with vascular risk factors including diabetes and hypertension but no history of stroke or transient ischemic attack (TIA), and 28 adults with "stroke mimics" such as migraine, meningitis, palsies, and intracranial hemorrhage due to aneurysm rupture. NR2 peptide levels were measured within 24 hours from symptom onset.

Healthy controls and those with vascular risk factors had NR2 peptide concentrations <0.25 and <0.4 mcg/L, respectively, while those with stroke mimics had mean concentrations of 0.5 mcg/L.

In contrast, acute ischemic stroke patients had concentrations that were significantly higher (>0.5 mcg/L) compared with all control groups (p<0.0001). The highest NR2 peptide levels were seen within 12 hours, with peak concentrations at one to three hours after symptom onset (mean 25.44 mcg/L; range 1.46-86.70 mcg/L).

At a cutoff point of 0.5 mcg/L, the NR2 peptide test had high diagnostic sensitivity, indicating true positive diagnosis of ischemic stroke, high specificity, meaning the correct identification of stroke mimics, and positive and negative predictive values, signifying the proportion of subjects with positive/negative NR2 peptide elevations who are correctly diagnosed.

Test performance at a cutoff point of 0.5 mcg/L

Performance measure	% (95% CI)
Sensitivity	98 (89.4-99.9)
Specificity	86.3 (78-92.3)
Positive predictive value	78 (65.5-87.3)
Negative predictive value	98.9 (93.9-99.9)

The results also suggested a significant correlation between NR2 peptide levels and cortical lesion size (<200 cc). However, researchers say this finding requires further validation.

"This is a simple test to do, and the preliminary data look excellent," Bettermann said. "The real key now is to validate it in a larger study population and we have applied to [the National Institutes of Health] NIH for funds to do this. . . . Ideally this is something you could do in the emergency room or even in the ambulance; it could be developed into a point-of-care finger stick test."

It might also be useful not only for stroke, but for transient ischemic attack. "In another study, we have some preliminary data that look promising," Bettermann noted.