Jun 8, 2018
The first SAFE Regional Conference this year gathered 20 participants from organisations covering Spain, Catalonia, Norway, Finland, Portugal, Greece, Iceland, Turkey, Israel and Latvia.
The agenda was focused on SAFE’s activities in 2017 and 2018, with a special emphasis on current SAFE projects, such as the Stroke Action Plan for Europe 2018-2030, SAFE Angels Initiative, Life with Spasticity and the new upcoming project for raising awareness on stroke risk factors, Stop Stroke from Happening.
Jon Barrick, SAFE President gave an interesting overview of SAFE political activities aimed towards politicians and EU policy makers, shortly reflecting the Burden of Stroke Report presented in 2017 and how it led to the Stroke Action Plan document, in cooperation with ESO. The full document of the Stroke Action Plan for Europe 2018-2030 is expected to be released for public by September this year.
A special session of the meeting were dedicated to the World Stroke Campaign 2018 and it’s topic, Life After Stroke, as it is closely tied to SAFE’s core goals, such as improving life conditions and level of care for people who survived stroke and their families.
SAFE Project and Operations Manager, Victoria Brewer, gave an update on SSOFT project and helped participants perform a user testing of the existing SSOFT Modules 1 and 2.
Harriklia Proios, SAFE Board member from Greece, presented and update on EU funded research projects in which SAFE is involved as a member of consortium. Once again, the importance of research dissemination was stressed out, explaining why SAFE members should continue to take active part in dissemination activities.
SAFE Board member from Israel, Pnina Rosenzveig chaired a session with individual SSO’s feedback on national activities and next steps.
Finally, SAFE had a guest workshop held by our sponsorship partner Boehringer Ingelheim. The workshop was about the next steps in the Angels Initiative project development, with a special focus on new and exciting branding ideas and approaches for a sustainable stroke awareness education of the target audience.
SAFE is appreciating support from the company Boehringer Ingelheim, given to us through an unconditional educational grant. The Boehringer Ingelheim is a sponsor of all this year’s Regional Conferences, the one just being held in Madrid, but also the upcoming two in Dublin (21st June) and Prague (28th June 2018).
Jun 8, 2018
First appeared on ScienceDaily.com
More than 2.5 million Americans are living with Atrial Fibrillation (AFib). AFib is an irregular heartbeat that can lead to blood clots, stroke, heart failure and other heart-related complications.
What doctors and researchers currently understand about treating AFib stems mainly from whether a patient has been diagnosed with the condition or not. University of Minnesota researchers are urging the medical community to take a closer look, specifically at AFib burden.
AFib burden refers to the amount of AFib that an individual has. The goal of the scientific statement published in the American Heart Association’s journal Circulation is to increase knowledge and awareness by healthcare professionals of effective, state-of-the-art science related to the causes, prevention, detection, management, and future research needs related to AFib burden.
“We hope to bring awareness to this concept of measuring the AFib burden and then to outline what we know about it,” said Lin Yee Chen, MD, MS, tenured associate professor, Department of Medicine at the University of Minnesota Medical School, “the hope then is to use that knowledge so more research can be done to fill in those gaps.”
AFib is associated with an elevated risk of stroke, and this statement also pushes for more research to refine risk classifications for stroke. Further understanding the relationship between AFib pattern or burden and stroke risk might result in deeper insights into stroke prevention.
“We could see an enormous benefit to our patient population once these standards are applied. And now is the time to do so,” said Chen.
Story Source: University of Minnesota Medical School. “A deeper understanding of AFib could lower risk.” ScienceDaily. ScienceDaily, 6 June 2018. <www.sciencedaily.com/releases/2018/06/180606143719.htm>.
Jun 7, 2018
A massive and extremely slow change in electrical potential is evidence of irreparable damage
First appeared on ScienceDaily.com
Researchers from Charité — Universitätsmedizin Berlin have analyzed the underlying electrophysiological indicators of subarachnoid hemorrhage, the second most common type of brain hemorrhage that can lead to ischemic stroke within a matter of days. Their findings, which have been published in the journal Brain, may lay the foundations for new stroke treatments.
Subarachnoid hemorrhage is a type of brain bleed that occurs in the area between the membranes surrounding the brain. Patients with subarachnoid hemorrhage can develop complications within approximately one week. Between one in three and one in four patients will develop symptoms of ischemic stroke, a type of stroke caused by an inadequate blood supply. This phenomenon occurs as the result of mechanisms triggered by the molecular breakdown products of the patient’s earlier hemorrhagic stroke. It sets off a wave of electrochemical depolarization, or ‘spreading depolarization’, within the brain tissue. Affected areas of the brain require large amounts of energy in order to restore normal conditions.
In healthy brains, this depolarization of nerve cells is linked to blood supply, meaning blood vessels widen in areas of the brain that are active. However, a subarachnoid hemorrhage may disrupt the signaling cascades between nerve cells and blood vessels, so that the depolarization of nerve cells causes extreme constriction of the blood vessels, which leads to spreading ischemia. Deprived of energy, the nerve cells are incapable of restoring normal electrochemical gradients. If depolarization persists for too long, affected nerve cells will begin to die off. Measurements of the electrical brain potential will then show an extreme and very gradual change , a process known as ‘negative ultraslow potential’, which is indicative of ‘terminal spreading depolarization’.
“Two months ago, we were able to show for the first time that terminal spreading polarization occurs in humans — namely in patients who had suffered cardiac arrest. Now we have been able to show that it also occurs in patients with cerebral infarctions after subarachnoid hemorrhage,” explains Prof. Dr. Jens Dreier of Charité’s Center for Stroke Research Berlin (CSB). Prof. Dreier and his team analyzed data from 11 patients, comparing their findings with results obtained from animal experiments. The waves of depolarization observed indicate disturbances of energy metabolism. The ‘negative ultraslow potential’ constitutes the electrophysiological correlate of infarction, and of tissue death due to an inadequate supply of blood.
Prof. Dreier emphasizes: “Measurements of spreading depolarization may prove as important to the development of interventions for patients with stroke, global ischemia and traumatic brain injury, as similar electrophysiological tools have proved in the past, in the areas of epilepsy or cardiology — because they make the underlying causes visible.”
Story Source: Charité – Universitätsmedizin Berlin. “Electrophysiological sign of cerebral infarction identified: A massive and extremely slow change in electrical potential is evidence of irreparable damage.” ScienceDaily. ScienceDaily, 29 May 2018. <www.sciencedaily.com/releases/2018/05/180529132142.htm>.
Jun 4, 2018
Written by Jelena Misita, SAFE Awareness and Advocacy Manager
Prof. Valery Feigin, photo credits: www.stroke.net.nz
I first met Prof. Valery Feigin in person in Gothenburg this May, when he visited SAFE stand at ESOC 2018. I knew him, of course, from the literature, with his name coming across many references. According to his official biography, this was hardly any wonder, as he had published over 600 research articles over his career and his publications have been cited over 30,000 times, within his prime research interest fields- prevention and management of stroke, epidemiology and traumatic brain injury.
Imagine my surprise when he suddenly appeared at a patient support organisation stand, shook my hand and said he’s started a website for patient support in New Zealand. I just had to tell him that in stroke world, he is nothing short of a celebrity and that we will be honoured to help him spread the news about his latest project. The project is in fact being realised through the New Zealand Stroke Education Trust, a charitable organisation based in New Zealand.
We set up an interview and I used the opportunity to ask him not only about his current project, but also about his view on the Stroke Action Plan for Europe 2018-2030, ICD-11 and how could these things lead to a real-life impact on stroke prevention, treatment and after-care. (more…)
Jun 2, 2018
Replacement neurons, blood vessels fill in stroke cavity; gel provides scaffolding
First appeared on ScienceDaily.com
In a first-of-its-kind finding, a new stroke-healing gel helped regrow neurons and blood vessels in mice with stroke-damaged brains, UCLA researchers report in the May 21 issue of Nature Materials.
“We tested this in laboratory mice to determine if it would repair the brain in a model of stroke, and lead to recovery,” said Dr. S. Thomas Carmichael, Professor and Chair of neurology at UCLA. “This study indicated that new brain tissue can be regenerated in what was previously just an inactive brain scar after stroke.”
The results suggest that such an approach may someday be a new therapy for stroke in people, said Dr. Tatiana Segura, a former Professor of Chemical and Biomolecular Engineering at UCLA who is now a professor at Duke University. Carmichael and Segura collaborated on the study.
The brain has a limited capacity for recovery after stroke and other diseases. Unlike some other organs in the body, such as the liver or skin, the brain does not regenerate new connections, blood vessels or new tissue structures. Tissue that dies in the brain from stroke is absorbed, leaving a cavity, devoid of blood vessels, neurons or axons, the thin nerve fibers that project from neurons.
To see if healthy tissue surrounding the cavity could be coaxed into healing the stroke injury, Segura engineered a gel to inject into the stroke cavity that thickens to mimic the properties of brain tissue, creating a scaffolding for new growth.
The gel is infused with molecules that stimulate blood vessel growth and suppress inflammation, since inflammation results in scars and impedes regrowth of functional tissue.
After 16 weeks, stroke cavities in mice contained regenerated brain tissue, including new neural networks — a result that had not been seen before. The mice with new neurons showed improved motor behavior, though the exact mechanism wasn’t clear.
“The new axons could actually be working,” said Segura. “Or the new tissue could be improving the performance of the surrounding, unharmed brain tissue.”
The gel was eventually absorbed by the body, leaving behind only new tissue.
This research was designed to explore recovery in acute stroke, or the period immediately following stroke — in mice, that is five days; in humans, that is two months. Next, Carmichael and Segura are determining if brain tissue can be regenerated in mice long after the stroke injury. More than 6 million Americans are living with the long-term outcomes of stroke, known as chronic stroke.
Story Source: University of California – Los Angeles. “Mice regrow brain tissue after stroke with bioengineered gel: Replacement neurons, blood vessels fill in stroke cavity; gel provides scaffolding.” ScienceDaily. ScienceDaily, 21 May 2018. <www.sciencedaily.com/releases/2018/05/180521131811.htm>.
