International Stroke Conference Digest - February 20, 2008 - (Page 8) 2008 isc digest | New Orleans | februAry 20 Symposium to explore the future of brain repair after stroke new and emeRging foRms of brain therapy that focus on repairing damage after stroke will be discussed this morning in a symposium titled “Clinical Approaches to Brain Repair after Stroke.” The session begins at 7:30 a.m. Hall B 2-2. Moderators Steven C. Cramer, MD, FAHA, and Sean I. Savitz, MD, FAHA, will join two other specialists in presenting a panoramic view of what the future holds in the field of stroke therapy. “Most of the time in stroke, we’ve been talking about clot-busters that open up a blocked pipe, or neuroprotectants, which help injured tissues survive the acute insult,” said Dr. Cramer, who is Associate Professor of Neurology and Anatomy & Neurobiology at the University of California, Irvine, and the Director of the school’s Clinical Stroke Program. “This is more about restoring brain function after the injury is already fixed and the dust is settled.” The session will address therapies that are being proven in the lab, as well as some in late-phase clinical trials on their way to becoming standards in a field where there really are no approved therapies for brain repair after stroke. “It is a critical area of research because of all the people who are disabled by stroke; it’s the leading cause of adult disability,” said Dr. Savitz. “Physical therapy is helpful but limited.” Following a stroke, patients survive an average of eight years with the disabilities caused by their stroke, motivating the search for ways to improve behavioral function after the injury has settled. “Lots of studies out there support the conclusion that restorative therapies can make an impact even when initiated days, weeks, or months after the injury is fixed,” Dr. Savitz, who is Co-director of the don’t know why,” Dr. Savitz said. “But that Dr. Cramer said. “I will tell clinicians to keep their eyes open because I don’t think it will Vasc u la r Neu rolog y P rogra m at t he is what we observed: People who were be long before one of these approaches, or University of Texas Houston Medical years out and their strokes had stabilized some combination of these approaches, is School, will discuss cell therapy, which and there was nothing more available to is primarily still a laboratory research them, with their physical therapy no longer standard of care.” All of these emerging therapies have concept with great potential for restorative working, and they had these transplants and some of them got better.” reached human trials to some extent, brain therapy Physical therapist and this session will Carolee J. Winstein, review the available PhD, PT, FAPTA, will data. discuss some cases of A lso during the improvement in stroke session, Dr. Cramer patients who had will discuss the efconst ra i nt-i nduced fect of altering neumovement t herapy rotransmitter levels (CIMT). on the repair of the brain after stroke. Spec i f ica l ly, she While the modulawill discuss the results tion of neurotransmitof the Ex trem it y ters is widely known Constra i nt-Induced to influence a number Therapy Evaluation of brain behaviors, it (EXCITE) clinical study has not been studied publ ished i n 2006. extensively in stroke. Th is st udy showed Steven C. Cramer, MD, FAHA Sean I. Savitz, MD, FAHA Dr. Cramer said there t hat t wo weeks of has been some indicaCIMT garnered major “It’s a relatively new field for stroke improvements that lasted more than a tion that increasing serotonin or dopamine may be of value in restorative therapy after recovery. I’m going to give an overview of year. why we would even think of doing this stroke, but it’s been studied very little. D r. W i n s t e i n i s a P r o f e s s o r o f “There’s pretty good evidence that if approach and where we are at this point, Biokinesiology and Physical Therapy at you hit the nervous system’s chemical which is really still in its infancy,” said Dr. the University of Southern California, components in just the right way you can Savitz, who is directing a translational Los Angeles. She’s also the Director of the make some behaviors get better and some research initiative in neuroprotection Motor Behavior and Neurorehabilitation behaviors get worse,” said Dr. Cramer, who and cell therapy for acute stroke. He is Laboratory at USC. is also Associate Clinical Director for the the recipient of an AHA Fellow to Faculty And finally, Leonardo Cohen, MD, will UCI Stem Cell Research Center and Director Transition Award and is a Howard Hughes discuss electromagnetic brain stimulation of the Neuroimaging Core of the Institute Early Career Investigator. as a restorative therapy after stroke. In his talk, Dr. Savitz will present the for Clinical Translational Science. Dr. Cohen is Senior Investigator for Dr. Cramer added that in clinical trials animal data available, as well as what has the Nationa l Institutes of Hea lth in there has been evidence that chemical been done in humans, and look at what the neuroscience and an elected member of modulators and the behavioral effects data suggests about cell therapy as a viable the American Neurological Association. they produce are definitely associated with therapy in brain recovery. A device for electromagnetic stimulation “There are patients who underwent of the brain is currently in phase three changes in brain function. “So in the last few years we’ve seen some exciting proof- pig cell transplantation, and some of those trials, and may be approved for use in the patients got better. On the other hand, we near future. of-concept studies,” he said. Alzheimer’s continued from page 1 cannot ignore this emerging reality.” The other side of the coin is that Alzheimer’s disease can cause stroke, Dr. Black noted. “Amyloid is a protein deposited in the brain in patients with Alzheimer’s disease, and it can also be deposited around the vessels, making the vessels friable and prone to bleed,” she explained. “Amyloid angiopathy is becoming a leading cause of cerebral hemorrhage.” Also during today’s symposium, David F. Cechetto, PhD, from London, Ontario, will discuss an animal model of amyloid toxicity in stoke and its implications. “People will find this research quite interesting and perhaps alarming. It appears that stroke has much more malignant outcome in transgenic animal models of Alzheimer’s disease,” Dr. Black said. Glenn Stebbins, PhD, from Chicago, will describe some imaging studies of white matter in patients with vascular cognitive impairment compared with those with Alzheimer’s disease. Christophe Tzourio, MD, PhD, from Paris, will address the epidemiology of mixed Alzheimer’s disease and cerebrovascular disease and describe trials in which antihypertensive treatment reduced the emergence of dementia. Finally, Dr. Black will discuss treatment options for patients with mixed Alzheimer’s disease and cerebrovascular disease. “Specific treatments for vascular dementia have not been approved by the FDA, but cogn itive en hancing agents are sometimes used off label. Studies show that cholinesterase inhibitors can be beneficial in mixed Alzheimer’s and cerebrovascular disease, and they suggest the drugs have modest cognitive benefits in patients with vascular dementia. I’ll summarize these studies,” Dr. Black said. “I’ll also talk about disease-modifying drugs in the pipeline for Alzheimer’s disease because they will be important for patients with mixed dementia as well. Some new anti-amyloid approaches look promising,” Dr. Black added. ISC Digest is published by TriStar Publishing, Inc. as a service to the attendees of the International Stroke Conference. ®2008, TriStar Publishing, Inc. 7285 W. 132nd Street, Suite 300 Overland Park, KS 66213 Phone: (913) 491-4200 Fax: (913) 491-4202 www.tristarpub.com http://www.tristarpub.com
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