At least we have one state that is working in the right direction. I have no idea how to influence this agency to work on neurons. California readers, some help here.
http://blogs.nature.com/news/2012/05/california-stem-cell-agency-shifts-toward-clinical-work.html
I only copied the first 4 paragraphs.
The California Institute of Regenerative Medicine (CIRM) voted on 24 May to accept a new strategic plan which
shrinks or eliminates support for basic research, facilities and
training, while funneling more of its funds toward clinical development.
“The first stage of CIRM was really exploring the field,” said Ellen
Feigal, senior vice president of R&D. “The next five years should be
one of more focus.” By July 2013, the agency hopes to have two
programmes approved for clinical trials in the United States.
During the past five years, nearly half of the approximately $1.3
billion awarded by the agency went toward building new research
facilities and training and career development. Looking ahead, of the
approximately $840 million to be awarded over the next five years,
about three fifths is slotted to go toward development research,
preparing stem cell-based therapeutics for clinical testing, with much
of the rest devoted to translational and basic research. (An additional
$650 million has been approved but not awarded; allocation is roughly an
average between previously awarded funds and future plans.)
No one spoke during a call for comments from the general public, and
the plan was approved by a voice vote with no objections. Board member
Jeff Sheehy voiced concerns about cutting off training and basic
research. CIRM president Alan Trounson and Ellen Feigal said that the
exact allocations could be determined at future meetings. There was
general acknowledgement that difficult funding decisions are ahead. “We
are now in the realm of trade-offs,” said Sheehy.
Also today, CIRM announced $69 million
of grants for translational research. “With these new awards, the agency
now has 52 projects in 33 diseases at varying stages of working toward
clinical trials,” said Jonathan Thomas, governing board chair, said in a
statement.
Friday, May 25, 2012
Thursday, May 24, 2012
Tired neurons caught nodding off in sleep-deprived rats
So maybe you don't really have cognitive problems after stroke, you just need enough sleep. Challenge your doctor on this one, see how up-to-date they are. I never got enough sleep in the hospital, every morning someone in my 4plex would get a blood draw at 7 am.
http://www.nih.gov/news/health/apr2011/nimh-27.htm
A new study in rats is shedding light on how sleep-deprived lifestyles might impair functioning without people realizing it. The more rats are sleep-deprived, the more some of their neurons take catnaps — with consequent declines in task performance. Even though the animals are awake and active, brainwave measures reveal that scattered groups of neurons in the thinking part of their brain, or cortex, are briefly falling asleep, scientists funded by the National Institutes of Health have discovered.
"Such tired neurons in an awake brain may be responsible for the attention lapses, poor judgment, mistake-proneness and irritability that we experience when we haven't had enough sleep, yet don’t feel particularly sleepy," explained Giulio Tononi, M.D., Ph.D., of the University of Wisconsin-Madison. "Strikingly, in the sleep-deprived brain, subsets of neurons go offline in one cortex area but not in another — or even in one part of an area and not in another."
Tononi and colleagues report their findings online in the April 28, 2011 issue of the journal Nature. Their study was funded in part by the NIH’s National Institute of Mental health and a NIH Director's Pioneer Award, supported through the Common Fund, and administered by NIMH and the National Institute on Neurological Disorders and Stroke.
Previous studies had hinted at such local snoozing with prolonged wakefulness. Yet little was known about how underlying neuronal activity might be changing.
To learn more, the researchers tracked electrical activity at multiple sites in the cortex as they kept rats awake for several hours. They put novel objects into their cages — colorful balls, boxes, tubes and odorous nesting material from other rats. The sleepier the rats got, more subsets of cortex neurons switched off, seemingly randomly, in various localities. These tired neurons' electrical profiles resembled those of neurons throughout the cortex during NREM or slow wave sleep. Yet, the rats overall EEG, a measure of brain electrical activity at the scalp, confirmed that they were awake, as did their behavior. So neuronal tiredness differs from more overt microsleep – 3-15-second lapses with eyes closing and sleep-like EEG — that is sometimes experienced with prolonged wakefulness. It is more analogous to local lapses seen in some forms of epilepsy, suggest the researchers.
However subtle, having tired neurons did interfere with task
performance. If neurons switched off in the motor cortex within a split
second before a rat tried to reach for a sugar pellet, it decreased its
likelihood of success by 37.5 percent. And the overall number of such
misses increased significantly with prolonged wakefulness. This suggests
that tired neurons, and accompanying increases in slow wave activity,
might help to account for the impaired performance of sleep-deprived
people who may seem behaviorally and subjectively awake.
Subsets of neurons going offline with longer wakefulness is, in many ways, the mirror image of progressive changes that occur during recovery sleep following a period of sleep deprivation. Tononi suggests that both serve to maintain equilibrium — part of the compensatory mechanisms that regulate sleep need. Just as sleep deprivation produces a brain-wide state of instability, it may also trigger local instability in the cortex, possibly by depleting levels of brain chemical messengers. So, tired neurons might nod off as part of an energy-saving or restorative process for overloaded neuronal connections.
"Research suggests that sleep deprivation during adolescence may have adverse emotional and cognitive consequences that could affect brain development," noted NIMH Director Thomas R. Insel, M.D. “"The broader line of studies to which this belongs, are, in part, considering changes in sleep patterns of the developing brain as a potential index to the health of neural connections that can begin to go awry during the critical transition from childhood to the teen years."
The mission of the NIMH is to transform the understanding and treatment of mental illnesses through basic and clinical research, paving the way for prevention, recovery and cure. For more information, visit the NIMH website.
NINDS (www.ninds.nih.gov) is the nation's leading funder of research on the brain and nervous system. The NINDS mission is to reduce the burden of neurological disease — a burden borne by every age group, by every segment of society, by people all over the world.
About the National Institutes of Health (NIH): NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit www.nih.gov.
http://www.nih.gov/news/health/apr2011/nimh-27.htm
A new study in rats is shedding light on how sleep-deprived lifestyles might impair functioning without people realizing it. The more rats are sleep-deprived, the more some of their neurons take catnaps — with consequent declines in task performance. Even though the animals are awake and active, brainwave measures reveal that scattered groups of neurons in the thinking part of their brain, or cortex, are briefly falling asleep, scientists funded by the National Institutes of Health have discovered.
"Such tired neurons in an awake brain may be responsible for the attention lapses, poor judgment, mistake-proneness and irritability that we experience when we haven't had enough sleep, yet don’t feel particularly sleepy," explained Giulio Tononi, M.D., Ph.D., of the University of Wisconsin-Madison. "Strikingly, in the sleep-deprived brain, subsets of neurons go offline in one cortex area but not in another — or even in one part of an area and not in another."
Tononi and colleagues report their findings online in the April 28, 2011 issue of the journal Nature. Their study was funded in part by the NIH’s National Institute of Mental health and a NIH Director's Pioneer Award, supported through the Common Fund, and administered by NIMH and the National Institute on Neurological Disorders and Stroke.
Previous studies had hinted at such local snoozing with prolonged wakefulness. Yet little was known about how underlying neuronal activity might be changing.
To learn more, the researchers tracked electrical activity at multiple sites in the cortex as they kept rats awake for several hours. They put novel objects into their cages — colorful balls, boxes, tubes and odorous nesting material from other rats. The sleepier the rats got, more subsets of cortex neurons switched off, seemingly randomly, in various localities. These tired neurons' electrical profiles resembled those of neurons throughout the cortex during NREM or slow wave sleep. Yet, the rats overall EEG, a measure of brain electrical activity at the scalp, confirmed that they were awake, as did their behavior. So neuronal tiredness differs from more overt microsleep – 3-15-second lapses with eyes closing and sleep-like EEG — that is sometimes experienced with prolonged wakefulness. It is more analogous to local lapses seen in some forms of epilepsy, suggest the researchers.
Rats with objects introduced into their cages to keep them awake. Source: Giulio Tononi, M.D., Ph.D., University of Wisconsin-Madison
Subsets of neurons going offline with longer wakefulness is, in many ways, the mirror image of progressive changes that occur during recovery sleep following a period of sleep deprivation. Tononi suggests that both serve to maintain equilibrium — part of the compensatory mechanisms that regulate sleep need. Just as sleep deprivation produces a brain-wide state of instability, it may also trigger local instability in the cortex, possibly by depleting levels of brain chemical messengers. So, tired neurons might nod off as part of an energy-saving or restorative process for overloaded neuronal connections.
"Research suggests that sleep deprivation during adolescence may have adverse emotional and cognitive consequences that could affect brain development," noted NIMH Director Thomas R. Insel, M.D. “"The broader line of studies to which this belongs, are, in part, considering changes in sleep patterns of the developing brain as a potential index to the health of neural connections that can begin to go awry during the critical transition from childhood to the teen years."
The mission of the NIMH is to transform the understanding and treatment of mental illnesses through basic and clinical research, paving the way for prevention, recovery and cure. For more information, visit the NIMH website.
NINDS (www.ninds.nih.gov) is the nation's leading funder of research on the brain and nervous system. The NINDS mission is to reduce the burden of neurological disease — a burden borne by every age group, by every segment of society, by people all over the world.
About the National Institutes of Health (NIH): NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit www.nih.gov.
Enabling Fluent Speech in Non-Fluent Aphasia
A great TEDx talk, 15 minutes, sounds like action observation for aphasia
TEDx Columbia, SC - Dr. Julius Fridriksson, Director of the Aphasia Laboratory at the University of South Carolina
http://www.youtube.com/watch?v=Cy6S7aMmUYo&feature=colikeRadically New Patented Technology Highly Effective In Reducing Cerebral Oedema
Sounds fascinating to be able to get unwanted fluid back into the bloodstream. Would it help me drain all my cerebrospinal fluid from my dead area so I can start angiogenesis and create a substrate for my migrating neurons?
Radically New Patented Technology Highly Effective In Reducing Cerebral Oedema
Researchers at Trinity College Dublin have reported the results of groundbreaking research into the prevention of cerebral oedema or swelling of the brain, a major cause of death in people who have sustained a traumatic injury to the brain, out of hospital cardiac arrest or stroke. The research, which is published this week in the international journal, Nature Communications, uses a radically new patented technology, developed in Ireland and termed, 'Neuronal Barrier Modulation' which has been shown in an animal model simulating human brain swelling, to be highly effective in reducing the dangerous effects of this condition, while improving cognitive outcome. The research was sponsored by the US Department of Defense and Enterprise Ireland.The researchers have devised a method of safely manipulating the blood vessels in the brain to allow for periodic opening of tight junction channels between cells lining the vessels. A simple medication can be injected into a peripheral vein, rendering the blood vessels in the brain marginally and reversibly permeable to tiny molecules and this procedure allows the fluid in the brain, largely comprising water, to efficiently drain back into the blood.
"Unfortunately, there has been little change in treatment of acute brain swelling over the past 80 years and this is a major cause of mortality in traumatic brain injury (TBI), stroke and out-of-hospital cardiac arrest," says Senior Author of the Nature Communications paper, Dr. Matthew Campbell, of the Ocular Genetics Unit at Trinity College Dublin. "We developed the technique initially for treatment of neuronal edema in cases where injury has occurred to the visual cortex, the region of the brain involved in vision, in view of our Unit's profile in vision research, however, the same method can be used in alleviating edema in all parts of the brain," says Dr. Campbell.
In Europe alone, brain injuries cause over 66,000 deaths while almost 1.6 million people are admitted to hospital each year. Similar numbers are affected by stroke and cardiac arrest. In fact, more people suffer a traumatic brain injury (TBI) each year than the numbers diagnosed with breast, lung, prostate, brain, and colon cancer combined.
"The medication is based on the use of RNA Interference, a demanding technology which has had a bumpy ride within the pharmaceuticals industry in recent years, and I am delighted that a highly effective and simply deployable therapeutic strategy has emerged based on this technology. There is now a clear path to clinical deployment," says Professor Pete Humphries, Director of the Ocular Genetics Unit at Trinity College Dublin, where the work was carried out.
"Malignant brain swelling as a consequence of cardiac arrest, head injury, stroke, and brain tumours is the single most common factor leading to death in Western society and plays a major role in worsening the outcome of those who survive. Given how common these conditions are, anything that could significantly reduce the effect of brain swelling is likely to have a profound impact on morbidity and mortality and will have reverberations though the public health system," continued co-author, neurologist, Dr Colin Doherty, MD, St James's Hospital, Dublin.
The technology the researchers have reported is planned to enter Phase I clinical trials both here, with neurologist Dr Colin Doherty and in the US along with the team's collaborator, neurosurgeon Professor Gerald Grant, at Duke University and will be developed by the recently established Irish Company, Avena Therapeutics Ltd. Veteran life-science investor and Executive Chairman of the Company, Jeremy L. Curnock Cook says: "This sort of thing doesn't happen too often and we have now been presented with a remarkable and exciting opportunity thanks to the Trinity researchers and their supporters both here and in the US".
Brain white matter tract integrity as a neural foundation for general intelligence
Abstract first then a blogger discussing it. Considering the size of my infarct I have to assume that a large part of my white matter was also destroyed. And if I could find a 3d map of the arteries of the brain I could figure it out. Help here please.
http://www.nature.com/mp/journal/vaop/ncurrent/full/mp201266a.html
General intelligence is a robust predictor of important life outcomes, including educational and occupational attainment, successfully managing everyday life situations, good health and longevity. Some neuronal correlates of intelligence have been discovered, mainly indicating that larger cortices in widespread parieto-frontal brain networks and efficient neuronal information processing support higher intelligence. However, there is a lack of established associations between general intelligence and any basic structural brain parameters that have a clear functional meaning. Here, we provide evidence that lower brain-wide white matter tract integrity exerts a substantial negative effect on general intelligence through reduced information-processing speed. Structural brain magnetic resonance imaging scans were acquired from 420 older adults in their early 70s. Using quantitative tractography, we measured fractional anisotropy and two white matter integrity biomarkers that are novel to the study of intelligence: longitudinal relaxation time (T1) and magnetisation transfer ratio. Substantial correlations among 12 major white matter tracts studied allowed the extraction of three general factors of biomarker-specific brain-wide white matter tract integrity. Each was independently associated with general intelligence, together explaining 10% of the variance, and their effect was completely mediated by information-processing speed. Unlike most previously established neurostructural correlates of intelligence, these findings suggest a functionally plausible model of intelligence, where structurally intact axonal fibres across the brain provide the neuroanatomical infrastructure for fast information processing within widespread brain networks, supporting general intelligence.
Blogger here:
http://theness.com/neurologicablog/index.php/the-aging-brain/
http://www.nature.com/mp/journal/vaop/ncurrent/full/mp201266a.html
General intelligence is a robust predictor of important life outcomes, including educational and occupational attainment, successfully managing everyday life situations, good health and longevity. Some neuronal correlates of intelligence have been discovered, mainly indicating that larger cortices in widespread parieto-frontal brain networks and efficient neuronal information processing support higher intelligence. However, there is a lack of established associations between general intelligence and any basic structural brain parameters that have a clear functional meaning. Here, we provide evidence that lower brain-wide white matter tract integrity exerts a substantial negative effect on general intelligence through reduced information-processing speed. Structural brain magnetic resonance imaging scans were acquired from 420 older adults in their early 70s. Using quantitative tractography, we measured fractional anisotropy and two white matter integrity biomarkers that are novel to the study of intelligence: longitudinal relaxation time (T1) and magnetisation transfer ratio. Substantial correlations among 12 major white matter tracts studied allowed the extraction of three general factors of biomarker-specific brain-wide white matter tract integrity. Each was independently associated with general intelligence, together explaining 10% of the variance, and their effect was completely mediated by information-processing speed. Unlike most previously established neurostructural correlates of intelligence, these findings suggest a functionally plausible model of intelligence, where structurally intact axonal fibres across the brain provide the neuroanatomical infrastructure for fast information processing within widespread brain networks, supporting general intelligence.
Blogger here:
http://theness.com/neurologicablog/index.php/the-aging-brain/
Think you might have Dementia? There's an app for that!
Obviously something for our stroke doctors to give us as a baseline since having a stroke increases your risk of Alzheimers. Who's going to get this into doctor training? A 2 min 10 second video. I don't care if it's the UK, good ideas need to be spread around.
Think you might have Dementia? There's an app for that!
Dietary fat types and 4-year cognitive change in community-dwelling older women
First the abstract and then the blogger explaining it.
http://onlinelibrary.wiley.com/doi/10.1002/ana.23593/abstract
http://onlinelibrary.wiley.com/doi/10.1002/ana.23593/abstract
Abstract
Objective:
A study was undertaken to relate dietary fat types to cognitive change in healthy community-based elders.
Methods:
Among
6,183 older participants in the Women's Health Study, we related intake
of major fatty acids (saturated [SFA], monounsaturated [MUFA], total
polyunsaturated [PUFA], trans-unsaturated) to late-life
cognitive trajectory. Serial cognitive testing, conducted over 4 years,
began 5 years after dietary assessment. Primary outcomes were global
cognition (averaging tests of general cognition, verbal memory, and
semantic fluency) and verbal memory (averaging tests of recall). We used
analyses of response profiles and logistic regression to estimate
multivariate-adjusted differences in cognitive trajectory and risk of
worst cognitive change (worst 10%) by fat intake.
Results:
Higher SFA intake was associated with worse global cognitive (p for linear trend = 0.008) and verbal memory (p
for linear trend = 0.01) trajectories. There was a higher risk of worst
cognitive change, comparing highest versus lowest SFA quintiles; the
multivariate-adjusted odds ratio (OR) with 95% confidence interval (CI)
was 1.64 (1.04–2.58) for global cognition and 1.65 (1.04–2.61) for
verbal memory. By contrast, higher MUFA intake was related to better
global cognitive (p for linear trend < 0.001) and verbal memory (p
for linear trend = 0.009) trajectories, and lower OR (95% CI) of worst
cognitive change in global cognition (0.52 [0.31–0.88]) and verbal
memory (0.56 [0.34–0.94]). Total fat, PUFA, and trans-fat intakes were not associated with cognitive trajectory.
Interpretation:
Higher
SFA intake was associated with worse global cognitive and verbal memory
trajectories, whereas higher MUFA intake was related to better
trajectories. Thus, different consumption levels of the major specific
fat types, rather than total fat intake itself, appeared to influence
cognitive aging. ANN NEUROL 2012;
http://www.drjohnm.org/2012/05/cycling-wed-will-eating-nuts-make-you-smarter/
http://www.drjohnm.org/2012/05/cycling-wed-will-eating-nuts-make-you-smarter/
Wednesday, May 23, 2012
Outcome In Chronic Stroke May Be Improved By Modifying Scar Tissue
Get this on the fast track to clinical trials. Millions are waiting for an answer.
Again its good to be a rat in stroke research. If we had a decent foundation it could sponsor trials and donations would flow in for this stuff. But they didn't say how far along this chronic phase was.
http://www.medicalnewstoday.com/releases/245672.php
New research from the Buck Institute for Research on Aging shows that modifying the scar tissue that develops following a stroke is a promising avenue for future treatments. The need for therapeutics for chronic stroke is compelling. There are 750,000 new strokes per year in the U.S., a leading cause of morbidity and mortality. Aside from physical and occupational therapy, treatments for the six million patients in the U.S. who suffer from chronic stroke are lacking; the vast majority of patients remain in an ongoing state of disability with little hope of return to normal function.
The research, published in the online edition of The Proceedings of the National Academy of Sciences, builds on ongoing spinal cord repair studies. Working in rats, scientists in the Greenberg laboratory infused the stroke cavity with either the enzyme chondroitinase ABC (ChABC) or the protein heparan sulfate proteoglycan glypican (glypican). In both cases the treatments improved outcome in the animals - they had less weakness and improved coordination.
Lead scientist, Justin Hill, MD, says both treatments reduced the size of the scar tissue that had formed following the stroke and essentially "woke up" neurons in the areas surrounding the injury, stimulating the growth of new neurites, which are the terminal extensions of nerves. "We think the scar tissue not only blocks off areas of the brain that are injured during stroke, we also believe the scar tissue secretes factors that impact the function of nearby neurons," said Hill. "Dissolving the scar may spur neurons to re-route connections around the area injured during the stroke." Researchers found that treatment with glypican increased the expression of fibroblast growth factor-2 (FGF-2) near the site of injury and that ChABC increased brain-derived neurotrophic factor (BDNF) expression, both of which have been shown to increase neuron size and survival.
"There are only a handful of laboratories that are focused on treatments for chronic stroke," said Buck faculty David Greenberg, MD, PhD. "Dr. Hill's research is groundbreaking in that it is the first to apply this research on spinal cord injury to stroke and uncovers some of the underlying mechanisms involved in improved function."
Future research is aimed at discovering possible drug candidates to help patients suffering from chronic stroke.
Again its good to be a rat in stroke research. If we had a decent foundation it could sponsor trials and donations would flow in for this stuff. But they didn't say how far along this chronic phase was.
http://www.medicalnewstoday.com/releases/245672.php
New research from the Buck Institute for Research on Aging shows that modifying the scar tissue that develops following a stroke is a promising avenue for future treatments. The need for therapeutics for chronic stroke is compelling. There are 750,000 new strokes per year in the U.S., a leading cause of morbidity and mortality. Aside from physical and occupational therapy, treatments for the six million patients in the U.S. who suffer from chronic stroke are lacking; the vast majority of patients remain in an ongoing state of disability with little hope of return to normal function.
The research, published in the online edition of The Proceedings of the National Academy of Sciences, builds on ongoing spinal cord repair studies. Working in rats, scientists in the Greenberg laboratory infused the stroke cavity with either the enzyme chondroitinase ABC (ChABC) or the protein heparan sulfate proteoglycan glypican (glypican). In both cases the treatments improved outcome in the animals - they had less weakness and improved coordination.
Lead scientist, Justin Hill, MD, says both treatments reduced the size of the scar tissue that had formed following the stroke and essentially "woke up" neurons in the areas surrounding the injury, stimulating the growth of new neurites, which are the terminal extensions of nerves. "We think the scar tissue not only blocks off areas of the brain that are injured during stroke, we also believe the scar tissue secretes factors that impact the function of nearby neurons," said Hill. "Dissolving the scar may spur neurons to re-route connections around the area injured during the stroke." Researchers found that treatment with glypican increased the expression of fibroblast growth factor-2 (FGF-2) near the site of injury and that ChABC increased brain-derived neurotrophic factor (BDNF) expression, both of which have been shown to increase neuron size and survival.
"There are only a handful of laboratories that are focused on treatments for chronic stroke," said Buck faculty David Greenberg, MD, PhD. "Dr. Hill's research is groundbreaking in that it is the first to apply this research on spinal cord injury to stroke and uncovers some of the underlying mechanisms involved in improved function."
Future research is aimed at discovering possible drug candidates to help patients suffering from chronic stroke.
Post-stroke rehab: Turning patients into dolphins
A novel use of mental imagery. I bet no clinic in the US will use this. Pinko therapy you know.
http://www.rt.com/news/russia-stroke-rehab-dolphins-973/
Before her appointment as Russia’s new Health Minister, Veronika Skvortsova used to help post-stroke patients with paralysis to recuperate through an illusion of becoming… a dolphin.
Research showed that through a virtually created illusion of moving like this marine mammal, a patient’s brain can be trained to regain control over the head and body. Together with two colleagues, Skvortsova offered post-stroke patients the chance to feel like dolphins with the help of special equipment.
A fully or partially paralyzed client dons a hi-tech helmet with special goggles and motion-sensing devices attached to the head, body and pelvis. With these, and computer software the patient receives the illusion of being plunged into water and moving like a dolphin.
“Sometimes, the human brain may be restored through an illusion of its normal activity,” Skvortsova said to the Russian Moskovsky Komsomolets daily.
Virtual reality can be used to recreate a person’s motions, lost after a stroke or other serious trauma. Patients receive a full illusion of successive motion – from the first baby movements of turning on their belly to crawling and walking.
Patients sense submerging and swimming, and even see their limbs moving. The virtual sensations help the brain to gradually regain lost functions, strengthening the impression that it is in full health.
The intensity of the workload and the patient’s reaction are monitored by motion-sensing devices and further computer-analyzed to choose an optimal personal program.
“As a result, contacts between nerve cells are restored, which facilitate post-stroke rehabilitation,” explained the Minister.
Veronika Skvortsova graduated from the Second Moscow State Medical Institute, then took postgraduate courses in clinical studies and neurological disorders. In 1994, Skvortsova was awarded the highest possible degree in neurology.
http://www.rt.com/news/russia-stroke-rehab-dolphins-973/
Before her appointment as Russia’s new Health Minister, Veronika Skvortsova used to help post-stroke patients with paralysis to recuperate through an illusion of becoming… a dolphin.
Research showed that through a virtually created illusion of moving like this marine mammal, a patient’s brain can be trained to regain control over the head and body. Together with two colleagues, Skvortsova offered post-stroke patients the chance to feel like dolphins with the help of special equipment.
A fully or partially paralyzed client dons a hi-tech helmet with special goggles and motion-sensing devices attached to the head, body and pelvis. With these, and computer software the patient receives the illusion of being plunged into water and moving like a dolphin.
“Sometimes, the human brain may be restored through an illusion of its normal activity,” Skvortsova said to the Russian Moskovsky Komsomolets daily.
Virtual reality can be used to recreate a person’s motions, lost after a stroke or other serious trauma. Patients receive a full illusion of successive motion – from the first baby movements of turning on their belly to crawling and walking.
Patients sense submerging and swimming, and even see their limbs moving. The virtual sensations help the brain to gradually regain lost functions, strengthening the impression that it is in full health.
The intensity of the workload and the patient’s reaction are monitored by motion-sensing devices and further computer-analyzed to choose an optimal personal program.
“As a result, contacts between nerve cells are restored, which facilitate post-stroke rehabilitation,” explained the Minister.
Veronika Skvortsova graduated from the Second Moscow State Medical Institute, then took postgraduate courses in clinical studies and neurological disorders. In 1994, Skvortsova was awarded the highest possible degree in neurology.
Efficiency of drug delivery enhanced by acoustic pressure during blood–brain barrier disruption induced by focused ultrasound
When we need to get drugs thru the blood-brain barrier we might be able to use this method.
Efficiency of drug delivery enhanced by acoustic pressure during blood–brain barrier disruption induced by focused ultrasound
Purpose: We evaluated the delivery efficiency of intravenously injected large molecular agents, before and after disruption of the blood–brain barrier (BBB-D), induced by focused ultrasound (FUS) using various acoustic parameters.
Materials and methods: Male Sprague-Dawley rats were injected intravenously with Evans blue (EB) before or after BBB-D induction by pulsed FUS. We used a 1.0 MHz pulsed FUS with four acoustic power settings and an ultrasound contrast agent (UCA) at four different doses to induce BBB-D resulting from cavitation. The permeability of the BBB was assessed quantitatively based on the extravasation of EB. Contrast enhanced magnetic resonance imaging (MRI) was used to monitor the gadolinium deposition associated with FUS. Histological analysis was performed to examine tissue damage.
Results: The accumulation of EB in rat brain was found to be dependent on acoustic power and UCA dosage, regardless of whether EB administration occurred before or after FUS-induced BBB-D. Administration of EB followed by sonication resulted in greater EB extravasation than that for rats subjected to sonication prior to EB injection. To reduce tissue damage, EB extravasation was enhanced by first administering EB by intravenous injection, followed by sonication at reduced acoustic power or UCA dosage. The normalized signal intensity change in rat brains that received the same dose of UCA and sonicated after gadolinium injection was significantly greater than in rats undergoing sonication followed by gadolinium administration. Moreover, contrast enhanced MRI showed a more precise distribution of gadolinium in the brain when gadolinium was administered before sonication.
Conclusion: We demonstrated that a compound administered prior to sonication treatment promotes extravasation of the sonicated region. Thus, it is possible to optimize ultrasound parameters for lower sonication and reduced UCA doses, to induce BBB-D while minimizing damage to normal brain tissue.
Technology can help PTs empower patients in regaining mobility
Found this thru Billy Ethridges site.
Technology can help PTs empower patients in regaining mobility
Gait Rehabilitation
My job as an inpatient rehab manager at Sheltering Arms Hospital in Richmond, VA, is to facilitate my team's ability to help patients realize this important but often difficult goal. Since I am also a clinician, I understand how challenging it can be to learn to walk again and also how crucial this skill is to quality of life.
Recently, I worked with a patient who had not walked in several weeks. She had a long hospital course with several surgical procedures, resulting in pain and dysfunction. When I asked this patient what her goals for physical therapy were, her answer was simple but familiar: "I just want to walk."
Although she was severely debilitated, I was determined to help her attain her goal. A rehab technician and I attempted to help her stand with a walker and move her legs, but after only a few steps we were all totally exhausted. If you are a PT in inpatient rehabilitation, this frustrating situation is probably one you know well.
Principles of motor learning and neuroplasticity tell us that repetition is essential for recovery.1,2 Yet how can a patient possibly learn and recover if he or she is only able to walk a few steps at a time? How can physical therapists help patients meet the goal to resume walking and recover faster using evidence-based practice?
The Role of a Rehab Manager
Although most of us take it for granted, the ability to walk independently is required for most daily activities. The majority of patients need to be able to walk fast enough to function in the community in order to return to prior level of mobility.
The unfortunate fact is that studies have shown only 7 percent of patients discharged from rehabilitation meet the criteria for community walking, which includes the ability to cross a road safely, and they continue to demonstrate gait patterns that deviate from the norm.3,4 This tells the therapy community that we, as caregivers and rehabilitation experts, could do better.
Part of my responsibility as an inpatient rehab manager is providing the finest tools and resources that enable therapists to deliver the best possible care to each patient. Yet there are hundreds of different devices on the market, and it can be difficult to determine which technology is the best fit for a clinic or specific patient populations.
Any new technology must be appropriate for the patient and be designed based on the most recent evidence in motor learning. The technology must also be easy to use; if a piece of equipment takes too long to set up or is difficult to operate, therapists simply will not use it. They want to use their time-and the patient's time-wisely.
Stepping Forward with Technology
At Sheltering Arms we are fortunate to have the resources to acquire new technologies to supplement physical therapy expertise. Our iWALK Recovery Center program includes inpatient and outpatient services built upon the latest research in assessment and intervention.
The center was created to provide the most advanced technologies available to help patients walk again. Our goal is to have a variety of equipment and technology to meet the needs of patients with a range of diagnoses and functional abilities, all in one place. Patients who have reached a plateau with other therapies or who have been living with debilitating conditions for years finally have a resource to make progress.
The iWALK therapy team is also trained in neurorecovery-without highly trained experts to effectively use and operate the technology, devices and equipment cannot deliver on their promise.
After all, these are just tools; without the clinical judgment and expertise of a therapist, they would be useless. The therapist determines the right tool for the right patient at the right time.
Choosing Your Tools
New technologies are designed based on principles of motor learning and the relatively new concept of neuroplasticity; it has not always been known that the brain is capable of modification after injury.
In the case of my patient mentioned above, this is the point where technology came into play for her rehabilitation. After the frustrating effort to help her take a few steps with a walker, we fit her with a harness and hooked it into a dynamic over-ground body weight support system.
 |
The over-ground body weight support system is just one example of technology that can be used to capitalize on the theories of neurorecovery while keeping patients safe and engaged in therapy.
Because it is a dynamic system and can be used over ground or over a treadmill, patients experience walking in a real-world environment and are safe from falling. Patients are even able to experience loss of balance by being able to fall up to six inches before the system "catches" them.
As recent research indicates, it is important for patients to experience error in order to promote learning in the neural pathways. Coupled with a split-belt treadmill, which uses the principle of motor adaptation to improve asymmetric gait patterns, many patients are able to recover much faster than previously possible.5
In addition, advances in functional electrical stimulation (FES) have resulted in the ability to cue and facilitate muscle activity during functional activities. For example, we frequently use a cuff that fits on the patient's lower leg and has three components that communicate with each other through wireless technology to stimulate the muscles used to lift the foot while walking. It is especially useful because it allows for real-time adjustments and adaptations according to the patient's gait pattern.
Recently, we started using a new expansion on the technology that was cleared by the FDA earlier this year. This includes a thigh cuff that works along with the lower leg cuff to stimulate the quad or hamstring muscles used during walking and allows for even greater facilitation of gait kinematics.
Although the technology was just commercially released and is new in our facility, patients are already seeing results from working with the new thigh cuff. Our therapists use these technologies frequently because they are easy to use and can be set up in less than 15 minutes and patients are motivated and engaged by their use.
While the ultimate resource is the expertise and judgment of the therapist, these kinds of advances in the rehabilitation tool kit enable patients to practice walking with appropriate kinematics earlier in their rehabilitation course and promote recovery of the central nervous system.6
Early rehabilitation has been associated with improved functional outcomes and quality of life following a stroke.7 Therapists need to have the right tools and expertise to help patients improve more quickly and ultimately attain a higher level of recovery.
At Sheltering Arms, our patients benefit from our ability to provide walking retraining earlier in their recovery process. When considering how to best approach patients hoping to walk again, it is important to consider the exciting advances in our constantly evolving field, and how to best marry technological power with clinical expertise.
Before even doing anything an objective assessment like this would be good.
Computerized gait analysis helps patients with brain injuries
Or:
Automatic identification of gait events using an instrumented sock
The article covers these types of technology:
Lite Gait except the harness connects to ceiling rails.
http://www.litegait.com/litegait.html
The picture is the Lokomat which I used and thought was wonderful, my doctor thought it was a waste of time, shows you what he doesn't know.
http://www.hocoma.com/en/products/lokomat/
The FES stuff referred to is something like the Bioness or Walkaide.
Split-belt treadmill here:
http://www.treadmilltalk.com/split-belt-treadmills.html
Other technology for walking that wasn't mentioned:
1. Hip Flexion Assist Orthosis
2. GaitMaster 5: The Mechanical Physical Therapist of the Future
3. ‘Exoskeleton’ Helps Paralyzed Stand, Take Steps
4. Walk Again Project
5. C-Mill: A Plug & Play Treadmill For Gait Training & Rehabilitation
6. powered AFOs
The future:
Body suit may soon enable the paralyzed to walk
Tuesday, May 22, 2012
Alcohol intake in the elderly affects risk of cognitive decline and dementia
You'll have to decide with your doctors help how to approach this.
At the bottom I have 3 additional posts on alcohol for your edification.
http://www.eurekalert.org/pub_releases/2012-05/bumc-aii052212.php
Alzheimer's disease (AD) and other types of dementia are most common in the very elderly, and are associated with huge health costs. With a rapidly ageing population throughout the world, factors that affect the risk of cognitive decline and dementia are of great importance. A review paper by Kim JW et al published in Psychiatry Investig 2012;9:8-16 on the association between alcohol consumption and cognition in the elderly provides an excellent summary of the potential ways in which alcohol may affect cognitive function and the risk of dementia, both adversely and favourably as alcohol may have both a neuro toxic and neuro protective effect, depending on the dose and drinking pattern. Longitudinal and brain imaging studies in the elderly show that excessive alcohol consumption may increase the risk of cognitive dysfunction and dementia, but regular low to moderate alcohol intake may protect against cognitive decline and dementia and provide cardiovascular benefits.
Studies published from 1971 to 2011 related to alcohol and cognition in the elderly were reviewed using a PubMed search. At present, there are no proven agents to prevent cognitive decline or dementia, although a number of prospective epidemiologic studies have shown a lower risk of such conditions among light to moderate drinkers in comparison with non-drinkers. Other studies have found that beneficial effects are seen only among certain sub-groups of subjects. A recent meta-analysis by Peters et al of subjects over the age of 65 in longitudinal studies concluded that light-to-moderate alcohol consumption, in comparison with abstinence, was associated with approximately 35-45% lower risk of cognitive decline or dementia.
This paper provides a summary of what is known about the mechanisms by which alcohol consumption, especially heavy drinking, can be neurotoxic, and how light-to-moderate drinking may help protect against cognitive decline and dementia. The authors state that their intent is to determine if there is an "optimal pattern of drinking" that may protect the elderly against such conditions.
At present, the mechanisms by which the moderate intake of wine and other alcoholic beverages reduces the risk of cardiovascular diseases are much better defined than they are for cognition. Forum members agree with the authors that further research is needed to evaluate a potential role that alcohol may play in reducing the risk of dementia.
Forum members also agree that, at present, the specific mechanisms of such putative protection are not well defined, and it would be premature to recommend light-to-moderate drinking for reducing the risk of dementia. On the other hand, current biomedical data supports the concept that regular, moderate intake of ethanol is not simply less dangerous for cognitive function, but is positively protective. This is the same conclusion reached by epidemiologic studies."
At the bottom I have 3 additional posts on alcohol for your edification.
http://www.eurekalert.org/pub_releases/2012-05/bumc-aii052212.php
Alzheimer's disease (AD) and other types of dementia are most common in the very elderly, and are associated with huge health costs. With a rapidly ageing population throughout the world, factors that affect the risk of cognitive decline and dementia are of great importance. A review paper by Kim JW et al published in Psychiatry Investig 2012;9:8-16 on the association between alcohol consumption and cognition in the elderly provides an excellent summary of the potential ways in which alcohol may affect cognitive function and the risk of dementia, both adversely and favourably as alcohol may have both a neuro toxic and neuro protective effect, depending on the dose and drinking pattern. Longitudinal and brain imaging studies in the elderly show that excessive alcohol consumption may increase the risk of cognitive dysfunction and dementia, but regular low to moderate alcohol intake may protect against cognitive decline and dementia and provide cardiovascular benefits.
Studies published from 1971 to 2011 related to alcohol and cognition in the elderly were reviewed using a PubMed search. At present, there are no proven agents to prevent cognitive decline or dementia, although a number of prospective epidemiologic studies have shown a lower risk of such conditions among light to moderate drinkers in comparison with non-drinkers. Other studies have found that beneficial effects are seen only among certain sub-groups of subjects. A recent meta-analysis by Peters et al of subjects over the age of 65 in longitudinal studies concluded that light-to-moderate alcohol consumption, in comparison with abstinence, was associated with approximately 35-45% lower risk of cognitive decline or dementia.
This paper provides a summary of what is known about the mechanisms by which alcohol consumption, especially heavy drinking, can be neurotoxic, and how light-to-moderate drinking may help protect against cognitive decline and dementia. The authors state that their intent is to determine if there is an "optimal pattern of drinking" that may protect the elderly against such conditions.
At present, the mechanisms by which the moderate intake of wine and other alcoholic beverages reduces the risk of cardiovascular diseases are much better defined than they are for cognition. Forum members agree with the authors that further research is needed to evaluate a potential role that alcohol may play in reducing the risk of dementia.
Forum members also agree that, at present, the specific mechanisms of such putative protection are not well defined, and it would be premature to recommend light-to-moderate drinking for reducing the risk of dementia. On the other hand, current biomedical data supports the concept that regular, moderate intake of ethanol is not simply less dangerous for cognitive function, but is positively protective. This is the same conclusion reached by epidemiologic studies."
Can alcohol make men smarter? Study suggests yes
Two Drinks a Day Reduce Mortality in Male Heart Attack Victims
Alcohol’s Impact On Heart And Stroke Risk May Differ For Men, Women
Monday, May 21, 2012
Gamma Oscillations in the Hippocampal Network
This goes with this, Brain rhythms are linked to learning
Someone needs to tell us if this is an alternate way to get neuroplasticity done.
Gamma Oscillations in the Hippocampal Network
We propose that slow gamma rhythms may facilitate memory retrieval and that fast gamma rhythms may promote hippocampal encoding of information about the current sensory environment.
Juvenile, but not adult exposure to high-fat diet impairs relational memory and hippocampal neurogenesis in mice
Who is going to compare this to the tanycytes?
New one here:
http://onlinelibrary.wiley.com/doi/10.1002/hipo.22032/abstract;jsessionid=44ED7389686486C24C131190D2D4E52C.d02t03?userIsAuthenticated=false&deniedAccessCustomisedMessage=
New one here:
http://onlinelibrary.wiley.com/doi/10.1002/hipo.22032/abstract;jsessionid=44ED7389686486C24C131190D2D4E52C.d02t03?userIsAuthenticated=false&deniedAccessCustomisedMessage=
Abstract
Increased consumption of high-fat diet (HFD) leads to obesity and adverse neurocognitive outcomes. Childhood and adolescence are important periods of brain maturation shaping cognitive function. These periods could consequently be particularly sensitive to the detrimental effects of HFD intake. In mice, juvenile and adulthood consumption of HFD induce similar morphometric and metabolic changes. However, only juvenile exposure to HFD abolishes relational memory flexibility, assessed after initial radial-maze concurrent spatial discrimination learning, and decreases neurogenesis. Our results identify a critical period of development covering adolescence with higher sensitivity to HFD-induced hippocampal dysfunction at both behavioral and cellular levels.Fat incites tanycytes to neurogenesis
G-Protein-Coupled Receptors in Adult Neurogenesis
The abstract only hints at possibilities. Sign the petition for access to research.
G-Protein-Coupled Receptors in Adult Neurogenesis
Abstract
The importance of adult neurogenesis has only recently been accepted, resulting in a completely new field of investigation within stem cell biology. The regulation and functional significance of adult neurogenesis is currently an area of highly active research. G-protein-coupled receptors (GPCRs) have emerged as potential modulators of adult neurogenesis. GPCRs represent a class of proteins with significant clinical importance, because approximately 30% of all modern therapeutic treatments target these receptors. GPCRs bind to a large class of neurotransmitters and neuromodulators such as norepinephrine, dopamine, and serotonin. Besides their typical role in cellular communication, GPCRs are expressed on adult neural stem cells and their progenitors that relay specific signals to regulate the neurogenic process. This review summarizes the field of adult neurogenesis and its methods and specifies the roles of various GPCRs and their signal transduction pathways that are involved in the regulation of adult neural stem cells and their progenitors. Current evidence supporting adult neurogenesis as a model for self-repair in neuropathologic conditions, adult neural stem cell therapeutic strategies, and potential avenues for GPCR-based therapeutics are also discussedThe role of Nogo-A in axonal plasticity, regrowth and repair
Man this seems simple, tell us what blocks nogo-A and we can send the researchers out to find out if it is useful in humans.
The role of Nogo-A in axonal plasticity, regrowth and repair
Abstract
Axonal
damage leads to permanent deficits in the adult central nervous system
(CNS) not only because of the weak intrinsic
ability of adult neurons to activate their growth program
but importantly also because of the presence of specific growth
inhibitors in the CNS tissue and the environment of the
damaged axons. The well-studied myelin-derived protein Nogo-A is
involved
in various cellular and molecular events contributing to the
failure of CNS axons to regrow and reconnect after transection.
Recent studies have shown that, by acting in a negative way
on the cytoskeleton and on the growth program of axotomized neurons,
Nogo-A exerts fast and chronic inhibitory effects on neurite
outgrowth. On the other hand, the blockade of Nogo-A results
in a marked enhancement of compensatory and regenerative
axonal extension in vivo; this enhancement is often paralleled by
significant functional recovery, for example, of locomotion
or skilled forelimb reaching after spinal cord or stroke lesions
in rats and monkeys. Surprisingly, the blockade of Nogo-A or
its receptor NgR in the hippocampus has recently been demonstrated
to enhance long-term potentiation. A role of Nogo-A in
synaptic plasticity/stability might therefore represent an additional,
new and important aspect of CNS circuit remodeling.
Function-blocking anti-Nogo-A antibodies are currently being tested in
a clinical trial for improved outcome after spinal cord
injury.
Notch signaling and neural connectivity
Let's listen in on notch and hear what signals its putting out. More on brain connectivity.
http://www.sciencedirect.com/science/article/pii/S0959437X12000470
The cell surface receptor Notch contributes to the development of nearly every tissue in most metazoans by controlling the fates and differentiation of cells. Recent results have now established that Notch also regulates the connectivity of the nervous system, and does so at a variety of levels, including specification of neuronal identity, division, survival and migration, as well as axon guidance, morphogenesis of dendritic arbors and weighting of synapse strength. To these ends, Notch engages at least two signal transduction pathways, one that controls nuclear gene expression and another that directly targets the cytoskeleton. Coordinating the many functions of Notch to produce neural structure is thus a pivotal aspect of building and maintaining the nervous system.
http://www.sciencedirect.com/science/article/pii/S0959437X12000470
The cell surface receptor Notch contributes to the development of nearly every tissue in most metazoans by controlling the fates and differentiation of cells. Recent results have now established that Notch also regulates the connectivity of the nervous system, and does so at a variety of levels, including specification of neuronal identity, division, survival and migration, as well as axon guidance, morphogenesis of dendritic arbors and weighting of synapse strength. To these ends, Notch engages at least two signal transduction pathways, one that controls nuclear gene expression and another that directly targets the cytoskeleton. Coordinating the many functions of Notch to produce neural structure is thus a pivotal aspect of building and maintaining the nervous system.
Scuba exercises help stroke survivor recover
In a presentation I did I put a picture of a scuba diver swimming with sharks to demonstrate Dangerous Stroke Rehab. It does occur.
http://www.standard.net/stories/2011/11/22/scuba-exercises-help-stroke-survivor-recover
http://www.standard.net/stories/2011/11/22/scuba-exercises-help-stroke-survivor-recover
A Clinton man is going beneath the surface of the water in hopes of someday becoming physically whole again.
"I see me being a whole person (in a couple of years)," said 48-year-old Mark Wager, who is using scuba diving as a form of physical therapy after having a stroke on Feb. 6, 2009.
During that incident, which occurred in Clearfield, he was arrested by Davis County sheriff's deputies on suspicion of driving while intoxicated. He was handcuffed and put into the back of a patrol car.
It was not until police took Wager to Davis Hospital and Medical Center in Layton for a blood draw that they discovered he had suffered a stroke. From there, Wager was flown by helicopter to University of Utah Medical Center, where he remained in recovery for weeks.
Wager's rehabilitation from his stroke continues, as twice weekly he attends two-hour scuba sessions in the pool of the George E. Wahlen Department of Veterans Affairs Medical Center in Salt Lake City.
Wager said the sessions are beginning to strengthen the muscles in his left arm, left leg and left side of his body, which he described as being "useless" at one time after the stroke.
But not anymore.
Wager, a former Hill Air Force Base aircraft mechanic who took medical leave from his job in May 2011, said his therapy regimen will, over time, allow him to regain full use of his left arm and leg.
"I'm using muscle I haven't used before," said Wager, who since September has regularly participated in the therapy sessions with veterans who are amputees as a result of war.
Wager said the therapy was recommended to him by a hospital doctor.
The physical therapy he was doing before taking to the water, Wager said, got him back on his feet, but did not give him the muscle improvement he was looking for.
"Even after two years, I had a lot of problems with my walking. Before I did the scuba diving, I used to have to wear a brace on my foot to support it. I don't have to wear a brace anymore, because I can use my ankle," he said.
Tonua Hamilton, a physical therapist at the VA hospital, said she recommended Wager enroll in the scuba program offered at the pool on the hospital campus after running into him in the hall of the hospital.
Hamilton said Wager was the first veteran in the rehabilitation program that began in May.
Wager's scuba therapy has given him more freedom of movement by "not having gravity as an enemy anymore," Hamilton said.
Wager also is receiving occupational therapy at the hospital, Hamilton said, resulting in his experiencing "some upper body strength and improved function in his (left) arm."
But the unique therapy Wager is using in his rehabilitation isn't any more unique than the details and events surrounding his stroke experience.
While suffering his stroke, which Wager suspects was brought on by a Gulf War illness, he was suspected by Davis sheriff's officials of driving while intoxicated.
Had it not been for the deputy who arrested him stopping at the Layton hospital for a blood draw instead of taking him directly to jail, Wager is uncertain what his fate may have been.
"They never apologized," he said of the sheriff's office.
As a result, Wager said, he has yet to forgive the five officers who responded to the scene that night.
Deputies asked him to step out of his vehicle so he could undergo a sobriety test, Wager said, but he collapsed while getting out of his vehicle and was unable to walk.
However, officials at the scene report a different version of what occurred.
When asked whether he had any medical problems, Wager told deputies he had fibromyalgia, according to reports.
Officials also asked Wager if he wanted to be transported to the hospital for further assessment, to which Wager replied he did not and signed the refusal form for transport in the ambulance that had arrived on scene, the report states.
Wager did not file any civil complaint against the deputies, but did make a formal request to the state Emergency Medical Services Board to require deputy paramedics be better trained in recognizing the difference between someone who is intoxicated and someone who is experiencing a stroke.
"I see me being a whole person (in a couple of years)," said 48-year-old Mark Wager, who is using scuba diving as a form of physical therapy after having a stroke on Feb. 6, 2009.
During that incident, which occurred in Clearfield, he was arrested by Davis County sheriff's deputies on suspicion of driving while intoxicated. He was handcuffed and put into the back of a patrol car.
It was not until police took Wager to Davis Hospital and Medical Center in Layton for a blood draw that they discovered he had suffered a stroke. From there, Wager was flown by helicopter to University of Utah Medical Center, where he remained in recovery for weeks.
Wager's rehabilitation from his stroke continues, as twice weekly he attends two-hour scuba sessions in the pool of the George E. Wahlen Department of Veterans Affairs Medical Center in Salt Lake City.
Wager said the sessions are beginning to strengthen the muscles in his left arm, left leg and left side of his body, which he described as being "useless" at one time after the stroke.
But not anymore.
Wager, a former Hill Air Force Base aircraft mechanic who took medical leave from his job in May 2011, said his therapy regimen will, over time, allow him to regain full use of his left arm and leg.
"I'm using muscle I haven't used before," said Wager, who since September has regularly participated in the therapy sessions with veterans who are amputees as a result of war.
Wager said the therapy was recommended to him by a hospital doctor.
The physical therapy he was doing before taking to the water, Wager said, got him back on his feet, but did not give him the muscle improvement he was looking for.
"Even after two years, I had a lot of problems with my walking. Before I did the scuba diving, I used to have to wear a brace on my foot to support it. I don't have to wear a brace anymore, because I can use my ankle," he said.
Tonua Hamilton, a physical therapist at the VA hospital, said she recommended Wager enroll in the scuba program offered at the pool on the hospital campus after running into him in the hall of the hospital.
Hamilton said Wager was the first veteran in the rehabilitation program that began in May.
Wager's scuba therapy has given him more freedom of movement by "not having gravity as an enemy anymore," Hamilton said.
Wager also is receiving occupational therapy at the hospital, Hamilton said, resulting in his experiencing "some upper body strength and improved function in his (left) arm."
But the unique therapy Wager is using in his rehabilitation isn't any more unique than the details and events surrounding his stroke experience.
While suffering his stroke, which Wager suspects was brought on by a Gulf War illness, he was suspected by Davis sheriff's officials of driving while intoxicated.
Had it not been for the deputy who arrested him stopping at the Layton hospital for a blood draw instead of taking him directly to jail, Wager is uncertain what his fate may have been.
"They never apologized," he said of the sheriff's office.
As a result, Wager said, he has yet to forgive the five officers who responded to the scene that night.
Deputies asked him to step out of his vehicle so he could undergo a sobriety test, Wager said, but he collapsed while getting out of his vehicle and was unable to walk.
However, officials at the scene report a different version of what occurred.
When asked whether he had any medical problems, Wager told deputies he had fibromyalgia, according to reports.
Officials also asked Wager if he wanted to be transported to the hospital for further assessment, to which Wager replied he did not and signed the refusal form for transport in the ambulance that had arrived on scene, the report states.
Wager did not file any civil complaint against the deputies, but did make a formal request to the state Emergency Medical Services Board to require deputy paramedics be better trained in recognizing the difference between someone who is intoxicated and someone who is experiencing a stroke.
Petition -Require free access over the Internet to scientific journal articles arising from taxpayer-funded research.
Sign the petition to require free access over the Internet to journal
articles arising from taxpayer-funded research. This will require you to
create an account at the White House petition website, confirm the
account by clicking on a link in your email, and then sign the petition
itself.
http://access2research.org/
This would simplify getting the same knowledge as our doctors should have.
The current access to abstracts is way too limiting.
http://access2research.org/
This would simplify getting the same knowledge as our doctors should have.
The current access to abstracts is way too limiting.
Low-Dose Vitamin D Prevents Muscular Atrophy and Reduces Falls and Hip Fractures in Women after Stroke: A Randomized Controlled Trial
I don't fit the title but if it can reduce atrophy for women its worth a try for me. A vitamin D deficiency also results in fatigue so I'm trying it for that also. Don't follow anything I do without talking to your doctor.
Low-Dose Vitamin D Prevents Muscular Atrophy and Reduces Falls and Hip Fractures in Women after Stroke: A Randomized Controlled Trial
Abstract:
Objective: Vitamin D supplementation is
suggested to reduce the risk of falls among ambulatory or
institutionalized elderly subjects. The present study was undertaken to
address the reduced risk of falls and hip fractures in patients with
long-standing stroke by vitamin D supplementation. Methods:
Ninety-six elderly women with poststroke hemiplegia were followed for
two years. Patients were randomly assigned to one of the two groups, and
48 patients received 1,000 IU ergocalciferol daily, and the remaining
48 received placebo. The number of falls per person and incidence of hip
fractures were compared between the two groups. Strength and tissue
ATPase of skeletal muscles on the nonparetic side were assessed before
and after the study. Results: At baseline, serum
25-hydroxyvitamin D levels were in the deficient range (<10 ng/ml) in
all patients; and vitamin D treatment enhanced serum 25-hydroxyvitamin D
and1,25-dihydroxyvitamin D levels. Vitamin D treatment accounted for a
59% reduction in falls (95% CI, 28–81%; p = 0.003). There were increases
in the relative number and size of type II muscle fibers and improved
muscle strength in the vitamin D-treated group. Hip fractures occurred
in 4 of 48 placebo group and 0 in 48 vitamin D2 group during the 2-year study period (log-rank, p = 0.049). Conclusion:
Vitamin D may increase muscle strength by improving atrophy of type II
muscle fibers, which may lead to decreased falls and hip fractures
Subscribe to:
Posts (Atom)