Ok, this has only been tested in rats but lets start tests in humans, No time to waste. Time is Brain
http://www.medicalnewstoday.com/releases/230863.php
Natural Neuroprotective Self-Repairs Brain Following Stroke
Stroke is a leading cause of long-term disability and death in the United States. A team of researchers - led by Gregory Bix, at Texas A&M College of Medicine, College Station - has identified a way to exploit one of the brain's self-repair mechanisms to protect nerve cells and enhance brain repair in rodent models of stroke. The authors suggest that this approach could provide a nontoxic treatment for stroke.
The most common form of stroke (ischemic stroke) occurs when a blood vessel that brings oxygen and nutrients to the brain becomes clogged, for example with a blood clot, causing nerve cells in the affected area to die rapidly. In their study, Bix and colleagues detected in rodent models of stroke elevated levels of domain V, a naturally occurring fragment of the molecule perlecan, suggesting it might have a natural role in repairing the brain after a stroke. When administered in these models 24 hours after stroke, perlecan domain V protected nerve cells from death and promoted blood vessel growth, a key component of brain repair. The authors therefore suggest that perlecan domain V could provide a therapy that improves stroke outcome by protecting nerve cells and enhancing brain repair.
TITLE: Perlecan domain V is neuroprotective and proangiogenic following ischemic stroke in rodents
Sunday, July 17, 2011
Clinical Trial Of New Stem Cell Therapy For Use In Patients Up To 19 Days After Stroke
Finally a stem cell trial in the US, I'm sure they could get lots of participants. Get going, Time is Brain you know.
http://www.medicalnewstoday.com/releases/231147.php
The first Texas patient has been enrolled by researchers at The University of Texas Health Science Center at Houston (UTHealth) in the country's first double-blind clinical trial studying the safety and efficacy of an innovative stem cell therapy that can be given up to 19 days after an ischemic stroke.
The Phase II study, cleared by the Federal Drug Administration, examines a regenerative therapy developed by Aldagen that uses a patient's own bone marrow stem cells. The therapy, called ALD-401, consists of stem cells that are identified using Aldagen's proprietary technology to isolate cells that express high levels of an enzyme that serve as a marker of stem cells. Studies found that these cells enhance recovery after stroke in mice. The cells are administered into the carotid artery.
"This represents a new approach using stem cells for stroke," said Sean Savitz, M.D., senior investigator for the multi-center study and associate professor of neurology at the UTHealth Medical School. "A major question in the field of stem cell research is whether we can extend the time window for administering stem cells. A longer window increases the number of patients that might be helped."
Preclinical research, including research at UTHealth, has suggested that stem cells can promote the repair of the brain after an ischemic stroke, which is caused by a blood clot in the brain. Stroke is a leading cause of disability and the fourth-leading cause of death in the United States, according to 2008 statistics reported by the Centers for Disease Control and Prevention.
The Houston resident (who cannot be identified by name at this time because of the study design) received either placebo or ALD-401 on June 8 at Memorial Hermann-Texas Medical Center after suffering a stroke May 23 while on a trip to California. Her stroke was caused by previously undiagnosed atrial fibrillation.
"We were waiting for our taxi at the hotel and I immediately couldn't talk and my husband said my face was drooping," said the 67-year-old cosmetics developer. "We were just three blocks from a major trauma center. I had an angel with me because if it had happened two hours later, I would have been on an airplane."
Once back in Houston, she was referred to Savitz' study by Erin Furr-Stimming, M.D., UTHealth assistant professor of neurology, who treats her for Parkinson's disease.
While she doesn't know whether or not she received the stem cells in the double-blind study, she didn't hesitate to join the trial.
"I did a lot of research on stem cells online. I was very excited when I heard about the trial. I wanted to participate in the research for me, if possible, and for other people behind me," she said.
Savitz and his research team are studying other stem cell therapies for acute stroke, and these must be administered within a few days of the stroke. One of those, a safety and efficacy trial using a patient's own bone marrow stem cells administered intravenously, is funded by the National Institutes of Health. UTHealth researchers in the Department of Pediatric Surgery also are studying the use of stem cells for pediatric traumatic brain injury.
Savitz' team is working to enroll patients at other area hospitals and facilities into the study, something that is possible because the cells can be administered up to 19 days after a stroke. The trial, funded by Aldagen, will enroll a total of 100 patients with unilateral (one-sided) cortical ischemic strokes. For information, call 713-500-7183 or email jennifer.m.garrett@uth.tmc.edu.
http://www.medicalnewstoday.com/releases/231147.php
The first Texas patient has been enrolled by researchers at The University of Texas Health Science Center at Houston (UTHealth) in the country's first double-blind clinical trial studying the safety and efficacy of an innovative stem cell therapy that can be given up to 19 days after an ischemic stroke.
The Phase II study, cleared by the Federal Drug Administration, examines a regenerative therapy developed by Aldagen that uses a patient's own bone marrow stem cells. The therapy, called ALD-401, consists of stem cells that are identified using Aldagen's proprietary technology to isolate cells that express high levels of an enzyme that serve as a marker of stem cells. Studies found that these cells enhance recovery after stroke in mice. The cells are administered into the carotid artery.
"This represents a new approach using stem cells for stroke," said Sean Savitz, M.D., senior investigator for the multi-center study and associate professor of neurology at the UTHealth Medical School. "A major question in the field of stem cell research is whether we can extend the time window for administering stem cells. A longer window increases the number of patients that might be helped."
Preclinical research, including research at UTHealth, has suggested that stem cells can promote the repair of the brain after an ischemic stroke, which is caused by a blood clot in the brain. Stroke is a leading cause of disability and the fourth-leading cause of death in the United States, according to 2008 statistics reported by the Centers for Disease Control and Prevention.
The Houston resident (who cannot be identified by name at this time because of the study design) received either placebo or ALD-401 on June 8 at Memorial Hermann-Texas Medical Center after suffering a stroke May 23 while on a trip to California. Her stroke was caused by previously undiagnosed atrial fibrillation.
"We were waiting for our taxi at the hotel and I immediately couldn't talk and my husband said my face was drooping," said the 67-year-old cosmetics developer. "We were just three blocks from a major trauma center. I had an angel with me because if it had happened two hours later, I would have been on an airplane."
Once back in Houston, she was referred to Savitz' study by Erin Furr-Stimming, M.D., UTHealth assistant professor of neurology, who treats her for Parkinson's disease.
While she doesn't know whether or not she received the stem cells in the double-blind study, she didn't hesitate to join the trial.
"I did a lot of research on stem cells online. I was very excited when I heard about the trial. I wanted to participate in the research for me, if possible, and for other people behind me," she said.
Savitz and his research team are studying other stem cell therapies for acute stroke, and these must be administered within a few days of the stroke. One of those, a safety and efficacy trial using a patient's own bone marrow stem cells administered intravenously, is funded by the National Institutes of Health. UTHealth researchers in the Department of Pediatric Surgery also are studying the use of stem cells for pediatric traumatic brain injury.
Savitz' team is working to enroll patients at other area hospitals and facilities into the study, something that is possible because the cells can be administered up to 19 days after a stroke. The trial, funded by Aldagen, will enroll a total of 100 patients with unilateral (one-sided) cortical ischemic strokes. For information, call 713-500-7183 or email jennifer.m.garrett@uth.tmc.edu.
Friday, July 15, 2011
Solving the worlds' stroke problems
Just got back from the Winnipeg Folk festival. I was able to have breakfast with Linda of Leading a healthy life blog.Linda even has a picture of us on her blog, god I'm getting gray and old. In 4.5 hours we solved lots of the stroke rehab problems. A couple of weeks earlier I had coffee with Bob from the StrokeNetwork and in 2.5 hours we also solved lots of the worlds stroke issues.
What a novel idea; Lets get 10-12 stroke survivors together for 2 days of discussion and we can come up with something much better than the weasel words that the World Stroke Organization put out after their Synergium.
http://oc1dean.blogspot.com/2011/05/stroke-working-toward-prioritized-world.html
Nanotubes inject stroke therapy into rats’ brains
I wish they would have listed the enzyme they are trying to stop from causing continued damages to neurons, I could then have linked it to some other therapies I have posted about.From another site came these lines:
At the molecular level, the genetic activation of the nucleic acid protein Caspase-3 – a member of the cysteine-aspartic acid protease (caspase) family – is a major factor in loss of neuronal tissue and associated apoptosis (programmed cell death).
http://anpron.eu/?p=10599
Carbon nanotubes (CNTs) have been used as a delivery vehicle for tiny pieces of RNA to minimise brain cell death during and after a stroke. Rats given the nanotube therapy performed better than controls in physical skills tests after a stroke was induced and the researchers believe that this treatment could be used to tackle other neurodegenerative diseases, although questions remain over the safety of the nanotube vehicle.
Stroke is the second biggest killer worldwide. When a patient has a stroke it results in traumatic brain injury. This injury leads to increased activity of an enzyme, which results in a concomitant rise in programmed cell death. Inhibiting this enzyme would result in fewer neurons dying after a stroke, which would, in theory, help the stroke victim to avoid some of the debilitating physical effects, such as difficulty walking. Unfortunately, it is very difficult to target the enzyme at the site of injury in the brain.
Carbon nanotubes act as a delivery vehicle for small pieces of RNA that help to prevent cell death in the brain after stroke
Now, scientists led by Tommaso Pizzorusso at the National Neuroscience Research Institute in Pisa, Italy and Kostas Kostarelos at the University of London, UK, think they have found a way to inhibit this enzyme in the brain. They used ammonium-functionalised multi-walled CNTs to deliver small interfering RNAs – nucleic acids which block gene expression – to stop production of this enzyme. Rats that received an injection of the CNT-siRNA complex directly into the brain performed better in food retrieval tests than controls, after a stroke was induced. Although the effects were more pronounced if the siRNAs were administered before the stroke, injecting them after the stroke is still beneficial.
Pizzorusso believes that the work proves nanocarriers can deliver siRNAs to treat stroke. ‘The type of nanocarrier is not so important, we need chemists to prepare nano-vehicles with the best biocompatibility, and the best abilities to carry and release the siRNA once in the cells,’ he says. He says that protecting neurons in this manner should be combined with research to obtain better function from the remaining neurons after stroke damage. This combination should preserve more brain cells and enable the preserved cells to work better.
‘Our overarching hypothesis is that if we take CNTs coated or conjugated with small molecules and inject them directly into tissue, these materials are capable of piercing the cells as if they were an extension of the syringe,’ Kostarelos says. While there may be debate about the carrier, this is one of the first CNT-based treatments to have piqued the interest of clinicians and it is an important step forward for nanomedicine, he adds. Kostarelos’s group is now looking at what happens to the CNTs after the treatment is administered, and says that this therapy could be used in other neurodegenerative diseases.
Vincent Rotello, an expert in nanomaterial drug delivery at the University of Massachusetts, Amherst, US, says that ‘localised administration provides a means of increasing therapeutic efficacy while minimising collateral effects. Questions of long-term toxicity of the CNTs remain; however, this therapeutic strategy could be readily applied to other vehicles.’
At the molecular level, the genetic activation of the nucleic acid protein Caspase-3 – a member of the cysteine-aspartic acid protease (caspase) family – is a major factor in loss of neuronal tissue and associated apoptosis (programmed cell death).
http://anpron.eu/?p=10599
Carbon nanotubes (CNTs) have been used as a delivery vehicle for tiny pieces of RNA to minimise brain cell death during and after a stroke. Rats given the nanotube therapy performed better than controls in physical skills tests after a stroke was induced and the researchers believe that this treatment could be used to tackle other neurodegenerative diseases, although questions remain over the safety of the nanotube vehicle.
Stroke is the second biggest killer worldwide. When a patient has a stroke it results in traumatic brain injury. This injury leads to increased activity of an enzyme, which results in a concomitant rise in programmed cell death. Inhibiting this enzyme would result in fewer neurons dying after a stroke, which would, in theory, help the stroke victim to avoid some of the debilitating physical effects, such as difficulty walking. Unfortunately, it is very difficult to target the enzyme at the site of injury in the brain.
Carbon nanotubes act as a delivery vehicle for small pieces of RNA that help to prevent cell death in the brain after stroke
Now, scientists led by Tommaso Pizzorusso at the National Neuroscience Research Institute in Pisa, Italy and Kostas Kostarelos at the University of London, UK, think they have found a way to inhibit this enzyme in the brain. They used ammonium-functionalised multi-walled CNTs to deliver small interfering RNAs – nucleic acids which block gene expression – to stop production of this enzyme. Rats that received an injection of the CNT-siRNA complex directly into the brain performed better in food retrieval tests than controls, after a stroke was induced. Although the effects were more pronounced if the siRNAs were administered before the stroke, injecting them after the stroke is still beneficial.
Pizzorusso believes that the work proves nanocarriers can deliver siRNAs to treat stroke. ‘The type of nanocarrier is not so important, we need chemists to prepare nano-vehicles with the best biocompatibility, and the best abilities to carry and release the siRNA once in the cells,’ he says. He says that protecting neurons in this manner should be combined with research to obtain better function from the remaining neurons after stroke damage. This combination should preserve more brain cells and enable the preserved cells to work better.
‘Our overarching hypothesis is that if we take CNTs coated or conjugated with small molecules and inject them directly into tissue, these materials are capable of piercing the cells as if they were an extension of the syringe,’ Kostarelos says. While there may be debate about the carrier, this is one of the first CNT-based treatments to have piqued the interest of clinicians and it is an important step forward for nanomedicine, he adds. Kostarelos’s group is now looking at what happens to the CNTs after the treatment is administered, and says that this therapy could be used in other neurodegenerative diseases.
Vincent Rotello, an expert in nanomaterial drug delivery at the University of Massachusetts, Amherst, US, says that ‘localised administration provides a means of increasing therapeutic efficacy while minimising collateral effects. Questions of long-term toxicity of the CNTs remain; however, this therapeutic strategy could be readily applied to other vehicles.’
Continuum: Lifelong Learning in Neurology
This article attempts to summarize the current understanding of stroke rehabilitation but fails to realize that the recovery percents do not consider the complete lack of understanding as to why the recovery is so low. This all comes back to the fact that stroke survivors do not get a damage diagnosis.
https://www.aan.com/elibrary/continuum/?event=home.showArticleOrAbstract&id=ovid.com:/bib/ovftdb/00132979-201106000-00013
part of the article;
NATURAL HISTORY AND PREDICTING RECOVERY AFTER STROKE
Most recovery of specific deficits (motor, sensory, language) occurs during the first 3 to 6 months after stroke(WHY?).2,3 There are exceptions, however, and documented improvements can occur many years after stroke in a cooperative patient with an intensive rehabilitation program.4 Recovery of functional abilities can generally be predicted soon after stroke. Severity of disability status at 1 month poststroke is generally a reliable proxy for final outcome.5 Some simple predictions are possible regarding motor recovery. If there is no voluntary movement in the upper extremity at 15 days or no measureable grip at 1 month, the prognosis for recovery of useful arm function is poor. If the patient can move his or her hip within a week, ambulation is usually possible, but often with the use of an assistive device or an ankle orthosis. Motor recovery almost always occurs initially in the proximal muscles of the upper and lower extremity and often occurs in a specific sequence, sometimes called the Brunnstrom stages of motor recovery (Table 8-1). Between 70% and 88% of patients with ischemic stroke have some degree of motor dysfunction6; however, long-term survivors have a good prognosis for motor recovery. In the Framingham Heart Study, 52% of individuals who survived at least 6 months had no residual weakness. Aphasia occurs in approximately 23% of patients following stroke.7,8 Again, much recovery occurs within 3 to 6 months after onset. Some rough generalizations can be made. By 6 months poststroke only 12% of patients have continued aphasia. Degree of recovery correlates with the initial severity of the aphasia,9 although functional communication may recover after 6 months in some cases of severe aphasia. Recovery from sensory perceptual and cognitive deficits generally follows the same pattern as motor and language difficulties. Neglect is present in as many as one-third of patients with acute stroke but resolves in most by 12 weeks.7 When neglect persists, it can become a limiting factor to functional recovery.
https://www.aan.com/elibrary/continuum/?event=home.showArticleOrAbstract&id=ovid.com:/bib/ovftdb/00132979-201106000-00013
part of the article;
NATURAL HISTORY AND PREDICTING RECOVERY AFTER STROKE
Most recovery of specific deficits (motor, sensory, language) occurs during the first 3 to 6 months after stroke(WHY?).2,3 There are exceptions, however, and documented improvements can occur many years after stroke in a cooperative patient with an intensive rehabilitation program.4 Recovery of functional abilities can generally be predicted soon after stroke. Severity of disability status at 1 month poststroke is generally a reliable proxy for final outcome.5 Some simple predictions are possible regarding motor recovery. If there is no voluntary movement in the upper extremity at 15 days or no measureable grip at 1 month, the prognosis for recovery of useful arm function is poor. If the patient can move his or her hip within a week, ambulation is usually possible, but often with the use of an assistive device or an ankle orthosis. Motor recovery almost always occurs initially in the proximal muscles of the upper and lower extremity and often occurs in a specific sequence, sometimes called the Brunnstrom stages of motor recovery (Table 8-1). Between 70% and 88% of patients with ischemic stroke have some degree of motor dysfunction6; however, long-term survivors have a good prognosis for motor recovery. In the Framingham Heart Study, 52% of individuals who survived at least 6 months had no residual weakness. Aphasia occurs in approximately 23% of patients following stroke.7,8 Again, much recovery occurs within 3 to 6 months after onset. Some rough generalizations can be made. By 6 months poststroke only 12% of patients have continued aphasia. Degree of recovery correlates with the initial severity of the aphasia,9 although functional communication may recover after 6 months in some cases of severe aphasia. Recovery from sensory perceptual and cognitive deficits generally follows the same pattern as motor and language difficulties. Neglect is present in as many as one-third of patients with acute stroke but resolves in most by 12 weeks.7 When neglect persists, it can become a limiting factor to functional recovery.
Hand-hacking lets you pluck strings like a musical pro
This could easily be used for finger rehab after stroke compared to the non-specific eStims out there today.
When will this become standard in therapy departments? I'll take bets; I would say 25 years. Prove me wrong.
http://www.newscientist.com/article/mg21028186.100-handhacking-lets-you-pluck-strings-like-a-musical-pro.html
WANT to learn a musical instrument, but can't find the time to practise? A device now under development can take control of your hand and teach you how to play a tune. No spirits of dead musicians are involved.
PossessedHand, being developed jointly by the University of Tokyo, Japan, and Sony Computer Science Laboratories, also in Tokyo, electrically stimulates the muscles in the forearm that move your fingers. A belt worn around that part of the subject's arm contains 28 electrode pads, which flex the joints between the three bones of each finger and the two bones of the thumb, and provide two wrist movements. Users were able to sense the movement of their hands that this produced, even with their eyes closed. "The user's fingers are controlled without the user's mind," explains Emi Tamaki of the University of Tokyo, who led the research.
Devices that stimulate people's fingers have been made before, but they used electrodes embedded in the skin, which are invasive, or glove-like devices that make it hard to manipulate an object. Tamaki claims that her device is far more comfortable. "The electric stimulations are similar to low-frequency massage stimulations that are commonly used," she says.
Having successfully hijacked a hand, the researchers tried to teach it how to play the koto, a traditional Japanese stringed instrument. Koto players wear different picks on three fingers, but pluck the strings with all five fingertips, so each finger produces a distinctive sound. A koto score tells players which fingers should be moved and when, and from this Tamaki and her team were able to generate instructions telling their device how and when to stimulate the wearer's muscles.
PossessedHand does not generate enough force to pluck the koto strings, but it could help novice players by teaching them the correct finger movements. Tamaki and her team found that two beginner players made a total of four timing errors when using PossessedHand, compared with 13 when playing unassisted. After prompting from the device, the players also made one less mistake about which finger to use.
Perhaps not surprisingly, the players found it unsettling to have the device move their hand by itself. "I felt like my body was hacked," said one. Tamaki is confident that people will get used to the idea once they see how useful it can be: "We believe convenient technology will overcome a feeling of fear."
As well as helping would-be musicians, PossessedHand could be used to rehabilitate people who have suffered a stroke or other injury that impairs muscle control. Therapists already use electrical muscle stimulation to help these people, but existing non-invasive devices can only achieve crude movements such as contracting the entire arm.
Henrik Gollee, who researches rehabilitation devices at the University of Glasgow, UK, says PossessedHand could help patients train a wider range of movements. "I was surprised by the level of fine movement they can actually achieve," he says.
Simon Holland, director of the Music Computing Lab at the Open University in Milton Keynes, UK, points out that there is a big difference between learning to play one song and being a competent musician. "You might learn a fingering and be able to reproduce that performance, without necessarily being able to perform simple variants," he says.
When will this become standard in therapy departments? I'll take bets; I would say 25 years. Prove me wrong.
http://www.newscientist.com/article/mg21028186.100-handhacking-lets-you-pluck-strings-like-a-musical-pro.html
WANT to learn a musical instrument, but can't find the time to practise? A device now under development can take control of your hand and teach you how to play a tune. No spirits of dead musicians are involved.
PossessedHand, being developed jointly by the University of Tokyo, Japan, and Sony Computer Science Laboratories, also in Tokyo, electrically stimulates the muscles in the forearm that move your fingers. A belt worn around that part of the subject's arm contains 28 electrode pads, which flex the joints between the three bones of each finger and the two bones of the thumb, and provide two wrist movements. Users were able to sense the movement of their hands that this produced, even with their eyes closed. "The user's fingers are controlled without the user's mind," explains Emi Tamaki of the University of Tokyo, who led the research.
Devices that stimulate people's fingers have been made before, but they used electrodes embedded in the skin, which are invasive, or glove-like devices that make it hard to manipulate an object. Tamaki claims that her device is far more comfortable. "The electric stimulations are similar to low-frequency massage stimulations that are commonly used," she says.
Having successfully hijacked a hand, the researchers tried to teach it how to play the koto, a traditional Japanese stringed instrument. Koto players wear different picks on three fingers, but pluck the strings with all five fingertips, so each finger produces a distinctive sound. A koto score tells players which fingers should be moved and when, and from this Tamaki and her team were able to generate instructions telling their device how and when to stimulate the wearer's muscles.
PossessedHand does not generate enough force to pluck the koto strings, but it could help novice players by teaching them the correct finger movements. Tamaki and her team found that two beginner players made a total of four timing errors when using PossessedHand, compared with 13 when playing unassisted. After prompting from the device, the players also made one less mistake about which finger to use.
Perhaps not surprisingly, the players found it unsettling to have the device move their hand by itself. "I felt like my body was hacked," said one. Tamaki is confident that people will get used to the idea once they see how useful it can be: "We believe convenient technology will overcome a feeling of fear."
As well as helping would-be musicians, PossessedHand could be used to rehabilitate people who have suffered a stroke or other injury that impairs muscle control. Therapists already use electrical muscle stimulation to help these people, but existing non-invasive devices can only achieve crude movements such as contracting the entire arm.
Henrik Gollee, who researches rehabilitation devices at the University of Glasgow, UK, says PossessedHand could help patients train a wider range of movements. "I was surprised by the level of fine movement they can actually achieve," he says.
Simon Holland, director of the Music Computing Lab at the Open University in Milton Keynes, UK, points out that there is a big difference between learning to play one song and being a competent musician. "You might learn a fingering and be able to reproduce that performance, without necessarily being able to perform simple variants," he says.
New exercise technology designed for athletes increases production of 'HGH'
I wonder if HGH would be useful in neurogenesis. In all my research I haven't come across HGH and stroke rehab yet.
http://www.smartplanet.com/video/new-exercise-technology-designed-for-athletes-increases-production-of-hgh/6246488?tag=nl.e662
At NASA Ames Research Park, scientist Peter Wasowski has developed an alternative exercise machine called Vasper. The user wears compression cuffs on the arms and legs and core-cooling panels on the chest and head. During exercise, the machine traps large amounts of lactic acid in the body, stimulating the pituitary gland and producing more HGH or human growth hormone.
http://www.smartplanet.com/video/new-exercise-technology-designed-for-athletes-increases-production-of-hgh/6246488?tag=nl.e662
At NASA Ames Research Park, scientist Peter Wasowski has developed an alternative exercise machine called Vasper. The user wears compression cuffs on the arms and legs and core-cooling panels on the chest and head. During exercise, the machine traps large amounts of lactic acid in the body, stimulating the pituitary gland and producing more HGH or human growth hormone.
Psychostimulant Drugs and Neuroplasticity
I don't think this is referring to neuroplasticity in the good sense that we want.
http://www.mdpi.com/1424-8247/4/7/976/pdf
Abstract: Drugs of abuse induce plastic changes in the brain that seem to underlie
addictive phenomena. These plastic changes can be structural (morphological) or synaptic
(biochemical), and most of them take place in the mesolimbic and mesostriatal circuits.
Several addiction-related changes in brain circuits (hypofrontality, sensitization, tolerance)
as well as the outcome of treatment have been visualized in addicts to psychostimulants
using neuroimaging techniques. Repeated exposure to psychostimulants induces
morphological changes such as increase in the number of dendritic spines, changes in the
morphology of dendritic spines, and altered cellular coupling through new gap junctions.
Repeated exposure to psychostimulants also induces various synaptic adaptations, many of
them related to sensitization and neuroplastic processes, that include up- or
down-regulation of D1, D2 and D3 dopamine receptors, changes in subunits of G proteins,
increased adenylyl cyclase activity, cyclic AMP and protein kinase A in the nucleus
accumbens, increased tyrosine hydroxylase enzyme activity, increased calmodulin and
activated CaMKII in the ventral tegmental area, and increased deltaFosB, c-Fos and AP-1
binding proteins. Most of these changes are transient, suggesting that more lasting plastic
brain adaptations should take place. In this context, protein synthesis inhibitors block the
development of sensitization to cocaine, indicating that rearrangement of neural networks
must develop for the long-lasting plasticity required for addiction to occur.
Self-administration studies indicate the importance of glutamate neurotransmission in
neuroplastic changes underlying transition from use to abuse. Finally, plastic changes in
the addicted brain are enhanced and aggravated by neuroinflammation and neurotrophic
disbalance after repeated psychostimulants.
http://www.mdpi.com/1424-8247/4/7/976/pdf
Abstract: Drugs of abuse induce plastic changes in the brain that seem to underlie
addictive phenomena. These plastic changes can be structural (morphological) or synaptic
(biochemical), and most of them take place in the mesolimbic and mesostriatal circuits.
Several addiction-related changes in brain circuits (hypofrontality, sensitization, tolerance)
as well as the outcome of treatment have been visualized in addicts to psychostimulants
using neuroimaging techniques. Repeated exposure to psychostimulants induces
morphological changes such as increase in the number of dendritic spines, changes in the
morphology of dendritic spines, and altered cellular coupling through new gap junctions.
Repeated exposure to psychostimulants also induces various synaptic adaptations, many of
them related to sensitization and neuroplastic processes, that include up- or
down-regulation of D1, D2 and D3 dopamine receptors, changes in subunits of G proteins,
increased adenylyl cyclase activity, cyclic AMP and protein kinase A in the nucleus
accumbens, increased tyrosine hydroxylase enzyme activity, increased calmodulin and
activated CaMKII in the ventral tegmental area, and increased deltaFosB, c-Fos and AP-1
binding proteins. Most of these changes are transient, suggesting that more lasting plastic
brain adaptations should take place. In this context, protein synthesis inhibitors block the
development of sensitization to cocaine, indicating that rearrangement of neural networks
must develop for the long-lasting plasticity required for addiction to occur.
Self-administration studies indicate the importance of glutamate neurotransmission in
neuroplastic changes underlying transition from use to abuse. Finally, plastic changes in
the addicted brain are enhanced and aggravated by neuroinflammation and neurotrophic
disbalance after repeated psychostimulants.
The Master Negative Regulator REST/NRSF Controls Adult Neurogenesis by Restraining the Neurogenic Program in Quiescent Stem Cells
And more information on neurogenesis. I wish I had enough smarts to put all the information on this together into a comprehensible article.
http://www.jneurosci.org/content/31/26/9772.abstract
Abstract
Transcriptional regulation is a critical mechanism in the birth, specification, and differentiation of granule neurons in the adult hippocampus. One of the first negative-acting transcriptional regulators implicated in vertebrate development is repressor element 1-silencing transcription/neuron-restrictive silencer factor (REST/NRSF)—thought to regulate hundreds of neuron-specific genes—yet its function in the adult brain remains elusive. Here we report that REST/NRSF is required to maintain the adult neural stem cell (NSC) pool and orchestrate stage-specific differentiation. REST/NRSF recruits CoREST and mSin3A corepressors to stem cell chromatin for the regulation of pro-neuronal target genes to prevent precocious neuronal differentiation in cultured adult NSCs. Moreover, mice lacking REST/NRSF specifically in NSCs display a transient increase in adult neurogenesis that leads to a loss in the neurogenic capacity of NSCs and eventually diminished granule neurons. Our work identifies REST/NRSF as a master negative regulator of adult NSC differentiation and offers a potential molecular target for neuroregenerative approaches.
http://www.jneurosci.org/content/31/26/9772.abstract
Abstract
Transcriptional regulation is a critical mechanism in the birth, specification, and differentiation of granule neurons in the adult hippocampus. One of the first negative-acting transcriptional regulators implicated in vertebrate development is repressor element 1-silencing transcription/neuron-restrictive silencer factor (REST/NRSF)—thought to regulate hundreds of neuron-specific genes—yet its function in the adult brain remains elusive. Here we report that REST/NRSF is required to maintain the adult neural stem cell (NSC) pool and orchestrate stage-specific differentiation. REST/NRSF recruits CoREST and mSin3A corepressors to stem cell chromatin for the regulation of pro-neuronal target genes to prevent precocious neuronal differentiation in cultured adult NSCs. Moreover, mice lacking REST/NRSF specifically in NSCs display a transient increase in adult neurogenesis that leads to a loss in the neurogenic capacity of NSCs and eventually diminished granule neurons. Our work identifies REST/NRSF as a master negative regulator of adult NSC differentiation and offers a potential molecular target for neuroregenerative approaches.
Breaking News: When One Hand Doesn't Wash the Other
Ok, this doesn't really apply to us unless we are medical practitioners. I remember getting a squeeze of Purell when I entered the PT sanctum and one handedly trying to get it to dry.
http://journals.lww.com/em-news/Fulltext/2011/07000/Breaking_News__When_One_Hand_Doesn_t_Wash_the.5.aspx
Who knew hand-washing could be so controversial? Donald M. Yealy, MD, didn't, but he does now.
Image...
Image ToolsWhen UPMC Presbyterian in Pittsburgh mounted a campaign to improve compliance in hand-washing with threats of stiff fines, the concept made its way into the media, with claims of thousand-dollar penalties being slapped on doctors who didn't comply. The reports were wrong, said Dr. Yealy, the chair of emergency medicine there. When a headline on one such article posed the question: “Fining Unwashed Hands — A Dirty Trick?” physicians lashed out. “At Utopia General Hospital, everyone who has patient contact washes their hands thoroughly before and after every encounter. I don't practice there. I practice in the real world,” one observed. (http://bit.ly/WashFine.)
No fines were actually implemented at UPMC Presbyterian, and were only to be imposed when the lack of hygiene occurred despite clear markings of the patient room and notice by a trained infection control employee. Since announcing the approach, no one failed to abide by the precautions or received a fine, and a recent pathogen outbreak was quelled, Dr. Yealy pointed out.
The effort at UPMC Presbyterian, which also involved “modeling” by physician and nursing leaders who washed hands prominently during patient care, helped increase compliance in the emergency department from below 50 percent to above 80 percent.
The Centers for Disease Control and Prevention has called hand-washing the most effective preventive measure for preventing hospital-acquired infection. But apparently it doesn't take much to get the negative feedback started on the subject of clean hands for safety's sake. After the New York Times published a seemingly objective and scientific look at the matter — explaining the dismal record of hand-washing in many health care settings and noting that new methods such as alcohol-detecting lapel badges that record a staff member's sanitation status might help boost the habit — readers from the health community posted messages both critical and defiant. (http://nyti.ms/kcM3Up.)
One took issue with the white coats and hospital gowns that are supposed to represent cleanliness, asserting the attire should be viewed as a possible source of contamination instead. “They wear their ‘scrubs' and other uniforms around infected patients in the hospital and then leave the hospital (wearing the garb), often getting onto crowded buses and trains. Doesn't this spread infections?” one wrote. Another complained that excessive hand-washing was injurious to personal health. “All winter, every winter, my hands hurt from cracks in the skin. Washing exacerbates this condition. Are there hospital workers who, like me, approach hand-washing with trepidation?”
The most frequently cited figure for adherence to hand-washing is 40 percent, and the most common reason for this low statistic is time pressure. (Infect Disease Clin North Am 2011;25[1]:21.) In fact, investigations show a direct relationship between hand-washing and high patient volume, according to Didier Pittet, a professor of medicine and the director of the disease control program at the University of Geneva Hospitals. He and colleagues have examined hand-washing in emergency and nonurgent care settings, and the relationship persists wherever it occurs, he said. (Emerg Infect Dis 2001;7[2]:234; http://1.usa.gov/lyGGmL.)
“Our findings suggest that habits cannot be overcome by reason [or] motivation alone, but instead the person needs to supplement the good intentions with specific ‘if-then' plans that spell out when and how they will break the habit,” said Thomas Webb, PhD, a lecturer in social health and psychology at the University of Sheffield in the United Kingdom.
Motivation is more complicated than is generally assumed. It involves several different internal questions: Can you do it, and are the resources available for doing it? Do you think it will work under these circumstances? And is it worth doing? It is the answer to that last question where motivation can crumble, said Scott Geller, PhD, a distinguished professor of psychology at Virginia Polytechnic Institute in Blacksburg.
Insurmountable interference — time crunch — may cause well-intentioned people like emergency physicians to answer “no” to that third question. “When no one is watching, self-motivation is essential,” he said. That's when personal ethics alone can spur correct acts. Severe stressors can quash that good intent, however. Say someone truly wants to protect patients from any possibility of infection, but is making a split-second decision to institute care instead of pausing for an alcohol wipe. If there are adverse consequences in addition to ethical considerations, the alcohol wipe is likely to be used, he said. This is why surveillance cameras at stoplights work. The same thing could apply to a medical setting, Dr. Geller noted.
In the UPMC Presbyterian emergency department, employees themselves monitored hand-washing, alerting each other when they didn't see it being done. But the hospital also hired ringers to pose as hospital staff and report hand-washing observations by moving round the hospital and ED without detection. “I never spotted any,” noted Dr. Yealy. “So apparently they really blend in.” The goal, he said, “was to raise the level of awareness and change behavior.”
The experience at UPMC Presbyterian has shown how placement of sanitizing stations can make a difference, he said. They seemed to serve as reminders to wash, and are most effective when put in high-traffic areas and in plain view at each bedside, Dr. Yealy observed. “I think it is really helpful to look at the engineering of hand-washing opportunities,” he said.
UPMC Presbyterian's hand-washing campaign is still underway. After all, even though compliance has doubled, “we want to get that last 15 percent or so,” Dr. Yealy said.
http://journals.lww.com/em-news/Fulltext/2011/07000/Breaking_News__When_One_Hand_Doesn_t_Wash_the.5.aspx
Who knew hand-washing could be so controversial? Donald M. Yealy, MD, didn't, but he does now.
Image...
Image ToolsWhen UPMC Presbyterian in Pittsburgh mounted a campaign to improve compliance in hand-washing with threats of stiff fines, the concept made its way into the media, with claims of thousand-dollar penalties being slapped on doctors who didn't comply. The reports were wrong, said Dr. Yealy, the chair of emergency medicine there. When a headline on one such article posed the question: “Fining Unwashed Hands — A Dirty Trick?” physicians lashed out. “At Utopia General Hospital, everyone who has patient contact washes their hands thoroughly before and after every encounter. I don't practice there. I practice in the real world,” one observed. (http://bit.ly/WashFine.)
No fines were actually implemented at UPMC Presbyterian, and were only to be imposed when the lack of hygiene occurred despite clear markings of the patient room and notice by a trained infection control employee. Since announcing the approach, no one failed to abide by the precautions or received a fine, and a recent pathogen outbreak was quelled, Dr. Yealy pointed out.
The effort at UPMC Presbyterian, which also involved “modeling” by physician and nursing leaders who washed hands prominently during patient care, helped increase compliance in the emergency department from below 50 percent to above 80 percent.
The Centers for Disease Control and Prevention has called hand-washing the most effective preventive measure for preventing hospital-acquired infection. But apparently it doesn't take much to get the negative feedback started on the subject of clean hands for safety's sake. After the New York Times published a seemingly objective and scientific look at the matter — explaining the dismal record of hand-washing in many health care settings and noting that new methods such as alcohol-detecting lapel badges that record a staff member's sanitation status might help boost the habit — readers from the health community posted messages both critical and defiant. (http://nyti.ms/kcM3Up.)
One took issue with the white coats and hospital gowns that are supposed to represent cleanliness, asserting the attire should be viewed as a possible source of contamination instead. “They wear their ‘scrubs' and other uniforms around infected patients in the hospital and then leave the hospital (wearing the garb), often getting onto crowded buses and trains. Doesn't this spread infections?” one wrote. Another complained that excessive hand-washing was injurious to personal health. “All winter, every winter, my hands hurt from cracks in the skin. Washing exacerbates this condition. Are there hospital workers who, like me, approach hand-washing with trepidation?”
The most frequently cited figure for adherence to hand-washing is 40 percent, and the most common reason for this low statistic is time pressure. (Infect Disease Clin North Am 2011;25[1]:21.) In fact, investigations show a direct relationship between hand-washing and high patient volume, according to Didier Pittet, a professor of medicine and the director of the disease control program at the University of Geneva Hospitals. He and colleagues have examined hand-washing in emergency and nonurgent care settings, and the relationship persists wherever it occurs, he said. (Emerg Infect Dis 2001;7[2]:234; http://1.usa.gov/lyGGmL.)
“Our findings suggest that habits cannot be overcome by reason [or] motivation alone, but instead the person needs to supplement the good intentions with specific ‘if-then' plans that spell out when and how they will break the habit,” said Thomas Webb, PhD, a lecturer in social health and psychology at the University of Sheffield in the United Kingdom.
Motivation is more complicated than is generally assumed. It involves several different internal questions: Can you do it, and are the resources available for doing it? Do you think it will work under these circumstances? And is it worth doing? It is the answer to that last question where motivation can crumble, said Scott Geller, PhD, a distinguished professor of psychology at Virginia Polytechnic Institute in Blacksburg.
Insurmountable interference — time crunch — may cause well-intentioned people like emergency physicians to answer “no” to that third question. “When no one is watching, self-motivation is essential,” he said. That's when personal ethics alone can spur correct acts. Severe stressors can quash that good intent, however. Say someone truly wants to protect patients from any possibility of infection, but is making a split-second decision to institute care instead of pausing for an alcohol wipe. If there are adverse consequences in addition to ethical considerations, the alcohol wipe is likely to be used, he said. This is why surveillance cameras at stoplights work. The same thing could apply to a medical setting, Dr. Geller noted.
In the UPMC Presbyterian emergency department, employees themselves monitored hand-washing, alerting each other when they didn't see it being done. But the hospital also hired ringers to pose as hospital staff and report hand-washing observations by moving round the hospital and ED without detection. “I never spotted any,” noted Dr. Yealy. “So apparently they really blend in.” The goal, he said, “was to raise the level of awareness and change behavior.”
The experience at UPMC Presbyterian has shown how placement of sanitizing stations can make a difference, he said. They seemed to serve as reminders to wash, and are most effective when put in high-traffic areas and in plain view at each bedside, Dr. Yealy observed. “I think it is really helpful to look at the engineering of hand-washing opportunities,” he said.
UPMC Presbyterian's hand-washing campaign is still underway. After all, even though compliance has doubled, “we want to get that last 15 percent or so,” Dr. Yealy said.
Monday, July 11, 2011
Biting flies and stroke rehab or mosquitos
This is one of those off the wall posts. While resting between sessions of tree cutup work, I would dangle my left arm over the arm rest and rest it on the ground. My reason is to let my arm muscles know they can relax but opportunistic flies would come by and give me painful bites on the arm and hand or just go straight through the sock If I had a really poor case of sensation this could be a wonderful therapy for reconnecting the pain receptors in the brain. For a longer term one you could try the scratching produced by mosquito bites. When I would go camping I would have to wear a mitten on my left hand to protect it from mosquito bites.
Tuesday, July 5, 2011
Scanner helps find traumatic brain injuries
This would be easily useable for finding penumbra or bleed drainage damage as a result of stroke. And then we could finally have a damage diagnosis that our therapists could use to set up therapies.
http://www.marinecorpstimes.com/news/2011/07/marine-scanner-traumatic-brain-injury-070211/
SAN DIEGO — An advanced, high-tech scanner is providing a team of Navy, Veterans Affairs Department and university researchers with detailed pictures of brain activity that will better identify traumatic brain injury, the signature but often-invisible war wound.
Moreover, said a lead researcher, an initial study involving 55 military members and veterans with mild or moderate TBI shows that the advanced imaging scanner — using a technique called magnetoencephalography, or MEG — also can reveal and identify post-traumatic stress disorder.
“We have some exciting data ... that the MEG potentially diagnoses PTSD,” said Mingxiong Huang, professor and associate director of the University of California, San Diego’s MEG Radiology Imaging Laboratory, in a June 1 interview.
The initial study involved 55 military and civilian patients, ages 18 to 45, with mild to moderate TBIs. The group includes 23 patients, mostly Marines, who endured blasts from improvised explosive devices, which are among the common injuries reported by Iraq and Afghanistan war veterans.
Huang said VA recently approved extending the study, which began in 2007, for another four years, and the research team, which includes UCSD professor Roland R. Lee and Dewleen Baker, a VA and Navy researcher, hopes to broaden the study with additional patients and expand its research toward better understanding what causes PTSD. The team plans to publish its initial study next month in a professional, peer-reviewed journal.
“Can we make the ‘invisible’ injury visible?” Huang said. “Being able to see the injury is really a key start to help understand how the brain recovers from TBI. The treatment and diagnosis of TBI and PTSD may be very different.”
Although the study is preliminary, researchers hope to help diagnose brain injuries in countless wounded military veterans, including those with less-obvious injuries from blasts, falls and concussions.
“Six to nine months after the injury, the majority of people with mild TBIs become symptom-free,” Huang said. “The brain, as a system, can recover.”
“But 20 percent of people with TBI have long-term symptoms,” he said, noting those patients will require additional therapy or medications, and some may need treatment and therapy for PTSD. “Part of the problem is we cannot see the injury,” he added.
Unlike an X-ray, the MEG system is a noninvasive machine and passively records electrical activity in brain tissue.
The scanner can locate abnormal areas of low-frequency waves, which are telltale signs of injured brain tissue.
“The brain is like a huge network [that] has to communicate with each other,” Huang said.
Mild and moderate TBIs, like concussions and “closed brain” wounds from blasts, often go undetected by more conventional imaging machines — including MRI and computerized tomography, or CT, scanners. An MRI can show bleeding, but in most cases, it doesn’t see damaged “axonal injuries” such as torn or shredded brain tissue that often mark mild TBIs, Huang wrote in an article he co-authored in the August 2009 issue of the Journal of Neurotrauma.
Although TBIs are considered neurological wounds, PTSD is a psychological disorder. But patients diagnosed with either share related symptoms tied to damaged tissue in specific parts of the brain. Huang said MEG scans of PTSD sufferers show injuries in the four main parts of the brain, including the amygdala and hippocampus, which control emotions, sensory responses and memory.
“With the MEG, you can visualize these areas that are injured,” he said.
In one case, a 17-year-old football player who suffered three concussions complained of headaches, dizziness, fatigue, poor memory and changes in speech and language — but several MRI and CT scans came up negative for TBI. The MEG scanner revealed injuries in two areas of his brain.
Another case of negative clinical MRI and CT scans involved a 27-year-old Marine who was knocked unconscious when his Humvee hit an IED. He later suffered from anxiety, irritability, poor memory and sleep, fatigue, dizziness and depression.
The Marine wasn’t diagnosed with PTSD, but a MEG scan showed brain injuries consistent with TBI, and possibly PTSD.
For months after he returned from Iraq, Wilson struggled with short-term memory, migraines and poor sleep; he said he knew he had a concussion and was frustrated when MRI and CT scans came up negative for TBI. The MEG scans, which Huang conducted, revealed TBI and showed him what was happening in his brain, which explained the problems he was having.
Wilson said those results helped him begin the healing process.
“For me, it was important to know what was PTSD and what was TBI,” he said.
He credits therapies with improving his functions and even easing his PTSD.
“It made everything else less severe, because it didn’t add to the anxiety and to the frustration,” he said. “I’ve become less hypervigilant, and I started sleeping better.”
Although the MEG scanners provide more detailed information than conventional MRI machines, there are far fewer of them available around the country. UCSD’s lab has the only working MEG scanner in California. Each MEG machine costs about $2.5 million, but there are higher operating costs, Huang said.
Although Wilson wasn’t part of Huang’s initial study, he said he hopes VA and the military expand the research and enable broader use of MEG scanners to help diagnose other wounded warriors, especially vets who are still struggling through problems and symptoms that remain undiagnosed.
“You have to sort it out, but it’s so hard to do that until you know what it is,” Wilson said.
http://www.marinecorpstimes.com/news/2011/07/marine-scanner-traumatic-brain-injury-070211/
SAN DIEGO — An advanced, high-tech scanner is providing a team of Navy, Veterans Affairs Department and university researchers with detailed pictures of brain activity that will better identify traumatic brain injury, the signature but often-invisible war wound.
Moreover, said a lead researcher, an initial study involving 55 military members and veterans with mild or moderate TBI shows that the advanced imaging scanner — using a technique called magnetoencephalography, or MEG — also can reveal and identify post-traumatic stress disorder.
“We have some exciting data ... that the MEG potentially diagnoses PTSD,” said Mingxiong Huang, professor and associate director of the University of California, San Diego’s MEG Radiology Imaging Laboratory, in a June 1 interview.
The initial study involved 55 military and civilian patients, ages 18 to 45, with mild to moderate TBIs. The group includes 23 patients, mostly Marines, who endured blasts from improvised explosive devices, which are among the common injuries reported by Iraq and Afghanistan war veterans.
Huang said VA recently approved extending the study, which began in 2007, for another four years, and the research team, which includes UCSD professor Roland R. Lee and Dewleen Baker, a VA and Navy researcher, hopes to broaden the study with additional patients and expand its research toward better understanding what causes PTSD. The team plans to publish its initial study next month in a professional, peer-reviewed journal.
“Can we make the ‘invisible’ injury visible?” Huang said. “Being able to see the injury is really a key start to help understand how the brain recovers from TBI. The treatment and diagnosis of TBI and PTSD may be very different.”
Although the study is preliminary, researchers hope to help diagnose brain injuries in countless wounded military veterans, including those with less-obvious injuries from blasts, falls and concussions.
“Six to nine months after the injury, the majority of people with mild TBIs become symptom-free,” Huang said. “The brain, as a system, can recover.”
“But 20 percent of people with TBI have long-term symptoms,” he said, noting those patients will require additional therapy or medications, and some may need treatment and therapy for PTSD. “Part of the problem is we cannot see the injury,” he added.
Meet the machine
The MEG system, a large machine that resembles a Transformers-size hair dryer, was originally designed for research into epilepsy, stroke and other brain disorders.Unlike an X-ray, the MEG system is a noninvasive machine and passively records electrical activity in brain tissue.
The scanner can locate abnormal areas of low-frequency waves, which are telltale signs of injured brain tissue.
“The brain is like a huge network [that] has to communicate with each other,” Huang said.
Mild and moderate TBIs, like concussions and “closed brain” wounds from blasts, often go undetected by more conventional imaging machines — including MRI and computerized tomography, or CT, scanners. An MRI can show bleeding, but in most cases, it doesn’t see damaged “axonal injuries” such as torn or shredded brain tissue that often mark mild TBIs, Huang wrote in an article he co-authored in the August 2009 issue of the Journal of Neurotrauma.
Although TBIs are considered neurological wounds, PTSD is a psychological disorder. But patients diagnosed with either share related symptoms tied to damaged tissue in specific parts of the brain. Huang said MEG scans of PTSD sufferers show injuries in the four main parts of the brain, including the amygdala and hippocampus, which control emotions, sensory responses and memory.
“With the MEG, you can visualize these areas that are injured,” he said.
In one case, a 17-year-old football player who suffered three concussions complained of headaches, dizziness, fatigue, poor memory and changes in speech and language — but several MRI and CT scans came up negative for TBI. The MEG scanner revealed injuries in two areas of his brain.
Another case of negative clinical MRI and CT scans involved a 27-year-old Marine who was knocked unconscious when his Humvee hit an IED. He later suffered from anxiety, irritability, poor memory and sleep, fatigue, dizziness and depression.
The Marine wasn’t diagnosed with PTSD, but a MEG scan showed brain injuries consistent with TBI, and possibly PTSD.
Finding answers
After now-retired Col. Gary Wilson survived an IED blast in Iraq, MRI and CT brain scans came up negative and showed normal functions despite the Marine officer’s symptoms, which included headaches, poor recollection and inattentiveness. In MEG scans, three parts of his brain “lit up” to reveal three injured areas that also reflected his symptoms, “so that explained very well the problems he was having,” Huang said.For months after he returned from Iraq, Wilson struggled with short-term memory, migraines and poor sleep; he said he knew he had a concussion and was frustrated when MRI and CT scans came up negative for TBI. The MEG scans, which Huang conducted, revealed TBI and showed him what was happening in his brain, which explained the problems he was having.
Wilson said those results helped him begin the healing process.
“For me, it was important to know what was PTSD and what was TBI,” he said.
He credits therapies with improving his functions and even easing his PTSD.
“It made everything else less severe, because it didn’t add to the anxiety and to the frustration,” he said. “I’ve become less hypervigilant, and I started sleeping better.”
Although the MEG scanners provide more detailed information than conventional MRI machines, there are far fewer of them available around the country. UCSD’s lab has the only working MEG scanner in California. Each MEG machine costs about $2.5 million, but there are higher operating costs, Huang said.
Although Wilson wasn’t part of Huang’s initial study, he said he hopes VA and the military expand the research and enable broader use of MEG scanners to help diagnose other wounded warriors, especially vets who are still struggling through problems and symptoms that remain undiagnosed.
“You have to sort it out, but it’s so hard to do that until you know what it is,” Wilson said.
Sunday, July 3, 2011
Dexamphetamine Improves Upper Extremity Outcome During Rehabilitation After Stroke: A Pilot Randomized Controlled Trial
So we can get high while getting rehab at the same time we take anti-depressants. I hope someone is figuring out the best therapy protocol for all this stuff..
http://nnr.sagepub.com/content/early/2011/06/28/1545968311405674.abstract
http://nnr.sagepub.com/content/early/2011/06/28/1545968311405674.abstract
Abstract
Background. For early inpatient stroke rehabilitation, the effectiveness of amphetamine combined with physiotherapy varies across studies. Objective. To investigate whether the recovery of activities of daily living (ADL, primary outcome) and motor function (secondary outcome) can be improved by dexamphetamine added to physiotherapy. Methods. In a double-blind, placebo-controlled trial, 16 patients, from 918 who were screened, were randomized to the experimental group (EG, dexamphetamine + physiotherapy) or control group (CG, placebo + physiotherapy). Both groups received multidisciplinary inpatient rehabilitation. Dexamphetamine (10 mg oral) or placebo was administered 2 days per week before physiotherapy. ADL and motor function were measured using the Chedoke–McMaster Stroke Assessment (CMSA) twice during baseline, every week during the 5-week treatment period, and at follow-up 1 week, 6 months, and 12 months after intervention. Results. The majority of ineligible patients had too little paresis, were on anticoagulants, or had a stroke >60 days prior to entry. Participants (EG, n = 7, age 70.3 ± 10 years, 5 women, 37.9 ± 9 days after stroke; CG, n = 9, age 65.2 ± 17 years, 3 women, 40.3 ± 9 days after stroke) did not differ at baseline except for the leg subscale. Analysis of variance from baseline to 1 week follow-up revealed significant improvements in favor of EG for subscales ADL (P = .023) and arm function (P = .020) at end of treatment. No adverse events were detected. Conclusion. In this small trial that was based on prior positive trials, significant gains in ADL and arm function suggest that the dose and timing of dexamphetamine can augment physiotherapy. Effect size calculation suggests inclusion of at least 25 patients per group in future studies (ClinicalTrials.gov number: NCT00572767).
Amitriptyline-Mediated Cognitive Enhancement in Aged 3×Tg Alzheimer's Disease Mice Is Associated with Neurogenesis and Neurotrophic Activity
While this is not directly related to stroke rehab, any research into how the brain works can't but help us stroke survivor
http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0021660s.
http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0021660s.
Abstract Top
Approximately 35 million people worldwide suffer from Alzheimer's disease (AD). Existing therapeutics, while moderately effective, are currently unable to stem the widespread rise in AD prevalence. AD is associated with an increase in amyloid beta (Aβ) oligomers and hyperphosphorylated tau, along with cognitive impairment and neurodegeneration. Several antidepressants have shown promise in improving cognition and alleviating oxidative stress in AD but have failed as long-term therapeutics. In this study, amitriptyline, an FDA-approved tricyclic antidepressant, was administered orally to aged and cognitively impaired transgenic AD mice (3×TgAD). After amitriptyline treatment, cognitive behavior testing demonstrated that there was a significant improvement in both long- and short-term memory retention. Amitriptyline treatment also caused a significant potentiation of non-toxic Aβ monomer with a concomitant decrease in cytotoxic dimer Aβ load, compared to vehicle-treated 3×TgAD controls. In addition, amitriptyline administration caused a significant increase in dentate gyrus neurogenesis as well as increases in expression of neurosynaptic marker proteins. Amitriptyline treatment resulted in increases in hippocampal brain-derived neurotrophic factor protein as well as increased tyrosine phosphorylation of its cognate receptor (TrkB). These results indicate that amitriptyline has significant beneficial actions in aged and damaged AD brains and that it shows promise as a tolerable novel therapeutic for the treatment of AD.Early Post-Stroke Cognition in Stroke Rehabilitation Patients Predicts Functional Outcome at 13 Months.
and another research study that really has no validity because they have not specified the starting point for any of the survivors. It would be helpful if they publically included the testing so all us survivors can either prove or disprove their hypothesis.
http://www.ncbi.nlm.nih.gov/pubmed/21720162?dopt=Abstract
http://www.ncbi.nlm.nih.gov/pubmed/21720162?dopt=Abstract
Abstract
Objective: To identify prognostic factors associated with functional outcome at 13 months in a sample of stroke rehabilitation patients. Specifically, we hypothesized that cognitive functioning early after stroke would predict long-term functional outcome independently of other factors. Methods: 163 stroke rehabilitation patients underwent a structured neuropsychological examination 2-3 weeks after hospital admittance, and their functional status was subsequently evaluated 13 months later with the modified Rankin Scale (mRS) as outcome measure. Three predictive models were built using linear regression analyses: a biological model (sociodemographics, apolipoprotein E genotype, prestroke vascular factors, lesion characteristics and neurological stroke-related impairment); a functional model (pre- and early post-stroke cognitive functioning, personal and instrumental activities of daily living, ADL, and depressive symptoms), and a combined model (including significant variables, with p value <0.05, from the biological and functional models). Results: A combined model of 4 variables best predicted long-term functional outcome with explained variance of 49%: neurological impairment (National Institute of Health Stroke Scale; β = 0.402, p < 0.001), age (β = 0.233, p = 0.001), post-stroke cognitive functioning (Repeatable Battery of Neuropsychological Status, RBANS; β = -0.248, p = 0.001) and prestroke personal ADL (Barthel Index; β = -0.217, p = 0.002). Further linear regression analyses of which RBANS indexes and subtests best predicted long-term functional outcome showed that Coding (β = -0.484, p < 0.001) and Figure Copy (β = -0.233, p = 0.002) raw scores at baseline explained 42% of the variance in mRS scores at follow-up. Conclusions: Early post-stroke cognitive functioning as measured by the RBANS is a significant and independent predictor of long-term functional post-stroke outcome.Friday, July 1, 2011
Chainsaws and stroke rehabilitation
STOP READING NOW. THIS IS A JOKE AND SARCASM. DO NOT ATTEMPT ANYTHING LIKE THIS WITHOUT YOUR DOCTORS PERMISSION. My dad wanted a butternut tree cut down and I wanted to help since I wanted a lot of the wood for woodturning. Dad is 84 and shouldn't really be running a chainsaw all day long, thats what younger sons like me are for.
My help was mostly piling branches and getting the foot-long pieces I wanted out of the way. Since I can't pick up any wood with two hands I would walk back and forth dozens of times with one piece of wood in my right hand. I have a cool looking ice tongs grabber that I use to pick up the hefty chunks of wood(20-40 lbs.) This came from eBay and I just noticed that they have another for sale. My walking deteriorates with the weight pulling me on the right side but it definitely strengthens the left leg. Dad jokingly said that I should use the chainsaw as therapy, my right hand would be the trigger finger and the left hand on top basically getting lots of vibrations and either pushing down or pulling it up. I can just see the therapy disclaimer, we are not responsible if the chainsaw gets away from you and cuts off one of your limbs. Side effects: hearing loss, massive bleeding, loss of limbs, fingers, death.
Fishing and stroke rehaB
I'm at my parents cabin by Upper Red Lake, Minnesota. Walleyes is the object of this vacation. This will be the third year I've done this. We troll with minnows on rods and reels. I have to use the old style closed face spinning reel because I can wrap my affected hand around the grip and use my good hand to reel up the line. The open face spinning reel is just the opposite, my good hand would be on the grip and my affected hand would have to try to reel in the line. That would be an exercise in futility. I caught and landed 3 walleyes the first night, didn't even have to hand the rod and reel off to someone else. Dad thinks the hand is getting better, it is but this year I haven't gotten a large enough fish to test the limits of the left hand. I have to fish with someone else along because I never would be able to get the minnow on the hook. Hey lets get a proposal to NINDS and have fishing be one of the proven hand therapies. And require therapy departments to have boats, motors and tackle.
I love this because the usual case is fishing in the morning, lunch, then an afternoon nap, dinner, a walk down the gravel road, card games using a block of wood with grooves in it to hold the cards, drive to the local bar/restaurant for wireless access to update blog, sleep.
I love this because the usual case is fishing in the morning, lunch, then an afternoon nap, dinner, a walk down the gravel road, card games using a block of wood with grooves in it to hold the cards, drive to the local bar/restaurant for wireless access to update blog, sleep.
Tuesday, June 28, 2011
Nicotinergic impact on focal and non-focal neuroplasticity induced by non-invasive brain stimulation in non-smoking humans
I think this says nicotine in patch form helps with neuroplasticity. 32 pages in all.
http://repository.peerproject.eu:8080/jspui/bitstream/123456789/15484/1/PEER_stage2_10.1038%252Fnpp.2010.227.pdf
Abstract
Nicotine improves cognitive performance and modulates neuroplasticity in brain networks. The
neurophysiological mechanisms underlying nicotine-induced behavioral changes have been
sparsely studied, especially in humans. Global cholinergic activation focuses plasticity in
humans. However, the specific contribution of nicotinic receptors to these effects is unclear.
Henceforth, we explored the impact of nicotine on non-focal neuroplasticity induced by
transcranial direct current stimulation (tDCS) and focal, synapse-specific plasticity induced by
paired associative stimulation (PAS) in healthy non-smoking individuals. Forty eight subjects
participated in the study. Each subject received placebo and nicotine patches combined with one
of the stimulation protocols to the primary motor cortex in different sessions. Transcranial
magnetic stimulation (TMS) - elicited motor evoked potential (MEP) amplitudes were recorded
as a measure of corticospinal excitability until the evening of the second day following the
stimulation. Nicotine abolished or reduced both PAS- and tDCS-induced inhibitory
neuroplasticity. Non-focal facilitatory plasticity was also abolished, whereas focal facilitatory
plasticity was slightly prolonged by nicotine. Thus, nicotinergic influence on facilitatory, but not
inhibitory plasticity mimics that of global cholinergic enhancement. Therefore, activating
nicotinic receptors has clearly discernable effects from global cholinergic activation. These
nicotine-generated plasticity alterations might be important for the effects of the drug on
cognitive function.
http://repository.peerproject.eu:8080/jspui/bitstream/123456789/15484/1/PEER_stage2_10.1038%252Fnpp.2010.227.pdf
Abstract
Nicotine improves cognitive performance and modulates neuroplasticity in brain networks. The
neurophysiological mechanisms underlying nicotine-induced behavioral changes have been
sparsely studied, especially in humans. Global cholinergic activation focuses plasticity in
humans. However, the specific contribution of nicotinic receptors to these effects is unclear.
Henceforth, we explored the impact of nicotine on non-focal neuroplasticity induced by
transcranial direct current stimulation (tDCS) and focal, synapse-specific plasticity induced by
paired associative stimulation (PAS) in healthy non-smoking individuals. Forty eight subjects
participated in the study. Each subject received placebo and nicotine patches combined with one
of the stimulation protocols to the primary motor cortex in different sessions. Transcranial
magnetic stimulation (TMS) - elicited motor evoked potential (MEP) amplitudes were recorded
as a measure of corticospinal excitability until the evening of the second day following the
stimulation. Nicotine abolished or reduced both PAS- and tDCS-induced inhibitory
neuroplasticity. Non-focal facilitatory plasticity was also abolished, whereas focal facilitatory
plasticity was slightly prolonged by nicotine. Thus, nicotinergic influence on facilitatory, but not
inhibitory plasticity mimics that of global cholinergic enhancement. Therefore, activating
nicotinic receptors has clearly discernable effects from global cholinergic activation. These
nicotine-generated plasticity alterations might be important for the effects of the drug on
cognitive function.
Monday, June 27, 2011
Role of transcription factors in neurogenesis after cerebral ischemia
The last line with all the factors listed sure sounds like a dedicated res
earcher could work for years on this stuff.
http://www.reference-global.com/doi/abs/10.1515/RNS.2011.034
earcher could work for years on this stuff.http://www.reference-global.com/doi/abs/10.1515/RNS.2011.034
Abstract
Studies have revealed that the adult mammalian brain has the capacity to regenerate some neurons after cerebral ischemia. And this perspective on neurogenesis adds to the conceptual framework for strategies for the repair of ischemia-induced brain injury, that is, if the effect of ischemia-induced neurogenesis is enhanced, then the recovery of brain function after stroke can be promoted. Neurogenesis is a multistep process that requires the proliferation of neural stem/progenitor cells, migration and that new cells differentiate, survive and integrate into existing neural networks. For that to occur, the same concerted action of various factors is needed, especially transcription factors which regulate the expression of many moleculars and interact with them to promote neurogenesis. This review article gives a brief overview of some transcription factors (NF-κB, Hes, STAT3, AP-1, CREB, HIF1, Pax6, Tcf/Lef, Gli, Sox2, Olig2, Dlx2, TLX, Bmi-1) in ischemia-induced neurogenesis.
The Pessimist's and Optimist's Views of Adult Neurogenesis
I'm not willing to spend $31.50 to find out what these scientists have to say., I wonder if one of my German readers could get the complete article if their government sponsored the research.
http://www.sciencedirect.com/science/article/pii/S0092867411006532
The reports by Bonaguidi et al. (in this issue of Cell) and Encinas et al. (in Cell Stem Cell) come to differing conclusions about whether and how the proliferation of radial glia-like stem cells of the adult hippocampus impacts their long-term potential for neurogenesis
http://www.sciencedirect.com/science/article/pii/S0092867411006532
The reports by Bonaguidi et al. (in this issue of Cell) and Encinas et al. (in Cell Stem Cell) come to differing conclusions about whether and how the proliferation of radial glia-like stem cells of the adult hippocampus impacts their long-term potential for neurogenesis
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