This is so f*cking stupid, this should have been a standard stroke protocol 30 years ago. Tells you how bad our stroke associations are.
http://www.ptproductsonline.com/2014/05/stroke-recovery-include-exercise-prescription-study-says/
Saturday, May 31, 2014
Taiko drumming for stroke recovery
Went to a Taiko drumming concert tonight and then the 'The Twilight Samurai' movie, both were great.
A great stroke association would have created a video of this drumming and focus on the arm and hand movements so you could get lots of action observation. And the music would be great for your recovery. A two-fer. But your stroke association won't do this, that would require thought and innovation.
These three guys at least have large enough drumsticks that I might be able to grasp them.
https://www.youtube.com/watch?v=C7HL5wYqAbU
Or these 11-13 youngsters.
https://www.youtube.com/watch?v=CsKqBy2uJ34
Or a full drum line.
https://www.youtube.com/watch?v=YNmXNc95ncU
There are classes only about 40 minutes from me. If I ever get hand grasp back and can lift my arm over my shoulder I would do this.
A great stroke association would have created a video of this drumming and focus on the arm and hand movements so you could get lots of action observation. And the music would be great for your recovery. A two-fer. But your stroke association won't do this, that would require thought and innovation.
These three guys at least have large enough drumsticks that I might be able to grasp them.
https://www.youtube.com/watch?v=C7HL5wYqAbU
Or these 11-13 youngsters.
https://www.youtube.com/watch?v=CsKqBy2uJ34
Or a full drum line.
https://www.youtube.com/watch?v=YNmXNc95ncU
There are classes only about 40 minutes from me. If I ever get hand grasp back and can lift my arm over my shoulder I would do this.
Vitamin D and inflammatory diseases
Is some of the aftereffects of stroke caused by inflammation? And would this help us? Doctor?
http://www.dovepress.com/articles.php?article_id=17054
Published Date May 2014
Volume 2014:7 Pages 69 - 87
Kai Yin, Devendra K Agrawal
Center for Clinical and Translational Science, Creighton University School of Medicine, Omaha, NE, USA
Abstract: Beyond its critical function in calcium homeostasis, vitamin D has recently been found to play an important role in the modulation of the immune/inflammation system via regulating the production of inflammatory cytokines and inhibiting the proliferation of proinflammatory cells, both of which are crucial for the pathogenesis of inflammatory diseases. Several studies have associated lower vitamin D status with increased risk and unfavorable outcome of acute infections. Vitamin D supplementation bolsters clinical responses to acute infection. Moreover, chronic inflammatory diseases, such as atherosclerosis-related cardiovascular disease, asthma, inflammatory bowel disease, chronic kidney disease, nonalcoholic fatty liver disease, and others, tend to have lower vitamin D status, which may play a pleiotropic role in the pathogenesis of the diseases. In this article, we review recent epidemiological and interventional studies of vitamin D in various inflammatory diseases. The potential mechanisms of vitamin D in regulating immune/inflammatory responses in inflammatory diseases are also discussed.
http://www.dovepress.com/articles.php?article_id=17054
Authors: Yin K, Agrawal DK
Published Date May 2014
Volume 2014:7 Pages 69 - 87
DOI: http://dx.doi.org/10.2147/JIR.S63898
| Received: |
11 March 2014 
|
|---|---|
| Accepted: | 08 April 2014 |
| Published: | 29 May 2014 |
Center for Clinical and Translational Science, Creighton University School of Medicine, Omaha, NE, USA
Abstract: Beyond its critical function in calcium homeostasis, vitamin D has recently been found to play an important role in the modulation of the immune/inflammation system via regulating the production of inflammatory cytokines and inhibiting the proliferation of proinflammatory cells, both of which are crucial for the pathogenesis of inflammatory diseases. Several studies have associated lower vitamin D status with increased risk and unfavorable outcome of acute infections. Vitamin D supplementation bolsters clinical responses to acute infection. Moreover, chronic inflammatory diseases, such as atherosclerosis-related cardiovascular disease, asthma, inflammatory bowel disease, chronic kidney disease, nonalcoholic fatty liver disease, and others, tend to have lower vitamin D status, which may play a pleiotropic role in the pathogenesis of the diseases. In this article, we review recent epidemiological and interventional studies of vitamin D in various inflammatory diseases. The potential mechanisms of vitamin D in regulating immune/inflammatory responses in inflammatory diseases are also discussed.
Friday, May 30, 2014
Treating anxiety can improve patients' sleep
Since survivors need as much sleep as possible this should be a priority. Our anxiety is caused by our doctors not giving us an objective diagnosis or any protocols that will get us to 100% recovery. Solve those damn problems and survivors will have much less anxiety and sleep better. I don't care how difficult this is. Step up to the damn plate and do your job.
http://www.clinicaladvisor.com/treating-anxiety-can-improve-patients-sleep/article/348974/?
Anxiety plays a part in many illnesses, and the effects of anxiety follow patients through their daily lives. More than 16 million people deal with some type of anxiety disorder, including social anxiety disorder, generalized anxiety disorder, obsessive-compulsive disorder, panic disorder and post-traumatic stress disorder.
Being a sleep specialist, I see anxiety most when it involves a patient's sleep, but anxiety doesn't stop after patients wake up in the morning. Anxiety has a huge impact on everyday life.
Patients with anxiety report being unable to complete tasks. They often drink or use drugs, feel isolated and stop participating in life. Emotionally, patients with anxiety can be nervous and fearful. Physically, they often experience palpitations, difficulty breathing, dizziness, sweating, restlessness and an inability to concentrate.
My patients with insomnia often have difficulty turning off their thoughts at bedtime, unable to stop worrying. These patients experience sleep panic attacks, and patients with PTSD often talk about their recurring nightmares.
Anywhere from 50% to 70% of patients with generalized anxiety disorder have difficulty sleeping. Because patients with anxiety often have disturbed sleep, they start having anxiety about their lack of sleep.
Polysomnograms of patients with anxiety show prolonged sleep onset, decreased sleep efficiency, and decreased deep (slow wave) sleep. Although patients do not usually complain of daytime sleepiness, they often complain of daytime fatigue.
Prescribing antidepressants and benzodiazepines is standard treatment. However, cognitive behavioral strategies are recommended to help patients manage their anxiety. Have the name of a trusted professional ready for recommending to patients diagnosed with anxiety.
Encourage patients to find pleasurable hobbies to engage in, participate in regular exercise, and focus on positive emotions. Meditation and yoga may also be helpful.
Treating sleep disorders in patients' with anxiety may help ease patients' worries. How do you treat your patients who have panic disorders? Are you doing anything differently?
Sharon M. O'Brien, MPAS, PA-C, is a practicing clinician with an interest is helping patients understand the importance of sleep hygiene and the impact of sleep on health.
http://www.clinicaladvisor.com/treating-anxiety-can-improve-patients-sleep/article/348974/?
Anxiety plays a part in many illnesses, and the effects of anxiety follow patients through their daily lives. More than 16 million people deal with some type of anxiety disorder, including social anxiety disorder, generalized anxiety disorder, obsessive-compulsive disorder, panic disorder and post-traumatic stress disorder.
Being a sleep specialist, I see anxiety most when it involves a patient's sleep, but anxiety doesn't stop after patients wake up in the morning. Anxiety has a huge impact on everyday life.
Patients with anxiety report being unable to complete tasks. They often drink or use drugs, feel isolated and stop participating in life. Emotionally, patients with anxiety can be nervous and fearful. Physically, they often experience palpitations, difficulty breathing, dizziness, sweating, restlessness and an inability to concentrate.
My patients with insomnia often have difficulty turning off their thoughts at bedtime, unable to stop worrying. These patients experience sleep panic attacks, and patients with PTSD often talk about their recurring nightmares.
Anywhere from 50% to 70% of patients with generalized anxiety disorder have difficulty sleeping. Because patients with anxiety often have disturbed sleep, they start having anxiety about their lack of sleep.
Polysomnograms of patients with anxiety show prolonged sleep onset, decreased sleep efficiency, and decreased deep (slow wave) sleep. Although patients do not usually complain of daytime sleepiness, they often complain of daytime fatigue.
Prescribing antidepressants and benzodiazepines is standard treatment. However, cognitive behavioral strategies are recommended to help patients manage their anxiety. Have the name of a trusted professional ready for recommending to patients diagnosed with anxiety.
Encourage patients to find pleasurable hobbies to engage in, participate in regular exercise, and focus on positive emotions. Meditation and yoga may also be helpful.
Treating sleep disorders in patients' with anxiety may help ease patients' worries. How do you treat your patients who have panic disorders? Are you doing anything differently?
Sharon M. O'Brien, MPAS, PA-C, is a practicing clinician with an interest is helping patients understand the importance of sleep hygiene and the impact of sleep on health.
What you wear can change your brain
So when will your hospital hand out Superman or Wonder Woman t-shirts to stroke survivors? If I were to put on a white doctors coat it would flatline my mental abilities.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=142322&CultureCode=en
Clothing affects our mental processes and perceptions which can change our minds and the way we think, according to research by Professor Karen Pine from the University of Hertfordshire.
When Professor Pine asked students to put on a Superman t-shirt there was a scientific reason behind the request. She wanted to know if the heroic clothing would change the students’ thinking. She found it boosted their impression of themselves and made them feel physically stronger. This, and other discoveries of how clothing can change our minds, is the topic of her new book called Mind What You Wear: The Psychology of Fashion.
Professor Karen Pine, from the department of Psychology at the University of Hertfordshire, explained: “When wearing a Superman t-shirt the students rated themselves as more likeable and superior to other students. When asked to estimate how much they could physically lift, those in a Superman t-shirt thought they were stronger than students in a plain t-shirt, or in their own clothing.”
This research, and other clothing research described in the book, shows how people’s mental processes and perceptions can be primed by clothing, as they internalise the symbolic meaning of their outer layers.
In Mind What You Wear, Professor Pine describes how women who were given a maths test performed worse when wearing a swimsuit than when wearing a sweater. She describes how putting on a white coat improved people’s mental agility, as their brain was primed to take on the mental capacities they associated with being a doctor.
Professor Pine’s book gives fascinating insights into the cognitive, social and emotional consequences of what we wear. Her previous research discovered that women are more likely to wear jeans when they are depressed. In this book she reveals that when women are stressed they wear less of their wardrobe, neglecting 90% of it, and the main reason women dress up is not to look attractive but to feel confident.
Professor Pine added: “As well as scientific research, my book also contains tips on how to feel happier and more confident with the right clothes, explaining not only that we are what we wear, but that we become what we wear.”
http://www.alphagalileo.org/ViewItem.aspx?ItemId=142322&CultureCode=en
Clothing affects our mental processes and perceptions which can change our minds and the way we think, according to research by Professor Karen Pine from the University of Hertfordshire.
When Professor Pine asked students to put on a Superman t-shirt there was a scientific reason behind the request. She wanted to know if the heroic clothing would change the students’ thinking. She found it boosted their impression of themselves and made them feel physically stronger. This, and other discoveries of how clothing can change our minds, is the topic of her new book called Mind What You Wear: The Psychology of Fashion.
Professor Karen Pine, from the department of Psychology at the University of Hertfordshire, explained: “When wearing a Superman t-shirt the students rated themselves as more likeable and superior to other students. When asked to estimate how much they could physically lift, those in a Superman t-shirt thought they were stronger than students in a plain t-shirt, or in their own clothing.”
This research, and other clothing research described in the book, shows how people’s mental processes and perceptions can be primed by clothing, as they internalise the symbolic meaning of their outer layers.
In Mind What You Wear, Professor Pine describes how women who were given a maths test performed worse when wearing a swimsuit than when wearing a sweater. She describes how putting on a white coat improved people’s mental agility, as their brain was primed to take on the mental capacities they associated with being a doctor.
Professor Pine’s book gives fascinating insights into the cognitive, social and emotional consequences of what we wear. Her previous research discovered that women are more likely to wear jeans when they are depressed. In this book she reveals that when women are stressed they wear less of their wardrobe, neglecting 90% of it, and the main reason women dress up is not to look attractive but to feel confident.
Professor Pine added: “As well as scientific research, my book also contains tips on how to feel happier and more confident with the right clothes, explaining not only that we are what we wear, but that we become what we wear.”
Thursday, May 29, 2014
Multi-sensory room helps those suffering from strokes
This enriched environment was reported for stroke way back in 2011 by Dr. Corbett. Only 3 years to do something so incredibly simple.
Does your hospital have one?
http://www.mysuncoast.com/news/local/multi-sensory-room-helps-those-suffering-from-strokes/article_be12276a-e6ae-11e3-a35e-0017a43b2370.html
Now a new multi-sensory room on the Suncoast helps stroke patients and others via neuro-rehabilitation.
Colors, lights, sounds and smells can awaken memories, like your favorite sunset on the gulf, mockingbirds, or a fresh cut lawn. And now a room dedicated to the senses helps Suncoast residents suffering stroke, dementia, and other conditions.
There is a soft blue light, a light citrus scent, and video projected on a wall. “When they walk in that room, their eyes light up,” says Heidi Brown, CEO of Kobernick Anchin Benderson.
The multi-sensory room at Anchin Pavilion makes a difference to residents, she says. “They're so excited to have the sights, and the smells, and the sounds that they're not having in the opportunity to experience on a day to day basis.”
Colors trigger emotions, but it’s not just the color that resident Helen Waldman likes. “It’s smooth, it feels smooth.”
She enjoys the nature scenes of butterflys. “And fish, because they're gentle.”
The variety of sensory stimulation helps many people, including those suffering stroke, says activities director April Moschini. “Usually people who have a stroke are affected on one side.”
Moving sand from one side to another incorporates both sides of the body. “Being able to use things that are tactile and using both of the sides of your body helps bring them back to baseline.”
The swinging chair awakens vestibular stimulation. “That is for somebody with limited mobility. It allows them to feel what it's like to move in space again.”
Registered nurse Judith Yaeger says she sneaks into the room every chance she gets to play with her personal favorite, the fiberoptic strands. “They change colors; they're not supposed to be warm, but they are a little warm, and they're just very relaxing, you can do all kinds of things with them.”
Moschini say dramatic changes occur with patients suffering aphasia, when a person's previous capacity to understand or express language is impaired. “They may suddenly be stimulated to be verbal, or vocalize something.”
Brown remembers the room’s effect on a specific non-verbal patient’s reaction. “She was actually able to smile and laugh, and have a conversation, and that's the benefit.”
Sensory perception and multi-sensory rooms and tools are used and help people with a number of conditions, including PTSD and brain trauma.
The multisensory room at Anchin Pavilion is open to the community, and receives outside clients by appointment. It is located at 1959 Honore Avenue in Sarasota.
Video at link.
Does your hospital have one?
http://www.mysuncoast.com/news/local/multi-sensory-room-helps-those-suffering-from-strokes/article_be12276a-e6ae-11e3-a35e-0017a43b2370.html
Now a new multi-sensory room on the Suncoast helps stroke patients and others via neuro-rehabilitation.
Colors, lights, sounds and smells can awaken memories, like your favorite sunset on the gulf, mockingbirds, or a fresh cut lawn. And now a room dedicated to the senses helps Suncoast residents suffering stroke, dementia, and other conditions.
There is a soft blue light, a light citrus scent, and video projected on a wall. “When they walk in that room, their eyes light up,” says Heidi Brown, CEO of Kobernick Anchin Benderson.
The multi-sensory room at Anchin Pavilion makes a difference to residents, she says. “They're so excited to have the sights, and the smells, and the sounds that they're not having in the opportunity to experience on a day to day basis.”
Colors trigger emotions, but it’s not just the color that resident Helen Waldman likes. “It’s smooth, it feels smooth.”
She enjoys the nature scenes of butterflys. “And fish, because they're gentle.”
The variety of sensory stimulation helps many people, including those suffering stroke, says activities director April Moschini. “Usually people who have a stroke are affected on one side.”
Moving sand from one side to another incorporates both sides of the body. “Being able to use things that are tactile and using both of the sides of your body helps bring them back to baseline.”
The swinging chair awakens vestibular stimulation. “That is for somebody with limited mobility. It allows them to feel what it's like to move in space again.”
Registered nurse Judith Yaeger says she sneaks into the room every chance she gets to play with her personal favorite, the fiberoptic strands. “They change colors; they're not supposed to be warm, but they are a little warm, and they're just very relaxing, you can do all kinds of things with them.”
Moschini say dramatic changes occur with patients suffering aphasia, when a person's previous capacity to understand or express language is impaired. “They may suddenly be stimulated to be verbal, or vocalize something.”
Brown remembers the room’s effect on a specific non-verbal patient’s reaction. “She was actually able to smile and laugh, and have a conversation, and that's the benefit.”
Sensory perception and multi-sensory rooms and tools are used and help people with a number of conditions, including PTSD and brain trauma.
The multisensory room at Anchin Pavilion is open to the community, and receives outside clients by appointment. It is located at 1959 Honore Avenue in Sarasota.
Video at link.
Early Mobilisation Following Stroke
These people still don't understand that therapy after the stroke is not where research should take place. You stop the neuronal cascade of death and that will result in much less death and disability. Once again we see that nothing exists as standardized stroke protocols. Why do I have to point out these fucking simplistic facts.
http://www.touchneurology.com/articles/early-mobilisation-following-stroke
Stroke is a sudden loss of cerebral blood flow caused either by occlusion (85 % of cases) or rupture of the cerebral artery manifesting with focal neurological deficits.1 One-third of stroke patients are younger than and two-thirds are older than 65 years of age.2 Stroke can have both immediate and ongoing physical consequences. Disability and mortality represent the most relevant clinical outcomes. The degree of disability varies from devastating outcome with total dependence on family/carer to minimal and manageable disability.3 Within 12 months of stroke, one-third of stroke patients will die and another third are left with restriction in performing simple activities of daily living (ADL). Considering the high prevalence of the disease, the burden of post-stroke disability is of primary public health importance, translating to a substantial cost worldwide. In the US in 2008, for example, the direct and indirect costs of stroke are estimated to be more than $65 billion.4 Much of this cost probably relates to the physical disability. Any treatment that improves functional outcome can significantly reduce disability and costs, setting regaining of functional independence, defined as improvement in mobility and activities of ADL, as an important goal.4 The potential for recovery varies substantially across stroke patients. Factors associated with poor functional recovery include stroke severity, age and, to a lesser extent, diabetes.5
Today, rehabilitation is recognised as a cornerstone of multidisciplinary stroke care and can reduce the number of patients who are left handicapped. Forty per cent of stroke patients require active rehabilitation services.3 In recent years, rehabilitation has been shown to influence both brain recovery and reorganisation, especially in relation to motor impairment. Comprehensive rehabilitation programmes appear to improve functional recovery over standard care in terms of speed and extent of recovery.6 It is noteworthy that neurological recovery is not linear and most of it occurs within the first 3–6 months, although some patients show recovery over prolonged timelines.
Rehabilitation intensity depends on the status of the patient and degree of disability. If the patient is unconscious, rehabilitation is passive to prevent contractions, pressure ulcers and to prevent distress when movement is regained.3 However, there is still debate regarding the optimal intensity of physical therapy following stroke, with conflicting results across the different studies ranging from no benefit to significant functional improvement.6 This discrepancy may reflect differences in methodology, patient selection and outcome scales.
The Rationale Behind Very Early Mobilisation
Very early mobilisation (VEM) is a distinctive characteristic of care that involves starting mobilisation, including sitting up, getting out of bed, standing and walking, early after stroke and continuing at frequent intervals. However, the exact meaning of VEM is not well established and varies between 1 day to 3 months following symptoms onset.7
Previous studies have shown that induction of neurotrophic factors is associated with neural repair within the first 2 weeks after stroke and, thus, may modulate greater plasticity that may restore function in the periinfarct tissue and supplementary motor areas.8 This experience dependent cortical plasticity has been well documented in normal and injured brains.7 It may also enable the brain to better respond to rehabilitation, suggesting that efficacy of therapy may vary considerably with the timeline of initiation. The interaction between plasticity and recovery is, however, complicated and individualistic; therefore, it is of importance to apply the appropriate rehabilitation strategy at the appropriate time. Efforts are being made to develop more efficient rehabilitate strategies that utilise current knowledge of cortical plasticity. In addition to enhancing plasticity, VEM may prevent complications with a high risk of causing harm such as deep vein thrombosis, pulmonary embolism, contractures, infections, sores, muscle atrophy and deterioration in cardiorespiratory function. The complications associated with immobility were shown to be responsible for 51 % of deaths in patients with cerebral infarction.9 In another analysis of stroke unit systems,9 stroke unit care appeared to reduce complications of immobility, and infections, in particular. Early mobilisation may also have important psychological effects on a patient’s motivation, well-being and quality of life.6
Another page and references at link.
http://www.touchneurology.com/articles/early-mobilisation-following-stroke
Stroke is a sudden loss of cerebral blood flow caused either by occlusion (85 % of cases) or rupture of the cerebral artery manifesting with focal neurological deficits.1 One-third of stroke patients are younger than and two-thirds are older than 65 years of age.2 Stroke can have both immediate and ongoing physical consequences. Disability and mortality represent the most relevant clinical outcomes. The degree of disability varies from devastating outcome with total dependence on family/carer to minimal and manageable disability.3 Within 12 months of stroke, one-third of stroke patients will die and another third are left with restriction in performing simple activities of daily living (ADL). Considering the high prevalence of the disease, the burden of post-stroke disability is of primary public health importance, translating to a substantial cost worldwide. In the US in 2008, for example, the direct and indirect costs of stroke are estimated to be more than $65 billion.4 Much of this cost probably relates to the physical disability. Any treatment that improves functional outcome can significantly reduce disability and costs, setting regaining of functional independence, defined as improvement in mobility and activities of ADL, as an important goal.4 The potential for recovery varies substantially across stroke patients. Factors associated with poor functional recovery include stroke severity, age and, to a lesser extent, diabetes.5
Today, rehabilitation is recognised as a cornerstone of multidisciplinary stroke care and can reduce the number of patients who are left handicapped. Forty per cent of stroke patients require active rehabilitation services.3 In recent years, rehabilitation has been shown to influence both brain recovery and reorganisation, especially in relation to motor impairment. Comprehensive rehabilitation programmes appear to improve functional recovery over standard care in terms of speed and extent of recovery.6 It is noteworthy that neurological recovery is not linear and most of it occurs within the first 3–6 months, although some patients show recovery over prolonged timelines.
Rehabilitation intensity depends on the status of the patient and degree of disability. If the patient is unconscious, rehabilitation is passive to prevent contractions, pressure ulcers and to prevent distress when movement is regained.3 However, there is still debate regarding the optimal intensity of physical therapy following stroke, with conflicting results across the different studies ranging from no benefit to significant functional improvement.6 This discrepancy may reflect differences in methodology, patient selection and outcome scales.
The Rationale Behind Very Early Mobilisation
Very early mobilisation (VEM) is a distinctive characteristic of care that involves starting mobilisation, including sitting up, getting out of bed, standing and walking, early after stroke and continuing at frequent intervals. However, the exact meaning of VEM is not well established and varies between 1 day to 3 months following symptoms onset.7
Previous studies have shown that induction of neurotrophic factors is associated with neural repair within the first 2 weeks after stroke and, thus, may modulate greater plasticity that may restore function in the periinfarct tissue and supplementary motor areas.8 This experience dependent cortical plasticity has been well documented in normal and injured brains.7 It may also enable the brain to better respond to rehabilitation, suggesting that efficacy of therapy may vary considerably with the timeline of initiation. The interaction between plasticity and recovery is, however, complicated and individualistic; therefore, it is of importance to apply the appropriate rehabilitation strategy at the appropriate time. Efforts are being made to develop more efficient rehabilitate strategies that utilise current knowledge of cortical plasticity. In addition to enhancing plasticity, VEM may prevent complications with a high risk of causing harm such as deep vein thrombosis, pulmonary embolism, contractures, infections, sores, muscle atrophy and deterioration in cardiorespiratory function. The complications associated with immobility were shown to be responsible for 51 % of deaths in patients with cerebral infarction.9 In another analysis of stroke unit systems,9 stroke unit care appeared to reduce complications of immobility, and infections, in particular. Early mobilisation may also have important psychological effects on a patient’s motivation, well-being and quality of life.6
Another page and references at link.
Increased risk of cognitive impairment 3 months after mild to moderate first-ever stroke: a Community-Based Prospective Study of Nonaphasic English-Speaking Survivors
Damn it all, more reason to stop the neuronal cascade of death.
http://www.ncbi.nlm.nih.gov/pubmed/12702832
http://www.ncbi.nlm.nih.gov/pubmed/12702832
Srikanth VK1, Thrift AG, Saling MM, Anderson JF, Dewey HM, Macdonell RA, Donnan GA; Community-Based Prospective Study of Nonaphasic English-Speaking Survivors.
Abstract
BACKGROUND AND PURPOSE:
Results of hospital-based studies indicate a high risk of cognitive impairment 3 months after stroke. There are no comprehensive data on this issue from prospective community-based studies comparing first-ever stroke patients with stroke-free subjects.METHODS:
We administered a comprehensive neuropsychological battery to 99 community-based nonaphasic survivors of first-ever stroke at 3 months and 99 age- and sex-matched (1:1) stroke-free individuals. Domain-specific cognitive deficits were identified by blinded neuropsychological consensus.METHODS:
Stroke patients were more likely to suffer any cognitive impairment (relative risk [RR], 1.5; 95% CI, 1.1 to 2.1) attributable mainly to a greater risk of single-domain cognitive impairment (RR, 2.8; 95% CI, 1.5 to 5.3) but not multiple-domain cognitive impairment (RR, 1.2; 95% CI, 0.8 to 1.9).CONCLUSIONS:
In this community-based study, a first-ever stroke of mild to moderate severity was associated with a significant risk of cognitive impairment at 3 months, even in the absence of clinical aphasia. This was due primarily to an increased risk of solitary deficits rather than generalized deficits.Current Perspectives in Post-stroke Cognitive Impairment
I couldn't make head or tails of what possible stroke protocols could come from this. Ask your doctor. Go to bottom for one highlighted line which is distressing, I've been using a 33% dementia chance from an Australian study.
http://www.touchneurology.com/articles/current-perspectives-post-stroke-cognitive-impairment
This article summarises the content of a symposium that
took place during the 21st World Congress of Neurology in Vienna,
Austria. It aims to describe the vascular and cellular processes that
are involved in the maintenance of the blood–brain barrier (BBB), the
cells involved in the neurovascular unit (NVU) and its dysfunction in
stroke resulting in poststroke cognitive impairment (PSCI) for many
patients. There is substantial variability in eported rates of PSCI and
this is largely a result of differing assessment methods used to assess
the condition and inconsistent treatments and times to treatment
initiation in different territories. The lack of agreed guidelines and
of consensus among healthcare professionals also contributes to variable
levels of diagnosis and treatment outcomes in PSCI. This article will
additionally consider these critical matters and discuss the development
of a new treatment approach for PSCI that has shown potential and is
being evaluated in clinical trials.
The Role of the Blood–Brain Barrier and the Neurovascular Unit in Cerebral Ischaemia An important concept in the development of stroke and consequent cognitive impairment is the fact that the brain has no reserve of energy or oxygen. It must therefore be constantly perfused through the normal blood supply to supply these factors and to remove metabolic products, particularly carbon dioxide. Any interruption in this continuous process is liable to have a serious effect on the brain region in which it occurs.1The BBB comprises a diverse set of cellular components some of which participate in the NVU. The interaction between these cells is important in the pathophysiology of PSCI and other neurological diseases (see Figure 1).2–4
The tissues of the central nervous system (CNS) make high metabolic demands of the vascular system and the microcirculation of the brain must be responsive to changing requirements.5,6 The NVU is central to this process and maintains a ‘metabolic coupling’ between brain activity and blood flow. In neurological disease or injury there is a danger of exposure to metabolic products that are toxic to brain tissue and may cause neuronal damage.4,7 ATP-sensitive potassium channels play a major role in sensing metabolic requirements and provide protection of brain tissues against these effects of neurological disease or injury.8 Some functional magnetic resonance imaging (fMRI) studies have suggested that following stroke there is an uncoupling between metabolic requirements, especially for oxygen and vascular supply and this can worsen outcomes.9
Within the NVU, astrocytes provide trophic support to neurons and maintain synaptic functions and dynamic signalling. The end-feet structures of astrocytes have a close contact with cerebral endothelial cells and provide a physical link to the microvasculature. Astrocytes are therefore uniquely positioned to exercise control over local changes in cerebral blood flow as well as regulating tight junction integrity.1,10,11 Pericytes are important in regulating blood flow by contracting or relaxing in response to vasoactive stimuli from surrounding cells.12,13
Microglial cells are cerebral monocytes with a stellate morphology and release a range of pro- and anti-inflammatory mediators but their role in the NVU is as yet, unclear.14–16 In response to changes in neuronal activity, perivascular-released neurotransmitters and other mediators can activate receptors on both smooth muscle cells and astrocytes to alter the tone of brain microvessels.17
Cellular communication within the NVU involves various signalling pathways of neurovascular coupling and interactions among astrocyte, vascular smooth muscle, neuronal and endothelial compartments. These processes comprise numerous factors including cytochrome P450 epoxygenase metabolites, signalling initiated by metabotropic glutamate receptor (mGluR) activation, potassium signalling, 20-hydroxyeicosatetraenoic acid (20-HETE acid) signalling, adenosine signalling, carbon monoxide signalling and calcium (Ca2+) efflux. In addition, the regulation of blood flow by astrocytes may involve both vasodilating and vasoconstricting components.18
Several neurotransmitters are important in vascular coupling in the NVU. Glutamate is the main excitatory neurotransmitter in the brain and may trigger responses via indirect signalling.19 The release of glutamate during neuronal activation may act on astrocytic mGluR receptors to increase Ca2+ in astrocytes and elicit a vasodilatory effect.20 Nitric oxide is released from activated neurons following N-methyl-D-aspartate (NMDA) receptor activation21 and is one of the major vasoactive substances whose role is of prime importance in maintaining endothelial homeostasis. Calcium waves are another form of neurotransmitters and are a type of non-electrical impulse in which increased blood flow results in greater intracellular Ca2+ concentrations in astrocytes and the signal is propagated by release of Ca2+ to surrounding cells or by extracellular ATP signalling.22
The variability of post-stroke cognition assessment methods is highlighted by the finding that in patients with MCI (without dementia) 3 months after a stroke varies from 17–66 % depending on the criteria used for testing.33
4 more pages and references at link.
http://www.touchneurology.com/articles/current-perspectives-post-stroke-cognitive-impairment
The Role of the Blood–Brain Barrier and the Neurovascular Unit in Cerebral Ischaemia An important concept in the development of stroke and consequent cognitive impairment is the fact that the brain has no reserve of energy or oxygen. It must therefore be constantly perfused through the normal blood supply to supply these factors and to remove metabolic products, particularly carbon dioxide. Any interruption in this continuous process is liable to have a serious effect on the brain region in which it occurs.1The BBB comprises a diverse set of cellular components some of which participate in the NVU. The interaction between these cells is important in the pathophysiology of PSCI and other neurological diseases (see Figure 1).2–4
The tissues of the central nervous system (CNS) make high metabolic demands of the vascular system and the microcirculation of the brain must be responsive to changing requirements.5,6 The NVU is central to this process and maintains a ‘metabolic coupling’ between brain activity and blood flow. In neurological disease or injury there is a danger of exposure to metabolic products that are toxic to brain tissue and may cause neuronal damage.4,7 ATP-sensitive potassium channels play a major role in sensing metabolic requirements and provide protection of brain tissues against these effects of neurological disease or injury.8 Some functional magnetic resonance imaging (fMRI) studies have suggested that following stroke there is an uncoupling between metabolic requirements, especially for oxygen and vascular supply and this can worsen outcomes.9
Within the NVU, astrocytes provide trophic support to neurons and maintain synaptic functions and dynamic signalling. The end-feet structures of astrocytes have a close contact with cerebral endothelial cells and provide a physical link to the microvasculature. Astrocytes are therefore uniquely positioned to exercise control over local changes in cerebral blood flow as well as regulating tight junction integrity.1,10,11 Pericytes are important in regulating blood flow by contracting or relaxing in response to vasoactive stimuli from surrounding cells.12,13
Microglial cells are cerebral monocytes with a stellate morphology and release a range of pro- and anti-inflammatory mediators but their role in the NVU is as yet, unclear.14–16 In response to changes in neuronal activity, perivascular-released neurotransmitters and other mediators can activate receptors on both smooth muscle cells and astrocytes to alter the tone of brain microvessels.17
Cellular communication within the NVU involves various signalling pathways of neurovascular coupling and interactions among astrocyte, vascular smooth muscle, neuronal and endothelial compartments. These processes comprise numerous factors including cytochrome P450 epoxygenase metabolites, signalling initiated by metabotropic glutamate receptor (mGluR) activation, potassium signalling, 20-hydroxyeicosatetraenoic acid (20-HETE acid) signalling, adenosine signalling, carbon monoxide signalling and calcium (Ca2+) efflux. In addition, the regulation of blood flow by astrocytes may involve both vasodilating and vasoconstricting components.18
Several neurotransmitters are important in vascular coupling in the NVU. Glutamate is the main excitatory neurotransmitter in the brain and may trigger responses via indirect signalling.19 The release of glutamate during neuronal activation may act on astrocytic mGluR receptors to increase Ca2+ in astrocytes and elicit a vasodilatory effect.20 Nitric oxide is released from activated neurons following N-methyl-D-aspartate (NMDA) receptor activation21 and is one of the major vasoactive substances whose role is of prime importance in maintaining endothelial homeostasis. Calcium waves are another form of neurotransmitters and are a type of non-electrical impulse in which increased blood flow results in greater intracellular Ca2+ concentrations in astrocytes and the signal is propagated by release of Ca2+ to surrounding cells or by extracellular ATP signalling.22
The variability of post-stroke cognition assessment methods is highlighted by the finding that in patients with MCI (without dementia) 3 months after a stroke varies from 17–66 % depending on the criteria used for testing.33
4 more pages and references at link.
Late-life cynical distrust, risk of incident dementia, and mortality in a population-based cohort
Your doctor should be warning you about your cynicism in conjunction with your 33% chance of getting dementia/Alzheimers post stroke.
http://www.neurology.org/content/early/2014/05/28/WNL.0000000000000528
http://www.neurology.org/content/early/2014/05/28/WNL.0000000000000528
- Elisa Neuvonen,
- Minna Rusanen, MD, PhD,
- Alina Solomon, MD, PhD,
- Tiia Ngandu, MD, PhD,
- Tiina Laatikainen, MD, PhD,
- Hilkka Soininen, MD, PhD,
- Miia Kivipelto, MD, PhD and
- Anna-Maija Tolppanen, PhD
- Correspondence to Dr. Tolppanen: anna-maija.tolppanen@uef.fi
-
Neurology 10.1212/WNL.0000000000000528
- Abstract
- Full Text (PDF)
- Also available:
- Data Supplement
Abstract
Objective: We investigated the association between late-life cynical distrust and incident dementia and mortality (mean follow-up times
of 8.4 and 10.4 years, respectively) in the Cardiovascular Risk Factors, Aging and Dementia Study.
Methods: Cynical
distrust was measured based on the Cook-Medley Scale and categorized
into tertiles. Cognitive status was evaluated
with a 3-step protocol including screening,
clinical phase, and differential diagnostic phase. Dementia was
diagnosed according
to DSM-IV criteria. Complete data on
exposure, outcome, and confounders were available from 622 persons (46
dementia cases) for the
dementia analyses and from 1,146 persons (361
deaths) for the mortality analyses. Age, sex, systolic blood pressure,
total
cholesterol, fasting glucose, body mass index,
socioeconomic background, smoking, alcohol use, self-reported health,
and APOE genotype were considered as confounders.
Results: Cynical
distrust was not associated with dementia in the crude analyses, but
those with the highest level of cynical distrust
had higher risk of dementia after adjusting for
confounders (relative risk 3.13; 95% confidence interval [CI]
1.15–8.55).
Higher cynical distrust was associated with
higher mortality in the crude analyses (hazard ratio 1.40; 95% CI
1.05–1.87) but
the association was explained by confounders
(adjusted hazard ratio 1.19; 95% CI 0.86–1.61).
Conclusions: Higher
cynical distrust in late life was associated with higher mortality, but
this association was explained by socioeconomic
position, lifestyle, and health status.
Association between cynical distrust and incident dementia became
evident when confounders
were considered. This novel finding suggests
that both psychosocial and lifestyle-related risk factors may be
modifiable targets
for interventions. We acknowledge the need for
larger replication studies.
10 Tips for Your Best Stroke Recovery by Ira Rashbaum, MD
These are f*cking appalling. Not a single one even suggests that your doctor has anything to do with your recovery. Your doctor is completely responsible for not having any therapies that stop the neuronal cascade of death. I would suggest billing your doctor $1000 for every neuron that dies post clot clearing or bleed stopping. At maybe 1 million neurons dying per minute, that's only $1 billion a minute. That might cause your doctor and hospital to focus their attention on solving the problem. Nothing else has worked.
http://www.everydayhealth.com/columns/health-answers/10-tips-for-the-best-stroke-recovery/
1. Seek urgent care immediately.
2. Keep your medical information handy.
3. Choose a top care center for your rehabilitation.
There are none, 10% full recovery is failure by any stretch of the imagination.
4. Eat well.
5. Compliance is key.
. 6. Exercise, but within your limits.
7. Limit stress.
8. Stay positive.
9. Do your homework.
10. Stay vigilant.
http://www.everydayhealth.com/columns/health-answers/10-tips-for-the-best-stroke-recovery/
1. Seek urgent care immediately.
2. Keep your medical information handy.
3. Choose a top care center for your rehabilitation.
There are none, 10% full recovery is failure by any stretch of the imagination.
4. Eat well.
5. Compliance is key.
. 6. Exercise, but within your limits.
7. Limit stress.
8. Stay positive.
9. Do your homework.
10. Stay vigilant.
The Many Roads to Cell Death: Gaining a Practical Understanding of Apoptosis, Necrosis, and Autophagy
You do expect all your doctors to attend this seminar for their next stroke patients? Don't you? Since it is way too late to save your neurons from the neuronal cascade of death.
You are invited to hear our panel of experts on
June 4, 2014, in this live, online educational seminar. For more information and complimentary registration
visit: webinar.sciencemag.org
- Date: Wednesday, June 4, 2014
Time: 12 Noon Eastern, 9 a.m. Pacific, 5 p.m. UK, 6 p.m. Central Europe
Duration: 1 hour
About This Webinar
Cell death is, ironically, an
essential part of life. In recent years, the study and understanding of
cell death pathways has been dramatically transformed by the insights
gained into non-apoptotic pathways, including necro-apoptosis and
autophagy, together with a deeper understanding of the mechanism of the
apoptotic cascade. New discoveries have been enabled by cutting-edge
technologies, particularly in the realm of cytometry and
cell-death–specific markers. In this webinar, the latest insights into
cell death pathways will be discussed, including the molecular markers
and cellular changes that characterize each pathway. Viewers will also
learn practical cytometry-based strategies for dissecting cell death
pathways, and how to use the data to better understand the
pathophysiology of diseases such as cancer as well as to uncover new
targets for drug discovery and development.
During the webinar, speakers will discuss:
- Review the latest insights into the different cell death pathways
- Present their own recent data and research on cell death mechanisms and impacts
- Describe techniques to detect and dissect cell death pathways
- Answer your questions live and in real time!
Participants:
John Abrams, Ph.D.
University of Texas
Southwestern Medical Center
Dallas, TX
John Abrams, Ph.D.
University of Texas
Southwestern Medical Center
Dallas, TX
William G. Telford, Ph.D.
National Institutes of Health
Bethesda, MD
National Institutes of Health
Bethesda, MD
Register at:
webinar.sciencemag.org
webinar.sciencemag.org
Questions? E-mail: webinar@aaas.org.
Produced by the Science/AAAS Custom Publishing Office and sponsored by EMD Millipore.
National Institute for Health and Care Excellence stroke rehabilitation guidance – is it useful, usable, and based on best evidence?
This is a simple question to answer. What are the results? How many patients get to 100% recovery? The answer to that will tell you if this is a failure or not. In the US statistics tell us that only 10% get to full recovery. Complete failure in any endeavor. Even if this is based on best evidence everyone associated with this needs to be fired.
http://cre.sagepub.com/content/28/6/523.abstract
http://cre.sagepub.com/content/28/6/523.abstract
- Avril Drummond, University of Nottingham, A Floor, South Block, Queen’s Medical Centre (QMC), Nottingham NG7 2HA, UK. Email: avril.drummond@nottingham.ac.uk
Abstract
In the UK, the National Institute for
Health and Care Excellence (NICE) is responsible for producing clinical
guidance based
on sound evidence. In 2013 they produced guidance
on Stroke Rehabilitation and this editorial outlines why this is not a
useful
guide for clinicians or commissioners. Primarily
this is because NICE used inappropriate methods; the methods used are
appropriate
for evaluating drugs, but are inappropriate when
applied to any complex intervention. Moreover, the actual
recommendations
are written in clinically unhelpful language.
Future rehabilitation guidance should
include ensuring that the team responsible for the guidance are all
familiar with and
understand the biospsychosocial model of illness
and the nature of the rehabilitation process (which is not synonymous
with
therapy), setting a relevant and appropriate scope
for a guideline, agreeing to use all evidence relevant to a particular
question, and using a more appropriate way to
evaluate evidence while recognising that rehabilitation is a complex
intervention.(This is accepting failure as ok, call your doctor out that that mindset will not be tolerated).
More Brain Bleeds With Stroke Drug in 'Real World'
Well shit, when will our stroke doctors consider using magnetic nanoparticles to deliver a much smaller bolus directly to the clot site?
http://www.medpagetoday.com/MeetingCoverage/AAPA/46014?
Do we have anyone out there with any brains at all?
http://www.medpagetoday.com/MeetingCoverage/AAPA/46014?
Do we have anyone out there with any brains at all?
Wednesday, May 28, 2014
More research for strokes - MoveOn petition by Joyce Hoffman of The Tales of a Stroke Patient
Sign please.
http://petitions.moveon.org/sign/more-research-for-strokes.fb48?
My comment;
The research should start with stopping the neuronal cascade of death. That would result in much less death and disability allowing therapists a much better chance of getting survivors to 100% recovery.
http://petitions.moveon.org/sign/more-research-for-strokes.fb48?
My comment;
The research should start with stopping the neuronal cascade of death. That would result in much less death and disability allowing therapists a much better chance of getting survivors to 100% recovery.
Stroke patient records help evaluate need for Integrative Medicine
This is so simple to explain why stroke patients go for Integrative, Complementary, Chinese, and other assorted quackery. Doctors have no objective diagnosis of the problems in your stroke and no repeatable way to get to 100% recovery. With that as a backdrop why wouldn't you listen to slick sellers of quackery?
http://medicalxpress.com/news/2014-05-patient-medicine.html
And they are doing it wrong by looking at 3-6 month period which is when spontaneous recovery is going to occur anyway. Absolutely nothing to do with the quackery being sold.
http://medicalxpress.com/news/2014-05-patient-medicine.html
And they are doing it wrong by looking at 3-6 month period which is when spontaneous recovery is going to occur anyway. Absolutely nothing to do with the quackery being sold.
Learning Early in Life May Help Keep Brain Cells Alive
One highlighted line is important because it implies that as soon as you get new neurons via neurogenesis you need to somehow incorporate them into your learning process (ie. use them). I'm sure your doctor has no clue how this can be accomplished so you'll have to teach them.
http://www.biosciencetechnology.com/news/2014/05/learning-early-life-may-help-keep-brain-cells-alive?
Using your brain – particularly during adolescence – may help brain cells survive and could impact how the brain functions after puberty.
According to a recently published study in Frontiers in Neuroscience, Rutgers behavioral and systems neuroscientist Tracey Shors, who co-authored the study, found that the newborn brain cells in young rats that were successful at learning survived while the same brain cells in animals that didn’t master the task died quickly.
“In those that didn’t learn, three weeks after the new brain cells were made, nearly one-half of them were no longer there,” said Shors, professor in the Department of Psychology and Center for Collaborative Neuroscience at Rutgers. “But in those that learned, it was hard to count. There were so many that were still alive.”
The study is important, Shors says, because it suggests that the massive proliferation of new brain cells most likely helps young animals leave the protectiveness of their mothers and face dangers, challenges and opportunities of adulthood.
Scientists have known for years that the neurons in adult rats, which are significant but fewer in numbers than during puberty, could be saved with learning, but they did not know if this would be the case for young rats that produce two to four times more neurons than adult animals.
By examining the hippocampus – a portion of the brain associated with the process of learning – after the rats learned to associate a sound with a motor response, scientists found that the new brain cells injected with dye a few weeks earlier were still alive in those that had learned the task while the cells in those who had failed did not survive.
“It’s not that learning makes more cells,” says Shors. “It’s that the process of learning keeps new cells alive that are already present at the time of the learning experience.”
Since the process of producing new brain cells on a cellular level is similar in animals, including humans, Shors says ensuring that adolescent children learn at optimal levels is critical.
“What it has shown me, especially as an educator, is how difficult it is to achieve optimal learning for our students. You don’t want the material to be too easy to learn and yet still have it too difficult where the student doesn’t learn and gives up,” Shors says.
So, what does this mean for the 12-year-old adolescent boy or girl?
While scientists can’t measure individual brain cells in humans, Shors says this study, on the cellular level, provides a look at what is happening in the adolescent brain and provides a window into the amazing ability the brain has to reorganize itself and form new neural connections at such a transformational time in our lives.
“Adolescents are trying to figure out who they are now, who they want to be when they grow up and are at school in a learning environment all day long,” says Shors. "The brain has to have a lot of strength to respond to all those experiences.”
http://www.biosciencetechnology.com/news/2014/05/learning-early-life-may-help-keep-brain-cells-alive?
Using your brain – particularly during adolescence – may help brain cells survive and could impact how the brain functions after puberty.
According to a recently published study in Frontiers in Neuroscience, Rutgers behavioral and systems neuroscientist Tracey Shors, who co-authored the study, found that the newborn brain cells in young rats that were successful at learning survived while the same brain cells in animals that didn’t master the task died quickly.
“In those that didn’t learn, three weeks after the new brain cells were made, nearly one-half of them were no longer there,” said Shors, professor in the Department of Psychology and Center for Collaborative Neuroscience at Rutgers. “But in those that learned, it was hard to count. There were so many that were still alive.”
The study is important, Shors says, because it suggests that the massive proliferation of new brain cells most likely helps young animals leave the protectiveness of their mothers and face dangers, challenges and opportunities of adulthood.
Scientists have known for years that the neurons in adult rats, which are significant but fewer in numbers than during puberty, could be saved with learning, but they did not know if this would be the case for young rats that produce two to four times more neurons than adult animals.
By examining the hippocampus – a portion of the brain associated with the process of learning – after the rats learned to associate a sound with a motor response, scientists found that the new brain cells injected with dye a few weeks earlier were still alive in those that had learned the task while the cells in those who had failed did not survive.
“It’s not that learning makes more cells,” says Shors. “It’s that the process of learning keeps new cells alive that are already present at the time of the learning experience.”
Since the process of producing new brain cells on a cellular level is similar in animals, including humans, Shors says ensuring that adolescent children learn at optimal levels is critical.
“What it has shown me, especially as an educator, is how difficult it is to achieve optimal learning for our students. You don’t want the material to be too easy to learn and yet still have it too difficult where the student doesn’t learn and gives up,” Shors says.
So, what does this mean for the 12-year-old adolescent boy or girl?
While scientists can’t measure individual brain cells in humans, Shors says this study, on the cellular level, provides a look at what is happening in the adolescent brain and provides a window into the amazing ability the brain has to reorganize itself and form new neural connections at such a transformational time in our lives.
“Adolescents are trying to figure out who they are now, who they want to be when they grow up and are at school in a learning environment all day long,” says Shors. "The brain has to have a lot of strength to respond to all those experiences.”
Gunshot victims to be suspended between life and death
An innovative and ground breaking stroke association would be in contact with numerous innovative stroke hospitals to see if applying this to stroke patients would help. But we have nothing like that and stroke patients die because of that lack of innovation.
http://www.newscientist.com/article/mg22129623.000-gunshot-victims-to-be-suspended-between-life-and-death.html#.U4ZEkxBc62V
http://www.newscientist.com/article/mg22129623.000-gunshot-victims-to-be-suspended-between-life-and-death.html#.U4ZEkxBc62V
NEITHER dead or alive, knife-wound or gunshot victims
will be cooled down and placed in suspended animation later this month,
as a groundbreaking emergency technique is tested out for the first
time.
Surgeons are now on call at the UPMC
Presbyterian Hospital in Pittsburgh, Pennsylvania, to perform the
operation, which will buy doctors time to fix injuries that would
otherwise be lethal.
"We are suspending life, but we don't like to call it suspended animation because it sounds like science fiction," says Samuel Tisherman, a surgeon at the hospital, who is leading the trial. "So we call it emergency preservation and resuscitation."
More at link.
13 Evidence-Based Medicinal Properties of Coconut Oil - brain boosting
I'm starting to use this for 2. Brain-Boosting
You'll have to ask your doctor for the details of the article from 2006. S/he should already be familiar with this because they should already be treating you for your 33% chance of getting dementia/Alzheimers post stroke.
http://wakeup-world.com/2012/09/05/13-evidence-based-medicinal-properties-of-coconut-oil/
2. Brain-Boosting
A now famous study, published in 2006 in the journal Neurobiology of Aging, showed that the administration of medium chain triglycerides (most plentifully found in coconut oil) in 20 subjects with Alzheimer’s disease or mild cognitive impairment, resulted in significant increases in ketone bodies (within only 90 minutes after treatment) associated with measurable cognitive improvement in those with less severe cognitive dysfunction.[i]
[i] Mark A Reger, Samuel T Henderson, Cathy Hale, Brenna Cholerton, Laura D Baker, G S Watson, Karen Hyde, Darla Chapman, Suzanne Craft . Effects of beta-hydroxybutyrate on cognition in memory-impaired adults. Neurobiol Aging. 2004 Mar;25(3):311-4. PMID: 15123336
You'll have to ask your doctor for the details of the article from 2006. S/he should already be familiar with this because they should already be treating you for your 33% chance of getting dementia/Alzheimers post stroke.
http://wakeup-world.com/2012/09/05/13-evidence-based-medicinal-properties-of-coconut-oil/
2. Brain-Boosting
A now famous study, published in 2006 in the journal Neurobiology of Aging, showed that the administration of medium chain triglycerides (most plentifully found in coconut oil) in 20 subjects with Alzheimer’s disease or mild cognitive impairment, resulted in significant increases in ketone bodies (within only 90 minutes after treatment) associated with measurable cognitive improvement in those with less severe cognitive dysfunction.[i]
[i] Mark A Reger, Samuel T Henderson, Cathy Hale, Brenna Cholerton, Laura D Baker, G S Watson, Karen Hyde, Darla Chapman, Suzanne Craft . Effects of beta-hydroxybutyrate on cognition in memory-impaired adults. Neurobiol Aging. 2004 Mar;25(3):311-4. PMID: 15123336
Chase your stroke recovery by drinking
Never follow what I say or do. Nothing here is clinically proven.
For your balance therapies; climb up on a high bar stool, drink 2 high alcohol content beers or 3 regular beers or wine, hop down and practice walking to the bathroom. Hopefully the bar is not too crowded, you'll need the room to stagger and sway your way there. Its kind of like this Saturday Morning Breakfast Cereal comic.
The Bayesian drinking game
You do have to challenge yourself to get better in your recovery, I just challenge myself in non-approved ways.
For your balance therapies; climb up on a high bar stool, drink 2 high alcohol content beers or 3 regular beers or wine, hop down and practice walking to the bathroom. Hopefully the bar is not too crowded, you'll need the room to stagger and sway your way there. Its kind of like this Saturday Morning Breakfast Cereal comic.
The Bayesian drinking game
You do have to challenge yourself to get better in your recovery, I just challenge myself in non-approved ways.
New design of a system that " interrogates " and shows how the brain relearns post stroke
If this works we may finally understand where functionality of dead areas goes to as it recovers. And we might then make repeatable therapy protocols.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=142245&CultureCode=en
Monitoring the rehabilitation of patients with neurological damage caused by a stroke, has encouraged Mexican scientists to work in the design and manufacture of a functional infrared spectroscopy (fNIRS -FD ) instrument capable of identifying the affected areas of the brain and the sites that were activated while analyzing the oxygen content in blood flow during therapy.
"It's a device consisting of a headband or helmet equipped with emitters and light detectors, oximeter (to measures oxygen levels), a monitor and software. Its operation is based on infrared light, which passes through the scalp to the skull leather and displays and “interrogates” brain activity in order to obtain information on cell metabolism, alterations in blood flow and amount of oxygen," explains Carlos Gerardo Treviño Palacios, researcher at the National Institute of Astrophysics, Optics and Electronics (INAOE) in Mexico.
He highlights that so far they are ending the development of an oximeter and software to display images. Also, they analyze information that will be provided to the base hardware and detectors, and work in the construction helmet. This will not only help rehabilitate patients, but will create a map of the brain to detect which parts are replacing areas that died in the motor cortex after stroke and watch how the body relearns with the help of rehabilitation.
"The aim is to build a non-invasive imaging system to avoid secluding the patient into a box camera during the shooting of brain “photography” with the limitations of the procedure , as happens with an MRI," says Treviño Palacios.
He notes that although the latter method also measures the concentration of oxygen, infrared spectroscopy despite having a lower resolution does not require the patient to lie still and requires only the use of a helmet, allowing the physician to observe brain activity and progress while continuing the patient’s rehabilitation therapy. Additional advantages are system portability and low cost.
"In parallel, we are looking for a fast optical signal, ie, a series of changes that occur a few milliseconds before the neuron is active in the images, which shows the action potential of the nerve cell," says the researcher at INAOE.
This project is jointly implemented by INAOE and the National Institute of Neurology and Neurosurgery of the Mexican Ministry of Health, where collaboration comes naturally to raise an investigation into an imaging modality based on the interaction of light with matter, after a previous collaboration where a rehabilitation therapy system was developed.
"The particular characteristics of the optical imaging system make it a unique tool in certain problems where the in-vivo and in- situ neuroimaging is required noninvasively and continuously for long periods of time. This is the case of the study of brain plasticity in patients going through motor rehabilitation, which should be monitored while practicing neuro-rehabilitation exercises during therapy sessions that can last from 45 minutes to an hour ," says Treviño Palacios. (Agencia ID)
http://www.alphagalileo.org/ViewItem.aspx?ItemId=142245&CultureCode=en
Monitoring the rehabilitation of patients with neurological damage caused by a stroke, has encouraged Mexican scientists to work in the design and manufacture of a functional infrared spectroscopy (fNIRS -FD ) instrument capable of identifying the affected areas of the brain and the sites that were activated while analyzing the oxygen content in blood flow during therapy.
"It's a device consisting of a headband or helmet equipped with emitters and light detectors, oximeter (to measures oxygen levels), a monitor and software. Its operation is based on infrared light, which passes through the scalp to the skull leather and displays and “interrogates” brain activity in order to obtain information on cell metabolism, alterations in blood flow and amount of oxygen," explains Carlos Gerardo Treviño Palacios, researcher at the National Institute of Astrophysics, Optics and Electronics (INAOE) in Mexico.
He highlights that so far they are ending the development of an oximeter and software to display images. Also, they analyze information that will be provided to the base hardware and detectors, and work in the construction helmet. This will not only help rehabilitate patients, but will create a map of the brain to detect which parts are replacing areas that died in the motor cortex after stroke and watch how the body relearns with the help of rehabilitation.
"The aim is to build a non-invasive imaging system to avoid secluding the patient into a box camera during the shooting of brain “photography” with the limitations of the procedure , as happens with an MRI," says Treviño Palacios.
He notes that although the latter method also measures the concentration of oxygen, infrared spectroscopy despite having a lower resolution does not require the patient to lie still and requires only the use of a helmet, allowing the physician to observe brain activity and progress while continuing the patient’s rehabilitation therapy. Additional advantages are system portability and low cost.
"In parallel, we are looking for a fast optical signal, ie, a series of changes that occur a few milliseconds before the neuron is active in the images, which shows the action potential of the nerve cell," says the researcher at INAOE.
This project is jointly implemented by INAOE and the National Institute of Neurology and Neurosurgery of the Mexican Ministry of Health, where collaboration comes naturally to raise an investigation into an imaging modality based on the interaction of light with matter, after a previous collaboration where a rehabilitation therapy system was developed.
"The particular characteristics of the optical imaging system make it a unique tool in certain problems where the in-vivo and in- situ neuroimaging is required noninvasively and continuously for long periods of time. This is the case of the study of brain plasticity in patients going through motor rehabilitation, which should be monitored while practicing neuro-rehabilitation exercises during therapy sessions that can last from 45 minutes to an hour ," says Treviño Palacios. (Agencia ID)
Migrating stem cells possible new focus for stroke treatment - pericytes
I'm sure your doctor and researcher know that one of the 6 causes of neuronal cascade of death is Capillaries that don't open due to pericytes not letting go.
So you need to remind them to be careful that solving that problem doesn't restrict this migration.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=142225&CultureCode=en
Two years ago, a new type of stem cell was discovered in the brain that has the capacity to form new cells. The same research group at Lund University in Sweden has now revealed that these stem cells, which are located in the outer blood vessel wall, appear to be involved in the brain reaction following a stroke.
The findings show that the cells, known as pericytes, drop out from the blood vessel, proliferate and migrate to the damaged brain area where they are converted into microglia cells, the brain’s inflammatory cells.
Pericytes are known to contribute to tissue repair in a number of organs, and the researchers believe that their reparative properties could also apply to the brain. The study shows for the first time that pericytes are directly involved in the reaction of the brain tissue after stroke.
“Pericytes are a fascinating cell type with many different properties and found at high density in the brain. It was surprising that a pericyte subtype is so strongly activated after a stroke. The fact that pericytes can be converted into microglia, which have an important function in the brain after a stroke, was an unexpected finding that opens up a new possibility to influence inflammation
associated with a stroke”, said Gesine Paul-Visse, neurologist at Lund University and senior author of the study.
Using a green fluorescent protein bound to the pericytes, the researchers were able to track the cells’ path to the damaged part of the brain. The migration takes place within a week after a stroke. When the cells reach the site of damage they are converted into microglia cells, the ‘cleaners’ of the central nervous system. Inflammation can, however, have both positive reparative effects and negative effects on the damaged tissue. The exact role of microglia cells in the regeneration after a stroke is not entirely clear, but we do know that pericytes play an important role in protecting the brain against disease and injury.
“We now need to elucidate how pericytes affect the brain’s recovery following a stroke. Our findings put pericytes in focus as a new target for brain repair and future research will help us understand more about the brain’s own defence and repair mechanisms.”
There is an urgent need for new drugs that can alleviate the harmful effects of a stroke as current treatment possibilities using thrombolysis are limited to the first hours following a stroke.
“Because inflammation following a stroke is an event that continues after the acute stage, we hope that targeting pericytes in the subacute phase after stroke, i.e. within a longer time window following the onset of stroke, may influence the outcome”, said Gesine Paul-Visse.
http://dx.doi.org/10.1007/s00401-014-1295-x
So you need to remind them to be careful that solving that problem doesn't restrict this migration.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=142225&CultureCode=en
Two years ago, a new type of stem cell was discovered in the brain that has the capacity to form new cells. The same research group at Lund University in Sweden has now revealed that these stem cells, which are located in the outer blood vessel wall, appear to be involved in the brain reaction following a stroke.
The findings show that the cells, known as pericytes, drop out from the blood vessel, proliferate and migrate to the damaged brain area where they are converted into microglia cells, the brain’s inflammatory cells.
Pericytes are known to contribute to tissue repair in a number of organs, and the researchers believe that their reparative properties could also apply to the brain. The study shows for the first time that pericytes are directly involved in the reaction of the brain tissue after stroke.
“Pericytes are a fascinating cell type with many different properties and found at high density in the brain. It was surprising that a pericyte subtype is so strongly activated after a stroke. The fact that pericytes can be converted into microglia, which have an important function in the brain after a stroke, was an unexpected finding that opens up a new possibility to influence inflammation
associated with a stroke”, said Gesine Paul-Visse, neurologist at Lund University and senior author of the study.
Using a green fluorescent protein bound to the pericytes, the researchers were able to track the cells’ path to the damaged part of the brain. The migration takes place within a week after a stroke. When the cells reach the site of damage they are converted into microglia cells, the ‘cleaners’ of the central nervous system. Inflammation can, however, have both positive reparative effects and negative effects on the damaged tissue. The exact role of microglia cells in the regeneration after a stroke is not entirely clear, but we do know that pericytes play an important role in protecting the brain against disease and injury.
“We now need to elucidate how pericytes affect the brain’s recovery following a stroke. Our findings put pericytes in focus as a new target for brain repair and future research will help us understand more about the brain’s own defence and repair mechanisms.”
There is an urgent need for new drugs that can alleviate the harmful effects of a stroke as current treatment possibilities using thrombolysis are limited to the first hours following a stroke.
“Because inflammation following a stroke is an event that continues after the acute stage, we hope that targeting pericytes in the subacute phase after stroke, i.e. within a longer time window following the onset of stroke, may influence the outcome”, said Gesine Paul-Visse.
http://dx.doi.org/10.1007/s00401-014-1295-x
“Virtual human” shows that stiff arteries can explain the cause of high blood pressure
Maybe you want to ask your doctor about these possible solutions to stiff arteries. Why would you listen to me? I'm a non-medical person.
You can test if you have stiff arteries here and here.
Watermelon juice reverses hardening of the arteries
Stiff arteries relax like younger blood vessels after taking alagebrium
http://www.alphagalileo.org/ViewItem.aspx?ItemId=142222&CultureCode=en
High blood pressure is highly age-related and affects more than 1 billion people worldwide. But doctors can’t fully explain the cause of 90 per cent of all cases. A computer model of a “virtual human” suggests that stiff arteries alone are enough to cause high blood pressure.
“Our results suggest that arterial stiffness represents a major therapeutic target. This is contrary to existing models, which typically explain high blood pressure in terms of defective kidney function,” says Klas Pettersen, a researcher at the Norwegian University of Life Sciences and first author of the study, recently published in PLOS Computational Biology.
High blood pressure is a major source of morbidity and mortality, because it makes individuals more prone to heart failure, stroke and kidney disease.
When blood pressure travels down the aorta from the heart, a special group of cells in the aortic wall, called baroreceptors, sense the pressure in this stretch of the aortic wall and send signals with this information to the nervous system.
If the blood pressure is too high, these cells send stronger signals and the body is able to lower blood pressure. However, if the aorta gets stiffer, as typically happens with age, this stretch of the aorta is not as sensitive as it once was in measuring blood pressure. Thus, although a person’s blood pressure may have increased, the baroreceptors do not signal as intensively as they should and the body does not get the message to lower blood pressure.
“With the stiffening of the wall that follows ageing, these sensors become less able to send signals that reflect the actual blood pressure. Our mathematical model predicts the quantitative effects of this process on blood pressure,” says Pettersen.
“If our hypothesis is proven right, arterial stiffness and baroreceptor signaling will become hotspot targets for the treatment of high blood pressure and the development of new medicines and medical devices,” says Stig W. Omholt from the Norwegian University of Science and Technology, who was the senior investigator of the research project.
With the use of existing experimental data and models of the aging human aorta, the researchers were able to show quantitatively how the stiffening of the aorta with age causes the baroreceptors to misinform the central nervous system about blood pressure, thus preventing the system from downregulating blood pressure. The model predictions were compared with data from the Nord-Trøndelag Health Study (HUNT2), which is comprised of information on the health history of 74,000 people, including blood sample collection from 65,000 people.
NTNU’s Omholt says that the study is a good example of how very complex human disease can be understood by use of mathematical models and thus allow for much better treatment strategies.
“If we are to succeed in developing predictive, preventive and participatory medicine envisioned by so many, there is no substitute for building much stronger transdisciplinary ties between the life sciences, the mathematical sciences and engineering across the whole spectrum of basic, translational and applied research. And mathematical models of the human physiology will be at the core of this development,” he says.
In September the Norwegian University of Science and Technology will host the biannual conference on the Virtual Physiological Human, where this research will be presented. http://www.ntnu.edu/vph2014
You can test if you have stiff arteries here and here.
Watermelon juice reverses hardening of the arteries
Stiff arteries relax like younger blood vessels after taking alagebrium
http://www.alphagalileo.org/ViewItem.aspx?ItemId=142222&CultureCode=en
High blood pressure is highly age-related and affects more than 1 billion people worldwide. But doctors can’t fully explain the cause of 90 per cent of all cases. A computer model of a “virtual human” suggests that stiff arteries alone are enough to cause high blood pressure.
“Our results suggest that arterial stiffness represents a major therapeutic target. This is contrary to existing models, which typically explain high blood pressure in terms of defective kidney function,” says Klas Pettersen, a researcher at the Norwegian University of Life Sciences and first author of the study, recently published in PLOS Computational Biology.
High blood pressure is a major source of morbidity and mortality, because it makes individuals more prone to heart failure, stroke and kidney disease.
When blood pressure travels down the aorta from the heart, a special group of cells in the aortic wall, called baroreceptors, sense the pressure in this stretch of the aortic wall and send signals with this information to the nervous system.
If the blood pressure is too high, these cells send stronger signals and the body is able to lower blood pressure. However, if the aorta gets stiffer, as typically happens with age, this stretch of the aorta is not as sensitive as it once was in measuring blood pressure. Thus, although a person’s blood pressure may have increased, the baroreceptors do not signal as intensively as they should and the body does not get the message to lower blood pressure.
“With the stiffening of the wall that follows ageing, these sensors become less able to send signals that reflect the actual blood pressure. Our mathematical model predicts the quantitative effects of this process on blood pressure,” says Pettersen.
“If our hypothesis is proven right, arterial stiffness and baroreceptor signaling will become hotspot targets for the treatment of high blood pressure and the development of new medicines and medical devices,” says Stig W. Omholt from the Norwegian University of Science and Technology, who was the senior investigator of the research project.
With the use of existing experimental data and models of the aging human aorta, the researchers were able to show quantitatively how the stiffening of the aorta with age causes the baroreceptors to misinform the central nervous system about blood pressure, thus preventing the system from downregulating blood pressure. The model predictions were compared with data from the Nord-Trøndelag Health Study (HUNT2), which is comprised of information on the health history of 74,000 people, including blood sample collection from 65,000 people.
NTNU’s Omholt says that the study is a good example of how very complex human disease can be understood by use of mathematical models and thus allow for much better treatment strategies.
“If we are to succeed in developing predictive, preventive and participatory medicine envisioned by so many, there is no substitute for building much stronger transdisciplinary ties between the life sciences, the mathematical sciences and engineering across the whole spectrum of basic, translational and applied research. And mathematical models of the human physiology will be at the core of this development,” he says.
In September the Norwegian University of Science and Technology will host the biannual conference on the Virtual Physiological Human, where this research will be presented. http://www.ntnu.edu/vph2014
Tuesday, May 27, 2014
3 Strategies for Combating Post-stroke Fatigue
NO, NO, NO This is putting all the responsibility for combatting fatigue on the patient. Dump that fucking monkey directly on your doctors' back. They need to actually do some work for once. Quote this Harvard Business Review article to them and never let a stroke recovery problem be allowed to stay on your back overnight.
Who's Got the Monkey?
3 Strategies for Combating Post-stroke Fatigue
1. Keep a fatigue diary.
2. Plan Your Activities.
3.Adjust Your Diet.
Driving challenges
I got a late start on the drive back to Minnesota, somehow missed the exit to interstate 80 which bypasses most of Chicago. So I ended up driving in rush hour traffic through Chicago just knowing in a general idea where to go. Even so it cut an hour off my driving time and only cost an extra $8.50. It's quite the sensation overload driving in such traffic. The drive back had numerous rainstorms and nighttime driving with the wipers at high speed and raindrops exploding on the sheets of water covering the road made it extremely hard to see the traffic lane you were supposed to be driving in.
Found out my sense of when the car is on the edge of losing control is intact. I passed a pickup truck by going into the right lane during a rainstorm just so I could see the road ahead. 90 mph was the point at which it was imperative to start slowing down. This sense has been quite useful driving in winter in Michigan.
The whole point of going to MN for the weekend was to check out the two storage lockers I was renting that my ex was putting my stuff into. A 5x15 costing $90 a month and a 10x20 costing $200 a month. I thought I was going to put everything into the larger locker but when we checked out the large one it only had 2 sea kayaks in it, my friend volunteered his garage to store them for now. And I picked up my Wellies for mucking about in the flooded trails I'm clearing. Snowshoes also came back, I steamed and bent these myself, real rawhide for the webbing.
This is my wrist holding the steering wheel. Contrary to first impressions the natural spasticity causes the wheel to turn counterclockwise, I spend all my time making sure my right hand counteracts that force. For extremely short periods of time I can control it enough to change CDs or drink some coffee with a straw, straw because it doesn't require me to tip my head back. My elbow is on the gel pad attached to the arm rest which forces my lats to relax. It was glued and velcroed on which of course will destroy the fabric.
New hope for stroke rehabilitation - anti-depressant fluoxetine - Prozac
What the hell is it going to take to get this into a standard stroke protocol? It's been out for a while in a small study - Antidepressants may help people recover from stroke even if they are not depressed, Ask your doctor exactly what proof they need before they try something new to help your recovery. And it better not be when the Joint Commission or Get With the Guidelines puts something new out. That answer will tell you if you have a pitifully poor stroke department head and a hospital not worth using.
http://www.georgeinstitute.org/media-releases/new-hope-for-stroke-rehabilitation
http://www.georgeinstitute.org/media-releases/new-hope-for-stroke-rehabilitation
Australian researchers are beginning a new study that looks at the
effects of the anti-depressant fluoxetine (also known as Prozac) on the
rehabilitation of stroke patients.
The new study, led by Associate Professor Maree Hackett of The George Institute for Global Research and co-principal investigator Graeme Hankey (Perth), comes after a small French study in 2010 that indicated that anti-depressants may help people move again after stroke.
This time, the study is large, involving 1600 people, and will take place in Australia and New Zealand where stroke is the second biggest killer after heart disease. In 2012, more than 420,000 Australians were living with the effects of stroke, with about 50,000 strokes occurring each year, or 1,000 strokes per week
“The French study showed that patients who were on the antidepressants were able to physically move much better than patients who were not on the medication,” said A/Prof Hackett.
“It may be that the medication helps patients because they are happier and therefore more likely to stick to their rehabilitation, or it may be that the medication is helping patients make new connections in their brains that are vital to movement.”
The study, which is underway in Western Australia, is about to begin recruiting patients in New South Wales and New Zealand.
A/Prof Hackett said the French study showed not just a small improvement for patients using the medication. “It resulted in such a large improvement it made the difference between whether patients could live unassisted or not.”
The study, however, finished after three months and did not follow up to find out whether patients regressed after being taken off the medication, or whether there were better outcomes from different doses or longer periods of medication, she said.
“We’re quite excited about the potential for this study to answer some really important questions. And if it works, this course of treatment may have potential for other types of injury.”
The trial is called AFFINITY, and is funded by NHMRC. A/Prof Hackett holds a Future Leader Fellowship through The Heart Foundation, which has funded her work on this project.
The new study, led by Associate Professor Maree Hackett of The George Institute for Global Research and co-principal investigator Graeme Hankey (Perth), comes after a small French study in 2010 that indicated that anti-depressants may help people move again after stroke.
This time, the study is large, involving 1600 people, and will take place in Australia and New Zealand where stroke is the second biggest killer after heart disease. In 2012, more than 420,000 Australians were living with the effects of stroke, with about 50,000 strokes occurring each year, or 1,000 strokes per week
“The French study showed that patients who were on the antidepressants were able to physically move much better than patients who were not on the medication,” said A/Prof Hackett.
“It may be that the medication helps patients because they are happier and therefore more likely to stick to their rehabilitation, or it may be that the medication is helping patients make new connections in their brains that are vital to movement.”
The study, which is underway in Western Australia, is about to begin recruiting patients in New South Wales and New Zealand.
A/Prof Hackett said the French study showed not just a small improvement for patients using the medication. “It resulted in such a large improvement it made the difference between whether patients could live unassisted or not.”
The study, however, finished after three months and did not follow up to find out whether patients regressed after being taken off the medication, or whether there were better outcomes from different doses or longer periods of medication, she said.
“We’re quite excited about the potential for this study to answer some really important questions. And if it works, this course of treatment may have potential for other types of injury.”
The trial is called AFFINITY, and is funded by NHMRC. A/Prof Hackett holds a Future Leader Fellowship through The Heart Foundation, which has funded her work on this project.
Woodtick stroke therapy
At the visit to a northern Minnesota cabin and land, numerous woodticks were pulled off of clothing. The challenge was to feel them on the affected side crawling up your body. I noticed two on my leg, but one got all the way to the back of the neck before being noticed. If you need even more challenge ask your therapist to provide mosquitos and see if you notice their tiny legs walking on your skin. For extra challenges see if you can feel the tiny air movement of the wings beating before they land. That will tell you that you have fully recovered sensation. Your therapist should know how many mosquito bites will be necessary before you become proficient at noticing them before they bite.
Oregon company's device lifts stroke patients' hopes
I'm somewhat suspicious, it seems to be around the 6 month period which would still correspond with spontaneous recovery. So with one anecdotal case you can't tell what caused the recovery. Which also means that the FDA doesn't know what it is doing when it approves the sale of devices like this.
http://www.nwcn.com/news/health/Oregon-companys-device-lifts-stroke-patients-hopes-260680021.html
The marketing of it as "another tool in the toolbox" matches Peter Levines' comments on how therapy tools are marketed to therapists.
http://www.nwcn.com/news/health/Oregon-companys-device-lifts-stroke-patients-hopes-260680021.html
The marketing of it as "another tool in the toolbox" matches Peter Levines' comments on how therapy tools are marketed to therapists.
The STROKE-O-MATIC 76
Steering Neuronal Growth Cones by Shifting the Imbalance between Exocytosis and Endocytosis
You do expect your doctor to know how to manipulate this axon guidance to redirect neurons around dead areas to connect up sections of your brain again? Don't you?
http://www.jneurosci.org/content/34/21/7165.short
http://www.jneurosci.org/content/34/21/7165.short
-
Author contributions: T.T., R.I., and H.K. designed research; T.T. and R.I. performed research; T.T. and R.I. analyzed data; T.T., R.I., and H.K. wrote the paper.
-
↵*T.T. and R.I. contributed equally to this work.
-
The Journal of Neuroscience, 21 May 2014, 34(21): 7165-7178; doi: 10.1523/JNEUROSCI.5261-13.2014
- Abstract
- Full Text
- Full Text (PDF)
Abstract
Extracellular molecular cues guide
migrating growth cones along specific routes during development of axon
tracts. Such processes
rely on asymmetric elevation of cytosolic Ca2+ concentrations across the growth cone that mediates its attractive or repulsive turning toward or away from the side with
Ca2+ elevation, respectively. Downstream of these Ca2+
signals, localized activation of membrane trafficking steers the growth
cone bidirectionally, with endocytosis driving repulsion
and exocytosis causing attraction. However, it
remains unclear how Ca2+ can differentially regulate these opposite membrane-trafficking events. Here, we show that growth cone turning depends on
localized imbalance between exocytosis and endocytosis and identify Ca2+-dependent signaling pathways mediating such imbalance. In embryonic chicken dorsal root ganglion neurons, repulsive Ca2+ signals promote clathrin-mediated endocytosis through a 90 kDa splice variant of phosphatidylinositol-4-phosphate 5-kinase
type-1γ (PIPKIγ90). In contrast, attractive Ca2+ signals facilitate exocytosis but suppress endocytosis via Ca2+/calmodulin-dependent
protein kinase II (CaMKII) and cyclin-dependent kinase 5 (Cdk5) that
can inactivate PIPKIγ90. Blocking
CaMKII or Cdk5 leads to balanced activation of
both exocytosis and endocytosis that causes straight growth cone
migration
even in the presence of guidance signals,
whereas experimentally perturbing the balance restores the growth cone's
turning
response. Remarkably, the direction of this
resumed turning depends on relative activities of exocytosis and
endocytosis,
but not on the type of guidance signals. Our
results suggest that navigating growth cones can be redirected by
shifting the
imbalance between exocytosis and endocytosis,
highlighting the importance of membrane-trafficking imbalance for axon
guidance
and, possibly, for polarized cell migration in
general.
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