Well I tried the bike thing again,Aug.3 failed spectactularily. I waited until now to post about this to make sure I was ok. I didn't follow thru on my plans, which was to have a friend over to help me. I looked at my initial success and didn't analyze it enough to figure out why it worked. I wrapped my left hand on the handlebar, grabbed the arbor with my right hand to get my right leg over the seat. The left pedal was at the bottom of the arc so I could easily get my left foot on the pedal. I pushed off with my right foot and got the right foot on the right pedal, however since it was at the top of the arc I didn't have any leverage to start pedaling. So I fell directly to my left smashing directly on my left hip. On concrete no less, my upper body fell into the flower garden. A woman walking by asked very concerned if I was ok. I assured her I was, I pried my left hand off the handle bar, got up and hobbled my bike back into the garage. What the difference between the two tries was that the earlier one had a slight downward slant from where I started so I started rolling downhill immediately, if I had waited for my friend to be around he could have given me enough of a push to get rolling. I hobbled into the house and as I'm walking in the living room I realize my head is spinning and if I don't sit down immediately I'll fall, I fall onto the couch and roll onto the floor(on my good side at least). While down there our rabbit comes by and sniffs me. I spent the rest of that day crawling on my hands/elbows and knees to get around. The next day I can at least use my single point cane to move around the house. Day 2 I am reduced to using my 4-point cane and very heavily leaning on it. So much that my right hand goes numb from the pressure on the nerves. I manage to drive my car to pick up some groceries and library books. That night I go to X-Men: First Class, good movie but sitting still for two hours stiffens me up and hobbling out of the theater is pretty bad. I thought I was slow before but now I am glacial, half-step every minute. It takes me 20 minutes to walk a block.I will be going to a doctor soon to make sure I didn't break my hip, movement while non weight-bearing is ok.So I now have skinned knees and floor burns on my left toes.
Conclusion: I didn't analyze why my first attempt worked and was too arrogant to think I needed help the second time if the first time worked. I was already imagining long bike rides on the converted rail lines near our house. Baby steps were needed and I went off into full speed running instead. I know there is a medical term for that inability to see our defects. I will have to remember that when I attempt to run.
Elderly patients with hip fracture with positive affect have better functional recovery over 2 years.
http://www.ncbi.nlm.nih.gov/pubmed/16866678
So I better have a positive attitude or I won't recover as well.
The xray showed no break, was offered an MRI to see if I had a hairline crack, but asked if treatment was different based on the outcome, the answer was no, so I didn't get an MRI. Saw an ortho doctor who said I probably got a hematoma in the bursa covering the head of my thigh bone.
But it does give me more therapy, sensation pain, trying to find its way back to the sensory cortex. And since my sensory cortex is intact, it is just the white matter underlying it that needs connecting and boy does pain work well for that. I shouldn't make light of this, it was stupid, as long as others don't try to follow me. Now 3+ weeks later I can finally sometimes walk without the cane again. I will try again, I'm obviously stroke-addled in that regard.
Wednesday, August 31, 2011
Permanent damage of stroke prevented by ‘vacuuming’ blood clots
Maybe this would have worked better than the tPA that didn't work for me. But actually the tPA probably worked but the cascade of neuronal death continued which probably was why I was so close to death.
http://clinicaltrials.gov/ct2/show/NCT00334061
http://clinicaltrials.gov/ct2/show/NCT00334061
This clinical evaluation is a prospective, single-arm, multi-center trial.
The purpose of this clinical evaluation is to assess the safety and effectiveness of the Penumbra System in the revascularization of patients presenting with acute ischemic stroke secondary to intracranial, large vessel, occlusive disease.
Images of how it works here:
http://images.pido71.multiply.com/content/movie/pido71:video:71/pido71/71.swf/dmip0vg0lCL+iZm6WgP+3A/STROKE.swf?nmid=84570847Tuesday, August 30, 2011
Rewiring the Brain After Traumatic Injury or Stroke
Hey, the six-million dollar man gets new brain hardware.
http://www.healthymagination.com/blog/rewiring-the-brain-after-traumatic-injury-or-stroke/
picture of the implant here:
http://www.neural-prosthesis.com/
I wonder if memories put in here would not be changed as they are reaccessed.
http://www.healthymagination.com/blog/rewiring-the-brain-after-traumatic-injury-or-stroke/
picture of the implant here:
http://www.neural-prosthesis.com/
I wonder if memories put in here would not be changed as they are reaccessed.
New Hope in the Fight Against Stroke - estrogen therapy
So I can see dozens of questions needing to be answered, make sure your researcher knows those questions.
http://magazine.nursing.jhu.edu/2011/08/new-hope-in-the-fight-against-stroke/
There’s new evidence that estrogen therapy could potentially reduce the severity of stroke. In studies involving rats, School of Nursing associate professor Marguerite Littleton-Kearney, DNSc, RN, FAAN, found that animals that received oral doses of estrogen for one month before suffering a “stroke” (having blood flow to their brains restricted) recovered more quickly than rats that did not get estrogen.
http://magazine.nursing.jhu.edu/2011/08/new-hope-in-the-fight-against-stroke/
There’s new evidence that estrogen therapy could potentially reduce the severity of stroke. In studies involving rats, School of Nursing associate professor Marguerite Littleton-Kearney, DNSc, RN, FAAN, found that animals that received oral doses of estrogen for one month before suffering a “stroke” (having blood flow to their brains restricted) recovered more quickly than rats that did not get estrogen.
Littleton-Kearney has long been interested in how female hormones like estrogen affect blood flow in the brains of women. “In general,” she notes, “women are less likely than men to have a stroke during their reproductive years, but after age 65, men and women suffer stroke at about the same rate. Unfortunately, our understanding of the role of estrogen in females during and immediately after stroke is quite limited.
She continues, “In our study of animals, we had always administered estrogen under the skin or intravenously, but most women take female hormones orally. So my research team initiated the first study of the effects of estrogen and progesterone on the size of stroke where the animals took the drug orally.”
She and her colleagues administered the hormones in quantities that simulate what a postmenopausal woman would typically ingest, feeding the rats their hormones in jelly each day for a month. After restricting blood flow to the brain for two hours, then allowing the blood to freely circulate for 24 hours, she examined the animals to measure the size of the stroke. Estrogen alone decreased the size of the stroke in the brain stem, while stroke was diminished in the cortex through use of both estrogen alone as well as a combination of estrogen and progesterone. Progesterone itself did not have any effect.
“In terms of normal blood flow to the brain, it is important that blood vessels be able to expand and contract—they must be responsive to the body’s natural vasodilators and vasoconstrictors,” says Littleton-Kearney. “Our initial studies examined only dilation of the blood vessels, so we recently conducted a study to find out whether the blood vessels’ ability to contract is affected by stroke as well.”
Littleton-Kearney found that after stroke, the vessels have difficulty contracting. Since previous studies had found difficulty with the dilation response, this finding was surprising.
“We know now that blood vessels are less responsive to both vasodilators and vasoconstrictors after stroke,” says Littleton-Kearney. “Estrogen appears to help blood vessels to be more responsive to both, helping them to expand and contract as necessary to regulate blood flow to the brain.”
Her findings were published in the April 2005 Journal of Cerebral Blood Flow and Metabolism. In the future, Littleton-Kearney hopes to better understand why estrogen has this effect, learn more about the effects of progesterone, and examine the differences between natural and synthetic hormones.
Design and Control of an Actuated Thumb Exoskeleton for Hand Rehabilitation Following Stroke
Pictures at the URL. Anything is helpful to get our hands back. I could use thumb help since my thumb does not spread 90 degrees to my first finger.
http://robolab.cse.unsw.edu.au/conferences/ICRA-2011/data/pape
rs/1170.pdf
Abstract— Chronic hand impairment is common following
stroke. This paper presents an actuated thumb exoskeleton
(ATX) to facilitate research in hand rehabilitation therapy. The
ATX presented in this work permits independent bi-directional
actuation in each of the 5 degrees-of-freedom (DOF) of the
thumb using a mechanism that has 5 active DOF and 3 passive
DOF. The ATX is able to provide considerable joint torques for
the user while still allowing backdrivability through flexible
shaft transmission. A prototype has been built and experiments
were conducted to evaluate the closed-loop position control.
Further improvement and future work are discussed.
I. INTRODUCTION
Hand impairment is a prevalent outcome for a variety of
neuromuscular disorders, such as stroke. Up to 795,000
people in the U.S. experience a stroke each year [1]. Of these,
60-75% will live beyond one year after the incidence,
resulting in a current stroke population of 6.5 million [1]-[2].
Arm function is acutely impaired in a large majority of those
diagnosed with stroke [3]-[5]. Furthermore, acute
hemiparesis presages chronic hemiparesis in over 40% of
individuals [3], [4]. Chronic deficits are prevalent in the distal
upper extremities, especially with regard to finger extension
[6].
This distal limb impairment can be especially disabling, as
proper hand function is crucial to manual exploration and
manipulation of the environment. Indeed, loss of hand
function due to neuromuscular disorders frequently prevents
effective self-care and limits employment opportunities. One
study reported that more than half of the subjects they
observed were dependent on others for help in the activities of
daily living six months post-stroke [7].
An assortment of interventions has been tried in an effort to
improve function or to treat the resulting peripheral
alterations following stroke. Those with the most success to
date tend to focus on repetitive practice. Indeed numerous
studies employing the constraint-induced technique, in which
focus is placed on intensive practice with the impaired arm
without using the less impaired arm, have shown
improvement in hand capabilities [8]-[9]. This supports the
observations in animal models of stroke in which practice
Furui Wang, Milind Shastri, Vikash Gupta and Nilanjan Sarkar are with
the Department of Mechanical Engineering, Vanderbilt University, Nashville,
TN, 37212, USA (email: {furui.wang, vikash.gupta, milind.shastri,
nilanjan.arkar}@Vanderbilt.edu).
Christopher L. Jones, Christian Osswald and Xuan Kang are with the
Department of Biomedical Engineering, Illinois Institute of Technology,
Chicago, IL, 60616, USA (email: jonechr@Iit.edu, cosswald@iit.edu,
xuankang@hotmail.com,).
Derek G. Kamper is with the Department of Biomedical Engineering,
Illinois Institute of Technology and the Rehabilitation Institute of Chicago,
Chicago, IL, 60611, USA (e-mail: d-kamper@northwestern.edu).
appears to be the primary factor leading to synaptogenesis
and brain plasticity [10]-[11].
Unfortunately, many stroke survivors do not possess
sufficient sensorimotor control to practice the desired
movements. For the upper extremity, robots have been
created to assist with therapeutic training of the wrist, arm and
shoulder [12]-[15]. It has been reported that robot-delivered
sensorimotor training enhanced the motor performance of the
exercised shoulder and elbow with improved functional
outcome [16] and that practicing with a robot that assisted
reaching movements helped the users learn how to generate
smoother unaided reaching trajectories [17].
In recent years, a number of devices have been developed
expressly for or applied to hand rehabilitation. These include
both commercial products, such as CyberGrasp (Immersion
Corporation, San Jose, CA), the Hand Mentor (Kinetic
Muscles Inc., Tempe, AZ) and the Amadeo System
(Tyromotion GmbH, Graz, Austria), and experimental
devices, such as Rutgers Master II-ND, HWARD and
HandCARE, among others [18]-[20].
Questions remain, however, as to how best to use robotic
devices to facilitate rehabilitation. Should the device assist or
resist movement? Should movement error actually be
augmented, as some have suggested [21]? Should emphasis
be placed on practice of movement of individual joints [22] or
on the coordination of multiple joints?
The majority of the systems developed for the hand do not
allow for independent control of each DOF of the
finger/thumb joints, making it difficult to answer these
questions. This is especially true for the thumb, which is
typically modeled with five degrees-of-freedom (DOF)
[23]-[24]. An 18 DOF hand device has been developed in
Japan for hand and wrist rehabilitation following stroke [20].
This device actuates 4 DOF for the thumb. The joint torques
that it can provide, however, are limited to roughly 0.3 N-m, a
value that may not be sufficient for resistive or perturbation
therapy paradigms.
Thus, in this work, we are designing an actuated thumb
exoskeleton (ATX) with 5 active DOF that allows
independent actuation of each DOF of the thumb. The ATX is
able to provide considerable torque to overcome the
excessive coactivation or increased stiffness in the affected
thumb. We present our first prototype of the ATX and initial
experimental results in this paper. The paper is organized as
follows: Section II describes the mechanical design of the
ATX; Section III presents the kinematic analysis; Section IV
introduces the real-time control system; Section V shows the
instrumentation and initial experimental results; and Section
VI discusses the necessary improvement and Section VII
concludes the paper and proposes future work.
http://robolab.cse.unsw.edu.au/conferences/ICRA-2011/data/pape
rs/1170.pdfAbstract— Chronic hand impairment is common following
stroke. This paper presents an actuated thumb exoskeleton
(ATX) to facilitate research in hand rehabilitation therapy. The
ATX presented in this work permits independent bi-directional
actuation in each of the 5 degrees-of-freedom (DOF) of the
thumb using a mechanism that has 5 active DOF and 3 passive
DOF. The ATX is able to provide considerable joint torques for
the user while still allowing backdrivability through flexible
shaft transmission. A prototype has been built and experiments
were conducted to evaluate the closed-loop position control.
Further improvement and future work are discussed.
I. INTRODUCTION
Hand impairment is a prevalent outcome for a variety of
neuromuscular disorders, such as stroke. Up to 795,000
people in the U.S. experience a stroke each year [1]. Of these,
60-75% will live beyond one year after the incidence,
resulting in a current stroke population of 6.5 million [1]-[2].
Arm function is acutely impaired in a large majority of those
diagnosed with stroke [3]-[5]. Furthermore, acute
hemiparesis presages chronic hemiparesis in over 40% of
individuals [3], [4]. Chronic deficits are prevalent in the distal
upper extremities, especially with regard to finger extension
[6].
This distal limb impairment can be especially disabling, as
proper hand function is crucial to manual exploration and
manipulation of the environment. Indeed, loss of hand
function due to neuromuscular disorders frequently prevents
effective self-care and limits employment opportunities. One
study reported that more than half of the subjects they
observed were dependent on others for help in the activities of
daily living six months post-stroke [7].
An assortment of interventions has been tried in an effort to
improve function or to treat the resulting peripheral
alterations following stroke. Those with the most success to
date tend to focus on repetitive practice. Indeed numerous
studies employing the constraint-induced technique, in which
focus is placed on intensive practice with the impaired arm
without using the less impaired arm, have shown
improvement in hand capabilities [8]-[9]. This supports the
observations in animal models of stroke in which practice
Furui Wang, Milind Shastri, Vikash Gupta and Nilanjan Sarkar are with
the Department of Mechanical Engineering, Vanderbilt University, Nashville,
TN, 37212, USA (email: {furui.wang, vikash.gupta, milind.shastri,
nilanjan.arkar}@Vanderbilt.edu).
Christopher L. Jones, Christian Osswald and Xuan Kang are with the
Department of Biomedical Engineering, Illinois Institute of Technology,
Chicago, IL, 60616, USA (email: jonechr@Iit.edu, cosswald@iit.edu,
xuankang@hotmail.com,).
Derek G. Kamper is with the Department of Biomedical Engineering,
Illinois Institute of Technology and the Rehabilitation Institute of Chicago,
Chicago, IL, 60611, USA (e-mail: d-kamper@northwestern.edu).
appears to be the primary factor leading to synaptogenesis
and brain plasticity [10]-[11].
Unfortunately, many stroke survivors do not possess
sufficient sensorimotor control to practice the desired
movements. For the upper extremity, robots have been
created to assist with therapeutic training of the wrist, arm and
shoulder [12]-[15]. It has been reported that robot-delivered
sensorimotor training enhanced the motor performance of the
exercised shoulder and elbow with improved functional
outcome [16] and that practicing with a robot that assisted
reaching movements helped the users learn how to generate
smoother unaided reaching trajectories [17].
In recent years, a number of devices have been developed
expressly for or applied to hand rehabilitation. These include
both commercial products, such as CyberGrasp (Immersion
Corporation, San Jose, CA), the Hand Mentor (Kinetic
Muscles Inc., Tempe, AZ) and the Amadeo System
(Tyromotion GmbH, Graz, Austria), and experimental
devices, such as Rutgers Master II-ND, HWARD and
HandCARE, among others [18]-[20].
Questions remain, however, as to how best to use robotic
devices to facilitate rehabilitation. Should the device assist or
resist movement? Should movement error actually be
augmented, as some have suggested [21]? Should emphasis
be placed on practice of movement of individual joints [22] or
on the coordination of multiple joints?
The majority of the systems developed for the hand do not
allow for independent control of each DOF of the
finger/thumb joints, making it difficult to answer these
questions. This is especially true for the thumb, which is
typically modeled with five degrees-of-freedom (DOF)
[23]-[24]. An 18 DOF hand device has been developed in
Japan for hand and wrist rehabilitation following stroke [20].
This device actuates 4 DOF for the thumb. The joint torques
that it can provide, however, are limited to roughly 0.3 N-m, a
value that may not be sufficient for resistive or perturbation
therapy paradigms.
Thus, in this work, we are designing an actuated thumb
exoskeleton (ATX) with 5 active DOF that allows
independent actuation of each DOF of the thumb. The ATX is
able to provide considerable torque to overcome the
excessive coactivation or increased stiffness in the affected
thumb. We present our first prototype of the ATX and initial
experimental results in this paper. The paper is organized as
follows: Section II describes the mechanical design of the
ATX; Section III presents the kinematic analysis; Section IV
introduces the real-time control system; Section V shows the
instrumentation and initial experimental results; and Section
VI discusses the necessary improvement and Section VII
concludes the paper and proposes future work.
Monday, August 29, 2011
assessing risk for both coronary heart disease (CHD) and ischemic stroke associated with atherosclerosis.
I know this points to a commercial site but ask your doctor if this could be useful.
http://www.plactest.com/
Learn more about your risk for stroke and cardiovascular disease prevention. Now there is a simple blood test that can help uncover hidden risk for heart attack and stroke. Discover how the PLAC Test can help your physician assess your risk for and prevent these events.
http://www.plactest.com/
Learn more about your risk for stroke and cardiovascular disease prevention. Now there is a simple blood test that can help uncover hidden risk for heart attack and stroke. Discover how the PLAC Test can help your physician assess your risk for and prevent these events.
Functional mapping of single spines in cortical neurons in vivo
Hey, in vivo means while living, so following this they can map individual neuron synapses. This is absolutely necessary for researchers to figure out exactly what occurs in neuroplasticity and neurogenesis. I know I shouldn't presume to tell the medical gods what to do and where to go but they are lost as far as stroke rehabilitation is concerned.
http://www.nature.com/nature/journal/vaop/ncurrent/full/nature10193.html
The individual functional properties and spatial arrangement of afferent synaptic inputs on dendrites have a critical role in the processing of information by neurons in the mammalian brain1, 2, 3, 4. Although recent work has identified visually-evoked local dendritic calcium signals in the rodent visual cortex5, sensory-evoked signalling on the level of dendritic spines, corresponding to individual afferent excitatory synapses, remains unexplored6. Here we used a new variant of high-resolution two-photon imaging7 to detect sensory-evoked calcium transients in single dendritic spines of mouse cortical neurons in vivo. Calcium signals evoked by sound stimulation required the activation of NMDA (N-methyl-D-aspartate) receptors. Active spines are widely distributed on basal and apical dendrites and pure-tone stimulation at different frequencies revealed both narrowly and widely tuned spines. Notably, spines tuned for different frequencies were highly interspersed on the same dendrites: even neighbouring spines were mostly tuned to different frequencies. Thus, our results demonstrate that NMDA-receptor-dependent single-spine synaptic inputs to the same dendrite are highly heterogeneous. Furthermore, our study opens the way for in vivo mapping of functionally defined afferent sensory inputs with single-synapse resolution.
http://www.nature.com/nature/journal/vaop/ncurrent/full/nature10193.html
The individual functional properties and spatial arrangement of afferent synaptic inputs on dendrites have a critical role in the processing of information by neurons in the mammalian brain1, 2, 3, 4. Although recent work has identified visually-evoked local dendritic calcium signals in the rodent visual cortex5, sensory-evoked signalling on the level of dendritic spines, corresponding to individual afferent excitatory synapses, remains unexplored6. Here we used a new variant of high-resolution two-photon imaging7 to detect sensory-evoked calcium transients in single dendritic spines of mouse cortical neurons in vivo. Calcium signals evoked by sound stimulation required the activation of NMDA (N-methyl-D-aspartate) receptors. Active spines are widely distributed on basal and apical dendrites and pure-tone stimulation at different frequencies revealed both narrowly and widely tuned spines. Notably, spines tuned for different frequencies were highly interspersed on the same dendrites: even neighbouring spines were mostly tuned to different frequencies. Thus, our results demonstrate that NMDA-receptor-dependent single-spine synaptic inputs to the same dendrite are highly heterogeneous. Furthermore, our study opens the way for in vivo mapping of functionally defined afferent sensory inputs with single-synapse resolution.
Murphy Corbett 2009 Neuroplasticity after stroke pdf
Dr.Carmichael of Carmichael Labs sent me this paper as part of his answer to my questions.
Murphy Corbett 2009 Neuroplasticity after stroke pdf
I already posted some stuff from Dale Corbett here:
Dr. Dale Corbett was proposing in 2011
I had not heard of Timothy H. Murphy but he has 55 references in Pubmed that I will have to start looking at.
The Human and Economic Burden of Poststroke Spasticity and Muscle Overactivity
God, I hope someone sends this to William M. Landau, the guy who doesn't believe spasticity needs treatment.
The Human and Economic Burden of Poststroke Spasticity and Muscle Overactivity
ABSTRACT
• Objective: To present an overview of the human
and economic burden of poststroke spasticity and
muscle overactivity.
• Methods: Literature review.
• Results: The burden of stroke for patients, their
caregivers, and society is enormous. Stroke can result
in markedly diminished quality of life (QOL), loss
of productivity, and considerable economic costs.
The subset of stroke patients who have poststroke
spasticity experience additional burdens. Patients
with poststroke spasticity represent at least 20% of
all stroke patients. Poststroke spasticity can manifest
in multiple ways, with potentially profound and detrimental
effects on patient function and QOL. The risk
of falling is higher among stroke patients than in the
general population, and even higher in poststroke
spasticity patients, with the consequent risk of fractures.
Estimated direct costs for poststroke spasticity
patients are 4 times higher than those for stroke
patients without residual spasticity.
• Conclusion: The burden of poststroke spasticity is
high in terms of treatment costs, QOL consequences,
caregiver burden, and the effects of comorbidities
such as falls and fractures.
Lots more at the URL.
Therapeutic Acqueous Oxygen
When I saw this in the homeopathy post I searched some more and found it at UCLA.
http://www.uclahealth.org/body.cfm?id=403&action=detail&ref=1354
although there is no definition or explanation of what they are trying except for this line:
The Therapeutic Acqueous Oxygen (TAO) Trial: using supersaturated liquid oxygen as a new stroke treatment. Can someone contact them and find out what they are trying to prove.
http://www.uclahealth.org/body.cfm?id=403&action=detail&ref=1354
although there is no definition or explanation of what they are trying except for this line:
The Therapeutic Acqueous Oxygen (TAO) Trial: using supersaturated liquid oxygen as a new stroke treatment. Can someone contact them and find out what they are trying to prove.
Chocolate good for the heart and brain, according to new meta-analysis
But they never tell us the cocoa content, so I'm sure that the bland parafin suffused chocolate does not count.
http://www.theheart.org/article/1268867.do?utm_campaign=newsletter&utm_medium=email&utm_source=20110829_20110829_ESC_PM_29Aug
Paris, France - In a city renowned for its love of food, it is only fitting that researchers presented the results of a new study in Paris, France, showing that chocolate is good for the heart and brain. In a presentation at the European Society of Cardiology (ESC) 2011 Congress, British investigators are reporting that individuals who ate the most chocolate had a 37% lower risk of cardiovascular disease and a 29% lower risk of stroke compared with individuals who ate the least amount of chocolate.
http://www.theheart.org/article/1268867.do?utm_campaign=newsletter&utm_medium=email&utm_source=20110829_20110829_ESC_PM_29Aug
Paris, France - In a city renowned for its love of food, it is only fitting that researchers presented the results of a new study in Paris, France, showing that chocolate is good for the heart and brain. In a presentation at the European Society of Cardiology (ESC) 2011 Congress, British investigators are reporting that individuals who ate the most chocolate had a 37% lower risk of cardiovascular disease and a 29% lower risk of stroke compared with individuals who ate the least amount of chocolate.
In the study, published online August 29, 2011 in BMJ to coincide with the ESC presentation, Dr Adriana Buitrago-Lopez (University of Cambridge, UK) and colleagues state: "Although overconsumption can have harmful effects, the existing studies generally agree on a potential beneficial association of chocolate consumption with a lower risk of cardiometabolic disorders. Our findings confirm this, and we found that higher levels of chocolate consumption might be associated with a one-third reduction in the risk of developing cardiovascular disease."
In this meta-analysis of six cohort studies and one cross-sectional study, overall chocolate consumption was reported, with investigators not differentiating between dark, milk, or white chocolate. Chocolate in any form was included, such as chocolate bars, chocolate drinks, and chocolate snacks, such as confectionary, biscuits, desserts, and nutritional supplements. Chocolate consumption was reported differently in the trials but ranged from never to more than once per day. Most patients included in the trials were white, although one study included Hispanic and African Americans and one study included Asian patients.
Of the seven studies, five trials reported a significant inverse association between chocolate intake and cardiometabolic disorders. For example, individual studies showed reductions in the risk of coronary heart disease (odds ratio 0.43; 95% CI 0.27-0.68), the risk of cardiovascular disease mortality (relative risk [RR] 0.50; 95% CI 0.32-0.78), and the risk of incident diabetes in men (hazard ratio 0.65; 95% CI 0.43-0.97).
Overall, the pooled meta-analysis results showed that high levels of chocolate consumption compared with the lowest levels of chocolate consumption reduced the risk of any cardiovascular disease 37% (RR 0.63; 0.44-0.90) and stroke 29% (RR 0.71; 0.52-0.98). There was no association between chocolate consumption and the risk of heart failure, and no association on the incidence of diabetes in women.
The researchers note that the findings corroborate the results of previous meta-analyses of experimental and observational studies in different populations showing a similar relationship between chocolate and cocoa consumption and cardiometabolic disorders.
"These favorable effects seem mainly mediated by the high content of polyphenols present in cocoa products and are probably accrued through the increasing bioavailability of nitric oxide, which subsequently might lead to improvements in endothelial function, reductions in platelet function, and additional beneficial effects on blood pressure, insulin resistance, and blood lipids," conclude Buitrago-Lopez and colleagues.
Sunday, August 28, 2011
You can't improve what you can't measure
It comes from a remark attributed to GALILEO, who said 'Count what is
countable, measure what is measurable. What is not measurable, make
measurable'."
Boy does this describe the brain and stroke effects and rehabilitation. We don't know exactly how neuroplasticity works so we can't figure out how to consistently duplicate it. This is where we hear the canard, ' All strokes are different, all stroke recoveries are different' If we can't measure the recovery we can't improve it.
countable, measure what is measurable. What is not measurable, make
measurable'."
Boy does this describe the brain and stroke effects and rehabilitation. We don't know exactly how neuroplasticity works so we can't figure out how to consistently duplicate it. This is where we hear the canard, ' All strokes are different, all stroke recoveries are different' If we can't measure the recovery we can't improve it.
Natural Stroke Prevention Herbal Remedies Natural Cure Stroke 2nd try
I couldn't help but post another one of these, found it by looking at how people get to my site.
This one, in my opinion, contains no factual data so don't expect anything useful. The original search was for this:
Obviously someone looking for magical recovery and susceptible to these claims.
http://www.dherbs.com/articles/strokes-116.html
A couple of the more fantastic lines here: read the article if you want to see what non-scientific information looks like.
This one, in my opinion, contains no factual data so don't expect anything useful. The original search was for this:
brain stroke recovery elixir
And my posting on nostroms from the 1800's was included in the results.Obviously someone looking for magical recovery and susceptible to these claims.
http://www.dherbs.com/articles/strokes-116.html
A couple of the more fantastic lines here: read the article if you want to see what non-scientific information looks like.
- The toxins and obstructions in the blood take up available room for oxygen and vital life essence (chi). When oxygen is cut off at the blood-brain barrier(Whoa, What??, that would kill you), stroke is the result.
- Metaphysically, strokes denote a feeling of (1) being cut off from your source, (2) constantly feeling trapped in between walls or barriers (a rock and a hard place), (3) feeling like you are not able to persevere through life's (actually 'society's') challenges, (4) feeling stagnant in life and unable to move forward, (5) feeling like giving up in regards to life, (6) Resistance, and (7) rejection of life.
- The greatest single herb you can take for prevention or remedy of a stroke is "Periwinkle." Periwinkle, botanically known as "vinca major," is a plant that naturally improves the blood flow to the brain area. It helps to arrest all excess bleeding disorders and is useful for hemorrhaging, excess menstrual flow, nosebleed, bleeding gums, and all other bleeding disorders. (attribution please)
- Other beneficial herbs for stroke prevention and remedy include: Cayenne, Ginger, Cinnamon, Butcher's Broom, Gotu Kola, Cranesbill, Goldenseal Root, Manjistha, Holy (Blessed) Thistle, Gingko Biloba, and Mullein Leaf. (attribution please)
- Because calcium is the most alkaline mineral in the mineral family, it helps to counteract acidity and bust up accumulated debris that stick to the arterial walls and thus open up clogged and obstructed arteries. Natural calcium-rich herbs include: Comfrey Root, Oatstraw, Horsetail, and Alfalfa. (attribution please)
- Liquid oxygen drops are very helpful in stroke prevention and remedy as a liquid oxygen solution will greatly increase oxygen in the body. Because of this reason, I refer to liquid oxygen as supplemental oxygen. For post-stroke prevention purposes, a stroke sufferer should add 25-30 drops of liquid oxygen to each glass of drinking water. Where the hell did this come from??
- Magnet therapy is very beneficial for stroke recovery. Magnets enhance circulation by causing minerals to spin in the blood and thus causing friction (heat) which causes blood vessels and arteries to dilate which improves and enhances circulation and thus blood, oxygen, and mineral flow. (I remember when I had to talk my parents out of getting a magnetic bed)
- The crystal Melanite, a variation of Garnet, is very helpful for stroke recovery. It can be used for elixir purpose or can be applied to the forehead.( Oh my god, Apply to forehead!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!)
- With the correct or proper knowledge and tools, you can most definitely successfully bounce back from a stroke and reclaim your health and vitality. (In my opinion, knowledge not from this site)
Saturday, August 27, 2011
Carmichael labs stroke rehabilitation information
Thanks to Nina at Mindpop for showing me the way to this site. So if you want an easier way to understand neuroplasticity and neurogenesis without having to wade through all my blathering posts, go here:
http://carmichaellab.neurology.ucla.edu/
Topics covered;
He even answered some questions I asked of him in an email.
http://carmichaellab.neurology.ucla.edu/
Topics covered;
He even answered some questions I asked of him in an email.
Improving poststroke recovery: Neuroplasticity and task-oriented training
Ask your neurologist for this book, s/he should have it in either print or ebook form. If not ask why not.
http://www.springerlink.com/content/t46807q158716287/
http://www.springerlink.com/content/t46807q158716287/
Abstract
Neurorehabilitation is a critical part of the overall process to achieve optimal outcome after stroke. Presently, the field of neurorehabilitation is in transition. New research suggesting novel approaches to optimize functional recovery after stroke is on the horizon, but clear knowledge of the underlying mechanisms of this recovery is still being unraveled. In practice, many rehabilitation centers continue to provide traditional compensatory rehabilitation training while many others are practicing newer, “task-oriented” approaches. A few centers are incorporating new technology, such as computer-based training devices or robotics, into rehabilitation care. This transition is happening because neuroscientific research has shown that neuroplastic changes in the cerebral cortex and in other parts of the central nervous system (CNS) are necessarily linked to motor skill retraining in the affected limbs. Task-oriented training that focuses on the practice of skilled motor performance is the critical link to facilitating neural reorganization and “rewiring” in the CNS. Therefore, whenever possible, task-oriented training at an intense level should be incorporated into the rehabilitation program of any patient with stroke-related motor deficits. Two such task-oriented therapies that should be available at all neurorehabilitation centers are constraint-induced movement therapy and body weight-supported treadmill training. The optimal intensity of training (frequency and duration) is still not clear but is certainly greater than that available in clinical programs. Therefore, the incorporation of automated training devices will be necessary in the future. However, the engineering necessary to make these devices effective, easy to use, affordable, and portable remains a challenge for the next decade of neurologic bioengineering research.
Discovery Of A Natural Protection Mechanism In Some Nerve Cells Could Benefit Stroke Victims
Someone should be able to come up with another hyperacute therapy based on these findings.
http://www.medicalnewstoday.com/releases/232868.php
Neuroscientists have identified a natural protection mechanism in some of the brain's nerve cells during the onset of stroke. The findings, published today [17 August] in the Journal of Neuroscience, could be used to develop treatments to protect other nerve cell types responsible for speech and movement.
Stroke - the third largest cause of death in the UK - causes disruption to the blood supply to the brain, depriving nerve cells of oxygen and nutrients. This leads to the death of nerve cells and the consequent loss of the brain's cognitive functions such as speech and movement. However, not all nerve cells are equally susceptible to stroke-induced damage.
The research, led by Dr Jack Mellor from the University of Bristol, examined two types of nerve cell in a part of the brain called the hippocampus - the region linked to memory and navigation. One of these cell types, the CA1 cell, is highly susceptible to damage after stroke whereas the other, the CA3 cell, is much more resistant despite many other similarities between the two cell types.
Dr Mellor, Senior Lecturer in the University's School of Physiology and Pharmacology, said: "We hope that if we can understand why some nerve cells are resistant to stroke damage we may be able to develop strategies to protect those cells that are sensitive."
The researchers found that the CA3 cells possess a mechanism for reducing their susceptibility during, and immediately after, a laboratory-based model for stroke. This mechanism involved making the CA3 cells less sensitive to the neurotransmitter glutamate, which is released in large quantities during stroke, by removing glutamate receptor proteins from the surface of these cells.
The removal of glutamate receptors was triggered by adenosine A3 receptors that are activated by very high levels of the neurotransmitter adenosine found only during stroke conditions. Interestingly, CA1 cells that are susceptible to stroke damage did not have adenosine A3 receptors and did not respond to the stroke model by removing surface glutamate receptors. The findings reveal that CA3 cells possess a mechanism for neuronal protection during stroke.
Dr Mellor added: "Historically, stroke has been very difficult to treat because of its unpredictability and the need to administer drugs within minutes of the onset of a stroke. These problems will not be overcome by our research but our findings do reveal a natural protection mechanism in some nerve cells, which may be useful in developing treatments to protect other nerve cell types."
http://www.medicalnewstoday.com/releases/232868.php
Neuroscientists have identified a natural protection mechanism in some of the brain's nerve cells during the onset of stroke. The findings, published today [17 August] in the Journal of Neuroscience, could be used to develop treatments to protect other nerve cell types responsible for speech and movement.
Stroke - the third largest cause of death in the UK - causes disruption to the blood supply to the brain, depriving nerve cells of oxygen and nutrients. This leads to the death of nerve cells and the consequent loss of the brain's cognitive functions such as speech and movement. However, not all nerve cells are equally susceptible to stroke-induced damage.
The research, led by Dr Jack Mellor from the University of Bristol, examined two types of nerve cell in a part of the brain called the hippocampus - the region linked to memory and navigation. One of these cell types, the CA1 cell, is highly susceptible to damage after stroke whereas the other, the CA3 cell, is much more resistant despite many other similarities between the two cell types.
Dr Mellor, Senior Lecturer in the University's School of Physiology and Pharmacology, said: "We hope that if we can understand why some nerve cells are resistant to stroke damage we may be able to develop strategies to protect those cells that are sensitive."
The researchers found that the CA3 cells possess a mechanism for reducing their susceptibility during, and immediately after, a laboratory-based model for stroke. This mechanism involved making the CA3 cells less sensitive to the neurotransmitter glutamate, which is released in large quantities during stroke, by removing glutamate receptor proteins from the surface of these cells.
The removal of glutamate receptors was triggered by adenosine A3 receptors that are activated by very high levels of the neurotransmitter adenosine found only during stroke conditions. Interestingly, CA1 cells that are susceptible to stroke damage did not have adenosine A3 receptors and did not respond to the stroke model by removing surface glutamate receptors. The findings reveal that CA3 cells possess a mechanism for neuronal protection during stroke.
Dr Mellor added: "Historically, stroke has been very difficult to treat because of its unpredictability and the need to administer drugs within minutes of the onset of a stroke. These problems will not be overcome by our research but our findings do reveal a natural protection mechanism in some nerve cells, which may be useful in developing treatments to protect other nerve cell types."
Develop a wearable ankle robot for in-bed acute stroke rehabilitation
Boy does this make a lot of sense, especially with all the downtime a survivor spends in bed with no therapy available. I used something similar to this when I was in a research study on ankle movement,
I was trying to follow a jagged line while in an MRI machine. It was difficult since I wasn't wearing my glasses and things were quite blurry. Pictures at the URL.
http://embc2011.embs.org/wp-content/uploads/2011/08/
unconference-demo-EMBS2011-RIC.pdf?
ACUTE stroke survivors are actively trained with activities helpful for recovery of mobility in only 13% of the time and they are left alone in more than 60% of the time in early post-acute rehabilitation window [1]. Considering the first few months post stroke is critical in stroke recovery (neuroplasticity) [2], there is a strong need for active movement therapy and manipulate/mobilize the joints early in acute stroke rehabilitation. This project seeks a feasible solution which can meet this clinic need and deliver well-controlled passive stretching and motivating active movement therapy with robotic assistance/resistance for better motor re-learning in acute stage.
I was trying to follow a jagged line while in an MRI machine. It was difficult since I wasn't wearing my glasses and things were quite blurry. Pictures at the URL.
http://embc2011.embs.org/wp-content/uploads/2011/08/
unconference-demo-EMBS2011-RIC.pdf?
ACUTE stroke survivors are actively trained with activities helpful for recovery of mobility in only 13% of the time and they are left alone in more than 60% of the time in early post-acute rehabilitation window [1]. Considering the first few months post stroke is critical in stroke recovery (neuroplasticity) [2], there is a strong need for active movement therapy and manipulate/mobilize the joints early in acute stroke rehabilitation. This project seeks a feasible solution which can meet this clinic need and deliver well-controlled passive stretching and motivating active movement therapy with robotic assistance/resistance for better motor re-learning in acute stage.
Lifetime economic burden of stroke
Lots of detail about the costs, maybe this needs a lot more exposure to influence persons of power that control what rehab research is done. I would have hoped that the WSO would be updating something like this every year.
Lifetime Cost of Stroke in the United States 1990
Results The lifetime cost per person of first strokes occurring in 1990 is estimated to be $228 030 for SAH, $123 565 for ICH, $90 981 for ISC, and $103 576 averaged across all stroke subtypes. Indirect costs accounted for 58.0% of lifetime costs. Aggregate lifetime cost associated with an estimated 392 344 first strokes in 1990 was $40.6 billion: $5.6 billion for SAH, $6.0 billion for ICH, and $29.0 billion for ISC.
Lifetime Cost of Stroke in the United States 1990
The most up to date analyses of
the economic burden of stroke in the United Kingdom estimated an
average per patient cost of £15,000 to £30,000 over the first five years
after stroke5 but does not provide the total aggregate cost of stroke in the
UK. A second study does calculate the overall cost of stroke care in
England to be £2.3 billion in 1995-96 with lifetime per patient costs
ranging from £2,000 to £62,000
http://www.nao.org.uk/idoc.ashx?docId=11ed54b8-babf-4c0e-aefc-2a09b55de4ae&version=-1
I'm sure there are lots more countries with information but they are hiding it. Come on get it out there.
Lifetime Cost of Stroke in the United States 1990
Results The lifetime cost per person of first strokes occurring in 1990 is estimated to be $228 030 for SAH, $123 565 for ICH, $90 981 for ISC, and $103 576 averaged across all stroke subtypes. Indirect costs accounted for 58.0% of lifetime costs. Aggregate lifetime cost associated with an estimated 392 344 first strokes in 1990 was $40.6 billion: $5.6 billion for SAH, $6.0 billion for ICH, and $29.0 billion for ISC.
Lifetime Cost of Stroke in the United States 1990
The Economic Burden of Stroke in the United Kingdom
Results: The model estimated that, for every patient who experiences a stroke, the cost to the NHS in the UK is £15 306 over 5 years and, when informal care costs are included, the amount increases to £29 405 (2001/2002 prices). The Economic Burden of Stroke in the United KingdomEstimating the lifetime economic burden of stroke according to the age of onset in South Korea: a cost of illness study
Results
The lifetime costs of stroke were estimated to be: 200.7, 81.9, and 16.4 million Korean won (1,200 KRW is approximately equal to one US dollar) for men who suffered a first stroke at age 45, 55 and 65 years, respectively, and 75.7, 39.2, and 19.3 million KRW for women at the same age. Estimating the lifetime economic burden of stroke according to the age of onset in South Korea: a cost of illness study US costs- The conditions and disabilities associated with stroke cost the United States between $30 billion and $40 billion a year.
- The average cost of care for a patient up to 90 days post-stroke is $15,000.
- The mean lifetime cost of ischemic stroke in the U.S. is an estimated $140,048. This cost includes inpatient care, rehabilitation, and follow-up care.
- As of 2005, stroke accounts for $57 billion in direct and indirect costs each year.
- The estimated direct and indirect cost of stroke for 2008 is $65.5 billion.
The most up to date analyses of
the economic burden of stroke in the United Kingdom estimated an
average per patient cost of £15,000 to £30,000 over the first five years
after stroke5 but does not provide the total aggregate cost of stroke in the
UK. A second study does calculate the overall cost of stroke care in
England to be £2.3 billion in 1995-96 with lifetime per patient costs
ranging from £2,000 to £62,000
http://www.nao.org.uk/idoc.ashx?docId=11ed54b8-babf-4c0e-aefc-2a09b55de4ae&version=-1
I'm sure there are lots more countries with information but they are hiding it. Come on get it out there.
Friday, August 26, 2011
Omega-3 fatty acids reduce stroke severity
So maybe we should be taking DHA - fish oil before and immediately after the stroke;
Before article here;
http://www.sciencecodex.com/omega3s_reduce_stroke_severity
After article here:
http://oc1dean.blogspot.com/2011/08/salutary-effects-of-dha-dietary.html
Before -
Before article here;
http://www.sciencecodex.com/omega3s_reduce_stroke_severity
After article here:
http://oc1dean.blogspot.com/2011/08/salutary-effects-of-dha-dietary.html
Before -
Quebec City, August 25, 2011—A diet rich in omega-3 fatty acids reduces the severity of brain damage after a stroke, according to a study conducted by Université Laval researchers. The team co-directed by professors Jasna Kriz and Frédéric Calon showed that the extent of brain damage following a stroke was reduced by 25% in mice that consumed DHA type omega-3s daily.
Researchers observed that the effects of stroke were less severe in mice that had been fed a diet rich in DHA for three months than in mice fed a control diet. In mice from the DHA group, they saw a reduction in the concentrations of molecules that stimulate tissue inflammation and, conversely, a larger quantity of molecules that prevent the activation of cell death.
"This is the first convincing demonstration of the powerful anti-inflammatory effect of DHA in the brain," underscored Frédéric Calon of Université Laval's Faculty of Pharmacy. This protective effect results from the substitution of molecules in the neuronal membrane: DHA partially replaces arachidonic acid, an omega-6 fatty acid known for its inflammatory properties.
"The consumption of omega-3s creates an anti-inflammatory and neuroprotective environment in the brain that mitigates damage following a stroke," summarized Jasna Kriz, of Université Laval's Faculty of Medicine. "It prevents an acute inflammatory response that, if not controlled, is harmful to brain tissue."
Professor Calon believes that this anti-inflammatory effect is likely transferable to humans. "Since DHA is readily available, inexpensive, and reduces the risk of a number of health problems without causing significant side effects, the risk–benefit ratio tends to favor the regular consumption of fish or DHA," he concluded.
Details of the study can be found on the website of the journal Stroke.
Wednesday, August 24, 2011
Studies of adult hippocampal neurogenesis in humans
I haven't gone thru all of these yet to see if this list contains all the research articles I've found. I follow this blogger. A roundabout way to find this since I follow www.quora.com the stroke a neurology sections
http://www.functionalneurogenesis.com/blog/2011/01/studies-of-adult-hippocampal-neurogenesis-in-humans/
http://www.functionalneurogenesis.com/blog/2011/01/studies-of-adult-hippocampal-neurogenesis-in-humans/
Tuesday, August 23, 2011
Stroke survivors: Naturopathic Medicine is the basis of your recovery
I guess all of us are missing the boat. You'll have to read the whole article at the URL if interested. I would expect a Nobel Prize for this if it is true.
This is only one paragraph;
By the time the stroke survivor even gets to physiotherapy, getting gone via the battery of tests and drugs in the hospital, his/her body is depleted of its crucial force(What???) and left with little power to " get off the ground".(What a total lack of understanding of the nature of stroke damage!) Naturopathic medicine is a blend of centuries old natural?? medicine with existing advances in the study of health. It covers all aspects of household wellness from prenatal to geriatric care. N.D.'s depend on patients to be an integral component of their own health. A Naturopathic team works together to discover the causes of illness and imbalance, rather than focusing on symptom management alone.
http://strokesymptomsformen.org/stroke-survivors-naturopathic-medicine-is-the-basis-of-your-recovery/
And they don't allow responses. Absolutely no scientific articles to back up the statements.
In my opinion, complete and absolute quackery, you would probably do just as well with these nostrums:
http://oc1dean.blogspot.com/2011/03/nostrums-for-apoplexy-rehab.html
This is only one paragraph;
By the time the stroke survivor even gets to physiotherapy, getting gone via the battery of tests and drugs in the hospital, his/her body is depleted of its crucial force(What???) and left with little power to " get off the ground".(What a total lack of understanding of the nature of stroke damage!) Naturopathic medicine is a blend of centuries old natural?? medicine with existing advances in the study of health. It covers all aspects of household wellness from prenatal to geriatric care. N.D.'s depend on patients to be an integral component of their own health. A Naturopathic team works together to discover the causes of illness and imbalance, rather than focusing on symptom management alone.
http://strokesymptomsformen.org/stroke-survivors-naturopathic-medicine-is-the-basis-of-your-recovery/
And they don't allow responses. Absolutely no scientific articles to back up the statements.
In my opinion, complete and absolute quackery, you would probably do just as well with these nostrums:
http://oc1dean.blogspot.com/2011/03/nostrums-for-apoplexy-rehab.html
Monday, August 22, 2011
Agmatine enhances neurogenesis by increasing ERK1/2 expression
More neurogenesis and a new word to understand - astrogenesis.
http://www.sciencedirect.com/science/article/pii/S0024320511003365
Our study aimed to demonstrate whether agmatine could regulate proliferation and cell fate determination of subventricular zone neural stem cells (SVZ NSCs).
SVZ NSCs were grown in the presence of epidermal growth factor (EGF) and basic fibroblast growth factor (bFGF) (20 ng/ml) until 4 days in vitro (DIV) and later the culture medium was replaced without EGF and bFGF until 11 DIV in the absence (EGF/bFGF+/−/Ag−) or presence of agmatine (EGF/bFGF+/−/Ag+). Another set SVZ NSCs were maintained with EGF and bFGF until 11 DIV without (EGF/bFGF+/+/Ag−) or with agmatine treatment (EGF/bFGF+/+/Ag+). Agmatine's effect on proliferation and cell death (H and PI staining and Caspase-3 immunostaining) was examined at DIV 4 and 11. Agmatine's (100 μM) effect on cell fate determination was confirmed by immunostaining and Western blot at 11 DIV.
Agmatine treatment reduced the neurosphere size and total cell count number dose-dependently in all the experimental groups both at DIV 4 and11. Immunoblotting and staining results showed that agmatine increased the Tuj1 and MAP2 and decreased the GFAP with no change in the Oligo2 protein expressions. This neurogenesis effect of agmatine seems to have a relation with ERK1/2 activation and anti-astrogenesis effect is thought to be related with the suppression of BMP 2,4 and SMAD 1,5,8 protein expression.
This model could be an invaluable tool to study whether agmatine treated SVZ NSC transplantation to the CNS injury could trigger neurogenesis and decrypt the full range of molecular events involved during neurogenesis in vivo as evidenced in vitro.
I like this last line.
http://www.sciencedirect.com/science/article/pii/S0024320511003365
Abstract
Aim
Our study aimed to demonstrate whether agmatine could regulate proliferation and cell fate determination of subventricular zone neural stem cells (SVZ NSCs).
Main methods
SVZ NSCs were grown in the presence of epidermal growth factor (EGF) and basic fibroblast growth factor (bFGF) (20 ng/ml) until 4 days in vitro (DIV) and later the culture medium was replaced without EGF and bFGF until 11 DIV in the absence (EGF/bFGF+/−/Ag−) or presence of agmatine (EGF/bFGF+/−/Ag+). Another set SVZ NSCs were maintained with EGF and bFGF until 11 DIV without (EGF/bFGF+/+/Ag−) or with agmatine treatment (EGF/bFGF+/+/Ag+). Agmatine's effect on proliferation and cell death (H and PI staining and Caspase-3 immunostaining) was examined at DIV 4 and 11. Agmatine's (100 μM) effect on cell fate determination was confirmed by immunostaining and Western blot at 11 DIV.
Key findings
Agmatine treatment reduced the neurosphere size and total cell count number dose-dependently in all the experimental groups both at DIV 4 and11. Immunoblotting and staining results showed that agmatine increased the Tuj1 and MAP2 and decreased the GFAP with no change in the Oligo2 protein expressions. This neurogenesis effect of agmatine seems to have a relation with ERK1/2 activation and anti-astrogenesis effect is thought to be related with the suppression of BMP 2,4 and SMAD 1,5,8 protein expression.
Significance
This model could be an invaluable tool to study whether agmatine treated SVZ NSC transplantation to the CNS injury could trigger neurogenesis and decrypt the full range of molecular events involved during neurogenesis in vivo as evidenced in vitro.
I like this last line.
The salutary effects of DHA dietary supplementation on cognition, neuroplasticity, and membrane homeostasis after brain trauma
I know this is mainly for TBI but heck survivors could become guinea pigs for this too.
I pointed out something similar in this post:
http://oc1dean.blogspot.com/2011/05/new-insights-into-gpr40-creb.html
The new article here:
http://www.liebertonline.com/doi/abs/10.1089/neu.2011.1872
The pathology of traumatic brain injury is characterized by failure in the capacity of neurons to metabolize energy, sustain synaptic function, and likely resulting in cognitive and emotional disorders. Based on the broad nature of the pathology, we have assessed the potential of the omega-3 fatty acid docosahexaenoic acid (DHA) to counteract the effects of concussive injury on important aspects of neuronal function and cognition. Fluid percussion injury (FPI) or sham injury was performed, and rats were then maintained on a diet high in DHA (1.2% DHA) for 12 days. We found that DHA supplementation, which elevates brain DHA contents, normalized levels of brain-derived neurotrophic factor (BDNF), synapsin I, cAMP responsive element-binding protein (CREB), and CaMKII, and improved learning ability in FPI rats. It is known that BDNF facilitates synaptic transmission and learning ability by modulating synapsin I, CREB, and CaMKII signaling. The DHA diet also counteracted the FPI-reduced manganese superoxide dismutase (SOD) and Sir2 (a NAD+ -dependent deacetylase. Given the involvement of SOD and Sir2 in promoting metabolic homeostasis, DHA may help the TBI brain by providing resistance to oxidative stress. Furthermore, DHA normalized levels of iPLA2 and syntaxin-3 which may help preserve membrane homeostasis and function after FPI. The overall results emphasize the potential of dietary DHA to counteract broad and fundamental aspects of the TBI pathology that can translate in preserved cognitive capacity.
I pointed out something similar in this post:
http://oc1dean.blogspot.com/2011/05/new-insights-into-gpr40-creb.html
The new article here:
http://www.liebertonline.com/doi/abs/10.1089/neu.2011.1872
The pathology of traumatic brain injury is characterized by failure in the capacity of neurons to metabolize energy, sustain synaptic function, and likely resulting in cognitive and emotional disorders. Based on the broad nature of the pathology, we have assessed the potential of the omega-3 fatty acid docosahexaenoic acid (DHA) to counteract the effects of concussive injury on important aspects of neuronal function and cognition. Fluid percussion injury (FPI) or sham injury was performed, and rats were then maintained on a diet high in DHA (1.2% DHA) for 12 days. We found that DHA supplementation, which elevates brain DHA contents, normalized levels of brain-derived neurotrophic factor (BDNF), synapsin I, cAMP responsive element-binding protein (CREB), and CaMKII, and improved learning ability in FPI rats. It is known that BDNF facilitates synaptic transmission and learning ability by modulating synapsin I, CREB, and CaMKII signaling. The DHA diet also counteracted the FPI-reduced manganese superoxide dismutase (SOD) and Sir2 (a NAD+ -dependent deacetylase. Given the involvement of SOD and Sir2 in promoting metabolic homeostasis, DHA may help the TBI brain by providing resistance to oxidative stress. Furthermore, DHA normalized levels of iPLA2 and syntaxin-3 which may help preserve membrane homeostasis and function after FPI. The overall results emphasize the potential of dietary DHA to counteract broad and fundamental aspects of the TBI pathology that can translate in preserved cognitive capacity.
Sunday, August 21, 2011
Synaptic plasticity in sleep: learning, homeostasis and disease.
So my reading of this is sleep can consolidate the therapy we do during the day. Although I do wonder about all the naps I could take everyday.
http://www.ncbi.nlm.nih.gov/pubmed/21840068
http://neuroskeptic.blogspot.com/2011/08/is-sleep-brain-defragmentation.html
http://www.ncbi.nlm.nih.gov/pubmed/21840068
Abstract
Sleep is a fundamental and evolutionarily conserved aspect of animal life. Recent studies have shed light on the role of sleep in synaptic plasticity. Demonstrations of memory replay and synapse homeostasis suggest that one essential role of sleep is in the consolidation and optimization of synaptic circuits to retain salient memory traces despite the noise of daily experience. Here, we review this recent evidence and suggest that sleep creates a heightened state of plasticity, which may be essential for this optimization. Furthermore, we discuss how sleep deficits seen in diseases such as Alzheimer's disease and autism spectrum disorders might not just reflect underlying circuit malfunction, but could also play a direct role in the progression of those disorders.
And this blogger has wonderful insights into along with some good pictures and charts.http://neuroskeptic.blogspot.com/2011/08/is-sleep-brain-defragmentation.html
Statins Not Suitable For Certain Patients: Study
Another reason to talk to your doctor about statins.
http://www.medindia.net/news/Statins-Not-Suitable-For-Certain-Patients-Study-89452-1.htm
But the Loyola neurologists say this benefit generally applies only to patients who have experienced ischemic strokes, which are caused by blood clots in brain vessels.
And even among ischemic stroke patients, there is a small subgroup that should be placed on statin therapy only "with circumspection," wrote Dr. Murray Flaster, an associate professor in the departments of Neurology and Neurological Surgery at Loyola University Chicago Stritch School of Medicine, and colleagues.
These patients are those who have had strokes in small blood vessels, have poorly controlled high blood pressure and consume more than one drink of alcohol per day.
The picture is more varied for the 15 percent of stroke patients who have had hemorrhagic strokes (caused by bleeding on or in the brain).
There are two types of hemorrhagic stroke: aneurysmal subarachnoid hemorrhage (SAH) and intracranial hemorrhage (ICH). An SAH stroke involves bleeding over the surface of the brain, while an ICH stroke involves bleeding inside the brain.
Read more: Statins Not Suitable For Certain Patients: Study | MedIndia http://www.medindia.net/news/Statins-Not-Suitable-For-Certain-Patients-Study-89452-1.htm#ixzz1ViN0Yxpp
http://www.medindia.net/news/Statins-Not-Suitable-For-Certain-Patients-Study-89452-1.htm
For many patients who has suffered strokes or heart attacks, cholesterol-lowering statin drugs can help to reduce the risk. But neurologists from Loyola University Health System have warned that statins may not be appropriate for certain categories of patients.
A landmark 2006 study known as SPARCL found that statins reduced the risk of subsequent strokes by 16 percent in patients who have experienced strokes or transient ischemic attacks (mini strokes).
A landmark 2006 study known as SPARCL found that statins reduced the risk of subsequent strokes by 16 percent in patients who have experienced strokes or transient ischemic attacks (mini strokes).
But the Loyola neurologists say this benefit generally applies only to patients who have experienced ischemic strokes, which are caused by blood clots in brain vessels.
And even among ischemic stroke patients, there is a small subgroup that should be placed on statin therapy only "with circumspection," wrote Dr. Murray Flaster, an associate professor in the departments of Neurology and Neurological Surgery at Loyola University Chicago Stritch School of Medicine, and colleagues.
These patients are those who have had strokes in small blood vessels, have poorly controlled high blood pressure and consume more than one drink of alcohol per day.
The picture is more varied for the 15 percent of stroke patients who have had hemorrhagic strokes (caused by bleeding on or in the brain).
There are two types of hemorrhagic stroke: aneurysmal subarachnoid hemorrhage (SAH) and intracranial hemorrhage (ICH). An SAH stroke involves bleeding over the surface of the brain, while an ICH stroke involves bleeding inside the brain.
Read more: Statins Not Suitable For Certain Patients: Study | MedIndia http://www.medindia.net/news/Statins-Not-Suitable-For-Certain-Patients-Study-89452-1.htm#ixzz1ViN0Yxpp
How to recover from a stroke
This is just my uninformed opinion so don't listen to me.
I answer like this on stroke forums.
It depends, but your medical staff has no clue on how to answer you. So here is my guideline, find out exactly what areas of your brain were in the bleed drainage area or penumbra. These should still be partially working, your neurologist should give you a map of what functions are in that area. Then get a map of what your dead brain looks like and the functions it supported. With a lot of hard work and neuroplasticity the damaged area can recover. The dead area is very problematic because you will need to move those functions to another area in your brain and no one can tell you how to do that. The 10% use of your brain is a myth, you do not have spare neurons lying around.
Waiting will not get you anywhere, recovery is extremely hard work that needs to continue until you die.
I answer like this on stroke forums.
It depends, but your medical staff has no clue on how to answer you. So here is my guideline, find out exactly what areas of your brain were in the bleed drainage area or penumbra. These should still be partially working, your neurologist should give you a map of what functions are in that area. Then get a map of what your dead brain looks like and the functions it supported. With a lot of hard work and neuroplasticity the damaged area can recover. The dead area is very problematic because you will need to move those functions to another area in your brain and no one can tell you how to do that. The 10% use of your brain is a myth, you do not have spare neurons lying around.
Waiting will not get you anywhere, recovery is extremely hard work that needs to continue until you die.
Saturday, August 20, 2011
Post-Stroke Care: A Comprehensive Approach
Another tidbit from here, 50 million survivors worldwide, what a huge market for neurogenesis and stem cells or extreme neuroplasticity.
http://www.physiciansweekly.com/Features/11_31/stroke_survivor_care.html
This whole article is depressing because it makes the assumption that only the medical staff needs to know this information. Another reason why the AHA needs to be taken over by survivors.
http://www.physiciansweekly.com/Features/11_31/stroke_survivor_care.html
This whole article is depressing because it makes the assumption that only the medical staff needs to know this information. Another reason why the AHA needs to be taken over by survivors.
According to the American Heart Association (AHA), approximately 50 million stroke survivors worldwide currently cope with significant physical, cognitive, and emotional deficits, and 25% to 74% of these survivors require some assistance. In the October 2010 issue of Stroke, the AHA published a comprehensive scientific statement on nursing and interdisciplinary rehabilitation care for stroke patients. The statement examines the coordination of care and summarizes the best available evidence for post-stroke therapies. Available at http://stroke.ahajournals.org, the statement is intended to help educate nurses and other members of the interdisciplinary team about the potential for recovery in the more chronic phases of stroke care. Healthcare professionals are often unaware of patients’ potential for improvement in the later phases of care.
“Healthcare professionals are often unaware of patients’ potential for improvement in the later phases of care.” What more do you need to know that you are on your own, do-it-yourself?
Research has shown that the mortality rate associated with stroke is highest in the first 30 days following the event. As such, it’s critical that stroke care be coordinated from the moment the patient hits the door through all phases of care. Clinicians can make measurable improvements with mortality and quality-of-life issues for these patients by initiating rehabilitation care as early as possible. The AHA statement outlines the role of key members of the interdisciplinary team and emphasizes the diverse skills that are necessary for post-stroke rehabilitation.
A Comprehensive Tool
The AHA statement provides an overview of the evidence for various screening tests and medical treatments, including traditional rehabilitation therapies and newer techniques, such as robot-assisted therapies, electrical stimulation, and weight-assisted treadmill devices. Physicians, nurses, and therapists can find a summary of virtually all treatments given for the rehabilitation of stroke, along with the level of evidence for benefit. It puts into context patients’ medical and functional limitations, as well as their social environment, access to healthcare, and family support. The AHA statement also provides the knowledge and support of how everyone caring for these patients can coordinate their efforts to improve quality of life.
Caregiver Support
Additionally, the AHA statement discusses approaches to personal and environmental factors and education and support for caregivers. Family members play a vital role in the long-term care of stroke patients. About 75% of stroke patients will be cared for by their family after their event. Caregivers should be active members of the interdisciplinary team with common shared goals for recovery and community reintegration. The statement addresses how these caregivers should be educated to optimize quality of life for patients and strategies to enhance their long-term caregiving capability.
Looking Ahead
Although the AHA statement presents sound evidence on managing stroke patients for the long term, several areas of research are lacking data and require greater emphasis. For example, the management of depression in the post-stroke phase and communication and cognition need more evidence-based data to guide clinicians. The hope is that more research will further assist our efforts in the care of these patients.
The Decline in Stroke Mortality Exploration of Future Trends in 7 Western European Countries
The last line in red here is the most important.http://stroke.ahajournals.org/content/42/8/2126.abstract
http://stroke.ahajournals.org/content/42/8/2126.abstract
Abstract
Background and Purpose—This article aims to make projections of future trends in stroke mortality in the Year 2030 based on recent trends in stroke mortality in 7 Western European countries.
Methods—Mortality data were obtained from national cause of death registries. Annual rates of decline in stroke mortality of 1980 to 2005 were determined for men and women in the United Kingdom, France, the Netherlands, and 4 Nordic countries on the basis of regression analysis. Estimated rates of decline were extrapolated until 2030. Cause-elimination life tables were used to determine the effect of stroke in 2030 in terms of potential gain in life expectancy. The absolute numbers of stroke deaths in 2030 were estimated using national population projections of Eurostat.
Results—In all countries, stroke mortality rates declined incessantly until 2005 among both men and women. If these trends were to continue, age-adjusted mortality rates would decline by approximately half between 2005 and 2030 with larger declines in France (approximately two thirds) and smaller declines in the Netherlands, Denmark, and Sweden (approximately one fourth). Similar rates of decline would be observed in terms of potential gain in life expectancy. Because of population aging, the absolute number of stroke deaths would decline slowly in the United Kingdom and France and stabilize or even increase in other countries.
Conclusions—In the near future, stroke may lose much of its effects on life expectancy but remain a frequent cause of death among elderly populations. The prevention of stroke-related disability instead of mortality may become increasingly more important.
So start working on testing all those hyperacute possibilities that stop the cascade of neuronal death.
Stem Cell Research in Stroke How Far From the Clinic?
the abstract just hints, send me the complete article.
http://stroke.ahajournals.org/content/42/8/2369.abstract
http://stroke.ahajournals.org/content/42/8/2369.abstract
Abstract
Stem cell-based approaches hold much promise as potential novel treatments to restore function after stroke. Studies in animal models have shown that stem cell transplantation can improve function by replacing neurons or by trophic actions, modulation of inflammation, promotion of angiogenesis, remyelination and axonal plasticity, and neuroprotection. Endogenous neural stem cells are also potential therapeutic targets because they produce new neurons after stroke. Clinical trials are ongoing but there is currently no proven stem cell-based therapy for stroke. Preclinical studies and clinical research will be needed to optimize the therapeutic benefit and minimize the risks of stem cells in stroke.
Stroke Declines From Third to Fourth Leading Cause of Death in the United States
I know this is good news but while they are congratulating themselves they are missing the huge problem of recovery and rehabilitation.
http://stroke.ahajournals.org/content/42/8/2351.abstract
http://stroke.ahajournals.org/content/42/8/2351.abstract
Abstract
Background and Purpose—Stroke recently declined from the third to the fourth leading cause of death in the United States, its first rank transition among sources of American mortality in nearly 75 years.
Methods—This is a narrative review supplemented by new analyses of Centers for Disease Control and Prevention National Vital Statistics Reports from 1931 to 2008.
Results—Historically, stroke transitioned from the second to the third leading cause of death in the United States in 1937, but stroke death rates were essentially stable from 1930 to 1960. Then a long, great decline began, moderate in the 1960s, precipitous in the 1970s and 1980s, and moderate again in the 1990s and 2000s. By 2008, age-adjusted annual death rates from stroke were three fourths less than the historic 1931 to 1960 norm (40.6 versus 175.0 per 100 000). Total actual stroke deaths in the United States declined from a high of 214 000 in 1973 to 134 000 in 2008. Improved stroke prevention, through control of hypertension, hyperlipidemia, and tobacco, contributed most greatly to the mortality decline with a lesser but still substantial contribution of improved acute stroke care. Persisting challenges include race–ethnicity, sex, and geographic disparities in stroke mortality; the burden of stroke disability; the expanding obesity epidemic and aging of the US population; and the epidemic of cerebrovascular disease in low- and middle-income countries worldwide.
Conclusions—The recent rank decline of stroke among leading causes of American death is testament to a half century of societal progress in cerebrovascular disease prevention and acute care. Renewed commitments are needed to preserve and broaden this historic achievement.
Restoring Neuronal Function After Stroke by Cell Replacement
I would love to read this complete article. Can someone send it to me.
http://stroke.ahajournals.org/content/42/8/2342.abstract
http://stroke.ahajournals.org/content/42/8/2342.abstract
Abstract
Background and Purpose—A major challenge to effective treatment after stroke is the restoration of neuronal function. In recent years, cell-based therapies for stroke have been explored in experimental animal models, and the results have suggested behavioral improvements. However, the anatomic targets of a cell-based stroke therapy and the relationship of cell grafts to post stroke reorganization are poorly understood, which results in difficulties defining strategies for neuronal substitution. Given that stroke causes a variety of secondary changes at locations beyond the infarct lesion, overcoming these difficulties is even more important.
Summary of Review We describe which brain structures and cell types are candidates for substitution and how new neuronal functionality could be implemented in a damaged brain by capitalizing on current concepts of post stroke plasticity.
I was hoping for more emphasis on neurogenesis.
Statins Promote the Growth of Experimentally Induced Cerebral Aneurysms in Estrogen-Deficient Rats
Another negative for statins. Ask your doctor for their take on it. They should know about this before you ask them, so if they don't tell you about this they are not keeping up on research. I know this is only on rats but that is no excuse for them.
http://stroke.ahajournals.org/content/42/8/2286.abstract
http://stroke.ahajournals.org/content/42/8/2286.abstract
Abstract
Background and Purpose—The pathogenesis of cerebral aneurysms is linked to inflammation, degradation of the extracellular matrix, and vascular wall apoptosis. Statins exert pleiotropic? effects on the vasculature, independent of their cholesterol-lowering properties. To explore the detailed pathogenesis of cerebral aneurysms, we examined their progression in a rat model and studied whether statins prevent their initiation and growth.
Methods—Cerebral aneurysms were induced in female rats subjected to hypertension, increased hemodynamic stress, and estrogen deficiency(so are males estrogen deficient all the time?). The development of aneurysm was assessed morphologically on corrosion casts. The effects of pravastatin (5, 25, or 50 mg/kg per day) and of simvastatin (5 mg/kg per day) on their aneurysms were studied. Human brain endothelial cells were also used to determine the effects of pravastatin.
Results—Pravastatin (5 mg/kg per day) reduced endothelial damage and inhibited aneurysm formation; there was an association with increased endothelial nitric oxide synthase (eNOS) levels and a decrease in human brain endothelial cell adhesion molecules. Unexpectedly, 25 mg/kg per day and 50 mg/kg per day pravastatin and 5 mg/kg per day simvastatin promoted aneurysmal growth, and high-dose pravastatin induced aneurysmal rupture. The deleterious effects exerted by these statins were associated with an increase in apoptotic caspase-3 levels and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL)-positive cells, suggesting that statins exert bidirectional effects.
Conclusions—Our results provide the first evidence that cerebral aneurysm growth is partly associated with apoptosis and issue a warning that statins exert bidirectional effects on cerebral aneurysms. Additional intensive research is necessary to understand better their mechanisms and to identify patients in whom the administration of statins may elicit deleterious effects.
Robotic Therapy and Learning Drug for Post-Stroke Rehabilitation
What is the learning drug?
http://www.youtube.com/watch?v=6FD9BbdVLM8
The guy in the video is pretty high functioning already, although it is hard to tell how much the orthotic arm is doing the work.
http://www.youtube.com/watch?v=6FD9BbdVLM8
The guy in the video is pretty high functioning already, although it is hard to tell how much the orthotic arm is doing the work.
Best Practices in Stroke Rehabilitation - webinar
I'm certainly not going to pay for this but maybe you should tell your therapists about it and then tell them to visit my blog for all the points they will miss. (not really sorry about being arrogant)
http://www.geriatricspt.org/pdfs/SoG-strokewebinar2011.pdf
The field of stroke rehabilitation is undergoing a major paradigm shift as a result of a number of
forces, including our understanding of neuroplasticity,(what about neurogenesis? it is the future) developments in neuroimaging to guide
treatment, and the emergence of evidence-based research in key specialties, such as physical
therapy. The National Stroke Association recognizes that physical therapists play a key role in
maximizing stroke rehabilitation and recovery and in promoting improvements to stroke
survivor quality of life. This 2-part webinar series will emphasize the practical application of new
research in stroke rehabilitation.
Webinar #1 Overview of Stroke, Its Impact on Patients and Gait Training
Topics to be covered:
• Pathophysiology
• Neuroplasticity and recovery (what does it mean to therapists in the trenches)
• Effective patient feedback information to promote effective interventions
• Gait training approaches (given the negative recent evidence from the LEAPS and LE robotic
trials)
• Body Weight-support Treadmill Training to Improve Walking
Webinar #2 Stroke Rehabilitation Training and Therapies
Topics to be covered:
• Sensorimotor Training and Upper Extremity Recovery
• Managing Spasticity to Maximize Rehabilitation Therapy (increase the emphasis on evidence based interventions that are therapist driven)(This would be entertaining to see)
• Impact of spasticity on rehabilitation - you missed William M. Landaus' screed against treating spasticity
• Physical modalities to improve spasticity: Positioning, splinting, etc.
• Medications to improve spasticity: Focal treatments to improve spasticity: Local Anesthetics,
Chemical Neurolysis, Chemodenervation
• Constraint-induced Movement Therapy, Mental Imagery (include both LE and UE and emphasize
modifications to CIT given its known limitations and limited clinical applicability for many
therapists "in the trenches")
• Electrical Stimulation and EMG Biofeedback and the Brain
Objectives
• Describe EBP with respect to each rehabilitation topic.
• Implement EBP in the practice setting related to each of the rehabilitation topics and describe potential problems and barriers to
implementation.
• Identify practical steps of implementing new rehabilitation strategies within your respective practice for improving stroke patient
outcomes.
• Summarize the importance of neuroplasticity in stroke recovery, and the effects of specific rehabilitation techniques on
neuroplasticity.
I personally think Peter Levines' seminar on the same topics would be a better use of your time and money.
http://www.geriatricspt.org/pdfs/SoG-strokewebinar2011.pdf
The field of stroke rehabilitation is undergoing a major paradigm shift as a result of a number of
forces, including our understanding of neuroplasticity,(what about neurogenesis? it is the future) developments in neuroimaging to guide
treatment, and the emergence of evidence-based research in key specialties, such as physical
therapy. The National Stroke Association recognizes that physical therapists play a key role in
maximizing stroke rehabilitation and recovery and in promoting improvements to stroke
survivor quality of life. This 2-part webinar series will emphasize the practical application of new
research in stroke rehabilitation.
Webinar #1 Overview of Stroke, Its Impact on Patients and Gait Training
Topics to be covered:
• Pathophysiology
• Neuroplasticity and recovery (what does it mean to therapists in the trenches)
• Effective patient feedback information to promote effective interventions
• Gait training approaches (given the negative recent evidence from the LEAPS and LE robotic
trials)
• Body Weight-support Treadmill Training to Improve Walking
Webinar #2 Stroke Rehabilitation Training and Therapies
Topics to be covered:
• Sensorimotor Training and Upper Extremity Recovery
• Managing Spasticity to Maximize Rehabilitation Therapy (increase the emphasis on evidence based interventions that are therapist driven)(This would be entertaining to see)
• Impact of spasticity on rehabilitation - you missed William M. Landaus' screed against treating spasticity
• Physical modalities to improve spasticity: Positioning, splinting, etc.
• Medications to improve spasticity: Focal treatments to improve spasticity: Local Anesthetics,
Chemical Neurolysis, Chemodenervation
• Constraint-induced Movement Therapy, Mental Imagery (include both LE and UE and emphasize
modifications to CIT given its known limitations and limited clinical applicability for many
therapists "in the trenches")
• Electrical Stimulation and EMG Biofeedback and the Brain
Objectives
• Describe EBP with respect to each rehabilitation topic.
• Implement EBP in the practice setting related to each of the rehabilitation topics and describe potential problems and barriers to
implementation.
• Identify practical steps of implementing new rehabilitation strategies within your respective practice for improving stroke patient
outcomes.
• Summarize the importance of neuroplasticity in stroke recovery, and the effects of specific rehabilitation techniques on
neuroplasticity.
I personally think Peter Levines' seminar on the same topics would be a better use of your time and money.
Wednesday, August 17, 2011
ImAble system for upper limb stroke rehabilitation
I wish they would post pictures of this, sounds like a type of comic book hero.
http://scholar.google.com/scholar_url?hl=en&q=http://ieeexplore.ieee.org/xpls/abs_all.jsp%3Farnumber%3D5971835&oi=scholaralrt&ct=alrt&cd=3&sa=X&scisig=AAGBfm0_5ooTvCNRI2n9qbRlJ5e3_Xpc3Q
http://scholar.google.com/scholar_url?hl=en&q=http://ieeexplore.ieee.org/xpls/abs_all.jsp%3Farnumber%3D5971835&oi=scholaralrt&ct=alrt&cd=3&sa=X&scisig=AAGBfm0_5ooTvCNRI2n9qbRlJ5e3_Xpc3Q
Abstract
ImAble is an integrated upper limb (UL) exercise system comprising three devices (Able-B, Able-M and Able-X) targeting UL rehabilitation using computer games and virtual reality (VR). The system can be tailored to different levels of ability and strength, depending on the presentation of the stroke. Results from pilot testing and case studies indicate a therapeutic benefit for both movement outcome and patient motivation.
A case study on muscle activation analysis in post-stroke rehabilitation patients
And now they can map the output from this to the instrumented sock and a powered AFO along with the Regent suit. And maybe with this the therapists could work with objective measures rather than subjective. Although this still does not absolve the neurologist from providing a damage diagnosis.
http://ieeexplore.ieee.org/xpl/freeabs_all.jsp?arnumber=5966777
http://ieeexplore.ieee.org/xpl/freeabs_all.jsp?arnumber=5966777
Abstract
The paper presents a case study based on a system for the monitoring of daily functions in post-stroke rehabilitation patients. The system is capable of monitoring some daily life functions of the patient, by providing to the rehabilitation experts information about the correct or wrong activation of the monitored muscles during those specific functions. The monitoring system consists of a wearable wireless device, equipped with electrogoniometers and electromyography sensors, and by a signal processing software. Preliminary experiments have been conducted on post-stroke patients.
Tuesday, August 16, 2011
Do you want to participate in clinical trials?
Become a guinea pig and ask the researchers you talk to if any of their trials are repeatable. The real question to ask is if they can guarantee that they will be able to duplicate the same type of damage in their subjects, penumbra damage to penumbra damage, dead brain to dead brain. If not, they are just another naked emperor.
http://trialx.com/
categories include;
http://trialx.com/
categories include;
- Stem Cell Mobilization Clinical Trials (1 Ongoing)
- Stem Cell Transplantation Clinical Trials (11 Ongoing)
- Stem Cells Clinical Trials (1 Ongoing)
- STEMI Clinical Trials (1 Ongoing)
- Stroke Clinical Trials (80 Ongoing)
- Stroke Acute Clinical Trials (4 Ongoing)
- Stroke Prevention Clinical Trials (1 Ongoing)
- Stroke With Hemiparesis Clinical Trials (1 Ongoing)
Attributable Risk Estimate of Severe Psoriasis on Major Cardiovascular Events
More knowledge for all you readers.
http://amjmed.blogspot.com/2011/08/attributable-risk-estimate-of-severe.html
Patients with severe psoriasis have an additional 6.2% absolute risk of major adverse cardiac events compared to the general population. This finding could have important therapeutic implications for cardiovascular risk stratification and prevention in patients with severe psoriasis.
Abstract
Background
Recent studies suggest that psoriasis, particularly if severe, may be a risk factor for major adverse cardiac events, such as myocardial infarction, stroke, and mortality from cardiovascular disease. We compared the risk of major adverse cardiac events between patients with psoriasis and the general population and estimated the attributable risk of severe psoriasis.
Methods
We performed a cohort study in the General Practice Research Database. Severe psoriasis was defined as receiving a psoriasis diagnosis and systemic therapy (N=3603). Up to 4 patients without psoriasis were selected from the same practices and start dates for each patient with psoriasis (N=14,330).
Results
Severe psoriasis was a risk factor for major adverse cardiac events (hazard ratio 1.53; 95% confidence interval, 1.26-1.85) after adjusting for age, gender, diabetes, hypertension, tobacco use, and hyperlipidemia. After fully adjusted analysis, severe psoriasis conferred an additional 6.2% absolute risk of 10-year major adverse cardiac events.
Conclusion
Severe psoriasis confers an additional 6.2% absolute risk of a 10-year rate of major adverse cardiac events compared with the general population. This potentially has important therapeutic implications for cardiovascular risk stratification and prevention in patients with severe psoriasis. Future prospective studies are needed to validate these findings.
http://amjmed.blogspot.com/2011/08/attributable-risk-estimate-of-severe.html
Patients with severe psoriasis have an additional 6.2% absolute risk of major adverse cardiac events compared to the general population. This finding could have important therapeutic implications for cardiovascular risk stratification and prevention in patients with severe psoriasis.
Abstract
Background
Recent studies suggest that psoriasis, particularly if severe, may be a risk factor for major adverse cardiac events, such as myocardial infarction, stroke, and mortality from cardiovascular disease. We compared the risk of major adverse cardiac events between patients with psoriasis and the general population and estimated the attributable risk of severe psoriasis.
Methods
We performed a cohort study in the General Practice Research Database. Severe psoriasis was defined as receiving a psoriasis diagnosis and systemic therapy (N=3603). Up to 4 patients without psoriasis were selected from the same practices and start dates for each patient with psoriasis (N=14,330).
Results
Severe psoriasis was a risk factor for major adverse cardiac events (hazard ratio 1.53; 95% confidence interval, 1.26-1.85) after adjusting for age, gender, diabetes, hypertension, tobacco use, and hyperlipidemia. After fully adjusted analysis, severe psoriasis conferred an additional 6.2% absolute risk of 10-year major adverse cardiac events.
Conclusion
Severe psoriasis confers an additional 6.2% absolute risk of a 10-year rate of major adverse cardiac events compared with the general population. This potentially has important therapeutic implications for cardiovascular risk stratification and prevention in patients with severe psoriasis. Future prospective studies are needed to validate these findings.
Will You Have A Heart Attack or Stroke? These Tests Might Tell
The carotid ultrasound would have found my problem, 80-85% blockage.
http://www.thebostonchannel.com/r/28878583/detail.html
(CNN) -- Most heart attacks strike with no warning, but doctors now have a clearer picture than ever before of who is most likely to have one, says Dr. Arthur Agatston, a Miami cardiologist and author of the best-selling South Beach diet books.Agatston says relatively new imaging tests give real-time pictures showing whether plaque is building up in key blood vessels, alerting doctor and patient to an increased risk of a potentially deadly heart attack."Unless you do the imaging, you are really playing Russian roulette with your life," he said.Agatston invented one of the imaging tests, the coronary calcium scan, which looks at plaque in the arteries leading to the heart. Plaque in these arteries is a red flag for a potential heart attack. (Agatston does not make any money from the coronary calcium scan.)The other imaging test Agatston recommends is an ultrasound of the carotid artery, looking at plaque in the main blood vessel leading to the brain. Plaque in the carotid artery is a sign of increased risk for a heart attack and stroke.Both tests are non-invasive and outpatient, although the calcium scan does expose the patient to the equivalent of several months of normal background radiation.One large federally funded study found the coronary calcium score a better predictor of coronary events like a heart attack than the traditional Framingham Risk Score, which considers age, cigarette smoking, blood pressure, total cholesterol and HDL, the "good" cholesterol.Agatston thinks the coronary calcium scan should be routinely scheduled at age 50, like a colonoscopy, or earlier for people with family histories of heart disease.Most hospitals now offer the imaging tests, some at less than $100 for both, and they are often covered by insurance.Cardiologists now generally use the calcium scan only for patients considered at intermediate risk for heart disease, determined by traditional measures such as cholesterol, blood pressure, lifestyle and family history.High-risk patients already receive such aggressive treatment as cholesterol-lowering statin medication, but many doctors don't think low-risk patients need to incur the expense or small dose of radiation that comes with a coronary calcium scan."There is a large group in the middle called intermediate risk, which may be as much as 50% of the population," said Dr. Erin Michos, a cardiologist at the Ciccarone Center for the Prevention of Heart Disease at Johns Hopkins UniversityA good candidate for a coronary calcium scan, she says, would be a 50-year-old man with slightly elevated cholesterol and a father who had a heart attack."Do you put this 50-year-old who has this family history on a statin medication with potential expense (and) side effects for the next four decades of his life, or do you further refine how far at risk he is?" she asked.A calcium score would answer that question, she says.There's a third test Agatston likes: a $65 blood test that looks at a patient's LDL, or bad cholesterol. LDL particles come in different sizes, and patients with a lot of small-particle LDL are more likely to build up plaque in their blood vessels, Agatston says. Alternately, patients with large LDL particles do not tend to accumulate plaque."There are a lot of little old ladies in their 80s with very high cholesterol who have squeaky clean vessels. They have very large particles, and they don't get into the vessel wall," Agatston says.These new tests give patients a chance to make major changes in their diet and lifestyle, and give doctors an opportunity to treat them with medication."One of the best-kept secrets in the country in medicine is the doctors who are practicing aggressive prevention are really seeing heart attacks and strokes disappear from their practices. It's doable," Agatston says.
http://www.thebostonchannel.com/r/28878583/detail.html
(CNN) -- Most heart attacks strike with no warning, but doctors now have a clearer picture than ever before of who is most likely to have one, says Dr. Arthur Agatston, a Miami cardiologist and author of the best-selling South Beach diet books.Agatston says relatively new imaging tests give real-time pictures showing whether plaque is building up in key blood vessels, alerting doctor and patient to an increased risk of a potentially deadly heart attack."Unless you do the imaging, you are really playing Russian roulette with your life," he said.Agatston invented one of the imaging tests, the coronary calcium scan, which looks at plaque in the arteries leading to the heart. Plaque in these arteries is a red flag for a potential heart attack. (Agatston does not make any money from the coronary calcium scan.)The other imaging test Agatston recommends is an ultrasound of the carotid artery, looking at plaque in the main blood vessel leading to the brain. Plaque in the carotid artery is a sign of increased risk for a heart attack and stroke.Both tests are non-invasive and outpatient, although the calcium scan does expose the patient to the equivalent of several months of normal background radiation.One large federally funded study found the coronary calcium score a better predictor of coronary events like a heart attack than the traditional Framingham Risk Score, which considers age, cigarette smoking, blood pressure, total cholesterol and HDL, the "good" cholesterol.Agatston thinks the coronary calcium scan should be routinely scheduled at age 50, like a colonoscopy, or earlier for people with family histories of heart disease.Most hospitals now offer the imaging tests, some at less than $100 for both, and they are often covered by insurance.Cardiologists now generally use the calcium scan only for patients considered at intermediate risk for heart disease, determined by traditional measures such as cholesterol, blood pressure, lifestyle and family history.High-risk patients already receive such aggressive treatment as cholesterol-lowering statin medication, but many doctors don't think low-risk patients need to incur the expense or small dose of radiation that comes with a coronary calcium scan."There is a large group in the middle called intermediate risk, which may be as much as 50% of the population," said Dr. Erin Michos, a cardiologist at the Ciccarone Center for the Prevention of Heart Disease at Johns Hopkins UniversityA good candidate for a coronary calcium scan, she says, would be a 50-year-old man with slightly elevated cholesterol and a father who had a heart attack."Do you put this 50-year-old who has this family history on a statin medication with potential expense (and) side effects for the next four decades of his life, or do you further refine how far at risk he is?" she asked.A calcium score would answer that question, she says.There's a third test Agatston likes: a $65 blood test that looks at a patient's LDL, or bad cholesterol. LDL particles come in different sizes, and patients with a lot of small-particle LDL are more likely to build up plaque in their blood vessels, Agatston says. Alternately, patients with large LDL particles do not tend to accumulate plaque."There are a lot of little old ladies in their 80s with very high cholesterol who have squeaky clean vessels. They have very large particles, and they don't get into the vessel wall," Agatston says.These new tests give patients a chance to make major changes in their diet and lifestyle, and give doctors an opportunity to treat them with medication."One of the best-kept secrets in the country in medicine is the doctors who are practicing aggressive prevention are really seeing heart attacks and strokes disappear from their practices. It's doable," Agatston says.
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