Deans' stroke musings

Changing stroke rehab and research worldwide now.Time is Brain!Just think of all the trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 493 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It's quite disgusting that this information is not available from every stroke association and doctors group.
My back ground story is here:http://oc1dean.blogspot.com/2010/11/my-background-story_8.html

Monday, April 30, 2012

Many medical decisions require shared decision making

This comes from KevinMDs blog. This should be extremely applicable to us in our rehabilitation journey. The problem is that there is no factual basis for  our therapies. we should be able to get something like;
This therapy has a 20% success rate when followed for 3 months.
vs. this therapy has a 50% success rate when followed for 6 months.
Until we get to that level of knowledge everything we do is just a shot in the dark. We can't accept the standard reply, 'All strokes are different, all stroke recoveries are different'. Thats just pure laziness on whomever said that to you.
http://www.kevinmd.com/blog/2012/04/medical-decisions-require-shared-decision-making.html

Treatment Options in Acute Ischemic Stroke - Cleveland Clinic

Another Online health chat with them.
Don't be polite, the world was not changed by polite people. Bring your questions on hyperacute treatments(I have 160 posts on them if you need inspiration) and hypothermia and cascade of death.  It should be easy to  overwhelm him with questions. Questions open on May 20 so you can submit them ahead of time. Be prepared with your questions when you register. I think I once had to register under 2 email ids to get all the questions in.
http://www.clevelandclinic.org/health/chatreg/ChatPage.aspx?ChatId=1367

Treatment Options in Acute Ischemic Stroke
Monday, May 21, 2012 - 12 Noon (Eastern Time)

M. Shazam Hussain
  • Neurological Institute
  • Cerebrovascular Center
  • Cleveland Clinic
Each year, more than half a million Americans suffer from strokes. A stroke, or “brain attack,” occurs when the blood supply is cut off from part of the brain. When this happens, the blood-deprived brain loses its supply of oxygen and nutrients. When the brain is deprived of blood for even a few minutes, it begins to die.

There are two types of stroke-ischemic and hemorrhagic. In ischemic strokes, brain arteries become blocked and prevent blood from nourishing the brain. In hemorrhagic strokes, brain arteries rupture from damage caused by high blood pressure and other risk factors or an aneurysm (an abnormal out pouching of a blood vessel) and cause blood to flood the brain, creating pressure that leads to brain-cell death.

There are many risk factors that increase the risk of stroke. Some factors can be controlled, while others cannot. Some of these factors include: high blood pressure, high cholesterol, heart disease, being overweight, heavy, drinking, smoking, diabetics and a family history of strokes.

Ways to reduce these risks include: not smoking, limiting alcohol intake, control your weight and blood pressure, finding out if you have an irregular heartbeat or a diseased carotid artery.

Immediate treatment of a stroke may limit or prevent brain damage. A thrombolytic agent or “clot buster” medication may be given within the first 4.5 hours of the onset stroke symptoms, and patients may also qualify for emergent endovascular therapy to try to open blocked blood vessels. It is critical to call 911 and get to the hospital quickly if you experience stroke symptoms. 
Show him all the untested possibilities
  1.  (What is the success rate of tPA? full recovery) Is Draculin available for use?
  2. Edaravone is used in Japan, why isn't it available here?
  3. Should anti-depressants be prescribed for all survivors to enhance rehabilitation? 
  4. Should  Tenecteplase be used in combination with tPA during ER treatment? 
  5.  There have been over 1000 treatments that worked in mice or rats that failed in humans, Why didn't we see more successes?
  6. Would it be possible to use magnetic nanoparticles to deliver tPA directly to the clot? Reducing the amount needed and the risk of bleeds.
  7. How long does the neuronal cascade of death continue in ischemic stroke? 
  8. Should hypothermia become the standard treatment in the ambulance?
  9. Which body cooling device do you think has the best chance of  becoming standard in the ambulance? core body cooler, drug cooler , brain helmet, nasal cooler , neck cooler?
  10. Is Enzogenol a possibility?
  11. What is the outlook for microrobots to travel in the bloodstream and remove clots? 


Take advantage of this chat to speak to a specialist about techniques, medications and treatment options after a stroke occurs from M. Shazam Hussain, M.D, who is involved in both medical and endovascular treatment of acute stroke patients.

The Cerebrovascular Center at Cleveland Clinic’s Neurological Institute integrates a multidisciplinary team of neurologists, neurosurgeons, neuroradiologists, neurointensivists and rehabilitation specialists who provide expert diagnosis and medical, endovascular and surgical management of all cerebrovascular conditions. Cleveland Clinic is a designated Primary Stroke Center.

A Primary Stroke Center is usually housed in a hospital where a group of medical professionals who specialize in stroke, work together to diagnose, treat, and provide early rehabilitation to stroke patients. The Joint Commission’s Certificate of Distinction for Primary Stroke Centers recognizes centers that make exceptional efforts to foster better outcomes for stroke care. The Cleveland Clinic Primary Stroke Center provides services that have critical elements to achieve long term success in improving outcomes. We provide quality care and effectively manage the unique and specialized needs of stroke patients.

M. Shazam Hussain, M.D, is the designated stroke center director and staff physician in the Cerebrovascular Center at Cleveland Clinic. He received his medical degree from University of Saskatchewan College of Medicine in Canada, and then went on to complete a residency and fellowship at University of Alberta Hospital Canada in neurology and vascular neurology. Dr. Hussain joined Cleveland Clinic for his final fellowship in endovascular surgical neuroradiology. His specialty interests include acute stroke therapy, cerebrovascular diseases and neuroimaging.

To make an appointment with Dr. Hussain or any other of the specialists in our Neurological Institute at Cleveland Clinic, please call 216.636.5860 or call toll-free at 866.588.2264. You can also visit us online at clevelandclinic.org/cerebrovascular.
This Health Chat will open on Sunday, May 20, 2012 to allow you to submit questions. We will try to answer as many questions as possible during the chat. Please create an account to attend the chat and submit your questions.

Sunday, April 29, 2012

Gummed-up memory: chewing gum impairs short-term recall.

You can ask your doctor to compare this one to the mastication induced arousal one I posted about earlier.
From http://io9.com/5905964/chewing-gum-can-mess-with-your-mind
comes this suggestion.
So what might explain these contradictory results? The scientists at Cardiff noted they used flavorless gum, while the past study used minty gum. Flavor might make a key difference — the brain might better remember tasks linked with pleasant experiences such as nice flavors.
http://www.ncbi.nlm.nih.gov/pubmed/22150606?dopt=Abstract

Abstract

Several studies have suggested that short-term memory is generally improved by chewing gum. However, we report the first studies to show that chewing gum impairs short-term memory for both item order and item identity. Experiment 1 showed that chewing gum reduces serial recall of letter lists. Experiment 2 indicated that chewing does not simply disrupt vocal-articulatory planning required for order retention: Chewing equally impairs a matched task that required retention of list item identity. Experiment 3 demonstrated that manual tapping produces a similar pattern of impairment to that of chewing gum. These results clearly qualify the assertion that chewing gum improves short-term memory. They also pose a problem for short-term memory theories asserting that forgetting is based on domain-specific interference given that chewing does not interfere with verbal memory any more than tapping. It is suggested that tapping and chewing reduce the general capacity to process sequences.

Saturday, April 28, 2012

Essential Oils for Blood Clots and Stroke -Warning

Beware, this is a commercial site with no listed human research to back up any of their statements. They also seem to want to get you to worry about the end-of-times when medical help won't be available.
http://essentialsurvival.org/essential-oils-blood-clots-stroke

Optogenetics: Stroke Rehabilitation

Interesting idea. I've always had at least 20 lbs. grip in my left hand., So I guess I wouldn't qualify. Would it work in reverse? Relaxing the spastic muscles?
http://rrg.utk.edu/resources/BME473/lectures/presentation_team_2.pdf
see page 6.

Ceresafe™ (Stroke Vaccine) - DO NOT BELIEVE

Found this though the blog ScienceRoll. A humor  site. I wonder if this is like Schrodingers' cat, Open the box and you kill the cat one time, the next time the cat lives. Those without computers/cell phones are SOL
http://www.quantummansite.com/catalog/ceresafe.php
With such a horrible condition affecting so many millions, it has become QuantumMAN™'s mission to eliminate this global menace by vaccinating those at risk. Having a revolutionary new stroke vaccine called CereSafe that is guaranteed 100% effective, QuantumMAN™ is armed to accomplish this mission.
CereSafe™ (Stroke Vaccine) programs your body in such a way that creates a biological terrain immune to stroke. You simply purchase CereSafe™ and receive a number of its Portal Access Keys™ (PAKs™). Accessing these PAKs™ via your personal computer, smartphone or tablet allows your body to quantumly receive (upload) CereSafe™'s master programs. Their directives repetitively transfer quantum biodata several times daily for exactly 10 days perfecting your biological terrain against any possibility of developing a stroke.
QuantumMan: Ceresafe
What Is "Quantum Teleportation?"
Admittedly quantum physics is weird especially the new reality technically called "quantum entanglement" which permits how two objects can be mysteriously entwined across great distances. The existence of the phenomenon of entanglement has been repeatedly affirmed over the years beginning in 1935 with physicists Erwin Schrodinger introducing the term of entanglement while Einstein and colleagues Podolsky and Rosen publishing their observations in Physical Review (SNL: 5/11/35). ZAG then developed its powerful technology utilizing this phenomenon that allows quantum bioinformation to be teleported around the globe via quantum computing. Entanglement is the basis of this ability to teleport quantum biodata from one physical location to another including the interface of the brain's neuro-network. Teleportation was first proposed in the scientific literature in 1993 by Charles Bennett and his colleagues. Teleportation was later experimentally verified in 1997 by Austrian quantum physicist Anton Zellinger and Colleagues in Nature.-

Access and participation in the community: a prospective qualitative study of driving post-stroke.

And I received no information on driving post-stroke. I wasn't going to ask either because they may have said no, which would have been hard to convince my spouse to allow me to drive then since the medical gods had spoken.
http://www.ncbi.nlm.nih.gov/pubmed/22035162

Abstract

Purpose: Loss of role as a driver significantly affects community participation; therefore, we aimed to explore the impact of driving issues post-stroke in community-dwelling stroke survivors. Methods: A longitudinal qualitative study of community-dwelling stroke survivors, using semi-structured interviews. Results: Twenty-two participants took part in 84 interviews over a 1-year period post-stroke. The majority of participants was independent and experienced few major depressive symptoms. ages ranged from 50 to 92 years. Emergent key themes included impact on quality of life, personal impacts, change to role performance and knowledge. Participants received inconsistent advice regarding return to driving. Confidence and availability determined public transport use. Conclusions: Driving advice should be standard practice prior to discharge. Allied health professionals can play an essential role in interventions addressing community participation, driver re-training and alternative transport use. Therapists have an important role in assisting stroke survivors to work through feelings of loss and in providing education concerning new skills to support this life transition.

Acupuncture for treatment of insomnia in patients with traumatic brain injury: a pilot intervention study.

I can't tell from the abstract if the control group had sham acupuncture or not. If not then the acupuncture group could easily be the placebo effect.
http://www.ncbi.nlm.nih.gov/pubmed/21386714

Abstract

OBJECTIVES:

: To assess the efficacy of acupuncture in treating insomnia in traumatic brain injury (TBI) survivors as compared to medication, to determine whether acupuncture has fewer cognitive and affective adverse effects than does medication.

PARTICIPANTS:

: Twenty-four adult TBI survivors, randomized to acupuncture or control arms.

SETTING:

: Outpatient rehabilitation clinic.

MEASURES:

: Insomnia Severity Index (degree of insomnia); actigraphy (sleep time); Hamilton Depression Rating Scale (depression); Repeatable Battery for the Assessment of Neuropsychological Status and Paced Auditory Serial Addition Test (cognitive function) administered at baseline and postintervention.

RESULTS:

: Sleep time did not differ between the treatment and control groups after intervention, whereas cognition improved in the former but not the latter.

CONCLUSION:

: Acupuncture has a beneficial effect on perception of sleep or sleep quality and on cognition in our small sample of patients with TBI. Further studies of this treatment modality are warranted to validate these findings and to explore factors that contribute to treatment efficacy.

Current evaluation of upper oesophageal sphincter opening in dysphagia practice: an international SLT survey

I didn't have this but you can get an idea of what your SLT goes thru to test you.
http://onlinelibrary.wiley.com/doi/10.1111/j.1460-6984.2011.00087.x/abstract;jsessionid=5828CA176375C6266285EB1007EA2A57.d01t03

Abstract

Background: The assessment of adequate upper oesophageal sphincter (UOS) opening during swallowing is an integral component of dysphagia evaluation.
Aims: To ascertain speech and language therapists’ (SLTs) satisfaction with current methods for assessing UOS function in people with dysphagia and to identify challenges encountered by SLTs with UOS evaluation.
Methods & Procedures: A survey was disseminated to 82 SLT managers in Ireland; to two dysphagia Special Interest Groups in the UK; and to the Royal College of Speech & Language Therapists’Bulletin periodical. A survey link was also posted on the American Speech and Hearing Association (ASHA) Division 13 (Dysphagia) web forum.
Outcomes & Results: Surveys from 224 SLTs with active dysphagia caseloads were included in data analysis. Only 17.9% (40/224) of SLTs were satisfied with the accuracy and reliability of UOS evaluations currently being employed in dysphagia practice. Satisfaction with current UOS evaluation was not associated with the level of clinical experience (r= 0.078; p= 0.246). Eighty-seven per cent (195/224) of SLTs working with dysphagia experience challenges in UOS evaluation. Challenges reported include lack of resources/equipment (55.9%), limited quantitative information (45.6%), lack of training (41%) and knowledge (39%) in UOS function, and limited multidisciplinary team involvement (34%).
Conclusions & Implications: SLTs across all levels of clinical experience are not satisfied with current UOS evaluation in dysphagia practice. Based on the specific challenges identified, recommendations to progress SLT evaluation of UOS function in people with dysphagia are proposed.

Friday, April 27, 2012

Training the brain: practical applications of neural plasticity from the intersection of cognitive neuroscience, developmental psychology, and prevention science.

Since this is so useful for us  I expect lots of interest in delivering this to all the stroke rehab instructors and textbook writers and the current medical staff.
http://www.ncbi.nlm.nih.gov/pubmed/21787037

Abstract

Prior researchers have shown that the brain has a remarkable ability for adapting to environmental changes. The positive effects of such neural plasticity include enhanced functioning in specific cognitive domains and shifts in cortical representation following naturally occurring cases of sensory deprivation; however, maladaptive changes in brain function and development owing to early developmental adversity and stress have also been well documented. Researchers examining enriched rearing environments in animals have revealed the potential for inducing positive brain plasticity effects and have helped to popularize methods for training the brain to reverse early brain deficits or to boost normal cognitive functioning. In this article, two classes of empirically based methods of brain training in children are reviewed and critiqued: laboratory-based, mental process training paradigms and ecological interventions based upon neurocognitive conceptual models. Given the susceptibility of executive function disruption, special attention is paid to training programs that emphasize executive function enhancement. In addition, a third approach to brain training, aimed at tapping into compensatory processes, is postulated. Study results showing the effectiveness of this strategy in the field of neurorehabilitation and in terms of naturally occurring compensatory processing in human aging lend credence to the potential of this approach.

Top 50 Brain Teasers and Games from Sharp Brains

Test yourself, Thanks to Brain Clock Blog
 http://www.sharpbrains.com/teasers/brain-games-and-teasers-top-50/
Be careful of this one;
8. Can you walk and chew gum at the same time?  Remember the mastication induced arousal?

Direct Stimulation of Adult Neural Stem/Progenitor Cells In Vitro and Neurogenesis In Vivo by Salvianolic Acid B

Some actual TCM research.
http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0035636

Introduction Top

Ischemic brain damage is one of the most dangerous ailments that lead to learning and memory disability, physical dysfunction and even death. Up to now, no effective treatment has been reported [1]. Neurons as terminally differentiated cells cannot regenerate after injury in traditional view. However, appropriate exercise training can facilitate some neurological function recovery after stroke in clinical practice [2], [3], with the evidence that neurogenesis occurs in the adult brain. Neural stem/precursor cells (NSPCs) had been found and confirmed in adult brain in past decades that it can differentiate into neurons or glial cells as a result of neurogenesis [4][7], NSPCs can be stimulated in several pathological conditions, such as neurological diseases, cerebral ischemic in adult brain, and many reports showed that they are an excellent candidate for developing therapeutic strategies to repair the injured CNS [8], [9]. Although the NSPCs would be stimulated to proliferation and differentiation during the brain injury, often this response is not sufficient to overcome the damage. It is essential to study the signalling mechanisms that are activated by small molecular materials in the NSPCs to enhance their response pharmacologically. NSPCs proliferation and neurogensis involves a series of intracellular signaling pathways [10], [11]. Among these pathways, the activation of Notch, mitogen-activated protein kinases (MAPKs) and phosphatidylinositol-3-kinase (PI3K)/Akt pathways are known to play major roles in cell growth and survival responses [12][14]. Numerous studies have shown that small molecular materials such as growth factors [15], retinoic acid [16] and Traditional Chinese Medicine (TCM) active constituent [17], [18] can regulate the biological characteristics of neural stem cell and promote neurogenesis. Therefore, regulation of neurogenesis by NSPCs is anticipated as a noble therapeutic strategy for brain damage.
Herbs have been used for treating diseases for centuries, and a lot of natural compounds that with neural beneficial from medicinal plants had been discovered [19]. Treatment of stroke by TCM has a wealth of clinical experience and theoretical basis, and a large number of effective clinical prescriptions have been accumulated. In recent years a large number of studies have shown that TCM prescription and its active ingredient can improve cerebral ischemic injury in experimental animal [20], [21]. Ginsenoside Rb1 and Rg1, for example, improved spatial learning and increase hippocampal synaptophysin level in mice [22]. Curcumin had been demonstrated to stimulate developmental and adult hippocampal neurogenesis, and a biological activity that may enhance neural plasticity and repair [23]. A recent report has shown that NeuroAid (MLC601 and MLC901), a Traditional Chinese Medicine is used in China for patients after stroke, reduced the increase in escape latency and in swim distance induced by ischemia [24]. With an extensive clinical experience, there are ample opportunities to discover natural compounds that effectively promote the proliferation of NSPCs and neurogenesis from TCM.

Results Top

Salvianolic acid B induced the proliferation of cultured NSPCs in vitro

Forty-five herbal compounds, which are extensively used clinically for treating stroke in China, were screened in an in vitro proliferation assay to identify compounds that could induce proliferation of NSPCs. As shown in Fig. 1, among these natural compounds screened, berberine and Sal B displayed marked activity promoting NSPCs proliferation. In the following study, the proliferative effect of berberine and Sal B were systematically investigated but the action of berberine was proved to be an illusion by BrdU incorporation assay (See Figure S1 in the Supporting Information).
To study the proliferation-inducing effect of Sal B in detail, we investigated effects of Sal B on the viability of NSPCs in vitro using the MTS assay, NSPCs were treated with Sal B at different concentrations and for different durations. We investigated Sal B at 5, 10, 20, 30, 40, 50 µM dose exposure for 24 hours, and at 20 µM dose incubated for 24, 48, 72 hours on promoting NSPCs proliferation. The results showed that the viability of NSPCs significantly increased as the dose (P<0.01, F(6, 35) = 103.06) and time increases (P<0.01, Fig. 2A–B). The number and size of neurospheres were increased by addition of 20 µM of Sal B (Figure 2C–D). These results suggested that Sal B significantly increased the viability of NSPCs in dose- and time- dependent manners.

Test-retest reliability of Motricity Index strength assessments for lower extremity in post stroke hemiparesis


I hadn't heard of this test. But this still needs to map these tests to a damage diagnosis to do any good.
Its only 4 pages long. Even Iran can do some decent research.
http://mjiri.tums.ac.ir/browse.php?a_id=481&slc_lang=en&sid=1&ftxt=1

















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Neural plasticity after spinal cord injury**

It also applies to stroke.
Full article here:
http://www.crter.org/NRR-E/2012/5k/386-391.pdf
INTRODUCTION
Over the past 30 years, the concepts of the central nervous system (CNS) have changed. The CNS is an organ with plasticity and has the ability to regulate and adapt after environmental transition or injury. Specifically, the uninjured neurons and axon lateral branches can grow in denervated regions to reconstruct neural circuits to compensate for impaired sensory and motor function[1]. Because the axonal lateral branch connection forms distal to the injury site, it avoids limitations to axonal growth and elongation due to an inhibitive environment in the injury site. However, the ability of axonal regeneration and elongation is limited in adult humans and other animals. Thus, improving neural plasticity is critical for repair of CNS injury. Increasing numbers of studies have confirmed that functional exercise targeting the denervated region, neurotrophic factor and transplantation of tissues and cells can effectively improve neural plasticity.
Retrieval strategy regarding articles included in this review is shown as follows.
Inclusion criteria: studies discussing advances in neural plasticity after spinal cord injury (SCI).
Exclusion criteria: outdated and repetitive studies were excluded.
Article inclusion: 231 articles were first collected, which were all published in English. The titles and abstracts were read, and 146 were excluded, including 35 repetitive studies. The remaining 52 English articles comprising 41 basic studies and animal experiments, and nine review articles were used for further analysis. These articles analyzed conditions for modulation of neural plasticity and reconstruction of the neural circuit and summarized methods for improving neural plasticity changes.
CONDITIONS FOR MODULATION OF NEURAL PLASTICITY AND RECONSTRUCTION OF NEURAL CIRCUITS
Due to the limitation of axonal regeneration in the adult injured CNS, spontaneous sensory and motor functional recovery after SCI has been regarded as reconstruction of neural circuits by axonal or dendritic elongation connections[2]. The reconstruction of neural circuits is generated in the spinal cord, brain stem, thalamus, and sensorimotor cortex[3], and is mainly comprised of synaptic reorganization, axonal sprouting, and neurogenesis.
Cool picture on the 3rd page.

Action observation and mirror neuron network: a tool for motor stroke rehabilitation.

So who is going to take responsibility to get this to all the stroke rehab instructors and textbooks and to all the existing stroke personell?
 http://www.ncbi.nlm.nih.gov/pubmed/22522432

Abstract

Mirror neurons are a specific class of neurons that are activated and discharge both during observation of the same or similar motor act performed by another individual and during the execution of a motor act. Different studies based on non invasive neuroelectrophysiological assessment or functional brain imaging techniques have demonstrated the presence of the mirror neuron and their mechanism in humans. Various authors have demonstrated that in the human these networks are activated when individuals learn motor actions via execution (as in traditional motor learning), imitation, observation (as in observational learning) and motor imagery. Activation of these brain areas (inferior parietal lobe and the ventral premotor cortex, as well as the caudal part of the inferior frontal gyrus [IFG]) following observation or motor imagery may thereby facilitate subsequent movement execution by directly matching the observed or imagined action to the internal simulation of that action. It is therefore believed that this multi-sensory action-observation system enables individuals to (re) learn impaired motor functions through the activation of these internal action-related representations. In humans, the mirror mechanism is also located in various brain segment: in Broca's area, which is involved in language processing and speech production and not only in centres that mediate voluntary movement, but also in cortical areas that mediate visceromotor emotion-related behaviours. On basis of this finding, during the last 10 years various studies were carry out regarding the clinical use of action observation for motor rehabilitation of sub-acute and chronic stroke patients.
Full 6 page article here: 
http://www.minervamedica.it/index2.t?show=R33Y9999N00A0161

Exoskeleton hand gives you robo-powered fingers

Someone could easily repurpose this for finger therapy - passive movement.
Festo's prototype robo-hand can operate machine manipulators from afar, and could help stroke victims regain use of their hands
http://news.cnet.com/8301-17938_105-57423204-1/exoskeleton-hand-gives-you-robo-powered-fingers/
 full article and video at the link.

Neuroscientists discover key protein responsible for controlling nerve cell protection - SUMO

This one is hard to understand.
http://www.pharmiweb.com/pressreleases/pressrel.asp?ROW_ID=57779
A key protein, which may be activated to protect nerve cells from damage during heart failure or epileptic seizure, has been found to regulate the transfer of information between nerve cells in the brain. The discovery, made by neuroscientists at the University of Bristol and published in Nature Neuroscience and PNAS, could lead to novel new therapies for stroke and epilepsy.
A key protein, which may be activated to protect nerve cells from damage during heart failure or epileptic seizure, has been found to regulate the transfer of information between nerve cells in the brain. The discovery, made by neuroscientists at the University of Bristol and published in Nature Neuroscience and PNAS, could lead to novel new therapies for stroke and epilepsy.
The research team, led by Professor Jeremy Henley and Dr Jack Mellor from Bristol’s Medical School, has identified a protein, known as SUMO, responsible for controlling the chemical processes which reduce or enhance protection mechanisms for nerve cells in the brain.
These key proteins produce subtle responses to the brain’s activity levels to regulate the amount of information transmitted by kainate receptors - responsible for communication between nerve cells and whose activation can lead to epileptic seizures and nerve cell death.
Protein function is controlled by altering their structure in processes that can be independent or inter-related including phosphorylation, ubiquitination and SUMOylation. In the present work it is shown that phosphorylation of kainate receptors on its own promotes their activity. However, phosphorylation also facilitates SUMOylation of kainate receptors that reduces their activity. Thus there is a dynamic and delicate interplay between phosphorylation and SUMOylation that regulates kainate receptor function.
This fine balance between phosphorylation and SUMOylation is dependent on brain activity levels where damaging activity that occurs during stroke or epilepsy will enhance SUMOylation and therefore reduce kainate receptor function to protect nerve cells.
Dr Mellor, Senior Lecturer from the University’s School of Physiology and Pharmacology, said: “Kainate receptors are a somewhat mysterious but clearly very important group of proteins that are known to be involved in a number of diseases including epilepsy. However, we currently know little about what makes kainate receptors so important. Likewise, we also know that SUMO proteins play an important role in neuroprotection. These findings provide a link between SUMO and kainate receptors that increases our understanding of the processes that nerve cells use to protect themselves from excessive and abnormal activity.”
Professor Henley added: “This work is important because it gives a new perspective and a deeper understanding of how the flow of information between cells in the brain is regulated. The team has found that by increasing the amount of SUMO attached to kainate receptors – which would reduce communication between the cells – could be a way to treat epilepsy by preventing over-excitation of the brain’s nerve cells.”
The research follows on from previous findings published in Nature that discovered SUMO proteins target the brain’s kainate receptors altering their cellular location.
The research teams comprised academics from the University of Bristol’s MRC Centre for Synaptic Plasticity and the Division of Neuroscience in the School of Physiology & Pharmacology and the School of Biochemistry. This work was supported by the Wellcome Trust, Biotechnology and Biological Sciences Research Council (BBSRC), European Research Council (ERC), Medical Research Council (MRC) and EMBO

Eye Disorder Tied to Stroke Risk

I don't think they have cause and effect down yet. Ask your doctor.
http://www.medpagetoday.com/Cardiology/Strokes/32382
Patients with age-related macular degeneration appear to be at risk for both ischemic and hemorrhagic stroke, researchers found.
Through an average follow-up of 13 years, middle-age individuals with the eye condition had a higher rate of any stroke (7.6% versus 4.9%), according to M. Kamran Ikram, MD, of the Singapore Eye Research Institute, and colleagues.
The difference was consistent for both ischemic stroke (6.4% versus 4.4%) and intracerebral hemorrhage (1.2% versus 0.4%), the researchers reported online in Stroke: Journal of the American Heart Association.
"These data provide further insight into common pathophysiological processes between age-related macular degeneration and stroke subtypes," they wrote.
Previous studies have examined the relationship between age-related macular degeneration and stroke, with some showing a positive association and others showing no correlation.
The current study included 12,216 middle-age individuals (ages 45 to 64) who had retinal photographs taken at the third examination visit of the Atherosclerosis Risk in Communities (ARIC) study.
Overall, 591 participants (4.9%) were diagnosed with age-related macular degeneration. Of those, 576 had early disease, defined as the presence of either soft drusen alone, retinal pigment epithelial depigmentation alone, or a combination of soft drusen with increased retinal pigment and/or retinal pigment epithelial depigmentation.
The rest had late disease, defined as the presence of exudative age-related macular degeneration or pure geographic atrophy.
Through follow-up, 619 of the participants (5.1%) had a stroke, including 548 cerebral infarctions, 57 intracerebral hemorrhages, and 14 subarachnoid hemorrhages.
Those with any age-related macular degeneration were about 50% more likely to have a stroke during follow-up (HR 1.51, 95% CI 1.11 to 2.06) after adjustment for age, sex, race, field center, mean arterial blood pressure, antihypertensive medications, fasting glucose, total cholesterol, HDL cholesterol, triglyceride levels, body mass index, atrial fibrillation, white blood cell count, cigarette smoking, and alcohol consumption.
The relationship was stronger for intracerebral hemorrhage (HR 2.64, 95% CI 1.18 to 5.87) than for ischemic stroke (HR 1.42, 95% CI 1.01 to 1.99).
"Recently, antivascular endothelial growth factor agents used in the treatment of neovascular age-related macular degeneration have been suggested to increase the risk of intracerebral hemorrhage," the authors noted. "Based on our findings, it appears that patients with [the eye disease] may already be at an increased risk of intracerebral hemorrhage and, thus, antivascular endothelial growth factor therapy could potentially increase this risk further."
"However," they added, "additional studies are needed to confirm this potential side effect of antivascular endothelial growth factor agents."
They acknowledged some limitations of the study, including the fact that the technique used for taking retinal photographs makes grading age-related macular degeneration more variable, the use of pictures from only one eye for each participant, and the low number of patients with late age-related macular degeneration.

Statins May Cut Stroke Mortality

But, but, but don't these people think about what they write before sending it out. What about this study that says about statins; Acute statin therapy improves survival after ischemic stroke
 So does the new study account for those who were on statins continuing to take statins? With that being the reason for improvement rather than pre-stroke use of statin.
The new study here:
 http://www.medpagetoday.com/MeetingCoverage/AANMeeting/32363
 Stroke patients who were on statin therapy at the time of their stroke appear to be significantly less likely to die in the hospital than patients who were not on the cholesterol-lowering drugs, researchers said here.
Among stroke patients on statins because of hypercholesterolemia, the early mortality was 2.1% compared with an early mortality of 12.5% among similar patients who were not treated with statins prior to admission for stroke (P<0.001), said Mohamed Al-Khaled, MD, a fellow in neurology at the University of Lübeck, Germany.
The difference in outcome also was seen for patients who did not have high cholesterol but were taking statins for other reasons, including heart disease and diabetes, Al-Khaled told MedPage Today at his poster presentation during the annual meeting of the American Academy of Neurology.
Among such patients who were on statins, in-hospital mortality was 2.5% while those with similar conditions who were not on statin therapy had an early mortality of 7% (P<0.001).
"Statin medication may reduce the early mortality and may have a neuroprotective effect in patients suffering from a stroke," Al-Khaled suggested. "Further studies are necessary to confirm this finding."
The research team investigated outcomes among 10,737 patients over a 42-month period -- beginning in 2007 -- who were diagnosed with ischemic stroke and were entered into the German Federal State of Schleswig-Holstein stroke registry.
During the mean hospital stay of 9 days, the researchers determined that overall, 4.8% of the patients succumbed to their strokes.
Among the patients in the registry, 5565 were also diagnosed with hypercholesterolemia. Al-Khaled reported that 88% of the patients with high cholesterol were treated with statins, and 24% of the patients who did not have high cholesterol also were treated with statin therapy.
The registry did not provide data on the type of statin used in the patients, he said.
"The early mortality was significantly lower in patients treated with statins than those who were not treated with statins, regardless of whether they had hypercholesterolemia," Al-Khaled said. "We were surprised to see that statin therapy among those who did not have high cholesterol appears to improve outcomes."
Al-Khaled reported that patients treated with statins also appeared to do better at discharge.
Among all patients on statin therapy upon admission, the discharge Modified Rankin Score was 2.1, compared with a score of 2.7 for patients who were not on statin therapy (P<0.001).
If the patients had high cholesterol, the discharge modified Rankin score was 2.1 at discharge for patients on statins, and 2.9 for patients not on statins at admission (P<0.001).
For patients who were on statins but who did not have high cholesterol, the discharge modified Rankin score averaged 2.1 compared with a 2.6 score for patients who were not on statins at admission (P<0.001).
"This type of phenomena has been reported before with statins," said Ralph Sacco, MD, chairman of the department of neurology at the University of Miami and a spokesperson for the American Heart Association.
"Nowadays, we are treating patients with heart disease or diabetes or other high-risk conditions with statins because in addition to their cholesterol-lowering properties, statins are know to reduce inflammation," Sacco told MedPage Today.
He said that the new data fits into previous findings that show when a person with a stroke comes in already on a statin, "you have better outcomes from those strokes, better 30-day outcomes, lower mortality. There are a number of studies, including this one, that do seem to confirm that patients who present with stroke while on statins may do a little better than those who are not on the drugs."

Thursday, April 26, 2012

Blood pressure breakthrough

I wish someone would explain why blood pressure is so important to prevent stroke when 85% of strokes are clots. But hey why should I know or care about it.
http://www.fox23news.com/content/healthalert/story/Blood-pressure-breakthrough/B9aR_F3_0U2F-zX9e4x2SQ.cspx
One in three adults have it.  And if left untreated, it can become a ticking time bomb. leading to heart disease, stroke or kidney failure.
It's high blood pressure. Something Caroline Lee wants to avoid.
"I'd like to think that I'm really active," Caroline said.
Caroline gets her blood pressure checked regularly, but now she can get an even better reading by testing what's happening in the large arteries close to her heart, known as central blood pressure. Normally, blood pressure is measured with a cuff in the upper arm for convenience, but recent studies show brachial blood pressure is not as accurate as central blood pressure for measuring your risk for disease.
 "Based on the change of your central pressure, you can find out what your risk of having heart disease are," Dr. Nicole Weinberg said.
 Being able to measure blood pressure in the aorta which is closer to the heart and brain is important because this is where high blood pressure can cause significant damage. Until now it could only be measured directly by surgically placing a catheter or pressure sensor into the aorta. But this new FDA approved machine, the Sphygmocor , is changing that. a sensor the size of a pen is pressed at the wrist.
"And through the pressure from your heart in the radial artery we are able to measure what the central pressures are," the doctor said.
In minutes, doctors can recommend either life style changes or drug therapy. As for Caroline.
 "I don't know exactly what it means to have 30 year old arteries, but I'm pretty happy about it," Caroline said.
Now she can get back to her active lifestyle.

The use of pedometers in stroke survivors: are they feasible and how well do they detect steps?

I used one for a while and I think it severely undercounted.
http://www.hubmed.org/display.cgi?uids=22373934&utm_source=feedburner&utm_medium=feed&utm_campaign=Feed%3A+nih%2Fbxxu+%28Stroke+rehabilitation%29&utm_content=Google+Feedfetcher
To determine (1) the feasibility of pedometers for stroke patients and (2) the level of agreement between pedometers and actual step count.Observational agreement study.Six stroke units.Independently mobile stroke patients (N=50) ready for hospital discharge.Patients were asked to apply 3 pedometers: 1 around the neck and 1 above each hip. Patients performed a short walk lasting 20 seconds, then a 6-minute walk test 6MWT. Video recordings determined the criterion standard step count.Agreement between the step count recorded by pedometers and the step count recorded by viewing the criterion standard video recordings of the 2 walks.Five patients (10%) needed assistance to put on the pedometers, and 5 (10%) could not read the step count. Thirty-nine (78%) would use pedometers again. Below a gait speed of about 0.5 m/s, pedometers did not generally detect steps. Agreement analyses showed that even above 0.5 m/s, pedometers undercounted steps for both the short walk and 6MWT; for example, the mean difference between the video recorder and pedometer around the neck was 5.93 steps during the short walk and 32.4 steps during the 6MWT.Pedometers are feasible but generally do not detect steps at gait speeds below about 0.5 m/s, and they undercount steps at gait speeds above 0.5 m/s.

Dark chocolate outperforms white chocolate in heart benefits study

Well there is no such thing as white chocolate (0 percent cocoa) .
http://www.ktvq.com/news/dark-chocolate-outperforms-white-chocolate-in-heart-benefits-study/
Previous research has linked eating dark chocolate to healthy heart benefits such as reduced risk for stroke and heart disease. A new study that compared dark chocolate against white chocolate adds to the evidence of why eating dark chocolate may help your health.
For the study, presented August 24 at the Experimental Biology 2012 conference in San Diego, researchers assigned 31 "fortunate" subjects to eat a daily serving of 50 grams of either dark chocolate (which contained 70 percent cocoa) or white chocolate (0 percent cocoa) for 15 days. The researchers performed a battery of blood tests on the participants before and after the study, and found those who ate dark chocolate had lower blood sugar (glucose) levels, lower levels of LDL (bad cholesterol) and higher levels of HDL (good) cholesterol.
Study author Dr. Mee Young Hong, associate professor of exercise and nutritional sciences at San Diego State University, told WebMD that dark chocolate eaters lowered their bad cholesterol by 20 percent and raised their good cholesterol by 20 percent.
The researchers concluded that dark chocolate may reduce the risk of heart disease by improving glucose levels and lipid profiles. This might be because dark chocolate contains more compounds called "flavanols" that have potent antioxidant and anti-inflammatory properties, they said. The effects from eating dark chocolate remained after scientists "bloomed" the chocolate, which is basically melting it and letting it settle.
But the researchers warn chocolate should be eaten in moderation since daily consumption adds saturated fat and calories to your diet. They realize that's no easy task since getting their study participants to limit their chocolate intake was hard enough.
"We had great compliance with our study subjects because everybody wanted to eat chocolate," the researchers wrote. "We actually had to tell them not to eat more than 50 grams a day."

Computer assisted stroke rehabilitation– the possibilities of distributed Virtual Reality.

For those who are fluent in Swedish you can read that here: Google says its German but what do I know
http://www.researchweb.org/is/gsb/ansokan/9716
Translation;

Summary

The aim is to develop and clinically deploy a system for rehabilitation after the acute phase of stroke. Stroke patients often use more than the healthy side to compensate for the loss of body function in the paralyzed side. They are likely to be a learned behavior persist if the individual only a limited use of the disabled upper limb. After the initial assessment identifies a training program, the patient sits in front of the computer and holding a computer mouse with full mobility in the three-dimensional space. The computer sees the patient as "virtual" 3D images of the exercises. Monitoring and evaluation is continuous. The results of the evaluation leads to changes in the management measures. All components of the system is fully developed. Our ambition is to create an optimal adherence to rehabilitation services by distributing the devices to patients or local centers.

Background

Patients with stroke may, depending on the damage location including have problems with various body functions (1, 2). Stroke patients often use more than the healthy side to compensate for the loss of body function in the paralyzed side. This can lead to problems in the body posture, balance, coordination, and strength, which leads to an abnormal motion. The scope ranges from the upper and lower extremity only to a small extent can be used, that the injured can move, but the movements are clumsy and uncoordinated. They are likely to be a learned behavior persist if the individual only limited uses such as the disabled upper limb (3, 4). After initial assessments that measure the ability to perform activities of daily life and various hand / arm function tests determined an individual training program. The patient sits in front of the computer and holding a computer mouse with full mobility in the three-dimensional space so that it can also be moved in depth. At the same time the so-called haptic technology it is possible to touch the virtual objects (5). The computer sees the patient as "virtual" 3D images of the exercises. All components of the system in prototypes or fully developed (6-8). Our ambition is to create economically viable conditions for an optimal adherence to rehabilitation after stroke by distributing units equipped with virtual reality, haptics and telemedicine for patients or local centers. Furthermore, elimination of tedious travel and some social costs.

Inpatient rehabilitation following stroke: amount of therapy received and associations with functional recovery

I wish these people would think before they set up research. You need to go to the reason therapy works first and that would be the amount of dead brain damage vs. penumbra damage. If its mostly penumbra damage then of course therapy will work. Dead brain damage  will likely not be recovered during inpatient therapy. It takes a long time to move functionality to another location.
http://informahealthcare.com/doi/abs/10.3109/09638288.2012.676145
Purpose: Canada’s Best Practice Recommendations for Stroke Care state that a minimum of one hour per day of each of the relevant core therapies be provided to patients admitted for inpatient rehabilitation. We examined whether this standard was met on a single, specialized stroke rehabilitation unit and if amount of therapy was an independent contributor to functional improvement. Methods: One-hundred and twenty-three, consecutive patients admitted to a 30-bed stroke rehabilitation program over a 6-month period with the confirmed diagnosis of stroke, were included. Workload measurement data were used to estimate the amount of therapy that patients received from core therapists during their inpatient stay. A multivariable model to predict Functional Independence Measure (FIM) gains achieved was also developed using variables that were significantly correlated with functional gain on univariate analysis. Results: On average, patients received 37 min of active therapy from both physiotherapists (PT) and occupational therapists (OT) and 13 min from speech-language pathologists per day. Admission FIM, length of stay, total OT and PT therapy time (hrs) were significantly correlated with FIM gain. In the final model, which explained 35% of the variance, admission FIM score and total amount of occupational therapy (OT) emerged as significant predictors of FIM gain. Conclusions: Patients admitted to a specialized rehabilitation unit received an average of 37 min a day engaged in therapeutic activities with both occupational and physical therapists. Although this value did not reach the standard of one hour, total amount of OT time contributed significantly to gains in FIM points during hospital stay.
Implications for Rehabilitation
  • Patients on an inpatient stroke rehabilitation unit received less than the standard of one hour of physiotherapy and occupational therapy per day.
  • Total amount of occupational therapy contributed significantly to gains in Functional Independence Measure points during hospital stay.



Wednesday, April 25, 2012

Whole-brain, time-locked activation with simple tasks revealed using massive averaging and model-free analysis

I think this means that the 10% use of the brain is blown completely out of the water. If you look at my colored fMRI scans further down in the blog you can see brightly colored active areas all over my brain when I was trying to move my ankle up and down to follow a cursor with my foot.
I'm not sure how I can use this information  but it's interesting.
http://www.pnas.org/content/109/14/5487

Abstract

The brain is the body's largest energy consumer, even in the absence of demanding tasks. Electrophysiologists report on-going neuronal firing during stimulation or task in regions beyond those of primary relationship to the perturbation. Although the biological origin of consciousness remains elusive, it is argued that it emerges from complex, continuous whole-brain neuronal collaboration. Despite converging evidence suggesting the whole brain is continuously working and adapting to anticipate and actuate in response to the environment, over the last 20 y, task-based functional MRI (fMRI) have emphasized a localizationist view of brain function, with fMRI showing only a handful of activated regions in response to task/stimulation. Here, we challenge that view with evidence that under optimal noise conditions, fMRI activations extend well beyond areas of primary relationship to the task; and blood-oxygen level-dependent signal changes correlated with task-timing appear in over 95% of the brain for a simple visual stimulation plus attention control task. Moreover, we show that response shape varies substantially across regions, and that whole-brain parcellations based on those differences produce distributed clusters that are anatomically and functionally meaningful, symmetrical across hemispheres, and reproducible across subjects. These findings highlight the exquisite detail lying in fMRI signals beyond what is normally examined, and emphasize both the pervasiveness of false negatives, and how the sparseness of fMRI maps is not a result of localized brain function, but a consequence of high noise and overly strict predictive response models.

Certified Stroke Centers Use More Thrombolysis

This makes it sound like a success, but in reading this they don't mention the actual success rate of complete recovery when tPA is used within the timeframes. I would be willing to bet because tPA does not have a very good success rate. Prevention of death vs. recovery would be a good measurement. Naked emperor and all. Time for your head to be rolling Dean.
http://www.medpagetoday.com/MeetingCoverage/AANMeeting/32348?utm_source=cardio-meetings&utm_medium=email&utm_content=mpt&utm_campaign=DCH
Use of tPA has been substantially higher in primary stroke centers certified by the Joint Commission compared with other facilities, although the gap has narrowed recently, a researcher said here.
Since the commission began certifying stroke centers in 2003, use of tPA at certified centers has ranged from 6% to nearly 8%, with a gradual increase through 2009, according to an analysis of National Inpatient Sample (NIS) data reported by Michael Mullen, MD, of the University of Pennsylvania.
The percentage was markedly lower in noncertified stroke centers throughout the study period, Mullen told attendees at the American Academy of Neurology's annual meeting. In 2009, the most recent year for NIS data, 3.3% of stroke patients at noncertified centers received tPA, he said. But that represented a substantial increase over time -- in 2004, only about 1.4% of patients got tPA.
Moreover, Mullen pointed out, certified stroke centers were different in many ways that would suggest a higher likelihood of administering thrombolytic therapies.
Certified centers were far more likely to be located in teaching hospitals and to be in nonrural areas, and they also were more likely to treat large numbers of patients annually, he reported:
  • Teaching hospital: 61.5% of certified centers, 35.1% of noncertified centers
  • Rural location: 1.6% of certified centers, 15.8% of noncertified centers
  • ≥300 cases per year: 69.0% of certified centers, 29.6% of noncertified centers
Many of the rural centers probably didn't have a neurologist on hand, commented session moderator Scott Silliman, MD, of Shands Jacksonville Hospital in Jacksonville, Fla.
Still, after adjusting for these factors as well as patient age, sex, race, comorbidities, insurance type, income (by ZIP code), and mortality propensity, the probability of getting tPA was still significantly higher in the certified stroke centers, with an odds ratio of 1.87 for the entire 6 years of the study (95% CI 1.62 to 2.17).
In line with the increase in tPA use in noncertified centers during the study period, the odds ratio for receiving tPA in certified centers declined -- from 2.95 in 2004 (95% CI 1.74 to 5.00) to 1.68 in 2009 (95% CI 1.36 to 2.16).
Mullen and colleagues had pulled NIS data on all patients with a primary diagnosis of ischemic stroke in states that publicly report hospitals' identity -- more than 320,000 patients, including about 63,000 treated in Joint Commission-certified centers.
A total of 37 states participate in the NIS but only 25 included hospital names in their stroke data from 2004 to 2009, with one additional state providing these data in 2009.
Clinicians have heard different stories about whether Joint Commission certification implies better care or outcomes. A report last year in the Journal of the American Medical Association found a significantly lower death rate in stroke patients admitted to certified centers.
But certification hinges on the ability to provide tPA, not on demonstrated adherence to guidelines or improvements in outcomes, and many clinicians remain skeptical about the benefits of tPA in stroke patients, especially those who come to the hospital later than 90 minutes after symptom onset.
Mullen said a notable lack in the NIS data is information on time to arrival -- a key factor in determining whether tPA is administered.
Silliman said it was encouraging to see that the rate of tPA used in noncertified centers had doubled during the study period. Mullen speculated that some of these centers may have participated in state-level certification programs or made other efforts to adopt guideline-recommended treatments.

Signaling Neurons Make Neighbor Cells "Want In"

So this is the belief in 'good' neurons. Is it helpful in more than memory neurons? full article at the link.
http://www.scientificamerican.com/article.cfm?id=keeping-up-with-the-neurons
Neurons, or nerve cells, each have a pair of projections—the axon and the dendrite, which transmit and receive impulses, respectively. The dendrite, a treelike structure, has several branches dotted with hundreds synaptic receiving terminals called "spines," each connected to the axons of scores of other neurons. When one of these spines receives stimulation (through the synapse it creates with another cell's axonal projection), the spine expands into the synapse, strengthening the link between its neuron and the other cell. This process of enhanced communication through a synapse is called long-term potentiation (LTP) and is thought to be the basis of learning.
Previous attempts to identify this process were stymied by inexact methods. Researchers primarily used electrical impulses, which do not allow for good spatial observation. Svoboda and study co-author Christopher Harvey, a graduate student in Svoboda's lab, used a more precise technique. They attached a light-absorbing chemical group to the neurotransmitter glutamate (an excitatory chemical messenger in the brain) at a particular synapse in a slice of a rat's hippocampus, the brain region responsible for short-term memory. When they trained a laser on the glutamate, it was freed from its light-absorbing molecular captor and thereby able to resume its function; it went to the dendritic spine in the synapse, allowing ions to enter the cell and an electrical signal to be generated.
As a result of this stimulation, the spine stretched farther into the synapse. Researchers did not find any evidence that neighboring spines had also expanded, but they did find that it took less stimulation—only 20 percent of the original prodding—to prompt any of the 20 spines within 10 microns (around four ten-thousandths of an inch) to undergo LTP. This effect appeared to last for five to 10 minutes, the scientists report.

“Housekeeping” Mechanism for Brain Stem Cells Discovered

So can we get the 'Good Housekeeping  Seal of Approval' protocol setup for this? I'm ready to release my stem cells anytime.
 http://www.newswise.com/articles/housekeeping-mechanism-for-brain-stem-cells-discovered?ret=/articles/list&category=medicine&page=1&search[status]=3&search[sort]=date+desc&search[section]=10&search[has_multimedia]=#
Researchers at Columbia University Medical Center (CUMC) have identified a molecular pathway that controls the retention and release of the brain’s stem cells. The discovery offers new insights into normal and abnormal neurologic development and could eventually lead to regenerative therapies for neurologic disease and injury. The findings, from a collaborative effort of the laboratories of Drs. Anna Lasorella and Antonio Iavarone, were published today in the online edition of Nature Cell Biology.
The research builds on recent studies, which showed that stem cells reside in specialized niches, or microenvironments, that support and maintain them.
“From this research, we knew that when stem cells detach from their niche, they lose their identity as stem cells and begin to differentiate into specific cell types,” said co-senior author Antonio Iavarone, MD, professor of Pathology and Neurology at CUMC.
“However, the pathways that regulate the interaction of stem cells with their niche were obscure,” said co-senior author Anna Lasorella, MD, associate professor of Pathology and Pediatrics at CUMC and a member of the Columbia Stem Cell Initiative.
In the brain, the stem cell niche is located in an area adjacent to the ventricles, the fluid-filled spaces within the brain. Neural stem cells (NSCs) within the niche are carefully regulated, so that enough cells are released to populate specific brain areas, while a sufficient supply is kept in reserve.
In previous studies, Drs. Iavarone and Lasorella focused on molecules called Id (inhibitor of differentiation) proteins, which regulate various stem cell properties. They undertook the present study to determine how Id proteins maintain stem cell identity.
The team developed a genetically altered strain of mice in which Id proteins were silenced, or knocked down, in NSCs. In the absence of Id proteins, mice died within 24 hours of birth. Their brains showed markedly lowered NSC proliferative capacity, and their stem cell populations were reduced.
Studies of NSCs from this strain of mice revealed that Id proteins directly regulate the production of a protein called Rap1GAP, which in turn controls Rap1, one of the master regulators of cell adhesion. The researchers found that the Id-Rap1GAP-Rap1 pathway is critical for the adhesion of NSCs to their niche and for NSC maintenance. “There may be other pathways involved, but we believe this is the key pathway,” said Dr. Iavarone. “There is good reason to believe that it operates in other kinds of stem cells, and our labs are investigating this question now.”
“This is a new idea,” added Dr. Lasorella. “Before this study, the prevailing wisdom was that NSCs are regulated by the niche components, conceivably through the release of chemical attractants such as cytokines. However, our findings suggest that stem cell identity relies on this mechanism.”
More research needs to be done before the findings can be applied therapeutically, Dr. Iavarone said. “Multiple studies show that NSCs respond to insults such as ischemic stroke or neurodegenerative diseases. If we can understand how to manipulate the pathways that determine stem cell fate, in the future we may be able to control NSC properties for therapeutic purposes.”
"Another aspect,” added Dr. Lasorella, “is to determine whether Id proteins also maintain stem cell properties in cancer stem cells in the brain. In fact, normal stem cells and cancer stem cells share properties and functions. Since cancer stem cells are difficult to treat, identifying these pathways may lead to more effective therapies for malignant brain tumors."
Stephen G. Emerson, MD, PhD, director of the Herbert Irving Comprehensive Cancer Center at NewYork-Presbyterian Hospital/Columbia University Medical Center, added that, "Understanding the pathway that allows stem cells to develop into mature cells could eventually lead to more effective, less toxic cancer treatments. This beautiful study opens up a wholly unanticipated way to think about treating brain tumors."
The paper is titled “Id proteins synchronize stemness and anchorage to the niche of neural stem cells.” Other contributors are Francesco Niola (CUMC), Xudong Zhao (CUMC), Devendra Singh (CUMC), Angelica Castano (CUMC), Ryan Sullivan (CUMC), Mario Lauria (Telethon Institute of Genetics and Medicine, Naples, Italy), Hyung-song Nam (Memorial Sloan-Kettering Cancer Center, New York),, Yuan Zhuang (Duke University Medical Center, Durham, North Carolina), Robert Benezra (Memorial Sloan-Kettering), and Diego Di Bernardo (Telethon Institute of Genetics and Medicine).
This research was supported by National Cancer Institute grants R01CA101644, R01CA131126, R01CA085628, and R01CA127643, and National Institute of Neurological Disorders and Stroke grant R01NS061776.
The authors declare no financial or other conflicts of interest.
Columbia University Medical Center provides international leadership in basic, pre-clinical and clinical research, in medical and health sciences education, and in patient care. The medical center trains future leaders and includes the dedicated work of many physicians, scientists, public health professionals, dentists, and nurses at the College of Physicians and Surgeons, the Mailman School of Public Health, the College of Dental Medicine, the School of Nursing, the biomedical departments of the Graduate School of Arts and Sciences, and allied research centers and institutions. Established in 1767, Columbia's College of Physicians and Surgeons was the first institution in the country to grant the M.D. degree and is among the most selective medical schools in the country. Columbia University Medical Center is home to the largest medical research enterprise in New York City and State and one of the largest in the United States.

Evidence-based guideline update: Pharmacologic treatment for episodic migraine prevention in adults

You'll have to get the complete article from your doctor.
http://www.neurology.org/content/78/17/1337.abstract?sid=17cfe656-7ccc-48d4-b062-383e6522ce00

Abstract

Objective: To provide updated evidence-based recommendations for the preventive treatment of migraine headache. The clinical question addressed was: What pharmacologic therapies are proven effective for migraine prevention?
Methods: The authors analyzed published studies from June 1999 to May 2009 using a structured review process to classify the evidence relative to the efficacy of various medications available in the United States for migraine prevention.
Results and Recommendations: The author panel reviewed 284 abstracts, which ultimately yielded 29 Class I or Class II articles that are reviewed herein. Divalproex sodium, sodium valproate, topiramate, metoprolol, propranolol, and timolol are effective for migraine prevention and should be offered to patients with migraine to reduce migraine attack frequency and severity (Level A). Frovatriptan is effective for prevention of menstrual migraine (Level A). Lamotrigine is ineffective for migraine prevention (Level A).

Tuesday, April 24, 2012

Experimental drug helps the brain recover from stroke -- in mice

You'll have to read the complete article at the link, copyrighted.
http://www.latimes.com/health/boostershots/la-heb-stroke-treatment-small-molecule-20120424,0,6344202.story
Though stroke is a major cause of long-term disability, the only proven treatment for patients is to dissolve a clot or stop the bleeding in the brain while the stroke is happening. Once it’s over, doctors and therapists can only offer rehabilitation to minimize the damage. The experimental drug being developed by scientists from Stanford University School of Medicine, Weill Cornell Medical College and UC San Francisco aims to change that.
The drug is designed to mimic a protein called brain-derived neurotrophic factor, or BDNF, which is thought to help stimulate growth of new neurons and make the brain “plastic,” or able to adapt to changes. BDNF works in cooperation with a receptor in the brain called TrkB. So the scientists set out to find a way to activate TrkB in hopes that doing so would mimic the action of BDNF and promote actual healing in the brain.
The researchers turned to a small molecule called LM22A-4 that – like BDNF – is known to bind to TrkB. The compound was made by a company called Ricerca Biosciences.
From another source:
 The results are promising because the compound wasn’t administered to the animals until a full three days after they had suffered strokes, noted Buckwalter. As such, the treatment – if proven effective in humans – could be particularly useful for patients who suffer strokes while sleeping or don’t readily recognize the symptoms and don’t get to the hospital fast enough for existing therapeutic agents to be administered.

Using placenta-derived stem cells for novel medical therapies

A TEDMED talk by Robert Hariri, MD, PhD, chief executive officer of Cellular Therapeutics Division at Celgene.
 http://scopeblog.stanford.edu/2012/02/using-placenta-derived-stem-cells-for-novel-medical-therapies/

Past research has suggested that human placentas are a rich source of stem cells that may prove useful in treating leukemia, heart disease and multiple sclerosis. In this TEDMED 2011 talk, Robert Hariri, MD, PhD, chief executive officer of Cellular Therapeutics Division at Celgene, discusses the challenges and potential benefits of transforming stem cells harvested from the placenta into novel medical therapies for a variety of conditions.
Previously: The placenta sacrifices itself to keep baby healthy in case of starvation, research shows and Program focuses on the treatment of placental disorders
Via Medgadget

Obesity and Your Brain

I couldn't find the real article behind this Lumosity email so take it with a grain of salt.

Can a steady diet of cheeseburgers change your brain? It might just be possible, according to a 2012 study from Nature Neuroscience that linked high fat diets to neurogenesis and obesity in mice.
Brain changes: good or bad?
Neurogenesis is the growth of new brain cells, and the adult neurogenesis observed by this study’s researchers is a rare form of brain change.

Neurogenesis is one manifestation of neuroplasticity, which can be promoted through good lifestyle choices—think of how Lumosity training builds connections that make everyday tasks easier, for example. On the other hand, poor lifestyle decisions might also  unfavorable results. The Johns Hopkins researchers in this study found that a high fat diet could trigger unwanted neurogenesis.(so where is the research link?)
High fat diets change the brain
The study put mice into two groups: those fed a normal diet and those who feasted regularly on high fat foods. After 1 month of chowing down, adult mice on high fat diets had quadruple the rate of new brain cell growth in the hypothalamus, a part of the brain responsible for regulating many metabolic processes.
But did neurogenesis also cause obesity? To answer this question, researchers irradiated the newly created portions of rats’ brains. Not only did radiation inhibit 85% of neurogenesis, but irradiated mice gained significantly less weight and fat mass compared to the group that kept their new neural growth—even though all of them stayed on the same high fat diet. Furthermore, irradiated mice used more energy and were more active despite their unhealthy diet.
Fighting obesity: current methods
The link between diet, obesity, and the brain is thought-provoking. But take it with a grain of salt: the connection has yet to be confirmed in humans. As we wait for more research, consider some current methods that could help change your eating habits.
Many scientists have pointed out that obesity often functions like an addiction to food in the brain. And a 2012 study from the University of Amsterdam found that challenging cognitive training lowered addiction symptoms in individuals with a drinking problem. People who trained not only drank less—they actually improved memory capacity as well.

Cell-death agents in stroke

The real title of the article is: 
N-terminally cleaved Bcl-xL mediates ischemia-induced neuronal death

Abstract


Transient global ischemia in rats induces delayed death of hippocampal CA1 neurons. Early events include caspase activation, cleavage of anti-death Bcl-2 family proteins and large mitochondrial channel activity. However, whether these events have a causal role in ischemia-induced neuronal death is unclear. We found that the Bcl-2 and Bcl-xL inhibitor ABT-737, which enhances death of tumor cells, protected rats against neuronal death in a clinically relevant model of brain ischemia. Bcl-xL is prominently expressed in adult neurons and can be cleaved by caspases to generate a pro-death fragment, ΔN-Bcl-xL. We found that ABT-737 administered before or after ischemia inhibited ΔN-Bcl-xL–induced mitochondrial channel activity and neuronal death. To establish a causal role for ΔN-Bcl-xL, we generated knock-in mice expressing a caspase-resistant form of Bcl-xL. The knock-in mice exhibited markedly reduced mitochondrial channel activity and reduced vulnerability to ischemia-induced neuronal death. These findings suggest that truncated Bcl-xL could be a potentially important therapeutic target in ischemic brain injury.

Raised blood pressure doesn’t cause heart problems if you are over 60

I can't find the real article so I don't really trust the source I have.
You have to sign up for free to access these.
WDDTY - What Doctors Don't Tell You
http://www.wddty.com/raised-blood-pressure-doesn-t-cause-heart-problems-if-you-are-over-60.html
Once you reach the age of 60, you will probably be told to start taking an antihypertensive, a drug to lower your blood pressure.  It’s one of the routine medications offered to older people as a just-in-case therapy – but the doctor couldn’t be more wrong, new research has discovered.
Raised blood pressure which is in the ‘high normal’ range becomes less of a risk factor as we get older, and doesn’t cause cardiovascular disease or coronary heart disease, as doctors have believed for the past 50 years or more.
Drugs to lower blood pressure should be given only to people who are younger than 60 years, say researchers from the Prevention of Metabolic Disorders Research Centre in Tehran, Iran.  There is still evidence that raised blood pressure in the middle-aged can cause serious health problems, they say.
Their findings were based on a major study of 6,273 people aged from 30 years and older, all with varying degrees of hypertension, who were monitored for more than nine years.
(Source: World Congress of Cardiology, April 20, 2012).

Migraine or stroke? Diagnostic test could provide answer

Could be quite useful, especially for those hypochrondriacs.
http://www.medcitynews.com/2012/04/migraine-or-stroke-diagnostic-test-could-provide-answer/
Researchers from the University of Cincinnati are behind a startup that’s developing a medical device to help emergency doctors diagnose a severe type of headache that could be a warning sign for stroke.
Xanthostat Diagnostics’ device would analyze cerebral spinal fluid to determine if patients are suffering from sentinel subarachnoid hemorrhage (SAH), a painful headache that can signal a stroke. If undiagnosed — or even sometimes when they’re diagnosed — these major hemorrhagic strokes can lead to death.

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Each year, roughly 1 million patients show up in emergency rooms with symptoms such as severe headache, nausea and dizziness. Emergency doctors must then determine the patient’s medical issue from among the three most likely: severe headache, meningitis or SAH, according to the University of Cincinnati (UC).“While there are only about 30,000 cases of SAH in the U.S. annually, the significant chance for the catastrophic or even fatal outcome that can result from misdiagnosis of these million patients annually make this one of the most important diagnostic decisions faced by emergency room physicians,” said Fred Beyette Jr., a UC professor and member of the Xanthostat team.
Doctors typically perform a spinal tap to obtain cerebral spinal fluid that is then subjected to a chemical assay to diagnose SAH. The problem with the chemical assay is that it takes several hours to deliver results and the presence of blood in the spinal fluid sample decreases the test’s accuracy.
Visual inspection of spinal fluid by physicians is another option, but that can be imprecise and is also subject to inaccuracy.
Xanthostat’s test would be an improvement on current practices because it delivers results faster and isn’t as susceptible to accuracy problems caused by blood, according to UC.
UC received a patent on Xanthostat’s core technology last year. The company has transitioned its diagnostic technology from a research-based proof-of-concept to a functional prototype.
Beyette and a UC spokeswoman didn’t respond to inquiries.

Monday, April 23, 2012

Cognitive and graded activity training can alleviate persistent fatigue after stroke: a randomized, controlled trial.

I'm not going to buy the full article to see if they list what the cognitive training consists of. I am concerned that this is just another compensatory protocol. I wish they would research exactly what is causing the fatigue before trying to come up with solutions. Cart before the horse and all.
https://www.medify.com/insights/article/22308241/cognitive-and-graded-activity-training-can-alleviate-persistent-fatigue-after-stroke-a-randomized-controlled-trial
BACKGROUND AND PURPOSE: Fatigue is a common, persistent consequence of stroke, and no evidence-based treatments are currently available to alleviate fatigue. A new treatment combining cognitive therapy (CO) with graded activity training (GRAT), called COGRAT, was developed to alleviate fatigue and fatigue-related symptoms. This study compared the effectiveness of the COGRAT intervention with a CO-only intervention after a 3-month qualification period without intervention.
METHODS: This randomized, controlled, assessor-blind clinical trial was conducted in 8 rehabilitation centers. Eighty-three stroke patients (>4 months after stroke) were randomly assigned to 12 weeks of CO or COGRAT after qualification. Seventy-three patients completed treatment and 68 were available at follow-up. Primary outcomes (Checklist Individual Strength-subscale Fatigue (CIS-f); self-observation list-fatigue (SOL-f)) and secondary outcomes (Hospital Anxiety and Depression Scale, Stroke-Adapted Sickness Impact Profile, SOL-pain, SOL-sleep-D, 6-minute walk test) were collected at baseline (before and after qualification period) and after treatment (immediate and 6-month follow-up).
RESULTS: The qualification period showed stable outcome measures. Both treatments showed significant beneficial effects on fatigue (CIS-f: η(p)(2)=0.48, P<0.001) and other outcomes (except pain and anxiety) with intention-to-treat analyses. Gains for the COGRAT group exceeded those in the CO group on number of individuals showing clinical improvement on the CIS-f (≥8 points: 58% versus 24%) and on physical endurance (η(p)(2)=0.20, P<0.001).
CONCLUSIONS: A 12-week cognitive therapy program can alleviate persistent fatigue after stroke. The best results are obtained when cognitive therapy is augmented with graded activity training. Clinical Trial Registration- URL: http://www.trialregister.nl. Unique identifier: NTR2704.

But ask your doctor to get the article to see if it might help.