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 438 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

Tuesday, October 21, 2014

Long Considered a Threat, Viagra May Help Treat Heart Disease

And why not use it for stroke?
This made it sound helpful, even though it was just in rats and during the first week:

Viagra and stroke rehab
Does your doctor know anything at all about your stroke rehab in the first week?

https://www.yahoo.com/health/long-considered-a-threat-viagra-may-help-treat-heart-100592190722.html

Science Shows How Piano Players' Brains Are Actually Different From Everybody Elses'

And if we had anything approaching a great stroke association we would be researching pianists that had a stroke and see how well they recover. But NO, we have crap for stroke associations.
http://mic.com/articles/91329/science-shows-how-piano-players-brains-are-actually-different-from-everybody-elses

Design of micro and nanoparticles to improve treatments for Alzheimer's and Parkinson's

If this is possible for other diseases we should have some stroke researchers smart enough to use this in treating stroke deficits. What is your doctor doing about this?
http://www.alphagalileo.org/ViewItem.aspx?ItemId=146390&CultureCode=en


Cold sores increases the risk of dementia

And is your doctor addressing this along with your 33% dementia chance post-stroke from an Australian study?  I remember having cold sores as a kid.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=146364&CultureCode=en
Infection with herpes simplex virus increases the risk of Alzheimer's disease. Researchers at Umeå University, Sweden, claim this in two studies in the journal Alzheimer’s & Dementia.
"Our results clearly show that there is a link between infections of herpes simplex virus and the risk of developing Alzheimer's disease. This also means that we have new opportunities to develop treatment forms to stop the disease," says Hugo Lövheim, associate professor at the Department of Community Medicine and Rehabilitation, Geriatric Medicine, Umeå University, who is one of the researchers behind the study. 
Alzheimer's disease is the most common among the dementia diseases. In recent years research has increasingly indicated that there is a possible connection between infection with a common herpes virus, herpes simplex virus type 1, and Alzheimer's disease.  A majority of the population carries this virus.  After the first infection the body carries the virus throughout your lifetime, and it can reactivate now and then and cause typical mouth ulcer. The hypothesis which links the herpes virus and Alzheimer's disease is based on that a weakened immune system among the elderly creates opportunities for the virus to spread further to the brain.  There this can in turn start the process which results in Alzheimer's disease.
Hugo Lövheim and Fredrik Elgh, professor at the Department of Virology, have now confirmed this link in two large epidemiological studies.  In one study, which is based on the Betula project, a study on ageing, memory and dementia, the researchers show that a reactivated herpes infection doubled the risk of developing Alzheimer's disease. This study had 3,432 participants who were followed for 11.3 years on average.  In another study, samples donated to the Medical Biobank at Umeå University from 360 people with Alzheimer's disease were examined and as many matched people who had not developed dementia.  The samples were taken on average 9.6 years before diagnosis.  This study showed an approximately doubled risk of developing Alzheimer's disease if the person was a carrier of the herpes virus.
"Something which makes this hypothesis very interesting is that now herpes infection can in principle be treated with antiviral agents. Therefore within a few years we hope to be able to start studies in which we will also try treating patients to prevent the development of Alzheimer's disease," says Hugo Lövheim.

Local Muscle Injection of Botulinum Toxin Type A Synergistically Improves the Beneficial Effects of Repetitive Transcranial Magnetic Stimulation and Intensive Occupational Therapy in Post-Stroke Patients with Spastic Upper Limb Hemiparesis

Have your doctor read this. I'm getting tired of pouring the same types of information into my brain.
http://www.karger.com/Article/Abstract/365005
Are they even considering that spasticity occurs in about 30% of patients?
Yamada N. · Kakuda W. · Kondo T. · Mitani S. · Shimizu M. · Abo M.

aDepartment of Rehabilitation Medicine, Jikei University School of Medicine, Minato-Ku, Tokyo and bShimizu Hospital, Kurayoshi, Tottori, Japan

Abstract

Background: The purpose of this study was to determine whether local injection of botulinum toxin type A (BoNT-A) into the spastic muscles has any added benefits to repetitive transcranial magnetic stimulation (RTMS)/occupational therapy (OT) in patients with spastic upper limb hemiparesis. Methods: The study subjects of 80 post-stroke patients with spastic upper limb hemiparesis (age: 60.2 ± 13.0 years, time after stroke: 55.3 ± 43.0 months), were divided into the BoNT-A plus RTMS/OT group and RTMS/OT group. BoNT-A was injected into the spastic muscles (total dose: 240 units) before RTMS/OT. The latter included 12 sessions of 40 min RTMS over the non-lesional hemisphere and 240-min intensive OT daily over 15 days. Spasticity was evaluated by the modified Ashworth scale (MAS) and the motor function of the affected upper limb was evaluated serially with Fugl-Meyer Assessment and Wolf Motor Function Tests. Results: Both groups showed significant improvements in spasticity and motor function. The addition of BoNT-A resulted in better improvement in FMA score and MAS of finger flexor muscles (p < 0.05). Conclusions: The triple-element protocol of local injection of BoNT-A into spastic finger muscles, RTMS and intensive OT, is a promising therapeutic program for post-stroke spastic upper limb hemiparesis, although its significance should be confirmed in randomized, placebo-controlled trials

New test to help brain injury victims recover

Will this be enough for your doctor to create stroke protocols to address your cognitive problems post-stroke?
http://www.alphagalileo.org/ViewItem.aspx?ItemId=146376&CultureCode=en
  • New SPANS assessment can help patients suffering from traumatic brain injury, aneurism, dementia, stroke and more between ages 18-74
  • Test suitable for measuring concentration, memory retention, motor performance, language skills and spatial awareness in patients
A dynamic new assessment for helping victims of trauma to the brain, including those suffering from progressive conditions such as dementia, has been developed by a clinical neuropsychologist at the University of Leicester.
The Short Parallel Assessments of Neuropsychological Status (SPANS) is the brainchild of Dr Gerald Burgess from the University of Leicester’s School of Psychology and has been designed to engage with patients suffering from a variety of brain injuries in order to aid in their recovery.
SPANS is unique in that it measures the cognitive skills of individuals with acquired brain injury and progressive neurological conditions in a user-friendly and concise way, taking patients an estimated 35 minutes to complete.
The assessment is capable of measuring seven key cognitive skills: orientation, attention and concentration, language, memory and learning, visuo-motor performance, efficiency and conceptual flexibility.
An alternate version is available, SPANS B, which complements SPANS A for reliable retesting of patients.
Both versions were developed based upon real neurological syndromes, such as aphasia, and common referral questions informed by Dr Burgess’s experience as a clinical psychologist in brain injury wards.
Dr Burgess said: “With SPANS clinicians now have a broader and more reliable assessment that is even more useful than most tests for tracking changes in cognitive skills over time. Patients are now more thoroughly assessed by a test that is less taxing on them than some other tests, so that their difficulties may be better understood.”
The test is suitable to be administered by a range of healthcare professionals, including clinical or research psychologists, occupational therapists, speech and language therapists, psychiatrists and neurologists.
During the development of SPANS Dr Burgess worked with Hogrefe, the publisher, who helped in collecting data and developing SPANS to a professional standard through production and marketing efforts.
Mr Roley Davis, Sales & Marketing Manager at Hogrefe said: “We are proud to have worked with Dr Burgess to bring this innovative new assessment to the market.  SPANS is a comprehensive and flexible test that will address the various needs of clinicians and researchers alike.  Hogrefe’s mission is to develop robust, valid and reliable assessments that address market need, and the SPANS is an excellent addition to our clinical portfolio. We look forward to hearing from people interested to know more about the assessment.”
For more information about SPANS visit Hogrefe’s website here: http://www.hogrefe.co.uk/spans.html
A paper about the development and use of SPANS is available here: http://www.hogrefe.co.uk/news/wp-content/uploads/2014/09/SPANS_overview.pdf
https://www.youtube.com/watch?v=WKvWfocqDJc

Want To Train Your Brain To Feel More Compassion? Here’s How

You might want the social workers at the hospital to train your relatives and friends in compassion towards you rather than judging you for not being who you used to be.
http://www.fastcoexist.com/3037045/want-to-train-your-brain-to-feel-more-compassion-heres-how

World Stroke Day - Only a Few Days Away!

An email from the National Stroke Association where they don't even acknowledge that everything in stroke is totally f*cked up.  If you don't even know you have a problem there is no way you can ever fix it.

Mr. Matt Lopez as Next CEO,  you have your work cut out for you. Lots to fix in your organization if you are to fulfill your mission statement.


Stroke Advocacy Network - Take Action

Dear dean,
Send an email to your representativesThe national and international effects of stroke are clear. In the United States, 795,000 people will experience a stroke every year. Globally, stroke will claim six million lives annually. World Stroke Day is right around the corner and we are still pushing members of Congress support the U.S. and global stroke community, but we need your help.
Congress has the ability to better the lives of stroke survivors and their loved ones, but some members of Congress are unaware of stroke’s prevalence. Please contact your legislators today and ask them to submit a statement to the record recognizing World Stroke Day. By promoting this international stroke awareness day, your legislators will learn more about the impact that stroke has on the lives of those in the stroke community.
Advocates from all over the nation are already reaching out to their members of Congress. Join your fellow advocates and contact your legislators today.
Contact your representatives in Congress with pre-written messages (which you can personalize). Help us help the entire stroke community—it only takes a minute to make a big difference!
Sincerely,
Signature of Angie Baker
Angie Baker
Manager, Policy Advocacy 

 0. There is no fast, easy and objective way to diagnose a stroke.
1. tPA may save your life but only has a 12% efficacy for full recovery.
2. Your neurologist doesn't have any concrete stroke protocols to save all the neurons that are dying in the first week.
3. Your neurologist or physiatrist doesn't have any clue about how to get you to full recovery. (Ask them exactly how to do it), you'll get excuses.
4. Only 10% get to full recovery.
5. No protocols to prevent your 33% chance of getting dementia post-stroke.
6. Nothing to alleviate your fatigue.
7. Nothing that will cure your spasticity.
8. Nothing on cognitive training unless you find this yourself.
9. No published stroke protocols.
10. No way to compare your stroke hospital results vs. other stroke hospitals.
Everything in stroke is a complete failure. 


























Personality Traits Predict the Onset of Disease

I'm sure your doctor is following this news and up-to-date on research. That would then entail telling you you need to change your personality to reduce your risk of disease.
Abstract here;
http://spp.sagepub.com/content/early/2014/10/13/1948550614553248.abstract
More readable article here;
The Best Personality Trait For Your Health

asthma drug, Xolair - Omalizumab May Elevate Risk of Cardiovascular, Cerebrovascular Adverse Events

Be careful out there.
http://www.docguide.com/omalizumab-may-elevate-risk-cardiovascular-cerebrovascular-adverse-events
A review of safety studies by the US Food and Drug Administration (FDA) suggests a slightly increased risk of cardiovascular and cerebrovascular adverse events among patients being treated with the asthma drug omalizumab (Xolair) than in those who were not treated with the drugs.
As a result, the FDA has added information about these potential risks to the drug label.
The review found no difference in the rates of cancer between those patients being treated with omalizumab and those who were not being treated with omalizumab. However, due to limitations in the 5-year study, the FDA cannot rule out a potential risk of cancer with omalizumab, so this information was added to the Warnings and Precautions section of the drug label.
Information for healthcare professionals:
• The FDA has added information about the findings of a slightly elevated risk of cardiovascular and cerebrovascular serious adverse events in omalizumab -treated patients to the Adverse Reactions section of the omalizumab label. The FDA has also added information about uncertain findings regarding a potential risk of cancer to the Warnings and Precautions section of the drug label.
• Periodically reassess the need for continued therapy with omalizumab based on the patient’s disease severity and level of asthma control.
• The appropriate duration of therapy for chronic idiopathic urticaria has not been evaluated. Periodically reassess the need for continued omalizumab therapy.
• Instruct patients receiving omalizumab not to decrease the dose or stop taking the drug or any other asthma medicines unless you instruct them to do otherwise.
• Provide and instruct patients to read the omalizumab patient Medication Guide before starting treatment and before starting each new prescription.
• Report adverse events involving omalizumab to the FDA MedWatch program.
Healthcare professionals and patients are encouraged to report adverse events or side effects related to the use of these products to the FDA's MedWatch Safety Information and Adverse Event Reporting Program: www.fda.gov/MedWatch/report.htm

Monday, October 20, 2014

How the Brain Rewires After Stroke - UCLA 2006

It is only 8 years old from UCLA. How is your doctor using this knowledge and updated protocols to help you recover? Has your doctor understood this at all?
http://www.uclahealth.org/body.cfm?id=502&action=detail&ref=44
Recent advances have provided vital clues that shed light on how the brain repairs and rewires itself, facilitating recovery from stroke. "We're beginning to understand exactly how the brain repairs itself after stroke," says S. Thomas Carmichael, M.D., UCLA neurologist. "We are identifying time windows in which certain repair processes are active.
Dr. Carmichael and researchers in his lab are studying the molecular and cellular mechanisms of axonal sprouting and stem cell responses to brain injury, and how these two processes of neuronal regeneration lead to repair of damaged brain circuits.
Using imaging techniques, researchers have determined that most of the recovery after stroke occurs in the tissues that border the nerve cells that die due to lack of blood supply and oxygen. In addition, researchers discovered which gene systems mediate the axonal sprouting. These findings offer two important clues about the biology of stroke recovery.
The brain operates as a set of circuits that control movement, thinking, emotion and behavior. A stroke interrupts or kills off certain circuits, causing debilitating paralysis as well as speech and cognitive problems and behavioral and emotional changes. Some spontaneous recovery does occur, however. For example, a patient may be unable to move his or her left side at all immediately following a stroke. Over time, usually about six months, some function returns. The circuits nearest the area damaged by the stroke naturally form new connections, routing around the damage and resulting in this recovery. "What is happening is the brain is remapping and reorganizing itself, and that is where recovery is occurring," Dr. Carmichael explains. "What we're trying to determine is if we can improve and enhance that recovery."
His research team found that nervous system injury induces expression of both growth-promoting and growth-inhibitory genes that together determine the location and degree of axonal sprouting. In the past, the extent of a patient's recovery depended upon the severity of the stroke. But new therapeutics may be able to boost the axonal sprouting process, allowing for the formation of more connections.
The brain could reroute its processes around the dead cells to restore more function. Children who suffer from stroke recover fully because their brains are still developing and are in a more plastic state, better able to make the circuit connections needed for repair. As humans grow and develop into adults, their brains solidify and lose that ability.
For years, researchers debated whether the adult brain could remap itself the way younger brains do. After researchers proved this did happen in adults, the second critical step was to find out how. As it turns out, the gene expression associated with axonal sprouting in the adult brain after stroke is unique, not like the axonal sprouting found in the peripheral or developing nervous systems. "This may give us clues as to why the adult brain is not as successful at rewiring itself as the peripheral and developing nervous system is," Dr. Carmichael says. "Obviously, most adult stroke patients don't recover well enough after stroke to resume normal function, yet children do. The fact that there is a unique growth program in the adult brain suggests that there may be unique targets at which we can aim new therapeutics."
Dr. Carmichael and his researchers are working to identify molecular targets to promote a neuronal growth program and induce increased axonal sprouting after stroke. Patients are taken through therapies that force them to walk more, use their arms more, or challenge their language function more completely. However, there are no drugs now that can be used to induce improved recovery after stroke.
"There needs to be a combination approach," Dr. Carmichael says. "If we were to develop a drug that enhanced sprouting, we could use that drug in combination with physical therapies that are the traditional mainstay of stroke rehabilitation."
The long-term goal is to move neurological rehabilitation closer to the acute stroke and marry the treatment of recovery to the treatment of the stroke itself.
"Epidemiological evidence has shown that most motor and sensory recovery is finished by the six-month mark," Dr. Carmichael says. "The goal of the molecular studies in stroke rehabilitation is to move the start of neural repair closer to the acute stroke itself, and to extend this limited time window for recovery well beyond six months."
Recommended Reading
Carmichael ST (2006) Cellular and molecular mechanisms of neural repair after stroke: making waves. Annal Neurol. 59:725-742.


Scientific Evidence Does Not Support 'Brain Game' Claims

Well shit. What are we supposed to do for our cognitive training to reduce our chances of getting dementia? What does your doctor suggest?
Ask for something specific. Not this crap statement, 'All strokes are different, all stroke recoveries are different'.
http://www.biosciencetechnology.com/news/2014/10/scientific-evidence-does-not-support-brain-game-claims?
The Stanford Center for Longevity joined today with the Max Planck Institute for Human Development in issuing a statement skeptical about the effectiveness of so-called "brain game" products. Signing the document were 69 scholars, including six from Stanford and cognitive psychologists and neuroscientists from around the world.
 
Laura Carstensen, a Stanford psychology professor and the director of the Center for Longevity, said as baby boomers enter their golden years, commercial companies are all too often promising quick fixes for cognition problems through products that are unlikely to produce broad improvements in everyday functioning.
 
More at link.

Sunday, October 19, 2014

How to Feel Happy Just By Walking Differently

Is your doctor going to recommend this instead of treating your depression?
http://www.spring.org.uk/2014/10/how-to-feel-happy-just-by-walking-differently.php

What good is it to do research and make new discoveries when no one pays any attention to the findings?

A quote from Musings of a Dinosaur
This is so true of stroke research. I don't know how many thousands of times I've pointed to research that looks like it might be useful to stroke patients and I bet not a single one of them has been implemented in any stroke doctors practice. We may as well go back to blood letting as a stroke prescription as discussed in the 1843 book, 'An Essay On The Nature and Treatment of Apoplexy'.
Ask your doctor why they haven't gone back to blood letting since they really haven't followed any later research?

Exploring a Neuroplasticity Model of Music Therapy

Don't just explore it, come up with a stroke protocol.
http://jmt.oxfordjournals.org/content/51/3/211.abstract
  1. Elizabeth L. Stegemöller, PhD, MT-BC
+ Author Affiliations
  1. Iowa State University
  1. Address correspondence concerning this article to Elizabeth L. Stegemöller, 240 Forker, Department of Kinesiology, Iowa State University, Ames IA, 50011.

Abstract

Background: Given that music therapists work across a wide range of disabilities, it is important that therapists have at least a fundamental understanding of the neurophysiology associated with the client/patient populations that they serve. Yet, there is a large gap of evidence regarding the neurophysiological changes associated with applying music as therapy.

Objective: The purpose of this article is to provide music therapists with a general background in neuroplasticity principles that can be applied to the use of music therapy with multiple populations.

Methods: This article will review literature on neuroplasticity and literature supporting the specific attributes of music therapy that apply to neuroplasticity. Finally, examples of how to use neuroplasticity principles to explain and support clinical music therapy will be provided.

Results: Using the material presented in this review, music therapists will be equipped with information to effectively communicate why music therapy works using three neuroplasticity principles; increase in dopamine, neural synchrony, and a clear signal.

Conclusion: Music therapy is a powerful tool to enhance neuroplasticity in the brain.

Baclofen facilitates sleep, neuroplasticity, and recovery after stroke in rats

Of course it's going to facilitate sleep, I hated it because it just caused massive amounts of fatigue and I couldn't see any progress in fixing any problems, spasticity or muscle movement.
http://onlinelibrary.wiley.com/doi/10.1002/acn3.115/full
  1. Aleksandra Hodor1,†,*,
  2. Svitlana Palchykova1,
  3. Francesca Baracchi1,
  4. Daniela Noain2 and
  5. Claudio L. Bassetti1
Article first published online: 14 OCT 2014
DOI: 10.1002/acn3.115

Abstract

Objective

Sleep disruption in the acute phase after stroke has detrimental effects on recovery in both humans and animals. Conversely, the effect of sleep promotion remains unclear. Baclofen (Bac) is a known non-rapid eye movement (NREM) sleep-promoting drug in both humans and animals. The aim of this study was to investigate the effect of Bac on stroke recovery in a rat model of focal cerebral ischemia (isch).

Methods

Rats, assigned to three experimental groups (Bac/isch, saline/isch, or Bac/sham), were injected twice daily for 10 consecutive days with Bac or saline, starting 24 h after induction of stroke. The sleep–wake cycle was assessed by EEG recordings and functional motor recovery by single pellet reaching test (SPR). In order to identify potential neuroplasticity mechanisms, axonal sprouting and neurogenesis were evaluated. Brain damage was assessed by Nissl staining.

Results

Repeated Bac treatment after ischemia affected sleep, motor function, and neuroplasticity, but not the size of brain damage. NREM sleep amount was increased significantly during the dark phase in Bac/isch compared to the saline/isch group. SPR performance dropped to 0 immediately after stroke and was recovered slowly thereafter in both ischemic groups. However, Bac-treated ischemic rats performed significantly better than saline-treated animals. Axonal sprouting in the ipsilesional motor cortex and striatum, and neurogenesis in the peri-infarct region were significantly increased in Bac/isch group.

Conclusion

Delayed repeated Bac treatment after stroke increased NREM sleep and promoted both neuroplasticity and functional outcome. These data support the hypothesis of the role of sleep as a modulator of poststroke recovery.

3D multi-channel bi-functionalized silk electrospun conduits for peripheral nerve regeneration

I don't see why your doctor isn't using something like this to reroute nerve signals around your dead brain areas. Or is your doctor a stick-in-the-mud? Hasn't read a research paper since medical school?
http://www.sciencedirect.com/science/article/pii/S1751616114003130
Choose an option to locate/access this article:
Check if you have access through your login credentials or your institution
Check access

Abstract

Despite technological advances over the past 25 years, a complete recovery from peripheral nerve injuries remains unsatisfactory today. The autograft is still considered the “gold standard” in clinical practice; however, postoperative complications and limited availability of nerve tissue has motivated the development of alternative approaches. Among them, the development of biomimetic nerve graft substitutes is one of the most promising strategies. In this study, multichanneled silk electrospun conduits bi-functionalized with Nerve Growth Factor (NGF) and Ciliary Neurotropic Factor (CNTF) were fabricated to enhance peripheral nerve regeneration. These bioactive guides consisting of longitudinally oriented channels and aligned nanofibers were designed in order to mimic the fascicular architecture and fibrous extracellular matrix found in native nerve. The simple use of the electrospinning technique followed by a manual manipulation to manufacture these conduits provides tailoring of channel number and diameter size to create perineurium-like structures. Functionalization of the silk fibroin nanofiber did not affect its secondary structure and chemical property. ELISA assays showed the absence of growth factors passive release from the functionalized fibers avoiding the topical accumulation of proteins. Additionally, our biomimetic multichanneled functionalized nerve guides displayed a mechanical behavior comparable to that of rat sciatic nerve with an ultimate peak stress of 4.0±0.6 MPa and a corresponding elongation at failure of 156.8±46.7%. Taken together, our results demonstrate for the first time our ability to design and characterize a bi-functionalized nerve conduit consisting of electrospun nanofibers with multichannel oriented and nanofibers aligned for peripheral regeneration. Our bioactive silk tubes thus represent a new and promising technique towards the creation of a biocompatible nerve guidance conduit.


Polyphenols from green tea prevent antineuritogenic action of Nogo-A via 67-kDa laminin receptor and hydrogen peroxide

I'm sure this is important somehow.
http://onlinelibrary.wiley.com/doi/10.1111/jnc.12964/abstract
Usha Gundimeda1, Thomas H. McNeill1, Barsegh A. Barseghian1, William Tzeng1, David Rayudu1, Enrique Cadenas2 and Rayudu Gopalakrishna1,* DOI: 10.1111/jnc.12964

Abstract

Axonal regeneration after injury to the CNS is hampered by myelin-derived inhibitors, such as Nogo-A. Natural products, such as green tea, which are neuroprotective and safe for long-term therapy, would complement ongoing various pharmacological approaches. In this study, using nerve growth factor-differentiated neuronal-like Neuroscreen-1 cells, we show that extremely low concentrations of unfractionated green tea polyphenol mixture (GTPP) and its active ingredient, epigallocatechin-3-gallate (EGCG), prevent both the neurite outgrowth-inhibiting activity and growth cone-collapsing activity of Nogo-66 (C-terminal domain of Nogo-A). Furthermore, a synergistic interaction was observed among GTPP constituents. This preventive effect was dependent on 67-kDa laminin receptor (67LR) to which EGCG binds with high affinity. The antioxidants N-acetylcysteine and cell-permeable catalase abolished this preventive effect of GTPP and EGCG, suggesting the involvement of sublethal levels of H2O2 in this process. Accordingly, exogenous sublethal concentrations of H2O2, added as a bolus dose (5 μM) or more effectively through a steady-state generation (1-2 μM), mimicked GTPP in counteracting the action of Nogo-66. Exogenous H2O2 mediated this action by bypassing the requirement of 67LR.

Taken together, these results show for the first time that GTPP and EGCG, acting through 67LR and elevating intracellular sublethal levels of H2O2, inhibit the antineuritogenic action of Nogo-A.


The Netrin/RGM Receptor, Neogenin, Controls Adult Neurogenesis by Promoting Neuroblast Migration and Cell Cycle Exit

Have you doctor understand this and create a stroke protocol to help you.
http://onlinelibrary.wiley.com/doi/10.1002/stem.1861/abstract
  1. Conor J. O'Leary,
  2. DanaKai Bradford,
  3. Min Chen,
  4. Amanda White,
  5. Daniel G. Blackmore and
  6. Helen M. Cooper*
DOI: 10.1002/stem.1861

ABSTRACT

A comprehensive understanding of adult neurogenesis is essential for the development of effective strategies to enhance endogenous neurogenesis in the damaged brain. Olfactory interneurons arise throughout life from stem cells residing in the subventricular zone of the lateral ventricle. Neural precursors then migrate along the rostral migratory stream (RMS) to the olfactory bulb. To ensure a continuous supply of adult-born interneurons, precursor proliferation, migration and differentiation must be tightly coordinated. Here we show that the netrin/RGM receptor, Neogenin, is a key regulator of adult neurogenesis. Neogenin loss-of-function (Neogt/gt) mice exhibit a specific reduction in adult-born calretinin interneurons in the olfactory granule cell layer. In the absence of Neogenin neuroblasts fail to migrate into the olfactory bulb and instead accumulate in the RMS. In vitro migration assays confirmed that Neogenin is required for Netrin-1-mediated neuroblast migration and chemoattraction. Unexpectedly, we also identified a novel role for Neogenin as a regulator of the neuroblast cell cycle. We observed that those neuroblasts able to reach the Neogt/gt olfactory bulb failed to undergo terminal differentiation. Cell cycle analysis revealed an increase in the number of S-phase neuroblasts within the Neogt/gt RMS and a significant reduction in the number of neuroblasts exiting the cell cycle, providing an explanation for the loss of mature calretinin interneurons in the granule cell layer. Therefore, Neogenin acts to synchronize neuroblast migration and terminal differentiation through the regulation of neuroblast cell cycle kinetics within the neurogenic microenvironment of the RMS. Stem Cells 2014

Does upper limb robot-assisted rehabilitation contribute to improve the prognosis of post-stroke hemiparesis?

I don't give a shit about your questions. What are some answers and protocols that will help stroke survivors? Why are these people even given research grants?
http://europepmc.org/abstract/med/25304657
,
Médecine physique et de réadaptation, unité de rééducation neurologique, CRF « Les Trois Soleils », 19, rue du Château, 77310 Boissise-Le-Roi, France. Electronic address: Ch.duret@les-trois-soleils.fr.
Highlight Terms
No biological terms identified
INTRODUCTION: Upper limb robot-assisted rehabilitation is a novel physical treatment for neurological motor impairments. During the last decade, this rehabilitation option utilizing technological tools has been evaluated in hemiparetic patients, mostly after stroke.

STATE OF ART: Studies at acute and chronic stages suggested good tolerance and a significant and persistent reduction of motor impairment; a real impact on disability has been shown in acute/sub acute patients.

PERSPECTIVES: Improved access to rehabilitation robots and an optimal use will probably(???) be associated with higher efficiency of rehabilitative work in the paretic upper limb.

CONCLUSIONS: Even if this treatment is still confined to a narrow circle of users, the device's biomechanical properties and clinical suggestions from the literature may show promise for the future of rehabilitation.

Saturday, October 18, 2014

One more reason to get a good night’s sleep - Jeff Iliff Neuroscientist

What is your doctors prescription for a sleep protocol to accomplish this brain cleanup task? Does taking sleeping pills help or hinder this task?  How efficiently do we want this cleanup to occur post-stroke? Does your doctor know any answers to your questions?
http://www.ted.com/talks/jeff_iliff_one_more_reason_to_get_a_good_night_s_sleep?
The brain uses a quarter of the body's entire energy supply, yet only accounts for about two percent of the body's mass. So how does this unique organ receive and, perhaps more importantly, rid itself of vital nutrients? New research suggests it has to do with sleep. 

Another great TED talk.

Brain Activity in Vegetative Patients

This may finally be an objective way to test for severe strokes. But you are going to have to call the hospital president to get something like this. I would never trust the stroke department head to do anything innovative like this. That president of the great stroke association would have every hospital president on speed dial and would be jawboning them on why their strokes heads are so damned fucking incompetent that a stroke survivor knows more about what should be occurring for stroke patients than they do.
http://theness.com/neurologicablog/index.php/brain-activity-in-vegetative-patients/

MicroRNAs and Chronic Fatigue Syndrome

Could this possily be one of the reasons we have so damn much fatigue that is untreatable?
Doctor, doctor What do you have to say?
http://questioning-answers.blogspot.com/2014/10/micrornas-and-chronic-fatigue-syndrome.html

Is Axon Guidance by Attraction and Repulsion, or by a Roll of the Dice?

When your axons are trying to find their way around damaged areas. Which stroke protocol is your doctor using? Attraction? or Repulsion?
I'd be willing to bet a lot of money that your doctor has no f*cking clue about this subject. 
http://wadsworthguidance.blogspot.com/2014/10/is-axon-guidance-by-attraction-and.html
Just a hint of some of the goodies your doctor needs to know about.


direction, X
probability
ventral
P(X = ventral)
anterior
P(X = ventral)
posterior
 P(X = ventral)
dorsal
 P(X = ventral)
  
In general, the probability distribution of variable X, the direction of outgrowth, is


It satisfies the following condition:
 
This just says that if all the probabilities for all the possible directions are added together the sum must equal 1.  
This little bit of probability theory is simple, but has profound implications.  It means that a guidance cue must affect the probability of outgrowth in more than one direction.  Since the sum of all the probabilities must equal 1, if a cue increases or decreases the probability of outgrowth in one direction it must alter the probability of outgrowth in another direction(s) as well.

 

Friday, October 17, 2014

World Stroke Day - Oct. 29

The focus of this day should be how incredibly F*CKED UP everything in stroke is.
The whole focus on F.A.S.T. is complete false advertising. tPA is given to maybe 5-10% of those eligible and of those that get it it works to completely reverse the stroke around 12% of the time. It probably will save your life like it did mine but truthfulness about this wouldn't make people feel good about the stroke associations. I consider the stroke associations a major part of the problem. No acknowledgement of the problems and deflection to news of reduced deaths by stroke which has almost nothing to do with them.


0. There is no fast, easy and objective way to diagnose a stroke.
Thornhill woman’s “stroke selfie” goes viral It was the second attack in two days — the first time she was sent home after being treated for stress.
Ohio hospital settles stroke misdiagnosis lawsuit
Pediatric Stroke Often Misdiagnosed, Treatment Delayed
Doctors tell boy, 15, he had a migraine after rugby tackle - but he was actually suffering a paralyzing stroke which nearly killed him
Factors Associated With Misdiagnosis of Acute Stroke in Young Adults
Investigation as Stafford Hospital - England - fails to spot stroke 
"Weekend effect" seen in large stroke study  
Amy on her 36 hour wait for a diagnosis.
1. tPA may save your life but only has a 12% efficacy for full recovery.
2. Your neurologist doesn't have any concrete stroke protocols to save all the neurons that are dying in the first week. The neuronal cascade of death is occurring in full force and I bet your doctor doesn't know about it and is doing nothing to stop it.
Like these 31 hyperacute possibilities
3. Your neurologist or physiatrist doesn't have any clue about how to get you to full recovery. (Ask them exactly how to do it), you'll get excuses.
4. Only 10% get to full recovery.
5. No protocols to prevent your 33% chance of getting dementia post-stroke.
6. Nothing to alleviate your fatigue. In one study, two years after their stroke 10 per cent of stroke survivors said they were always tired and 30 per cent said they were sometimes tired. In another study, at least 12 months after their stroke, 50 per cent of stroke survivors said tiredness was their main problem.

7. Nothing that will cure your spasticity.
Spasticity following a stroke occurs in about 30% of patients


8. Nothing on cognitive training unless you find this yourself.
9. No published stroke protocols.
If there are any out there I haven't found them.
10. No way to compare your stroke hospital results vs. other stroke hospitals.
Everything in stroke is a complete failure. And that should be the focus of the World Stroke Day, not  the feel good crap you are going to hear. 

Myelin Vital for Learning New Practical Skills

If this is truly the case, what is your doctor doing to make sure you have enough myelin to recover your skills? Anything at all?
http://www.biosciencetechnology.com/news/2014/10/myelin-vital-learning-new-practical-skills?
New evidence of myelin’s essential role in learning and retaining new practical skills, such as playing a musical instrument, has been uncovered by UCL research. Myelin is a fatty substance that insulates the brain's wiring and is a major constituent of "white matter." It is produced by the brain and spinal cord into early adulthood as it is needed for many developmental processes, and although earlier studies of human white matter hinted at its involvement in skill learning, this is the first time it has been confirmed experimentally.
The study in mice, published in Science, shows that new myelin must be made each time a skill is learned later in life and the structure of the brain’s white matter changes during new practical activities by increasing the number of myelin-producing cells. Furthermore, the team say once a new skill has been learnt, it is retained even after myelin production stops. These discoveries could prove important in finding ways to stimulate and improve learning, and in understanding myelin’s involvement in other brain processes, such as in cognition.
For a child to learn to walk or an adult to master a new skill such as juggling, new brain circuit activity is needed and new connections are made across large distances and at high speeds between different parts of the brain and spinal cord. For this, electrical signals fire between neurons connected by “axons”– thread-like extensions of their outer surfaces which can be viewed as the "wire" in the electric circuit. When new signals fire repeatedly along axons, the connections between the neurons strengthen, making them easier to fire in the same pattern in future. Neighboring myelin-producing cells called oligodendrocytes (OLs) recognize the repeating signal and wrap myelin around the active circuit wiring. It is this activity-driven insulation that the team identified as essential for learning.
The team demonstrated that young adult mice need to make myelin to learn new motor skills but that new myelin does not need to be produced to recall and perform a pre-learned skill. They tested the ability of mice to learn to run on a complex wheel with irregularly spaced rungs. The study looked at thirty-six normal mice and thirty-two mice with a drug-controlled genetic switch to prevent new OLs and myelin from being made. They found the mice that were prevented from producing new myelin could not master the complex wheel, whereas those that could produce myelin did learn, with differences between the two groups’ abilities seen after only two hours of practice.
A second experiment looked at mice that were first allowed to learn to run on the complex wheel before being treated with the drug to prevent further myelin production. When the mice were later re-introduced to the complex wheel, they were immediately able to run at top speed without having to spend time re-learning. This shows that the inability to make new myelin did not affect the mouse’s running ability and that new myelin is not required to remember and perform a skill once learned; it is required only during the initial learning phase.
"From earlier studies of human white matter using advanced MRI technology, we thought OLs and myelin might be involved in some way in skill learning, so we decided to attack this idea experimentally. We were surprised how quickly we saw differences in the ability of mice from each group to learn how to run on complex wheel, which shows just how fast the brain can respond to wrap newly-activated circuits in myelin and how this improves learning. This rapid response suggests that a number of alternative axon pathways might already exist in the brain that could be used to drive a particular sequence of movements, but it quickly works out which of those circuits is most efficient and both selects and protects its chosen route with myelin," said Lead Researcher and Professor Bill Richardson, director of the UCL Wolfson Institute for Biomedical Research.
Richardson added: “We think these findings are really exciting as they open up opportunities to investigate the role of OLs and myelin in other brain processes, such as cognitive activities (like navigating through a maze), to see if the requirement for new myelin is general or specific to motor activity. I’m keen to find out the precise sequence of changes to OLs and myelin during learning and whether these changes are needed more in some parts of the brain than others, which might shed light on some of the mysteries still surrounding how the brain adapts and learns throughout life.”

High-Tech Way to Diagnose Stroke

This is just a job saving initiative for neurologists. Fairly soon the  Qualcomm Tricorder X Prize will make this totally obsolete. Don't expect your neurologist to embrace this change, I bet you will need to call the hospital president directly to accomplish this change since I'm sure the stroke department head will not want to embrace technology that will lead to less doctors needed in the department.
http://www.wcvb.com/Sponsors/bethisrael/hightech-way-to-diagnose-stroke/28320644
What is TeleNet:Stroke Service:
TeleNet: Stroke service is a program that allows community hospitals to get an immediate diagnosis and treatment to a patient suspected of stroke. By collaborating with neurologic specialists, hospitals in the network can improve care while keeping a patient close to home, using this high-tech system.
Dr. Cole points out most community hospitals do not have a neurologist on-site 24 hours a day, 7 days a week.  But with TeleNet:Stroke, Dr. Cole says now a specialist can actually see, examine and interact with the patient in real time, enabling the team to make an accurate decision to administer medication and develop a treatment plan.
“We can quickly, accurately, and efficiently evaluate stroke patients to determine if they are candidates for thrombolytic therapy,” says Dr. Cole.

What Do Mirror Neurons Really Do? (BSP 112)

From Dr. Ginger Campbell interviewing Dr. Gregory Hickok
What is your doctor doing with this to help your recovery? 
What Do Mirror Neurons Really Do? (BSP 112)
Ever since their chance discovery back in 1992 mirror neurons have captured the imagination of both scientists and nonscientists, but their actual role remains mostly speculative. In The Myth of Mirror Neurons: The Real Neuroscience of Communication and Cognition Dr. Gregory Hickok (UC-Irvine) explains why the most popular theory is probably wrong. He also provides a fascinating account of how science is really done and the sobering lesson that scientists can fall prey to the same cognitive biases (and tendencies toward laziness) that plague all humans.
I first discussed the discovery of mirror neurons back in BSP 35 when I featured  Mirrors in the brain: How our minds share actions, emotions, and experience (2008) by Giacomo Rizzolatti and Corrado Sinigaglia. At that time what I found most fascinating was that since mirror neurons fire both when a subject (usually a monkey) performs an action and when a similar action is observed, this proves that single neurons are not necessarily purely motor or purely sensory. This surprising discovery seems to have been overshadowed in the rush to use mirror neurons to explain everything from autism to language evolution.
The latest Brain Science Podcast  (BSP 112) features an interview with Dr. Gregory Hickok. BSP 35 is also available for FREE via the Brain Science Podcast Mobile APP.

This is probably only available free for the next couple of months.

Ohio hospital settles stroke misdiagnosis lawsuit

One would think that this would initiate objective diagnosis research. Like these sixteen.
Although the assumption that earlier diagnosis would have prevented damage is not based on any medical action that I can think of.
http://www.toledoblade.com/Courts/2013/03/02/UTMC-agrees-to-pay-499-900-to-settle-lawsuit.html
The University of Toledo Medical Center has agreed to pay $499,900 to a patient for failing to diagnose and treat his bleeding on the brain that led to a stroke.
The Court of Claims of Ohio approved the settlement agreement Wednesday.
Adrian Fitzgerald of Toledo, who was a patient at the former Medical College of Ohio Hospital on Aug. 4, 2011, cited several incidences of negligence and medical malpractice during his hospital stay, including negligent administration of heparin; negligent failure to appropriately monitor him; negligent failure to timely and appropriately follow up on the results of a CT scan, and negligent failure to timely and appropriately report the results of a CT scan to the ordering physician and/or the physician in charge of the patient’s care.
In his complaint filed Jan. 7, Mr. Fitzgerald said he is “permanent and partially” disabled and had serious injuries including “traumatic brain injury, damage to the left visual field of both eyes, and loss of motor function.”
The complaint also cites the “loss of services and consortium” for his wife and two sons.
UTMC released a written statement about the settlement.
“At UTMC, patients’ and their families’ privacy is our priority. It is our internal policy not to discuss the details or facts surrounding their personal health care, even though some of the information is available due to the public nature of our institution,” the statement said “UTMC, in settling a matter of this nature, is making no admission of liability.”

Cost of informal caregiving associated with stroke among the elderly in the United States

And if we had a great stroke association we could reduce the caregiving needs substantially by having stopped the neuronal cascade of death.  Cause and effect is so important that I wish our stroke medical staff understood the concept and used it.
http://www.neurology.org/content/early/2014/10/10/WNL.0000000000000986.short?rss=1
  1. Guijing Wang, PhD
  1. Correspondence to Dr. Joo: hj528176@gmail.com
  1. Neurology 10.1212/WNL.0000000000000986
  1. Also available:
  2. Data Supplement

Abstract

Objectives: We estimated the informal caregiving hours and costs associated with stroke.
Methods: We selected persons aged 65 years and older in 2006 and who were also included in the 2008 follow-up survey from the Health and Retirement Study. We adapted the case-control study design by using self-reported occurrence of an initial stroke event during 2006 and 2008 to classify persons into the stroke (case) and the nonstroke (control) groups. We compared informal caregiving hours between case and control groups in 2006 (prestroke period for case group) and in 2008 (poststroke period for case group) and estimated incremental informal caregiving hours attributable to stroke by applying a difference-in-differences technique to propensity score–matched populations. We used a replacement approach to estimate the economic value of informal caregiving.
Results: The weekly incremental informal caregiving hours attributable to stroke were 8.5 hours per patient. The economic value of informal caregiving per stroke survivor was $8,211 per year, of which $4,356 (53%) was attributable to stroke. At the national level, the annual economic burden of informal caregiving associated with stroke among elderly was estimated at $14.2 billion in 2008.
Conclusions: Recent changes in public health and social support policies recognize the economic burden of informal caregiving. Our estimates reinforce the high economic burden of stroke in the United States and provide up-to-date information for policy development and decision-making.

Thursday, October 16, 2014

Seven Surprising Facts About Stroke

This is appalling that it doesn't discuss what should be the focus, that everything in stroke is a complete f*cking failure. See the bottom for my list of problems in stroke
http://www.newswise.com/articles/seven-surprising-facts-about-stroke
In recognition of World Stroke Day Oct. 29, Loyola University Medical Center neurologist Jose Biller, MD, lists seven surprising things you may not know about strokes.
Time is brain. During a stroke, 32,000 brain cells per second (1.9 million per minute) die. But if a patient receives timely treatment, the damage can be minimized. So it’s critically important to know the warning signs and symptoms of a stroke. However . . .
One in three Americans can’t name even a single stroke warning sign. These warning signs include sudden: numbness or weakness of the leg, arm or face; confusion or trouble understanding; trouble seeing in one or both eyes; trouble walking, dizziness, loss of balance or coordination; or severe headache with no known cause. An easy way to remember signs and symptoms is FAST. F: Face drooping. A: Arm weakness. S: Speech difficulty. T: Time to call 9-1-1 if any of these symptoms are present.
Strokes are surprisingly common in young people. And more young people are showing risk factors for such strokes. Between 532,000 and 852,000 people ages 18 to 44 in the United States have had a stroke. And between 1995-96 and 2007-08, U.S. hospital discharges for stroke among patients ages 15 to 44 increased by amounts ranging from 23 percent to 53 percent, depending on age and gender, according to a report, co-authored by Biller, in the journal Neurology.
Strokes are also common in presidents. Ten U.S. presidents likely suffered strokes, according to a study Biller and colleagues published in the Journal of Stroke and Cerebrovascular Diseases. Woodrow Wilson, Franklin Roosevelt and Dwight Eisenhower suffered strokes while in office, and Roosevelt’s stroke was fatal. Seven other presidents suffered apparent strokes after leaving office: John Tyler, Millard Fillmore, John Quincy Adams, Andrew Johnson, Chester Arthur, Richard Nixon and Gerald Ford.
How sex triggered a stroke. In the Journal of Stroke and Cerebrovascular Diseases, Biller and colleagues described an unusual case of a woman who suffered a stroke during sexual intercourse. Doctors believe a small clot formed in one of the veins in her thigh, broke loose and traveled to the right atrium (upper right pumping chamber). Pressure changes in the heart, triggered by sexual intercourse, enabled the clot to travel, through a hole in her heart, from the right atrium to the left atrium. From there, the clot traveled up to the brain and triggered a stroke.
The worst possible stroke. Among the most feared and devastating strokes are ones caused by blockages in the brain's critical basilar artery system. When not fatal, basilar artery strokes can cause devastating deficits, including head-to-toe paralysis called “locked-in syndrome,” according to a review article in MedLink Neurology by Biller and colleagues.
A character in "The Count of Monte Cristo," described as a "corpse with living eyes," had what appears to be locked-in syndrome. More recently, the book and movie "The Diving Bell and the Butterfly" describe a journalist with locked-in syndrome. He was mentally intact, but able to move only his left eyelid. He composed a moving memoir by picking out one letter at a time as the alphabet was slowly recited.
Neck manipulation may be associated with stroke. Treatments that involve neck manipulation may be associated with strokes, according to an American Heart Association Scientific Statement written by Biller and other leading stroke experts.
A small tear in a neck artery, called a cervical dissection, is among the most common causes of strokes in young and middle-aged adults. A dissection can lead to a blood clot that travels to the brain and triggers a stroke. Sudden movements that hyperextend or rotate the neck can cause a cervical dissection. Some maneuvers used by health practitioners also extend and rotate the neck. (Like chiropractic neck adjustments)
“Although a cause-and-effect relationship between these therapies and cervical dissection has not been established and the risk is probably low, a dissection can result in serious neurological injury,” Dr. Biller said. “Patients should be informed of this association before undergoing neck manipulation.”
World Stroke Day was established by the World Stroke Organization in 2006 to help spread public awareness of the world's high stroke risk and stroke prevalence. The theme of the 2014 World Stroke Day is women and stroke. Women have a higher stroke mortality rate than men. Six in ten stroke deaths occur in women, largely due to strokes occurring later in life in women, when strokes are more dangerous.
Biller is an internationally known expert on strokes(supposedly). He is professor and chair of the Department of Neurology of Loyola University Chicago Stritch School of Medicine.


0. There is no fast, easy and objective way to diagnose a stroke.
1. tPA may save your life but only has a 12% efficacy for full recovery.
2. Your neurologist doesn't have any concrete stroke protocols to save all the neurons that are dying in the first week.
3. Your neurologist or physiatrist doesn't have any clue about how to get you to full recovery. (Ask them exactly how to do it), you'll get excuses.
4. Only 10% get to full recovery.
5. No protocols to prevent your 33% chance of getting dementia post-stroke.
6. Nothing to alleviate your fatigue.
7. Nothing that will cure your spasticity.
8. Nothing on cognitive training unless you find this yourself.
9. No published stroke protocols.
10. No way to compare your stroke hospital results vs. other stroke hospitals.
Everything in stroke is a complete failure. 

Scorpion Venom Heat-Resistant Peptide (SVHRP) Enhances Neurogenesis and Neurite Outgrowth of Immature Neurons in Adult Mice by Up-Regulating Brain-Derived Neurotrophic Factor (BDNF)

This can join snake venom.

Intravenous Ancrod for Treatment of Acute Ischemic Stroke

Biting back - snake venom contains toxic clotting factors

 

Or tick spit

A tick’s spit leads to an entire lesson in blood clotting

Or bat saliva

vampire bat saliva

 


http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0109977#pone-0109977-g007


Tao Wang equal contributor,

    Shi-Wei Wang equal contributor,

    Yue Zhang,

    Xue-Fei Wu,

    Yan Peng,

    Zhen Cao,

    Bi-Ying Ge,

    Xi Wang,

    Qiong Wu,

    Jin-Tao Lin,

    Wan-Qin Zhang,

    Shao Li mail,

    Jie Zhao mail

    Published: October 09, 2014
    DOI: 10.1371/journal.pone.0109977

    Article
    About the Authors
    Metrics
    Comments
    Related Content

    Abstract
    Introduction
    Materials and Methods
    Results
    Discussion
    Author Contributions
    References

    Reader Comments (0)
    Figures

Abstract

Scorpion venom heat-resistant peptide (SVHRP) is a component purified from Buthus martensii Karsch scorpion venom. Although scorpions and their venom have been used in Traditional Chinese Medicine (TCM) to treat chronic neurological disorders, the underlying mechanisms of these treatments remain unknown. We applied SVHRP in vitro and in vivo to understand its effects on the neurogenesis and maturation of adult immature neurons and explore associated molecular mechanisms. SVHRP administration increased the number of 5-bromo-2’-dexoxyuridine (BrdU)-positive cells, BrdU- positive/neuron-specific nuclear protein (NeuN)-positive neurons, and polysialylated-neural cell adhesion molecule (PSA-NCAM)-positive immature neurons in the subventricular zone (SVZ) and subgranular zone (SGZ) of hippocampus. Furthermore immature neurons incubated with SVHRP-pretreated astrocyte-conditioned medium exhibited significantly increased neurite length compared with those incubated with normal astrocyte-conditioned medium. This neurotrophic effect was further confirmed in vivo by detecting an increased average single area and whole area of immature neurons in the SGZ, SVZ and olfactory bulb (OB) in the adult mouse brain. In contrast to normal astrocyte-conditioned medium, higher concentrations of brain-derived neurotrophic factor (BDNF) but not nerve growth factor (NGF) or glial cell line-derived neurotrophic factor (GDNF) was detected in the conditioned medium of SVHRP-pretreated astrocytes, and blocking BDNF using anti-BDNF antibodies eliminated these SVHRP-dependent neurotrophic effects. In SVHRP treated mouse brain, more glial fibrillary acidic protein (GFAP)-positive cells were detected. Furthermore, immunohistochemistry revealed increased numbers of GFAP/BDNF double-positive cells, which agrees with the observed changes in the culture system. This paper describes novel effects of scorpion venom-originated peptide on the stem cells and suggests the potential therapeutic values of SVHRP.