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

Saturday, August 31, 2013

Building a modern stroke system

I saw lots of articles esposing this. Chest-beating congratulatory thumping. This is actually a piece of shit, absolutely nothing that can be measured and nothing that says that tPA is a failure or even any mention of stopping the neuronal cascade of deathGawd the stupidity.
http://www.theheart.org/article/1575265.do?utm_medium=email&utm_source=20130831_ESC_EN&utm_campaign=newsletter

European Society of Cardiology kicked off its 5-day meeting

And with 32,000 attendees and all that supposed brainpower I bet they have no stroke survivor talking to them, telling them they know jackshit about where stroke research and rehab should be going. No planning/no strategy means absolutely no progress being made. That coming tsunami of strokes will roll right over them, killing them and us in the process.
http://spo.escardio.org/default.aspx?eevtid=60

Norfolk nurse’s warning after suffering stroke following bungee jump

That is one activity I never considered doing.
http://www.eveningnews24.co.uk/news/norfolk_nurse_s_warning_after_suffering_stroke_following_bungee_jump_1_2360690

Black Tea Linked with Reduced Risk of Heart Attack, Stroke and Tooth Decay

A news report from Austria that I'm sure your doctor is following.
http://austriantribune.com/informationen/132339-black-tea-linked-reduced-risk-heart-attack-stroke-and-tooth-decay

Folic Acid Supplements Cut Stroke Risk

Two separate news reports on this. Or go to your font of knowledge and ask your doctor what to do. They will be able to locate the actual research report and tell you what to do and where to go.
http://abcnews.go.com/Health/Healthday/story?id=4507384&page=1

http://www.newsfix.ca/2013/08/31/folic-acid-supplements-may-undercut-stroke-risk/

Friday, August 30, 2013

Stroke systems of care essential to reducing deaths, disabilities

And once again our stroke associations prove they are only press release orgs. You will notice nothing in here that is concrete and actionable. Not like my 30 actions in the immediate aftermath of my next stroke. Once again proving their incompentency. Nothing in here will prepare for the coming tsunami of stroke.
http://newsroom.heart.org/news/stroke-systems-of-care-essential-to-reducing-deaths-disabilities?preview=52bb
Statement Highlights:
  • The American Heart Association/American Stroke Association has identified several key elements needed for systems of care to effectively reduce stroke-related deaths and disability.
  • The systems should quickly and appropriately address patients’ needs from when stroke symptoms appear and EMS is called, during transport to and treatment in the hospital and through rehabilitation.
Embargoed for release at 3 p.m. CT/4 p.m. ET, Thursday, Aug. 29, 2013
DALLAS, Aug. 29, 2013 — Several key elements in systems of care can reduce stroke deaths and disabilities, according to a new American Heart Association/American Stroke Association policy statement published in its journal Stroke.
Stroke is the number four cause of death and a leading cause of adult disability in the United States. On average, every 4 minutes someone dies of a stroke.
The  policy statement addresses patients’ care from the time stroke symptoms are identified, to the emergency medical services’ (EMS) response, to the transport and treatment in the hospital and rehabilitation.
Recommendations include:
  • Develop public education programs to improve awareness of stroke symptoms and the need to call 9-1-1 to get to the hospital quickly for treatment.(But tPA only gives you a 30% better chance at a better recovery. Who is coming up with something better?)
  • Ensure EMS personnel can quickly assess stroke patients and get them to the hospital with appropriate care within 15-20 minutes.
  • Establish protocols to optimize the transfer of patients between hospitals offering different levels of care and within the different departments of a hospital.
  • Support the certification of stroke centers that follow treatment guidelines designed to improve patient care and outcomes. (Why? those guidelines need updating)
  • Use telemedicine, especially in rural areas, to ensure patients have 24/7 access to consultation and care.
The association also calls for patients to have access to post-stroke care, including rehabilitation and nursing services, regardless of their financial status or socio-economic background.
Authors of the statement also address issues related to adequate reimbursement for stroke treatment and care and the need for quality improvement and public reporting initiatives.
The American Heart Association/American Stroke Association has long supported and helped  develop stroke systems of care. Public awareness and patient resources include the F.A.S.T. campaign and the Together to End Stroke program. The association certifies stroke centers and provides many quality improvement tools for healthcare providers and resources to help people learn more about stroke hospitals in their communities.
Information on the statement authors and disclosures are on the manuscript.
For the latest heart and stroke news, follow @HeartNews on Twitter.
For stroke science, follow Stroke at @StrokeAHA_ASA.

Transgenic Overproduction of Omega-3 Polyunsaturated Fatty Acids Provides Neuroprotection and Enhances Endogenous Neurogenesis after Stroke

Who is going to take this and come up with translational stroke protocols for us?
Or are our stroke associations going to continue to sit on their asses?
http://www.ncbi.nlm.nih.gov/pubmed/23971733

Source

Department of Neurology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA. chenj2@upmc.edu.

Abstract

Strokes are devastating as there are no current therapies to prevent the long term neurological deficits that they cause. Soon after ischemic stroke, there is proliferation and differentiation of neural stem/progenitor cells as an important mechanism for neuronal restoration. However, endogenous neurogenesis by itself is insufficient for effective brain repair after stroke as most newborn neurons do not survive. One fascinating strategy for stroke treatment would thus be maintaining the survival and/or promoting the differentiation of endogenous neural stem/progenitor cells. Using transgenic (Tg) mice over-expressing the C. elegans fat-1 gene encoding an enzyme that converts endogenous omega-6 to omega-3 polyunsaturated fatty acids (n-3 PUFAs), we showed that fat-1 Tg mice with chronically elevated brain levels of n-3 PUFAs exhibited less brain damage and significantly improved long-term neurological performance compared to wild type littermates. Importantly, post-stroke neurogenesis occurred more robustly in fat-1 Tg mice after focal ischemia. This was manifested by enhanced neural stem cell proliferation/differentiation and increased migration of neuroblasts to the ischemic sites where neuroblasts matured into resident neurons. Moreover, these neurogenic effects were accompanied by significantly increased oligodendrogenesis. Our results suggest that n-3 PUFA supplementation is a potential neurogenic and oligodendrogenic treatment to naturally improve post-stroke brain repair and long-term functional recovery.

Statins may reduce MI stroke incidence in elderly with no history of CVD

But did they consider this?
higher cholesterol levels may predict longevity, rather than mortality, in the elderly. 

I'm sure your doctor can resolve the conundrum.
---------------------------------------------------------------------------------------------------------------
http://www.healio.com/cardiology/stroke/news/online/%7B356a1f47-6797-424c-a4f7-c9f7961d0cdf%7D/statins-may-reduce-mi-stroke-incidence-in-elderly-with-no-history-of-cvd
Results of a new meta-analysis that assessed statin use in elderly patients with no history of CVD indicate a reduced risk for MI and stroke, but no treatment effect on all-cause mortality, CV mortality or new cancer onset.
The meta-analysis included results from eight randomized, placebo-controlled trials of 24,674 participants (57.3% men; mean age, 73 years; mean follow-up, 3.5 years). All studies compared statins vs. placebo and reported outcomes of participants aged at least 65 years who had no history of CVD. Two studies focused on elderly individuals, while the other six had subgroups of elderly individuals. Outcomes of interest were all-cause mortality, CV mortality, MI, stroke and onset of new cancer.
MI occurred in 2.7% of participants assigned statins vs. 3.9% assigned placebo, for a 39.4% difference in risk (RR=0.606; 95% CI, 0.434-0.847). Stroke occurred in 2.1% of those assigned statins vs. 2.8% assigned placebo, for a 23.8% difference in risk (RR=0.762; 95% CI, 0.626-0.926), according to the study findings.
However, the analysis yielded little difference in risk for all-cause mortality (RR=0.941; 95% CI, 0.856-1.035), CV mortality (RR=0.907; 95% CI, 0.686-1.199) or risk for new onset of cancer (RR=0.989; 95% CI, 0.851-1.151) among participants assigned statins vs. those assigned placebo. The incidence of new cancer onset was 5.4% for both statin-treated and placebo-treated patients.
The researchers found no evidence of publication bias or evidence that effect modifiers such as sex, diabetes and hypertension affected the meta-analysis.
“The findings of the present meta-analysis provide evidence for treatment of subjects at high CVD risk and older than 65 years, and may be relevant for upgrading the level of recommendation for treatment in this age group in future guidelines,” Gianluigi Savarese, MD, of Federico II University in Naples, Italy, and colleagues concluded.

Parental Stroke Increases Stroke Risk in Children

But have they even correlated the same type of stroke to parent/child? I would have to tell my daughter not to do any type of twisting injury to the neck. Thats stupid, she just needs to make sure that she doesn't allow plaque buildup in arteries.
Maybe by;
1.Watermelon juice reverses hardening of the arteries
2.Statins Tame Plaque Inflammation
3 .Peptide Inhibitor of NF-κB Translocation Ameliorates Experimental Atherosclerosis
4. All About Monocyte Migrations
5. Targeting Arterial Plaque
 
http://www.tele-management.ca/2013/08/parental-stroke-increases-stroke-risk-in-children-2/
After heart disease and cancer, stroke is the third leading cause of death in the United States. In addition to modifiable risk factors such as high blood pressure, cigarette smoking, and obesity, non-modifiable risk factors such as increasing age, male gender, and previous history of stroke or heart attack contribute to the risk of stroke. Data from the Framingham Heart Study demonstrates that parental stroke before the age of 65 triples the risk of stroke among children.
Previous research has varied in its findings regarding the relationship between family history of stroke and stroke risk. Using data from the Framingham Heart Study, researchers from Boston University and their colleagues analyzed data on 3443 individuals with no history of stroke whose parents had a known stroke status by the age of 65. Among this study group, a total of 106 parental strokes were documented by the age of 65 and 128 strokes were documented among the offspring. Statistical analysis revealed that the risk of stroke was increased by as much as three times in individuals who had at least one parent with stroke by the age of 65.
While previous studies have been inconsistent in verifying the importance of family history of stroke as a risk factor for stroke, the current findings are based on long term in-person observation across multiple generations of family members. While further research is needed to identify and understand the genes responsible for stroke risk, it does seem that obtaining a family history is an important component of estimating an individual’s risk for stroke.

Galantamine Slashes Heart Attacks and Death

For your doctor to analyze and report back to you.
http://www.life-enhancement.com/magazine/article/2908-galantamine-slashes-heart-attacks-and-death
A new study has found that subjects taking the highest recommended doses of cholinesterase inhibitors (ChEIs)—including donepezil (at 10 mg/day), rivastigmine (at 6 mg/day), and galantamine (at 24 mg/day)—had significantly lower levels of myocardial infarction (MI, aka heart attack) or significantly reduced risk of death from any cause.1 The research was conducted at Karolinska University Hospital, Stockholm, Sweden where over 7000 subjects (mean age 79 years) from the Swedish Dementia Registry with the diagnoses of Alzheimer’s dementia or Alzheimer’s mixed dementia since 2007 were followed for a mean period of 503 days.
In the study, those who used ChEI, compared to those who did not, experienced:

  • 38% lower risk of heart attack
  • 26% lower risk of death from stroke and other cardiovascular diseases
  • 36% lower risk of death from any cause
More at link.

Thursday, August 29, 2013

Cure stroke with magic

A search term that found my blog. It was eighth in line. I'm hoping that these searches were not serious.
These two search results actually assume magic works.

A Magic Remedy from China Can Cure Stroke Paralysis 

A Magic Remedy for Treatment for Stroke Victims

 

These are using Appeal to tradition to try to prove their case.

(also known as argumentum ad antiquitatem, appeal to antiquity, or appeal to common practice) is a common fallacy in which a thesis is deemed correct on the basis that it correlates with some past or present tradition. The appeal takes the form of "this is right because we've always done it this way."

 

And why hasn't your doctor been using this magic? Conspiracy anyone? Stroke is needed because those 15 million strokes a year employ millions of people. The world economy might collapse without all this disability and death. 

 

NFL reaches concussion settlement

And after spending 765 million they could possibly prevent a lot of this from my 2 free ideas.
765 million dollars of stupidity.
http://www.usatoday.com/story/sports/nfl/2013/08/29/nfl-concussion-settlement-judge-anita-brody-tony-dorsett-jim-mcmahon-junior-seau/2727483/
Pretreatment like this;

Effect of fish oil supplementation in a rat model of multiple mild traumatic brain injuries

or interventions after the concussions.
Dietary Strategy to Repair Plasma Membrane After Brain Trauma Implications for Plasticity and Cognition
The NFL has enough money to employ as least one good researcher who could find and push these solutions.  But they seem to be just as naked as the medical emperors.

Stem-like Cells from Blood Show Promise for Stroke

Tested in rats, we'll need a great stroke association to push for human clinical trials, otherwise this will never get done.
http://ewireinformer.com/stem-like-cells-from-blood-show-promise-for-stroke/007

Intravenous Minocycline in Acute Stroke

I put this in my list of 31 things I was going to demand after my next stroke.
Notice the discrepancy between results and conclusion.

http://stroke.ahajournals.org/content/44/9/2493.abstract.html?etoc

A Randomized, Controlled Pilot Study and Meta-analysis

  1. David Blacker, FRACP
+ Author Affiliations
  1. From the Stroke Unit, Royal Perth Hospital, Perth, Australia (E.K., D.A.P., G.J.H., A.C.); Stroke Unit, Swan District Hospital, Perth, Australia (T.R.B.); and the Department of Radiology (J.v.H.) and Stroke Unit (D.B.), Sir Charles Gairdner Hospital, Perth, Australia.
  1. Correspondence to Edith Kohler, MD, Stroke Unit, Royal Perth Hospital, Perth, Western Australia, Australia. E-mail Edith_Kohler@hotmail.com

Abstract

Background and Purpose—Minocycline, in animal models and 2 small randomized controlled human trials, is a promising neuroprotective agent in acute stroke. We analyzed the efficacy and safety of intravenous minocycline in acute ischemic and hemorrhagic stroke.
Methods—A multicenter prospective randomized open-label blinded end point evaluation pilot study of minocycline 100 mg administered intravenously, commenced within 24 hours of onset of stroke, and continued 12 hourly for a total of 5 doses, versus no minocycline. All participants received routine stroke care. Primary end point was survival free of handicap (modified Rankin Scale, ≤2) at day 90.
Results—Ninety-five participants were randomized; 47 to minocycline and 48 to no minocycline. In the intention-to-treat population, 29 of 47 (65.9%) allocated minocycline survived free of handicap compared with 33 of 48 (70.2%) allocated no minocycline (rate ratio, 0.94; 95% confidence interval, 0.71–1.25 and odds ratio, 0.73; 95% CI, 0.31–1.71). A meta-analysis of the 3 human trials suggests minocycline may increase the odds of handicap-free survival by 3-fold (odds ratio, 2.99; 95% CI, 1.74–5.16) but there was substantial heterogeneity among the trials.
Conclusions—In this pilot study of a small sample of acute stroke patients, intravenous minocycline was safe but not efficacious. The study was not powered to identify reliably or exclude a modest but clinically important treatment effect of minocycline. Larger trials would improve the precision of the estimates of any treatment effect of minocycline.
Clinical Trial Registration—URL: http://www.anzctr.org.au. Unique identifier: ACTRN12612000237886.

In-Hospital Risk Prediction for Post-stroke Depression

But why do we care about predicting post-stroke depression? Do we not have consensus that all survivors should get anti-depression drugs because they lead to a better recovery?
Antidepressants may help people recover from stroke even if they are not depressed
"Taken together, the available data make a strong case for the prophylactic use and effectiveness of antidepressants post stroke," the researchers said.

Does no one think at all? Is everyone in the stroke world stupid?
http://stroke.ahajournals.org/content/44/9/2441.abstract.html?etoc


Development and Validation of the Post-stroke Depression Prediction Scale

  1. Marieke J. Schuurmans, RN, PhD
+ Author Affiliations
  1. From the Department of Rehabilitation, Nursing Science and Sports, Rudolf Magnus Institute of Neuroscience, University Medical Centre Utrecht, Utrecht, The Netherlands (J.M.d.M.-v.G., T.B.H., E.L., M.J.S.); Faculty of Healthcare, University of Applied Sciences Utrecht, Utrecht, The Netherlands (R.G.A.E.); and Julius Center for Health Sciences and Primary Care, Utrecht University, Utrecht, The Netherlands (D.E.G.).
  1. Correspondence to Janneke M. de Man-van Ginkel, RN, PhD, Division Neurosciences, UMC Utrecht, W01.121, Heidelberglaan 100, 3584 XC Utrecht, The Netherlands. E-mail J.M.deMan@umcutrecht.nl

Abstract

Background and Purpose—The timely detection of post-stroke depression is complicated by a decreasing length of hospital stay. Therefore, the Post-stroke Depression Prediction Scale was developed and validated. The Post-stroke Depression Prediction Scale is a clinical prediction model for the early identification of stroke patients at increased risk for post-stroke depression.
Methods—The study included 410 consecutive stroke patients who were able to communicate adequately. Predictors were collected within the first week after stroke. Between 6 to 8 weeks after stroke, major depressive disorder was diagnosed using the Composite International Diagnostic Interview. Multivariable logistic regression models were fitted. A bootstrap-backward selection process resulted in a reduced model. Performance of the model was expressed by discrimination, calibration, and accuracy.
Results—The model included a medical history of depression or other psychiatric disorders, hypertension, angina pectoris, and the Barthel Index item dressing. The model had acceptable discrimination, based on an area under the receiver operating characteristic curve of 0.78 (0.72–0.85), and calibration (P value of the U-statistic, 0.96). Transforming the model to an easy-to-use risk-assessment table, the lowest risk category (sum score, <−10) showed a 2% risk of depression, which increased to 82% in the highest category (sum score, >21).
Conclusions—The clinical prediction model enables clinicians to estimate the degree of the depression risk for an individual patient within the first week after stroke.
Key Words:

Systolic Blood Pressure During Acute Stroke Is Associated With Functional Status and Long-term Mortality in the Elderly

Your doctor needs to reconcile the differences between this report and these four other ones.
1. Detrimental effect of blood pressure reduction in the first 24 hours of acute stroke onset
 2. Early Intensive Blood-Pressure Lowering Improves Recovery in Patients With Acute Intracerebral Haemorrhage
 3. Detrimental effect of blood pressure reduction in the first 24 hours of acute stroke onset
 4. External Counterpulsation Augments Blood Pressure and Cerebral Flow Velocities in Ischemic Stroke Patients With Cerebral Intracranial Large Artery Occlusive Disease

 You better start asking now, you don't want to get to the emergency room and find out the doctors don't know anything about treating blood pressuse during your stroke and the immediate aftermath. 
Otherwise you are just letting your doctor kill your neurons by omission. The Joint Commission should be doing this if they were any good.


http://stroke.ahajournals.org/content/44/9/2434.abstract.html?etoc

change the world of stroke rehab

My response to an email I got.

I kinda feel like a prophet crying in the wilderness and the people that need to hear me are in the cities with their ears covered over. If every survivor created a blog we would have 15 million plus blogs and that presence would overwhelm the medical world. One would think stroke associations would be for us but they aren't, they are meant for doctors and survivors are just their means of getting money. We really need for every survivor to challenge their medical staff about why they know so little about stroke recovery. Sorry about ranting but there is nothing in the stroke world that can't be improved  vastly. And that's what this blog is about - to change the world of stroke rehab.

This is an almost impossible task, but I'm having fun tweaking the noses of the medical world.

G-CSF Fails to Benefit Acute Ischemic Stroke Patients

I wrote about this in Feb. 2012, why was a new trial needed?
Neutropenia Drug Falls Flat for Acute Stroke

http://www.tctmd.com/show.aspx?id=119920 
Key Points:
  • At 90 days, mortality similar with vs. without G-CSF in acute ischemic stroke patients
  • Modified Rankin score, NIHSS score, infarct volume also similar between groups
  • Study fails to translate preclinical promise to clinical benefit, authors say
 Table at link.

Mouth implant to save stroke victims from brain damage

I missed this when it came out three years ago -Bad boy Dean, no dessert for you tonight. Have any of your doctors followed up on this?
http://www.dailymail.co.uk/health/article-1330020/Mouth-implant-save-stroke-victims-brain-damage.html
A tiny device implanted in the roof of the mouth of stroke ­victims could boost their chances of making a full recovery.
The implant, slightly bigger than a grain of rice, works by stimulating nerves in the skull responsible for making blood vessels dilate, or widen.
As the vessels expand, they allow more blood to flow to the damaged part of the brain, bypassing the clot that caused the stroke. This stops the brain from being deprived of oxygen for so long that it is left permanently damaged.
Initial tests suggest the new treatment might be able to prevent brain damage if given up to 24 hours after a stroke has occurred. (Current treatments involve injecting clot-busting drugs into the brain, but are fully effective only if given within three hours of a stroke.)
The implant takes just 30 minutes to put in and can remain in the mouth for a few hours or several weeks.
The new device, developed by Israeli firm BrainsGate, could transform treatment of ischaemic strokes.


Rest at link.

Nike Fuelband

This might be better than the pedometers most of us have used. But I'm not going to spend $149 just to track my physical activity. I already know I'm not doing enough. I would be willing to bet you would have to wear it on your good arm to have any hope of correct movement activity.
http://store.nike.com/us/en_us/pd/fuelband/pid-669575/pgid-670534
The Nike+ FuelBand is an activity tracker that is worn on the wrist. As part of the Quantified Self movement, the Fuelband allows its wearers to track their physical activity, steps taken daily, and amount of calories burned

Wednesday, August 28, 2013

Moderate Hypothermia Inhibits Brain Inflammation and Attenuates Stroke-Induced Immunodepression in Rats

But what about this research that says that
An Analysis of 146 Contradicted Medical Practices including hypothermia
And it also may not be accounting for
the rodent model in inflammation is not the same as humans.
But other than those flaws its interesting. 
Ask your doctor to analyze all this and give their considered opinion - 5 pages double spaced, in one week.
----------------------------------------------------------------------------------

http://onlinelibrary.wiley.com/doi/10.1111/cns.12160/abstract;jsessionid=07153B593F41C32F76FEDD98F1C781A6.d03t04?systemMessage=Wiley+Online+Library+will+be+disrupted+on+31+August+from+10%3A00-12%3A00+BST+%2805%3A00-07%3A00+EDT%29+for+essential+maintenance&userIsAuthenticated=false&deniedAccessCustomisedMessage=

Keywords:

  • Focal cerebral ischemia;
  • Hypothermia;
  • Immunodepression;
  • Inflammation;
  • Leukocytes

Summary

Aims

Stroke causes both brain inflammation and immunodepression. Mild-to-moderate hypothermia is known to attenuate brain inflammation, but its role in stroke-induced immunodepression (SIID) of the peripheral immune system remains unknown. This study investigated the effects in rats of moderate intra-ischemic hypothermia on SIID and brain inflammation.

Methods

Stroke was induced in rats by permanent distal middle cerebral artery occlusion combined with transient bilateral common carotid artery occlusion, while body temperature was reduced to 30°C. Real-time PCR, flow cytometry, in vitro T-cell proliferation assays, in vivo delayed-type hypersensitivity (DTH) reaction and confocal microscopy were used to study SIID and brain inflammation.

Results

Brief intra-ischemic hypothermia helped maintain certain leukocytes in the peripheral blood and spleen and enhanced T-cell proliferation in vitro and delayed-type hypersensitivity in vivo, suggesting that hypothermia reduces SIID. In contrast, in the brain, brief intra-Ischemic hypothermia inhibited mRNA expression of anti-inflammatory cytokine IL-10 and proinflammatory mediators INF-γ, TNF-α, IL-2, IL-1β and MIP-2. Brief intra-Ischemic hypothermia also attenuated the infiltration of lymphocytes, neutrophils (MPO+ cells) and macrophages (CD68+ cells) into the ischemic brain, suggesting that hypothermia inhibited brain inflammation.

Conclusions

Brief intra-ischemic hypothermia attenuated SIID and protected against acute brain inflammation.

Migraine and structural changes in the brain

See what your doctor can help you with this. They can afford the $571.20 annual cost for this journal.
http://www.neurology.org/content/early/2013/08/28/WNL.0b013e3182a6cb32.abstract?sid=ec43234d-2f87-4dcd-befb-0adc9d400f17

A systematic review and meta-analysis

  1. Messoud Ashina, MD, PhD
  1. Correspondence to Dr. M. Ashina: ashina@dadlnet.dk
  1. Neurology 10.1212/WNL.0b013e3182a6cb32
  1. Also available:
  2. Data Supplement

Abstract

Objective: To evaluate the association between migraine without aura (MO) and migraine with aura (MA) and 3 types of structural brain abnormalities detected by MRI: white matter abnormalities (WMAs), infarct-like lesions (ILLs), and volumetric changes in gray and white matter (GM, WM) regions.
Methods: PubMed as well as the reference lists of identified studies and reviews were used to identify potentially eligible studies through January 2013. Candidate studies were reviewed and eligible studies were abstracted. Pooled odds ratios (OR) and 95% confidence intervals (CI) were calculated for WMAs and ILLs.
Results: Six population-based and 13 clinic-based studies were identified. The studies suggested that structural brain changes, including WMAs, silent ILLs, and volumetric changes in GM and WM regions, were more common in migraineurs than in control groups. The results were strongest for MA. The meta-analysis of WMAs showed an association for MA (OR 1.68; 95% CI 1.07–2.65; p = 0.03) but not for MO (OR 1.34; 95% CI 0.96–1.87; p = 0.08). The association of ILLs was greater for MA (OR 1.44; 95% CI 1.02–2.03; p = 0.04) than for MO, but no association was found for MA (p = 0.52) and MO (p = 0.08) compared to controls.
Conclusion: These data suggest that migraine may be a risk factor for structural changes in the brain. Additional longitudinal studies are needed to determine the differential influence of migraine without and with aura, to better characterize the effects of attack frequency, and to assess longitudinal changes in brain structure and function.

Should everyone over 65 take a statin?

Well how many people do they want to make stupid?
Or all the other side effects;
Myopathy.
diabetes risk.
Lung Damage in Smokers
higher cholesterol levels may predict longevity, rather than mortality, in the elderly.
Do Statins Make It Tough to Exercise?
How they can cause sexual dysfunction 
50% likelier to develop age-related cataracts
increased risk of intracerebral hemorrhage (ICH)
statins produce mild muscle injury
risk of musculoskeletal injury
This is all just to keep you informed, I'm sure your doctor can rattle all these off for you and explain exactly why you need statins. Don't listen to anything I have to say, I just point out stuff for your doctor to explain. That's why they are paid the big bucks.

Read it all at the link.
http://medicalxpress.com/news/2013-08-statin.html
This paragraph is one of the main reasons for doing it.
In these trials, which compared statins and placebos in patients followed for an average of three and a half years, statins reduced the risk of heart attack by about 29 percent and stroke by nearly 24 percent, the researchers found.

But why not a marijuana bud a day for a 50% stroke risk reduction?

Scientists grow replicas of 'mini human brains' from stem cells

I couldn't figure out where the actual research was published so you'll have to read this at FoxNews.
http://www.foxnews.com/health/2013/08/28/scientists-grow-mini-human-brains-from-stem-cells/?

Thinking with your gonads: testosterone and cognition

A question for your doctor. Is testosterone deprivation the cause of your memory and cognition problems? Because you lowered your cholesterol?
http://www.sciencedirect.com/science/article/pii/S1364661305003578
  • Department of Behavioral Neuroscience, Oregon Health & Science University CR131, 3181 SW Sam Jackson Park Road, Portland, OR 97239, USA

Sex hormones play a crucial role during brain development, but do they modulate or maintain cognition throughout life? Despite several million prescriptions annually for testosterone supplementation, we do not really know the answer. Here I review recent evidence that testosterone alters neural activity essential for learning and memory, and plays an important role as a neuroprotective agent in aging. In particular, testosterone deprivation is associated with poor memory in men and replacement can enhance memory and spatial cognition. However, there is little evidence that testosterone selectively affects only those cognitive domains where sex differences in performance have been found. There are also gaps in our knowledge surrounding the individual cognitive processes altered by testosterone, their neural basis, and the degree to which testosterone affects cognitive performance in women.
 This figure from the abstract bings up even more questions for your doctor. How does cholesterol lowering drugs affect your testosterone levels and cognition?

Full-size image (19 K)Figure 2. Testosterone is a hormone that is metabolized from cholesterol. Thus, its production can be influenced at several metabolic steps. In addition, it can be further metabolized to form estradiol or other androgen molecules. When testosterone affects cognition, it is not known in most instances whether this is as an androgen or via its conversion to estradiol.

Football - Heads Up: Good play or good ploy?

Safety concerns about tackling in youth football. Notice they say nothing about pretreatment like this;
Effect of fish oil supplementation in a rat model of multiple mild traumatic brain injuries

or interventions after the concussions.
Dietary Strategy to Repair Plasma Membrane After Brain Trauma Implications for Plasticity and Cognition
The NFL has enough money to employ as least one good researcher who could find and push these solutions.  But they seem to be just as naked as the medical emperors.

KINESTHETIC IMAGERY TRAINING OF FORCEFUL MUSCLE CONTRACTIONS INCREASES BRAIN SIGNAL AND MUSCLE STRENGTH

And your great stroke association would followup this with research on survivors. Otherwise this will never get done. What do you expect? You're screwed, nobody cares except for other survivors who hope that your recovery will miraculously extend to them thru quantum entanglement  or maybe worm-holes.
http://scholar.google.com/scholar_url?hl=en&q=http://www.frontiersin.org/Human_Neuroscience/10.3389/fnhum.2013.00561/abstract&sa=X&scisig=AAGBfm2LaQ8Pj1AZ-JibABYR8t_09-wbMQ&oi=scholaralrt

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  • 1Health and Kinesiology, University of Texas at San Antonio, USA
  • 2Physical Medicine and Rehabilitation, Cleveland Clinic, USA
  • 3Biomedical Engineering, Cleveland Clinic, USA
  • 4 Kessler Foundation Research Center, USA
The purpose of this study was to compare the effect of training using internal imagery (IMI; also known as kinesthetic imagery or first person imagery) with that of external imagery (EMI; also known as third-person visual imagery) of strong muscle contractions on voluntary muscle strengthening. Eighteen young, healthy subjects were randomly assigned to one of three groups (6 in each group): internal motor imagery (IMI), external motor imagery (EMI), or a no-practice control (CTRL) group. Training lasted for 6 weeks (~15 min/day, 5 days/week). The participants’ right arm elbow-flexion strength, muscle electrical activity and movement-related cortical potential (MRCP) were evaluated before and after training. Only the IMI group showed significant strength gained (10.8%) while the EMI (4.8%) and CTRL (-3.3%) groups did not. Only the IMI group showed a significant elevation in MRCP on scalp locations over both the primary motor (M1) and supplementary motor cortices (EMI group over M1 only) and this increase was significantly greater than that of EMI and CTRL groups. These results suggest that training by IMI of forceful muscle contractions was effective in improving voluntary muscle strength without physical exercise. We suggest that the IMI training likely strengthened brain-to-muscle (BTM) command that may have improved motor unit recruitment and activation, and led to greater muscle output. Training by internal motor imagery of forceful muscle contractions may change the activity level of cortical motor control network, which may translate into greater descending command to the target muscle and increase its strength.

Tuesday, August 27, 2013

More Stroke Patients Now Get Clot-Busting Drug

Finally some important info about tPA in this report.
http://wrkf.org/post/more-stroke-patients-now-get-clot-busting-drug
The selected info;
"That's very encouraging," study author Dr. Deepak Bhatt tells Shots. "That's a very large increase. But 23 percent of eligible patients still aren't getting it."
Alteplase treatment doesn't guarantee a good outcome. But studies have shown that 30 percent of stroke patients who get it have less long-term disability(I obviously fell into the 70%), and some patients have remarkable recoveries. Twelve percent recover with little or no disability.

This is still incredibly appalling, whomever is still only pushing tPA should be fired. Only baseball players can get by with a 30% success rate, and no one should stay employed at 12%.  Fire them all, stroke survivors would do  much better at creating and executing a strategy for making stroke recovery better.

Why Animal Experimentation Doesn't Work -- Reason 2: Animals Don't Get Human Diseases

This neurologist lists 3 strikes as to why stroke testing in animals doesn't work. She missed the most important strike.
The rodent model in inflammation is not the same as humans.
there have been more than 1,000 drugs (So what are they?)aimed at preventing brain damage that have failed to work in people, even though they worked well in mice or rats, said study researcher Dr. Michael Tymianski, of the Toronto Western Hospital Research Institute in Canada.
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Reason 1 is here; 
Why Animal Experimentation Doesn't Work -- Reason 1: Stressed Animals Yield Poor Data
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Reason 2 is here;
Why Animal Experimentation Doesn't Work -- Reason 2: Animals Don't Get Human Diseases
Selected paragraphs are here:
Let's take a look at stroke experiments in animals to examine how they strike out. In humans, stroke is usually caused by the gradual narrowing of a blood vessel to the brain by atherosclerosis or by a blood clot that developed in another part of the body. Animals in labs don't naturally get strokes. Experimenters artificially induce strokes by methods such as clamping off major blood vessels in animals' brains or artificially inserting clots into their vessels. Here are the problems with this:


Strike 1: Artificially inducing stroke in animals does not recreate the complex physiology that causes the natural disease in humans, which may develop over decades.
Diseases are diseases in context. In humans, stroke is usually linked to pre-disposing conditions such atherosclerosis, high blood pressure, and diabetes.


Strike 2: Animal stroke models don't usually include the underlying conditions, which contribute to human stroke.
Experimenters try to recreate the underlying human conditions such as diabetes in animals. However, these underlying conditions are usually also artificially induced in animals, and as we saw with diabetes, are often wrong anyway.
Strike 3: Artificially inducing in animals the underlying conditions that lead to human stroke does not replicate the processes that occur in humans.
Recognition of each difference between animal models and human diseases leads to renewed efforts to eliminate these differences. But in trying to recreate the complex physiology behind the human diseases, experimenters try to reproduce the complex physiology of the underlying conditions, which are just as difficult to accomplish. Thus animal experimenters are continuously going around in circles.
Stroke is probably one of the easiest human diseases to try to recreate in animals. Yet, over 150 stroke drugs found effective in animal stroke models failed in humans (1).
1. Macleod M. What can systematic review and meta-analysis tell us about the experimental data supporting stroke drug development? Int J Neuroprot Neuroregener 2005; 1: 201

Systemic administration of exosomes released from mesenchymal stromal cells promote functional recovery and neurovascular plasticity after stroke in rats

Whom is going to take this and create a human research trial? ASA, NSA? Never, we need our great stroke association.
http://www.ncbi.nlm.nih.gov/pubmed/23963371

Source

Department of Neurology, Henry Ford Health Sciences Center, Henry Ford Hospital, Detroit, Michigan, USA.

Abstract

Here, for the first time, we test a novel hypothesis that systemic treatment of stroke with exosomes derived from multipotent mesenchymal stromal cells (MSCs) promote neurovascular remodeling and functional recovery after stroke in rats. Adult male Wistar rats were subjected to 2 hours of middle cerebral artery occlusion (MCAo) followed by tail vein injection of 100 μg protein from MSC exosome precipitates or an equal volume of vehicle phosphate-buffered saline (PBS) (n=6/group) 24 hours later. Animals were killed at 28 days after stroke and histopathology and immunohistochemistry were employed to identify neurite remodeling, neurogenesis, and angiogenesis. Systemic administration of MSC-generated exosomes significantly improved functional recovery in stroke rats compared with PBS-treated controls. Axonal density and synaptophysin-positive areas were significantly increased along the ischemic boundary zone of the cortex and striatum in MCAo rats treated with exosomes compared with PBS control. Exosome treatment significantly increased the number of newly formed doublecortin (a marker of neuroblasts) and von Willebrand factor (a marker of endothelial cells) cells. Our results suggest that intravenous administration of cell-free MSC-generated exosomes post stroke improves functional recovery and enhances neurite remodeling, neurogenesis, and angiogenesis and represents a novel treatment for stroke.Journal of Cerebral Blood Flow & Metabolism advance online publication, 21 August 2013; doi:10.1038/jcbfm.2013.152.

Transplanting stem cells with "buddies" improves their chance of survival

From Stem Cells Freak. Are our researchers using this to keep our neurons alive? As compared to this possibility?
http://www.oc1dean.blogspot.com/2013/08/hydrogel-matrix-to-support-stem-cell.html

The new one here;
http://www.stemcellsfreak.com/2013/08/transplanting-stem-cells-with-buddies.html

Triple dissociation of attention networks in stroke according to lesion location

Your doctor can come up with some protocols for this. ASK  I know my doctor did nothing about this. My attention was so bad I once fell asleep listening to my speech therapist.
http://www.neurology.org/content/81/9/812.abstract?sid=7b7456af-c9a4-4426-b8f6-4cae6e552b3d
  1. Paul Bentley, MRCP, PhD
  1. Correspondence to Dr. Bentley: p.bentley@imperial.ac.uk
  1. Neurology vol. 81 no. 9 812-820

Abstract

Objective: To determine whether behavioral dissociations and interactions occur between the attentional functions—alerting, orienting, and conflict resolution—depending upon stroke location and to determine the approximate proportion of patients who can be classified into 1 of these 3 anatomical networks.
Methods: We recruited 110 anatomically unselected acute stroke patients and 62 age-matched controls. Subjects underwent the attention network test (ANT), which provides a measure of each attention type. Their performance was related to lesion anatomy on MRI using a voxel-lesion mapping approach.
Results: Patients as a whole performed poorer than controls, but there were no group differences in the size of attentional effects. Specific deficits in 1 of the 3 ANT-tested functions were found in the following lesion locations: alerting deficiency with bilateral anteromedial thalamus and upper brainstem (17% of patients); orienting impairment with right pulvinar and right temporoparietal cortex (15%); conflict resolution with bilateral prefrontal and premotor areas (23%). Lesions to right frontoparietal regions also modified interactions among the 3 types of attention.
Conclusions: More than half of all stroke patients can be expected to have a lesion location classifiable into 1 of the 3 principal attention networks. Our results have potential implications for therapy personalization in focal brain diseases including stroke.

Relationship Between Occurrence of Surgical Complications and Hospital Finances

We can probably make the same assumption for stroke patients. There is no incentive to reduce stroke disability during the neuronal cascade of death because that would reduce the need for all those billable hours for speech, OT, PT and the many neurologist consults that are worthless. Fee for service will never lead to innovation. Fee for results might do that, at least it would be more likely to be beneficial to patients.
Abstract here;
 http://jama.jamanetwork.com/article.aspx?articleid=1679400
Dr. John M discussing it in a blog post about his speciality, Atrial fibrulation.

New post up on theHeart.org: Fee-for-service, AF treatment and the untangling of knots…

Monday, August 26, 2013

What is your doctor doing the first week you are in the hospital for your stroke?

This is a very serious question. If they are doing nothing then your doctor is a problem you need to solve. Demand to know what s/he is going to do about the neuronal cascade of death. Its from Jan. 2009 so that will tell you a lot about their incompetence.  I would suggest telling them they will not get paid unless they get off their ass and do something positive.
My suggestions with references are here;
What I am going to insist I get after my next stroke

Then ask your doctor how many neurons they are killing; Calculations are provided in this post.

How many neurons is your doctor responsible for killing/not saving?
Sounds like a class action suit that your neurons would have a good chance of winning if they were alive, but they were killed to make sure they couldn't testify in the RICO case.

But since I am not medically trained I should not be listened too and should never point out the nakedness of the medical emperor.


Sorry about that, I was feeling especially ranty today.
Yes, I am still outraged.

Hydrogel Matrix to Support Stem Cell Survival After Brain Transplantation in Stroke

I just focused on the brain transplantation in the title, but its about saving injected stem cells into the brain. What does your doctor think of this?
Are they doing any thinking at all?
http://nnr.sagepub.com/content/24/7/636.short
  1. Jin Zhong, PhD
    1. David Geffen School of Medicine at UCLA, Los Angeles, CA, USA
  1. Albert Chan, MD
    1. David Geffen School of Medicine at UCLA, Los Angeles, CA, USA
  1. Leeron Morad
    1. David Geffen School of Medicine at UCLA, Los Angeles, CA, USA
  1. Harley I. Kornblum, MD, PhD
    1. David Geffen School of Medicine at UCLA, Los Angeles, CA, USA
  1. Guoping Fan, PhD
    1. David Geffen School of Medicine at UCLA, Los Angeles, CA, USA
  1. S. Thomas Carmichael, MD, PhD
    1. David Geffen School of Medicine at UCLA, Los Angeles, CA, USA, scarmichael@mednet.ucla.edu

Abstract

Stroke is a leading cause of adult disability. Stem/progenitor cell transplantation improves recovery after stroke in rodent models. These studies have 2 main limitations to clinical translation. First, most of the cells in stem/progenitor transplants die after brain transplantation. Second, intraparenchymal approaches target transplants to normal brain adjacent to the stroke, which is the site of the most extensive natural recovery in humans. Transplantation may damage this tissue. The stroke cavity provides an ideal target for transplantation because it is a compartmentalized region of necrosis, can accept a high volume transplant without tissue damage, and lies directly adjacent to the most plastic brain area in stroke. However, direct transplantation into the stroke cavity has caused massive death in the transplant. To overcome these limitations, the authors tested stem/progenitor transplants within a specific biopolymer hydrogel matrix to create a favorable environment for transplantation into the infarct cavity after stroke, and they tested this in comparison to stem cell injection without hydrogel support. A biopolymer hydrogel composed of cross-linked hyaluronan and heparin sulfate significantly promoted the survival of 2 different neural progenitor cell lines in vitro in conditions of stress and in vivo into the infarct cavity. Quantitative analysis of the transplant and surrounding tissue indicates diminished inflammatory infiltration of the graft with the hydrogel transplant. This result indicates that altering the local environment in stem cell transplantation enhances survival and diminishes cell stress. Stem cell transplantation into the infarct cavity within a pro-survival hydrogel matrix may provide a translational therapy for stroke recovery.