The Honor Roll of Best Hospitals 2014-15

If we had anything approaching a great stroke association these hospitals would also be ranked on stroke statistics; 30-day deaths, 100% recovery, tPA complete success rate, accurate stroke diagnosis upon first entry to the system. But since we have crap for stroke associations each individual will need to call up their local hospitals and do all this analysis and comparison work themselves. Good luck and stop swearing at me for pointing out how fucking badly our stroke associations and stroke hospitals are run.
https://www.yahoo.com/health/the-honor-roll-of-best-hospitals-2014-15-91772859252.html
The 2014-15 Honor Roll: 

17. Barnes-Jewish Hospital/Washington University

Location: St. Louis

Honor Roll Points: 9

Highest rankings: Pulmonology (#9), Nephrology (#11), Neurology & Neurosurgery (#11), Urology (#11), Ophthalmology (#12).

16. Mount Sinai Hospital

Location: New York

Honor Roll Points: 10

Highest rankings: Geriatrics (#2); Gastroenterology & GI Surgery (#9); Cardiology & Heart Surgery (#10); Ear, Nose & Throat (#10).


15. NYU Langone Medical Center

Location: New York

Honor Roll Points: 10

Highest rankings: Orthopedics (#4), Rheumatology (#6), Geriatrics (#8), Neurology & Neurosurgery (#8).

14. Duke University Hospital

Location: Durham, North Carolina

Honor Roll Points: 11

Highest rankings: Cardiology & Heart Surgery (#4), Pulmonology (#5), Ophthalmology (#6).

12. (tie) UPMC-University of Pittsburgh Medical Center

Location: Pittsburgh

Honor Roll Points: 11

Highest rankings: Ear, Nose & Throat (#7); Gastroenterology & GI Surgery (#7); Rheumatology (#9).

12. (tie) Cedars-Sinai Medical Center

Location: Los Angeles

Honor Roll Points: 11

Highest rankings: Gastroenterology & GI Surgery (#6), Orthopedics (#7), Cardiology & Heart Surgery (#8).

11. University of Washington Medical Center

Location: Seattle

Honor Roll Points: 12

Highest rankings: Rehabilitation (#4), Cancer (#6), Diabetes & Endocrinology (#10).

10. Northwestern Memorial Hospital

Location: Chicago

Honor Roll Points: 13

Highest rankings: Diabetes & Endocrinology (#8), Urology (#9), Neurology & Neurosurgery (#10).

9. Brigham and Women’s Hospital

Location: Boston

Honor Roll Points: 15

Highest rankings: Gynecology (#2), Cancer (#4), Cardiology & Heart Surgery (#5), Nephrology (#5), Rheumatology (#5).

8. UCSF Medical Center

Location: San Francisco

Honor Roll Points: 17

Highest rankings: Nephrology (#4), Diabetes & Endocrinology (#5), Neurology & Neurosurgery (#5).

7. Hospitals of the University of Pennsylvania-Penn Presbyterian
Location: Philadelphia

Honor Roll Points: 19

Highest rankings: Ear, Nose & Throat (#3); Cardiology & Heart Surgery (#7); Pulmonology (#7).


6. New York-Presbyterian University Hospital of Columbia and Cornell

Location: New York

Honor Roll Points: 22

Highest rankings: Psychiatry (#2), Neurology & Neurosurgery (#2), Cardiology & Heart Surgery (#3), Rheumatology (#3), Nephrology (#3).

5. UCLA Medical Center

Location: Los Angeles

Honor Roll Points: 23

Highest rankings: Geriatrics (#3), Urology (#4), Gastroenterology & GI Surgery (#5), Ophthalmology (#5).

4. Cleveland Clinic

Location: Cleveland

Honor Roll Points: 26

Highest rankings: Cardiology & Heart Surgery (#1), Urology (#1), Diabetes & Endocrinology (#2), Gastroenterology & GI Surgery (#2), Nephrology (#2), Rheumatology (#2).

3. Johns Hopkins Hospital

Location: Baltimore

Honor Roll Points: 26

Highest rankings: Rheumatology (#1); Ear, Nose & Throat (#2); Neurology & Neurosurgery (#3), Urology (#3); Ophthalmology (#3); Psychiatry (#3).

2. Massachusetts General Hospital

Location: Boston

Honor Roll Points: 28

Highest rankings: Psychiatry (#1), Diabetes & Endocrinology (#3), Gastroenterology & GI Surgery (#3).

1. Mayo Clinic

Location: Rochester, Minnesota

Honor Roll Points: 29

Highest rankings: Diabetes & Endocrinology (#1); Ear, Nose & Throat (#1); Gastroenterology & GI Surgery (#1); Geriatrics (#1); Gynecology (#1); Nephrology (#1); Neurology & Neurosurgery (#1); Pulmonology (#1).

Footprints to Cognitive Decline and Alzheimer’s Are Seen in Gait

I guess I'll have to first get my walking ability fairly normal  so my doctors can look at my gait deterioration when it comes time to evaluate my cognitive state. Does your doctor even know about your 33% dementia chance post-stroke from an Australian study? 
I will however prevent my dementia by these totally unapproved ways.
Dementia prevention 19 ways

http://www.nytimes.com/2012/07/17/health/research/signs-of-cognitive-decline-and-alzheimers-are-seen-in-gait.html

Five studies presented at the Alzheimer’s Association International Conference in Vancouver this month provide striking evidence that when a person’s walk gets slower or becomes more variable or less controlled, his cognitive function is also suffering.

Thinking skills like memory, planning activities or processing information decline almost in parallel with the ability to walk fluidly, these studies show.

In other words, the more trouble people have walking, the more trouble they have thinking.

Researchers Testing Possible Benefits of Brain Stimulation in Stroke Rehab

I couldn't participate in one of these at the University of Minnesota because it required some volitional extension of the fingers. And since my motor control area for the fingers is dead this type of therapy is useless for me.  Try it you may like it.
http://healthnews.uc.edu/news/?/24831/

Researchers on the University of Cincinnati medical campus are testing the possible benefits of brain stimulation on hand and arm function for stroke recovery patients.

The clinical trial, known as NICHE (for Navigated Inhibitory rTMS to Contralesional Hemisphere), is recruiting participants who have had a stroke in the past year. It involves a combination of occupational therapy and a method of non-invasive brain stimulation called transcranial magnetic stimulation (TMS). (rTMS is repetitive transcranial magnetic stimulation.)

UC is one of 12 sites for the study, all in the United States. Principal investigators for the UC site are Kari Dunning, PT, PhD, an associate professor and epidemiologist in the College of Allied Health’s Department of Rehabilitation Sciences and director of the Neural Excitability, Therapeutics and Recovery (NET Recovery) lab, and Brett Kissela, MD, MS, Albert Barnes Voorheis Professor and Chair of Neurology and Rehabilitation Medicine in the College of Medicine and a member of the UC Neuroscience Institute.

"There is evidence that people who have sustained a stroke can improve arm movement following stimulation to the brain using TMS,” says Dunning. "Our aim is to test this approach and quantify the results.”

Dunning explains that TMS can reduce or increase brain activity. By using it to reduce brain activity on the uninjured side of the brain, she says, the injured side is forced to work harder and might have a better chance of recovering.

The study will use a navigated brain stimulation device manufactured by Nexstim Ltd., which is funding the trial. Dunning and Kissela report no conflicts.

Participants will be divided into two groups, one of which will receive rTMS treatment and the other receiving sham (placebo) rTMS. Both groups will receive task-oriented rehabilitation from a licensed therapist. It is a randomized, controlled, double-blinded study, which means that neither participants nor investigators know which treatment is being used.

The therapy will be provided for six weeks, and primary outcomes assessed six months later.

To qualify, participants must be 18 or older, have had their stroke three to 12 months prior to enrollment in the study and have hand and arm weakness on one side of their body. Exclusion criteria include implanted devices such as pacemakers or defibrillators, pregnancy, depression and active alcohol abuse.

The therapy and treatments are free of charge. Participants will be compensated over the follow-up period.

Hospital elevator buttons carry more bacteria than toilet surfaces

And since we are very likely to  need to use the elevators because of our impaired walking ability let your doctor or therapist push the buttons for you. They can handle any infection much better than you can.
http://www.fiercehealthcare.com/story/hospital-elevator-buttons-carry-more-bacteria-toilet-surfaces/2014-07-08?
Canadian researchers at the University of Toronto found that bacteria commonly colonize on elevator buttons, although most pathogens were not clinically relevant, according to a study published in Open Medicine.
Researchers swabbed 120 elevator buttons and 96 toilet surfaces over separate intervals at three large, urban teaching hospitals on weekends and weekdays in Toronto, Ontario. They swabbed the up and down buttons on the outside of the elevator, along with the ground floor and a randomly selected upper-level floor button, while they swabbed the handles of the bathroom door, the privacy latch on the door and the toilet flusher.

5 Low-cost Alternatives for Stroke Therapy

I'm sorry but this is just once again dumping all the recovery needs onto survivors. Because your in-patient rehabilitation was not even close to being successful, your doctor and therapists basically have to let you figure out the rest of your rehab on your own. What a crock of shit for all survivors.
http://www.strokesmart.org/new?id=241
From rebuilding your muscles to working out your brain, recovering from a stroke is a combination of challenging both body and mind. While physical therapy is a common and often successful form of rehabilitation post-stroke, continuing treatment in the months and years after can be pricey, even with health insurance.
These five treatment alternatives won’t break the bank and might even lead you to discovering a new hobby while continuing your recovery.
Check out community calendars. Many local resources and organizations offer affordable, or even free, activities. Look for:
• Classes available through your city’s parks and recreation department
• Continuing adult education programs through local schools
• Outdoor recreation groups
These can be valuable resources for discovering new activities that combine both physical and mental challenges advantageous to stroke recovery. From group hikes to archery lessons, the activities can aid recovery and also give you an outlet to socialize.
Volunteer. Whether it’s for a stroke support group, a stroke center at a local hospital or another cause, donating your time can not only help other survivors, but can also have a positive impact on your own recovery.
Work your brain. There are many activities that can exercise your brain, and most are free and easy to find.
• Read a book
• Make your best attempt at the Sunday crossword puzzle
• Write letters
Even playing a video game can exercise your brain. Recent research found that video games may also help improve arm motor function, with success rates up to five times higher than typical physical therapy.
Hire a personal trainer. Although a more expensive option, a fitness expert at a local gym is a great option to continue your physical therapy and improve your overall health. It’s a great way to get regular exercise and strengthen parts of your body affected by the stroke.
Stick together. Sharing your stroke experiences with other survivors and socializing regularly will likely improve your positive outlook, which can do wonders for recovery. And many stroke support groups are free of charge. To find a stroke support group near you, visit National Stroke Association’s national registry here.

New York legalizes medical marijuana

Worthless piece of crap as far as usefulness for stroke survivors.
The list for eligibility was significantly reduced during this week’s negotiations. Only patients with the following would be eligible for a medical marijuana prescription:
- Cancer
- Positive status for human immunodeficiency virus or acquired immune deficiency syndrome (HIV-AIDS)
- Amyotrophic lateral sclerosis (ALS, or Lou Gherig’s disease)
- Parkinson's disease
- Multiple sclerosis
- Damage to the nervous tissue of the spinal cord  (This is as close to stroke we can get, as long as we consider the brain an extension of the spinal cord)
- Epilepsy
- Inflammatory bowel disease
- Neuropathies
- Huntington's disease
http://www.cnn.com/2014/07/07/health/new-york-medical-marijuana/
What should be available for us;
13 reasons to use it post-stroke. 

But then I'm just a stupid stroke survivor who obviously knows less than these legislators and governor Cuomo and whatever brilliant medical minds are advising them.

A case-control study on red meat consumption and risk of stroke among a group of Iranian adults

But then there is this observational study from Japan. Ask your doctor.

Study: Protein from meat, fish may help men age well

http://www.docguide.com/case-control-study-red-meat-consumption-and-risk-stroke-among-group-iranian-adults?

Shakeri F, Beykverdi M, Keshteli A, Esmaillzadeh A; Public Health Nutrition 1-7 (Jun 2014)

Tags:

• Diabetes
• Dyslipidemia
• Hypertension
• Stroke

Read/Add Comments(2) | Email This | Print This | PubMed | Get Full Text

OBJECTIVE We aimed to examine the association between red meat consumption and stroke in a group of Iranian adults.
DESIGN A hospital-based case-control study.
SETTING The study included stroke patients and hospital-based controls. Usual dietary intakes of participants were assessed by means of a validated 168-item semi-quantitative FFQ. Total red meat consumption was calculated by summing up the consumption of red, processed and visceral meats.

SUBJECTS One hundred and ninety-five cases were stroke patients hospitalized in the neurology ward and 195 controls were recruited from patients hospitalized in other wards with no history of cerebrovascular diseases or neurological disorders.

RESULTS Participants with stroke were older, more likely to be male and less likely to be obese. Individuals in the highest tertile of red meat intake were 119 % more likely to have stroke (OR=2·19; 95 % CI 1·33, 3·60) compared with those in the lowest tertile. After controlling for age, sex and total energy intake, the association between red meat consumption and stroke was strengthened (OR=2·72; 95 % CI 1·53, 4·83). This association remained significant even after further controlling for physical activity and smoking as well as dietary intakes. Additional adjustments for BMI, diabetes, hypertension and hyperlipidaemia did not influence the association significantly (OR=2·51; 95 % CI 1·19, 5·09).

CONCLUSIONS Consumption of red meat was associated with greater odds of having stroke in a group of Iranian adults.

Can stroke survivors with severe upper arm disability achieve clinically important change in arm function during inpatient rehabilitation? A multicentre, prospective, observational study

It is only USD 27.50/EUR 20.00 . Will your doctor spend that piddling amount of money to solve your chronic spasticity problem? 
http://iospress.metapress.com/content/am72n140571l5pq2/

PDF (79.9 KB)HTMLFirst Page Preview

Authors

Kathryn S. Hayward¹, Suzanne S. Kuys², Ruth N. Barker^{3, 4}, Sandra G. Brauer¹

¹Division of Physiotherapy, School of Health and Rehabilitation Sciences, The University of Queensland, Brisbane, Australia
²School of Rehabilitation Sciences, Griffith University, Gold Coast, Australia 4217; and Allied Health Research Collaborative, The Prince Charles Hospital, Brisbane, Australia
³Discipline of Physiotherapy, School of Public Health Tropical Medicine and Rehabilitation Sciences, James Cook University, Townsville, Australia
⁴Community Rehab Northern Queensland, Townsville Mackay Medicare Local, Townsville, Australia

Abstract

BACKGROUND: Severe arm disability is considered to indicate poor potential to recover arm function. OBJECTIVE: Determine if stroke survivors with severe upper arm disability can achieve a clinically important change in arm function on discharge from inpatient rehabilitation. METHODS: 618 stroke survivors from 16 inpatient rehabilitation units were assessed on admission and discharge using the Motor Assessment Scale Item 6 Upper Arm Function (MAS6). Admission scores defined participants with severe (MAS6 ≤2) and mild/moderate (MAS6 >2) upper arm disability. A clinically important improvement was evaluated according to: 1) statistical significance; 2) minimal clinical importance difference (MCID); and 3) shift in disability status i.e., severe to mild/moderate. Achievers of a MCID and shift were compared to non-achievers. RESULTS: Stroke survivors with severe upper arm disability (n = 226) demonstrated a significant improvement in arm function (p < 0.001) at discharge. A MCID was achieved by 68% (n = 155) and a shift from severe to mild/moderate upper arm disability on discharge by 45% (n = 102) of participants. Achievers had a significantly shorter interval from stroke onset to inpatient rehabilitation admission (p < 0.002). CONCLUSION: Stroke survivors with severe upper arm disability can achieve clinically important improvements during inpatient rehabilitation.

Efficacy of Adjunctive Extra Virgin Coconut Oil Use in Moderate to Severe Alzheimer’s Disease

I would expect this to be blasted to all doctors working with dementia patients. What is the downside? I'm taking coconut oil to prevent dementia. However don't listen to me.

Efficacy of Adjunctive Extra Virgin Coconut Oil Use in Moderate to Severe Alzheimer’s Disease

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Gandotra S^1*, Kour J¹ and Van der Waag A²

¹Consultant Psychiatrist, Mental Health Foundation, St. Maarten, Dutch Caribbean, Netherlands

²Retired Family Physician, Mullet Bay Clinic, St. Maarten, Dutch Caribbean, Netherlands

Corresponding Author :

Sachin Gandotra, MBBS, DPM, MD (Psychiatry)
Consultant Psychiatrist, Mental Health Foundation
St. Maarten, Dutch Caribbean, Netherlands
Tel: 1721-5205557
E-mail: sachincip@gmail.com

Received May 06 2014; Accepted May 29 2014; Published June 12 2014

Citation: Gandotra S, Kour J and Van der Waag A (2014) Efficacy of Adjunctive Extra Virgin Coconut Oil Use in Moderate to Severe Alzheimer’s Disease. Int J Sch Cog Psychol 1:108. doi: 10.4172/1234-3425.1000108

Copyright: © 2014 Gandotra S, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Related article at
Pubmed Scholar Google

Visit for more related articles at
International Journal of School and Cognitive Psychology

Abstract

Background: 

Ketogenic compounds derived from medium chain triglyceride (MCT) oils have been claimed to have beneficial health effects in the Alzheimer’s disease (AD] mainly attributed to its medium chain triglycerides. AD is known to have been characterized by early and region specific decline in cerebral glucose metabolism. It is hypothesized that Alzheimer brain tends to preferentially utilize ketones generated from medium chain triglycerides in light of decreased glucose metabolism to improve cognition. Extra virgin coconut oil with predominance of MCT content was used in subjects with moderate to severe AD to examine its efficacy in improving cognitive performance. 

Methods: 

Daily oral administration of extra virgin coconut oil (20 gm) was evaluated in 31 subjects with predominantly moderate to severe AD diagnosed as per DSM IV TR criteria for AD in a 6 week trial using quasi experimental non randomized pre-post intervention design. Subjects were on a normal diet and continued taking approved AD medications. Primary cognitive end points were mean change from baseline in the AD Assessment Scale-Cognitive subscale [ADAS-Cog], and Clinicians Interview based Impression of Change Plus Caregivers input [CIBIC-Plus]. Active oil administration continued for 4 weeks from baseline with successive ratings on measures of cognitive change at 2, 4 and 6 weeks respectively. 

Results: 

There was a significant difference between the ADAS-Cog scores from baseline over repeated ratings at 2, 4 and 6 weeks (Mauchly’s Chi Square Χ2 = 61.1, ε=0.4, F =14, p=0.00, η2=0.31). Post hoc comparisons of ADAS-Cog scores from baseline at 4 and 6 weeks were similar [At 4 weeks, Mean difference=4.1, P=0.00, C.I= (1.4-6.7); at 6 weeks, Mean difference=4.1, p=0.00, C.I= (1.0-7.2). The response rate of CIBIC-Plus defined as improved or no change was significantly improved over successive ratings from 2 weeks to 6 weeks (Cochran’s Q=22.5, df=2, P=.00). No statistically significant difference could be noted for the total cholesterol, Triglycerides and LDL fractions over the study trial except for the HDL fraction over repeated measures at 4 and 6 weeks over baseline (Mauchly’s Chi Square Χ2 (df=2)=6.5, ε=0.8, F (df 1.6, 49.9)=6.4, p=0.005, η2=0.17).  

Conclusions: 

Addition of adjunctive coconut oil is likely to have beneficial effects in cognitive performance for those suffering from moderate to severe AD and the effects were sustained for at least 2 weeks after the oil administration stopped. No deleterious effects on the overall lipid profile could be elicited.

Oxidative Stress and the Use of Antioxidants in Stroke

Your doctor will need to read this all. It talks about ebselen, Normobaric oxygen, lubeluzole, nitric oxide, Mitoquinone. I sure your doctor can rattle off all the research with these compounds and why none of it can be used for your recovery. There are only 211 supporting research articles for this writeup. 

Oxidative Stress and the Use of Antioxidants in Stroke

Rachel Shirley ^†, Emily N. J. Ord ^† and Lorraine M. Work *

Institute of Cardiovascular & Medical Sciences, College of Medical, Veterinary & Life Sciences, University of Glasgow, BHF GCRC, 126 University Place, Glasgow G12 8TA, UK; E-Mails: Rachel.Shirley@glasgow.ac.uk (R.S.); Emily.Ord@glasgow.ac.uk (E.N.J.O.)

^†

These authors contributed equally to this work.

*

Author to whom correspondence should be addressed; E-Mail: Lorraine.Work@glasgow.ac.uk; Tel.: +44-141-330-5869; Fax: +44-141-330-5339.

Received: 24 February 2014; in revised form: 8 May 2014 / Accepted: 14 May 2014 /
Published: 3 July 2014

Abstract

: Transient or permanent interruption of cerebral blood flow by occlusion of a cerebral artery gives rise to an ischaemic stroke leading to irreversible damage or dysfunction to the cells within the affected tissue along with permanent or reversible neurological deficit. Extensive research has identified excitotoxicity, oxidative stress, inflammation and cell death as key contributory pathways underlying lesion progression. The cornerstone of treatment for acute ischaemic stroke remains reperfusion therapy with recombinant tissue plasminogen activator (rt-PA). The downstream sequelae of events resulting from spontaneous or pharmacological reperfusion lead to an imbalance in the production of harmful reactive oxygen species (ROS) over endogenous anti-oxidant protection strategies. As such, anti-oxidant therapy has long been investigated as a means to reduce the extent of injury resulting from ischaemic stroke with varying degrees of success. Here we discuss the production and source of these ROS and the various strategies employed to modulate levels. These strategies broadly attempt to inhibit ROS production or increase scavenging or degradation of ROS. While early clinical studies have failed to translate success from bench to bedside, the combination of anti-oxidants with existing thrombolytics or novel neuroprotectants may represent an avenue worthy of clinical investigation. Clearly, there is a pressing need to identify new therapeutic alternatives for the vast majority of patients who are not eligible to receive rt-PA for this debilitating and devastating disease.

Keywords:

anti-oxidant; stroke; oxidative stress

1. Introduction

In addition to being the second leading cause of death worldwide [1], stroke is also the leading cause of acquired adult disability [2]. Stroke therefore has a very large socioeconomic impact with one third of all stroke patients requiring permanent residential care, costing the NHS in the UK £3.8 billion per annum [3]. The only approved pharmacological intervention for stroke is intravenous administration of the thrombolytic, recombinant tissue plasminogen activator (rtPA), within 4.5 h of the onset of ischaemia [4]. This short therapeutic window results in only 2%–5% of all stroke patients receiving this intervention with successful reperfusion of the brain occurring in only 50% of that cohort [5], as such this is a disease with largely unmet clinical needs. Ischaemic stroke (as opposed to haemorrhagic stroke) results from an atherothrombotic or embolic blockage to a cerebral artery and accounts for ~80% of all stroke cases. Finding a new pharmacological treatment for stroke is incredibly complex for a number of reasons. The brain is a highly metabolically active organ that relies on constant oxygen and glucose supply from the circulation. The brain accounts for 2% of the total body but requires 20% O₂ and 2% of the entire body’s glucose consumption, although it performs no mechanical work or external secretory activity [6]. Storage of energy and metabolites within the brain is extremely low and as such the brain is exceptionally sensitive to interruptions in blood flow [7]. Although the brain is protected from systemic toxins under normal physiological conditions by the blood-brain barrier (BBB), this is broken down during cerebral ischaemia allowing infiltration of inflammatory mediators and other potentially toxic molecules. Following the onset of ischaemia numerous pathways contribute to brain injury, there is extensive crosstalk between these deleterious pathways with them also, in the main, existing as positive feedback loops serving to amplify insult. In what is the most significant challenge of stroke treatment, the majority of damage occurs within minutes and the acute hours following cerebral ischaemia and as such, stroke treatment at present remains mainly preventative. Here, we will discuss the source and consequence of reactive oxygen species (ROS) imbalance following cerebral ischaemia/reperfusion before considering anti-oxidant strategies attempted clinically based on the pre-clinical evidence for each. What is clear is that while the contributory role of ROS in stroke cannot be disputed, the relative merit of anti-oxidant therapy alone has yet to be established and combined therapy may be where agents modulating the balance of ROS prove beneficial.

You will need your doctor to compare and contrast  this previous one;

A 'switch' in Alzheimer's and stroke patient brains that prevents the generation and survival of neurons

To the new one here:

Aerobic exercise effects on neuroprotection and brain repair following stroke: A systematic review and perspective

• Mark W. Austin^a,
• Michelle Ploughman^{a, ,} ,
• Lindsay Glynn^b,
• Dale R. Corbett^c

Choose an option to locate/access this article:

Check if you have access through your login credentials or your institution

Check access

Purchase $35.95

• 

 Show more

DOI: 10.1016/j.neures.2014.06.007

Get rights and content

---

Highlights

•

Exercise 24–48 h post-stroke reduced lesion volume more than later onset exercise.

•

Post-stroke exercise effects on the older brain and in the long term are not known.

•

Moderate intensity is most effective in reducing lesion volume.

•

Moderate intensity exercise decreases inflammation and increases neurogenesis.

•

Higher intensity exercise increases angiogenesis in perilesional area and striatum.

---

Abstract

Aerobic exercise (AE) enhances neuroplasticity and improves functional outcome in animal models of stroke, however the optimal parameters (days post-stroke, intensity, mode, and duration) to influence brain repair processes are not known. We searched PubMed, CINAHL, PsychInfo, the Cochrane Library, and the Central Register of Controlled Clinical Trials, using predefined criteria, including all years up to July 2013 (English language only). Clinical studies were included if participants had experienced an ischemic or hemorrhagic stroke. We included animal studies that utilized any method of global or focal ischemic stroke or intracerebral hemorrhage. Any intervention utilizing AE-based activity with the intention of improving cardiorespiratory fitness was included. Of the 4250 titles returned, 47 studies (all in animal models) met criteria and measured the effects of exercise on brain repair parameters (lesion volume, oxidative damage, inflammation and cell death, neurogenesis, angiogenesis and markers of stress). Our synthesized findings show that early-initiated (24–48 h post-stroke) moderate forced exercise (10 m/min, 5–7 days per week for about 30 min) reduced lesion volume and protected perilesional tissue against oxidative damage and inflammation at least for the short term (4 weeks). The applicability and translation of experimental exercise paradigms to clinical trials are discussed.

 

 

Neuroaid - MLC 901, A Traditional Chinese Medicine Induces Neuroprotective and Neuroregenerative Benefits After Traumatic Brain Injury in Rats

I don't have a good enough scientific background to see if this research is valid and reverses the previous negative results for stroke.

---------------------------------------------------------------------------

Neuroaid - It’s sold in 25 countries and 20,000 people have taken it, but herbal remedy proves no better than placebo in trial

Chinese herbal remedy for stoke[sic] recovery no better than placebo

CAM taking advantage of stroke patients 

Neuroaid and stroke rehab 

And Peter Levines' comments on it here: 

Neuroaid: Partial Truth and Petty Theft

---------------------------------------------------------------------------

  The TBI Neuroaid result here:

Neuroaid - MLC 901, A Traditional Chinese Medicine Induces Neuroprotective and Neuroregenerative Benefits After Traumatic Brain Injury in Rats

• H. Quintard^{a, b},
• T. Lorivel^a,
• C. Gandin^a,
• M. Lazdunski^a,
• C. Heurteaux^{a, ,}

 Show more

DOI: 10.1016/j.neuroscience.2014.06.047

Under a Creative Commons license

  Open Access

---

Highlights

•

MLC901 prevented the serum increase of two biomarkers S100B and NSE.

•

MLC901 reduced the infarct volume up to 2 hours post-TBI.

•

MLC901 prevented the edema formation and assists resolution, via the aquaporin 4.

•

MLC901 induced an increase of neurogenesis and gliogenesis around the lesion.

•

MLC901 reduced cognitive deficits induced by TBI.

---

Abstract

Traumatic brain injury is a frequent and clinically highly heterogeneous neurological disorder with large socioeconomic consequences. NeuroAid (MLC601 and MLC901), a Traditional Medicine used in China for patients after stroke has been previously reported to induce neuroprotection and neuroplasticity. This study was designed to evaluate the neuroprotective and neuroregenerative effects of MLC901 in a rat model of traumatic brain injury (TBI). TBI was induced by a moderate lateral fluid percussion applied to the right parietal cortex. MLC901 was injected intraperitoneally at 2 hours post-TBI, and then administered in drinking water at a concentration of 10 mg/ml until sacrifice of the animals. The cognitive deficits induced by TBI were followed by using the “what-where-when” task, which allows the measurement of episodic-like memory. MLC901 treatment decreased brain lesions induced by TBI. It prevented the serum increase of S100B and NSE, which may be markers to predict the neurologic outcome in human patients with TBI. MLC901 reduced the infarct volume when injected up to 2 hours post-TBI, prevented the edema formation and assisted its resolution, probably via the regulation of aquaporin 4. These positive MLC901 effects were associated with an upregulation of VEGF as well as an increase of endogenous hippocampal neurogenesis and gliogenesis around the lesion. Furthermore, MLC901 reduced cognitive deficits induced by TBI. Rats subjected to TBI displayed a suppression of temporal order memory, which was restored by MLC901. This work provides evidence that MLC901 has neuroprotective and neurorestorative actions, which lead to an improvement in the recovery of cognitive functions in a model of traumatic brain injury.

Comparative Analysis Electroencephalographic of Alpha, Beta and Gamma Bands of a Healthy Individual and One with Hemiparesis

I can see absolutely no use of this for survivors and I doubt your doctor will either.  Someone could enlighten us all.
Comparative Analysis Electroencephalographic of Alpha, Beta and Gamma Bands of a Healthy Individual and One with Hemiparesis

Dionis de Castro Dutra Machado^{1) 2) 4)}, Glenda Crispim Lima^{1) 2)}, Rodrigo Souza dos Santos^{1) 2)}, Amanda Júlia Bezerra Ramos^{1) 2)}, Cáio César Menezes de Sousa^{1) 2)}, Rayele Pricila Moreira dos Santos¹⁾, Karyna Kelly Oliveira Coelho^{1) 2)}, Mauricio Cagy⁴⁾, Marco Orsini³⁾, Victor Hugo Bastos^{1) 2)}

1) Department of Physical Therapy, Federal University of Piauí: Av. São Sebastião, 2819-64202-020, Parnaíba, PI, Brazil 2) Brain Mapping and Functionality Laboratory (LAMCEF), Federal University of Piauí, Brazil 3) Master Program of the Rehabilitation Science, UNISUAM, Brazil 4) Brain Mapping and Sensory Motor Integration Laboratory, Federal University of Rio de Janeiro (IPUB/UFRJ), Brazil

Released on J-STAGE June 30, 2014  

Keywords: Electroencephalography, Hemiparetic, Rehabilitation

• Full Text PDF [540K]

• Abstracts
• References(18)

[Purpose] The study analyzed the electroencephalographic (EEG) data of the central cortical areas, during execution of the motor gestures of feeding, activation of the system of mirror neurons, and imagery between a right hemiparetic volunteer (RHV) and a healthy volunteer (HV). [Subjects and Methods] The volunteers’ EEG data were recorded with their eyes open for 4 minutes while they performed five experimental tasks. [Results] The alpha band, absolute power value of HV was lower than that of RHV. In the beta band, during the practice condition, there was an increase in the magnitude of the absolute power value of HV at T3, possibly because T3 is representative of secondary motor areas that work with cortical neurons related to planning and organizing sequence of movements performed by the hands. The gamma band is related to the state of preparation for movement and memory. The results of this study indicate that there was increased activation of the gamma frequency band of HV. [Conclusion] The findings of this study have revealed the changes in pattern characteristics of each band which may be associated with the brain injury of the hemiparetic patient. 

Even the 4 page full text did nor provide any understanding at all.

PTSD Awareness Day: The Future of Treatment

Is your doctor even aware of PTSD from stroke or any of these solutions?
http://danablog.org/2014/06/27/ptsd-awareness-future-of-treatment/
Although they do only focus on war survivors and make no mention of  marijuana for PTSD.

Joi Ito: Want to innovate? Become a "now-ist"

Somehow YOU are going to have to convince  the head of your hospital stroke department that they need to get off their asses and innovate some solutions to all the stroke problems out there.
Are they waiting for the dinosaurs to innovate something new at the Joint Commission with their  Comprehensive Stroke Center, or  Primary Stroke Center designations? That is a complete waste of time.
Or are they waiting for the American Stroke Association Get With the Guidelines?
Neither of these are going to occur unless YOU start screaming in their faces.
Problems needing solutions in stroke:
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1. There is no fast, easy and objective way to diagnose a stroke. Maybe when the Qualcomm Tricorder X Prize is available. A number of friends have waited hours in ERs until stroke symptoms have visibly manifested themselves.
http://oc1dean.blogspot.com/2013/11/34-teams-are-building-medical.html

2. Only 10% get to almost full recovery.
http://www.ninds.nih.gov/disorders/stroke/stroke_rehabilitation.htm
3. 12% tPA efficacy
http://wrkf.org/.../more-stroke-patients-now-get-clot-busting-drug
4. Nothing being done to stop the neuronal cascade of death during the first week.
http://newswire.rockefeller.edu/2009/01/15/discovery-could-help-scientists-stop-the-death-cascade-after-a-stroke/
5. No one knows how to cure spasticity.
6.  No one knows how to cure fatigue.
7. F.A.S.T is actually a failure because even at its best tPA is only delivered to 33% of those eligible and then of those that get it it only works 12% of the time.
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The TED talk on innovation here:
http://www.ted.com/talks/joi_ito_want_to_innovate_become_a_now_ist?utm_source=newsletter_daily&
“Remember before the internet?” asks Joi Ito. “Remember when people used to try to predict the future?” In this engaging talk, the head of the MIT Media Lab skips the future predictions and instead shares a new approach to creating in the moment: building quickly and improving constantly, without waiting for permission or for proof that you have the right idea. This kind of bottom-up innovation is seen in the most fascinating, futuristic projects emerging today, and it starts, he says, with being open and alert to what’s going on around you right now. Don’t be a futurist, he suggests: be a now-ist. 

Rethink Your Thoughts about Thinking

Your thinker just got blasted by a stroke. What the hell is your doctor doing to help you recover?
http://www.scientificamerican.com/article/rethink-your-thoughts-about-thinking/
Targeting metacognition—our beliefs about thoughts—might alleviate mood disorders and even schizophrenia. IE. depression and anxiety.

Peer support for stroke survivors: a case study

I'm sorry but this is just once again dumping all the recovery needs onto survivors. Don't doctors have to do a damn thing to help you recover? Like maybe figuring out how to stop the neuronal cascade of death?


http://www.biomedcentral.com/1472-6963/14/256

Dorothy Kessler^12*†, Mary Egan^12† and Lucy-Ann Kubina^1†

• * Corresponding author: Dorothy Kessler dkessler@bruyere.org
• † Equal contributors

Author Affiliations

¹ Bruyère Research Institute, 43 Bruyère St, Ottawa, ON K1N 5C8, Canada
² School of Rehabilitation Sciences, University of Ottawa, 451 Smyth Rd, Ottawa, ON K1H 8M5, Canada

For all author emails, please log on.

BMC Health Services Research 2014, 14:256  doi:10.1186/1472-6963-14-256

The electronic version of this article is the complete one and can be found online at: http://www.biomedcentral.com/1472-6963/14/256

Received:	21 August 2013
Accepted:	10 June 2014
Published:	16 June 2014

© 2014 Kessler et al.; licensee BioMed Central Ltd.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited.

Abstract

Background

Innovative and sustainable programs are required to support the well-being of stroke survivors. Peer support is a potentially low cost way to enhance well-being of recent stroke survivors and the well-being and community reintegration of their peer supporters. This article describes the perceptions of stroke survivors, care partners, peer supporters, and professionals of an individual peer support program.

Methods

An instrumental case study design was used to examine a volunteer peer support program that provides acute care visits and telephone follow-up post-discharge. In particular, a) type of support provided, b) benefits for the stroke survivor and care partner, c) potential harms to the stroke survivor, d) impact of providing support on the peer supporter, and e) required processes were considered. Semi-structured interviews were carried out with 16 new stroke survivors and 8 care partners immediately following hospital discharge and then 6 months later, and with 7 peer supporters, 3 program co-ordinators and 4 health professionals to gather feedback from multiple stakeholders.

Results

Emotional, affirmational and informational support were perceived as being offered by the peer supporters. Peer visits were perceived as providing encouragement, motivation, validation, and decreased feelings of being alone. However, the visits were not perceived as beneficial to all stroke survivors. The impact on the peer supporters included increased social connections, personal growth, enjoyment, and feelings of making a difference in the lives of others. Involvement of the healthcare team, peer supporter training and a skilled coordinator were crucial to the success this program.

Conclusions

Peer support can potentially enhance service to stroke survivors and promote community reintegration for peer volunteers. Further research is needed to determine the preferred format and timing of peer support, and the characteristics of stroke survivors most likely to benefit.

A 'switch' in Alzheimer's and stroke patient brains that prevents the generation and survival of neurons

This is a fascinating conundrum since nitric oxide has many health benefits. You'll have to have your doctor sort out all the claims and provide you with the way to go. Don't  let your doctor dismiss your questions without providing a clear answer to all the linked research.

You do expect your doctor to actually know something about your stroke recovery? Don't you?

We are really f*cking screwed if we can't use exercise to create neurogenesis because the same process that creates new neurons also creates NO that prevents neurogenesis?
Damnable Catch-22.

What is your doctors solution? 

Vigorous treadmill exercise improves reactivity of cerebral arterioles and reduces brain injury following transient focal ischemia - In rats

Exercise creates NO.

Enhanced endothelial nitric oxide production impairs cerebrovascular tone after brain trauma

How Mouthwash Can Affect Stroke Risk

Chlorhexidine kills nitrite production in your body, which prevents blood vessels from dilating.

Research Focuses on Beet Juice After Stroke

Creation of nitric oxide via Breath of Fire

 

The role of nitric oxide in pre-synaptic plasticity and homeostasis

 

  Physical activity improves long-term stroke outcome via endothelial nitric oxide synthase-dependent augmentation of neovascularization and cerebral blood flow.

 

  Sun's blood pressure benefits 'may outdo cancer risks'

 

 Nasal NO is known to be increased 15-to20 fold by humming compared with quiet exhalation.

  The role of nitric oxide in pre-synaptic plasticity and homeostasis

  Benefits of Nose Breathing & Nitric Oxide

Tea, flavonoids, and cardiovascular health: endothelial protection

A comparative study of NONOate based NO donors: Spermine NONOate is the best suited NO donor for angiogenesis

Atherosclerosis: Evolving Vascular Biology and Clinical Implications

Pleiotropic effects of statins include improvement of endothelial dysfunction, increased nitric oxide bioavailability, antioxidant properties, inhibition of inflammatory responses, and stabilization of atherosclerotic plaques.  

Intranasal pyrrolidine dithiocarbamate decreases brain inflammatory mediators and provides neuroprotection after brain hypoxia–ischemia in neonatal rats

Inhibition of inducible nitric oxide synthase after brain HI reduced brain tissue loss.

Effect of a single intrastriatal rotenone injection on oxidative stress and neurodegeneration in the rat brain

I'm not sure I'd want a pesticide injected into my brain even if nitric oxide and CoQ10 increased.

Modulation of Adult Neurogenesis by the Nitric Oxide System

Efficacy of Nitric Oxide in Stroke' (ENOS) study 

Inhaled Nitric Oxide Protects Males But not Females from Neonatal Mouse Hypoxia–Ischemia Brain Injury 

 

  Inhaled Nitric Oxide Protects Males But not Females from Neonatal Mouse Hypoxia–Ischemia Brain Injury

 

  Regulation of Injury-Induced Neurogenesis by Nitric Oxide

 

 Nitric Oxide and the Biological Cascades Underlying Increased Neurogenesis, Enhanced Learning Ability, and Academic Ability as an Effect of Increased Bouts of Physical Activity

  Inhalation of nitric oxide could help improve blood flow to ischemic brain

  Nitric oxide-induced calcium release via ryanodine receptors regulates neuronal function

 

  Cerebrovascular protection by various nitric oxide donors in rats after experimental stroke

 

Nitric oxide-induced calcium release via ryanodine receptors regulates neuronal function

Don't do your own research on this, your doctor needs to take the lead. This is all provided to you so you can ask your doctor leading questions. 

The new research here:

http://medicalxpress.com/news/2014-07-alzheimer-patient-brains-survival-neurons.html
A new study by researchers at Sanford-Burnham Medical Research Institute (Sanford-Burnham) has identified a chemical "switch" that controls both the generation of new neurons from neural stem cells and the survival of existing nerve cells in the brain. The switch that shuts off the signals that promote neuron production and survival is in abundance in the brains of Alzheimer's patients and stroke victims. The study, published July 3 in Cell Reports, suggests that chemical switch, MEF2, may be a potential therapeutic target to protect against neuronal loss in a variety of neurodegenerative diseases, such as Alzheimer's, Parkinson's and autism.

"We have shown that when nitric oxide (NO)—a highly reactive free radical—reacts with MEF2, MEF2 can no longer bind to and activate the genes that drive neurogenesis and neuronal survival," said Stuart Lipton, M.D., Ph.D., director and professor in the Neuroscience and Aging Research Center at Sanford-Burnham, and a practicing clinical neurologist. "What's unique here is that a single alteration to MEF2 controls two distinct events—the generation of new neurons and the survival of existing neurons," added Lipton, who is senior author of the study.
In the brain, transcription factors are critical for linking external stimuli to protein production, enabling neurons to adapt to changing environments. Members of the MEF2 family of transcription factors have been shown to play an important role in neurogenesis and neuronal survival, as well as in the processes of learning and memory. And, mutations of the MEF2 gene have been associated with a range of neurodegenerative disorders, including Alzheimer's and autism.
The process of NO-protein modifications—known as S-nitrosylation—was first described by Lipton and collaborators some 20 years ago. S-nitrosylation has important regulatory functions under normal physiological conditions throughout the body. However, with aging, environmental toxins, or stress-related injuries, abnormal S-nitrosylation reactions can occur, contributing to disease pathogenesis.
"Our laboratory had previously shown that S-nitrosylation of MEF2 controlled neuronal survival in Parkinson's disease," said Lipton. "Now we have shown that this same reaction is more ubiquitous, occurring in other neurological conditions such as stroke and Alzheimer's disease. While the major gene targets of MEF2 may be different in various diseases and brain areas, the remarkable new finding here is that we may be able to treat each of these neurological disorders by preventing a common S-nitrosylation modification to MEF2.
"The findings suggest that the development of a small therapeutic molecule—one that can cross the blood-brain barrier and block S-nitrosylation of MEF2 or in some other way increase MEF2 transcriptional activity—could promote new brain cell growth and protect existing cells in several neurodegenerative disorders," added Lipton.
"We have already found several such molecules in our high-throughput screening and drug discovery efforts, so the potential for developing new drugs to attack this pathway is very exciting," said Lipton.

Personality And Heart Attacks - A New Look

You'll have to ask your doctor, hospital and stroke association what the correlation is between personality and stroke. It would seem to be an obvious line of study but our stroke associations will do nothing about this.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=143440&CultureCode=en
A new study published in the current issue of Psychotherapy and Psychosomatics has addressed the relationship between personality and heart attacks. Distressed (type D) personality (TDP), characterized by high negative affectivity (NA) and social inhibition (SI), along with depression, anxiety and other negative affects (such as demoralization, hopelessness, pessimism and rumination) have been implicated as potential risk factors for coronary artery disease. While some evidence suggests that the NA dimension of TDP overlaps at least partially with depression, other studies underline how ‘TDP refers to a chronic, more covert form of distress that is distinct from depression'.
In this study, Authors aimed to clarify whether, among never depressed patients at their first acute coronary syndrome (ACS), there is an overlap between the constructs of TDP and depression, evaluating the stability of NA and SI 6 months after the ACS, and their relationship with depressive symptoms. Patients consecutively admitted to the Coronary Intensive Care Unit of the University Hospital of Parma between January 2009 and March 2012 who had their first ACS and no history of major depression (MD) or other psychiatric disorders, were included.
During the follow-up period 30 patients developed depressive symptoms (MD: n = 12; minor depression (md): n = 18), whereas 220 subjects maintained a nondepressive condition throughout the study period. At baseline the NA and SI levels were higher in subjects who developed depression than in patients who did not. However, at the baseline evaluation 19 patients without previous depressive episodes already satisfied the criteria for md. Interestingly, at baseline these subjects showed higher levels of NA and SI than subjects without md. Among patients who developed depression (n = 30) HADS scores significantly changed during the 6-month follow-up: both anxiety and depression scores increased from baseline to the second month of follow-up and then decreased. The same pattern of change was observed for the NA score, whereas the SI score did not vary during follow-up. In nondepressed patients, both HADS depression and anxiety scores and NA score significantly decreased throughout the follow-period, whereas the SI did not change.
In this study, the overlap between depressive psychopathology and NA features is suggested by the course of these two dimensions over time. Indeed, in both depressed and nondepressed patients, NA levels were not stable during the 6-month follow-up, but they changed along with the variation of HADS scores. This finding suggests that the NA dimension is sensitive to mood-state, because its levels increase and decrease according to the fluctuation of severity of depressive and anxious symptoms. This result supports the view that the disposition to experience and report negative emotions (NA) can be sensitive to mood-state. Therefore, the presence of depressive state is crucial when assessing TDP, since NA and anhedonic depression are partially overlapping and co-varying constructs.