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 27, 2016

Calcium supplementation and risk of dementia in women with cerebrovascular disease

Be careful out there.
http://www.mdlinx.com/internal-medicine/medical-news-article/2016/08/22/cerebrovascular-disease-calcium-supplementation-dementia/6824758/?
Neurology®, 08/22/2016
This longitudinal population–based study coordinated to describe the association between calcium supplementation with the development of dementia in women with cerebrovascular disease after a 5–year follow–up. The study found that calcium supplementation may increase the risk of developing dementia in elderly women. These findings need to be confirmed, because this sample was relatively small and the study was observational.

Methods

  • The authors derived this sample from the Prospective Population Study of Women and H70 Birth Cohort Study in Gothenburg, Sweden.
  • They included 700 dementia–free women aged 70–92 years.
  • The women underwent comprehensive neuropsychiatric and somatic examinations, at baseline in 2000–2001, and at follow–up in 2005–2006.
  • They performed a CT scan in 447 participants at baseline.
  • They collected information on the use and dosage of calcium supplements, and diagnosed dementia according to DSM–III–R criteria.

Results

  • As compare to women not given supplementation (n = 602), the women who treated with calcium supplements (n = 98) were at a higher risk of developing dementia (odds ratio [OR] 2.10, 95% confidence interval [CI] 1.01–4.37, p = 0.046) and the subtype stroke–related dementia (vascular dementia and mixed dementia) (OR 4.40, 95% CI 1.54–12.61, p = 0.006).
  • As per this stratified analyses, calcium supplementation was connected with the development of dementia in groups with a history of stroke (OR 6.77, 95% CI 1.36–33.75, p = 0.020) or presence of white matter lesions (OR 2.99, 95% CI 1.28–6.96, p = 0.011), but not in groups without these conditions.
Go to PubMed Go to Abstract Print Article Summary Cat 2 CME Report

Does Moderate Alcohol Consumption Improve Brain Function?

The BrainBlogger does a much better job than I to write about the benefits of alcohol.  I like these couple of lines:
Studies show that moderate alcohol intake can reduce the risk of cardiovascular diseases, dementia, depression, stroke, breast and colon cancer.
The results of this study show that the aggregation of beta-amyloid in the human brain is lower among beer drinkers. Only beer.
Compared to abstainers, moderate drinkers have a larger hippocampus and better episodic memory.
I'm sure your doctor will never agree to prescribe alcohol just like they will never agree to prescribe marijuana or ectasy. This is why you are completely on your own for your stroke rehab. Your options are being censored. And the worst part is your doctor doesn't have any clue about what they are missing(unknown unknowns) that might help you.

Effects of alteplase for acute stroke on the distribution of functional outcomes

They still don't bother to tell you that tPA getting to full recovery has a horrifying 88% failure rate. Damn I hate these 'happy talk' research articles. Because of this fucking 'happy talk' no one is looking for a better replacement.
http://www.mdlinx.com/internal-medicine/medical-news-article/2016/08/23/confidence-interval-odds-ratio-stroke-thrombolytic/6828728/?
Stroke, 08/23/2016
The clinicians intended to evaluate the effects of alteplase for acute stroke on the distribution of functional outcomes. The study reveal that treatment with intravenous alteplase started within 4.5 hours of stroke onset increases the chance of achieving an improved level of function for all patients across the age spectrum, including the over 80s and across all severities of stroke studied; the earlier that treatment is initiated, the greater the benefit.

Methods

  • From 9 randomized trials, prespecified pooled analysis of 6756 patients comparing alteplase vs. placebo/open control.
  • For this study, ordinal logistic regression models assessed treatment differences after adjustment for treatment delay, age, stroke severity, and relevant interaction term(s).

Results

  • Treatment with alteplase was favourable for a delay in treatment extending to 4.5 hours after stroke onset, with a greater benefit with earlier treatment.
  • The study reveal that, neither age nor stroke severity significantly affected the slope of the relationship between benefit and time to treatment initiation.
  • As per the study, for the observed case mix of patients treated within 4.5 hours of stroke onset (mean 3 hours and 20 minutes), the net absolute benefit from alteplase (ie, the difference between those who would do better if given alteplase and those who would do worse) was 55 patients per 1000 treated (95% confidence interval, 13–91; P=0.004).

Coffee and green tea consumption in relation to brain tumor risk in a Japanese population

I'm sure you've heard of all the greatness of green tea. This is not an endorsement, just more information for you. And my favorite(coffee) was also good.
www.mdlinx.com/internal-medicine/medical-news-article/2016/08/26/brain-tumor/6834884/?
International Journal of Cancer, 08/26/2016
 Ogawa T, et al. – In a Japanese population, this study assessed the relationship amongst coffee and greed tea intake and brain tumor risk, study authors recommended that coffee consumption may decrease the danger of brain tumor, including that of glioma.

Methods

  •  In the Japan Public Health Center-based Prospective Study (JPHC Study), the researchers assessed a cohort of 106,324 subjects (50,438 men and 55,886 women).
  • From 1990 for Cohort I and 1993 for Cohort II until December 31, 2012, subjects were followed.
  • During the study period, 157 (70 men and 87 women) newly diagnosed cases of brain tumor were distinguished.  
  • Using a Cox proportional hazards regression model, hazard ratio (HR) and 95% confidence intervals (95%CIs) for the relationship between coffee or green tea consumption and brain tumor risk were surveyed. 

Results

  •  Researchers found a significant inverse relationship between coffee consumption and brain tumor risk in both total subjects (≥3 cups/day; HR=0.47, 95%CI=0.22-0.98) and in women (≥3 cups/day; HR=0.24, 95%CI=0.06-0.99), although the number of cases in the highest category was small.
  • It was also observed that glioma risk tended to diminish with higher coffee consumption (≥3 cups/day; HR=0.54, 95%CI=0.16-1.80).  
  •  
  • As per the findings, no affiliation was seen between green tea and brain tumor risk.

Sleep-time blood pressure: Unique sensitive prognostic marker of vascular risk and therapeutic target for prevention

Is your doctor figuring out how to get your sleep-time blood pressure? And update your chronotherapy protocol?
http://www.smrv-journal.com/article/S1087-0792%2816%2930007-7/fulltext?rss=yes

Summary

Correlation between blood pressure (BP) and target organ damage, vascular risk, and long-term patient prognosis is stronger for measurements derived from around-the-clock ambulatory BP monitoring (ABPM) than in-clinic daytime ones. Numerous studies consistently substantiate the asleep BP mean is both an independent and much better predictor of cardiovascular disease (CVD) risk than either the awake or 24 h means. Elevated sleep-time BP, i.e., sleep-time hypertension, which can only be diagnosed by around-the-clock ABPM, is much more common than suspected, not only in patients with sleep disorders, but, among others, in those who are elderly or have type 2 diabetes, chronic kidney disease, or resistant hypertension. Hence, medical guidelines increasingly recommend ABPM to make the accurate differential diagnosis of hypertension versus normotension and recognize the marked clinical importance of adequate management of sleep-time BP. The ingestion time, according to circadian rhythms, of hypertension medications of six different classes and their combinations significantly impacts their beneficial, particularly on sleep-time BP control, and/or adverse effects. The MAPEC (monitorización ambulatoria para predicción de eventos cardiovasculares (i.e., ambulatory blood pressure monitoring for prediction of cardiovascular events)) study was the first prospective randomized treatment-time investigation designed to test the worthiness of bedtime chronotherapy with ≥1 conventional hypertension medications to specifically target attenuation of asleep BP. This 5.6 y median follow-up outcomes trial found the bedtime chronotherapy strategy most advantageous, resulting in the differential reduction of total CVD events by 61% and decrease of major CVD events – CVD death, myocardial infarction, and ischemic and hemorrhagic stroke – by 67%. The MAPEC study plus other earlier conducted less refined trials document the asleep BP mean is the most significant prognostic marker of CVD morbidity and mortality. It further substantiates attenuation of the asleep BP mean by a bedtime hypertension treatment strategy entailing the entire daily dose of ≥1 hypertension medications significantly reduces CVD risk, both in the general hypertension population and in more vulnerable patients, i.e., those diagnosed with chronic kidney disease, diabetes, and resistant hypertension.

Friday, August 26, 2016

Combined Action Observation and Motor Imagery Neurofeedback Up-Regulates Contralateral Sensorimotor Activity

Whoa, three big words to confuse us peons; Up-regulates, Contralateral, Sensorimotor. I don't think researchers even want us to read research which is why they obsfucate their blatherings.
https://dalspace.library.dal.ca/handle/10222/72090
Author
Friesen, Christopher
 
Motor imagery (MI) and action observation have proven to be efficacious adjuncts to traditional physiotherapy, to enhance motor recovery from stroke. Recently, researchers have used a combined approach called imagined imitation (II), where an individual watches a motor task being performed, while simultaneously imagining they are performing the movement. While neurofeedback (NFB) has been used extensively with MI to improve patients’ ability to modulate sensorimotor activity and enhance motor recovery, the feasibility of using NFB with II is unknown. This project tested whether healthy controls could modulate sensorimotor lateralization during II-NFB of a unilateral handshake using electroencephalography, and whether this ability transferred to subsequent MI. Thirty-two subjects, receiving real or sham NFB attended four sessions where they engaged in II-NFB training and subsequent MI. Results showed the NFB group demonstrated more sensorimotor activity during sessions three and four, and that this NFB effect transferred to subsequent MI.
 

Rehabilitation of motor function after stroke: a multiple systematic review focused on techniques to stimulate upper extremity recovery

You can have your therapist go thru this. Way too small for me and I'm not qualified to comment on this.

Rehabilitation of motor function after stroke: a multiple systematic review focused on techniques to stimulate upper extremity recovery

Myeloperoxidase inhibition increases neurogenesis after ischemic stroke

What protocol does your doctor have to increase your neurogenesis? How does s/he know that neurogenesis is working? Does your doctor know ONE DAMN THING ABOUT NEUROGENESIS?
http://jpet.aspetjournals.org/content/early/2016/08/22/jpet.116.235127.abstract

  1. John W. Chen1,*
+ Author Affiliations
  1. 1 MGH;
  2. 2 Massachusetts General Hospital
  1. *Address correspondence to: jwchen@mgh.harvard.edu

Abstract

The relationship between inflammation and neurogenesis in stroke is currently not well understood. Focal ischemia enhances cell proliferation and neurogenesis in the neurogenic regions including the subventricular zone (SVZ), dentate gyrus (DG) as well as non-neurogenic striatum, cortex in the ischemic hemisphere. Myeloperoxidase (MPO) is a potent oxidizing enzyme secreted during inflammation by activated leukocytes and its enzymatic activity is highly elevated after stroke. In this study, we investigated whether inhibition of MPO activity by a specific irreversible inhibitor, 4-aminobenzoic acid hydrazide (ABAH) or MPO-/- mice can increase neurogenesis after transient middle cerebral artery occlusion (tMCAO) in mice. ABAH administration increased the number of proliferating 5-bromo-2' deoxyuridine (BrdU)-positive cells expressing markers for neural stems cells, astrocytes, neuroprogenitors (Nestin), and neuroblasts (doublecortin) in the ischemic SVZ, anterior SVZ (aSVZ), striatum and cortex. MPO inhibition also increased levels of brain-derived neurotrophic factor (BDNF), phospho-cAMP response element-binding protein (pCREB Ser133), acetylated H3 (AcH3), and NeuN to promote neurogenesis in the ischemic SVZ. ABAH treatment also increased chemokine CXC receptor 4 (CXCR 4) expression in the ischemic SVZ. MPO-deficient mice treated with vehicle or ABAH both showed similar effects on the number of BrdU+ cells in the ischemic hemisphere, demonstrating that ABAH is specific to MPO. Taken together, our results underscore a detrimental role of MPO activity to post-ischemia neurogenesis and that a strategy to inhibit MPO activity can increase cell proliferation and improve neurogenesis after ischemic stroke.

The Big Dirty Secret Every Doctor Knows

This paragraph from there is instructive: Not being allowed to question the process. In stroke that leads to disaster where survivors haven't been progressing in decades because no one tells the emperor that he has no clothes. No one challenges the 'experts'.
http://www.medpagetoday.com/Cardiology/CardioBrief/59481?xid=fb_p_ms

But the responsibility for eminence-based medicine goes well beyond the elite coterie of experts. The real problem is the culture of medicine, which rewards the hubris of eminence and actively punishes or offers subtle disincentives to anyone who question this process.

ASA recommends 24/7, intense multi-disciplinary treatment

Can't even find those guidelines on the ASA website so I could specify exactly how bad they are.
Fucking useless because guidelines don't tell exactly what to do. That is what protocols are for. 
http://www.wibw.com/content/news/New-stroke-rehab-guidelines-aim-to-get-patients-back-on-feet-391363771.html
TOPEKA, Kan. (WIBW) - Already a heart attack survivor, Diana Houser had another scare in early August.
"I just knew I needed help," she said of the symptoms that brought her to the emergency room at Stormont-Vail in Topeka.
Diana suffered a mild stroke. In the weeks since, she's worked hard to get back on her feet, as an in-patient at Kansas Rehabilitation Hospital.
"I couldn't walk very well, couldn't speak very well," she said of her condition when she first checked in. "We started kind of from the beginning over it seemed to me."
The journey through in-patient therapy falls in line with the American Heart Assoc. and American Stroke Assoc.'s first-ever guidelines for adult stroke rehab. They recommend 24/7, intense multi-disciplinary treatment.
"What the rehabilitation phase focuses on is regaining that quality of life, addressing the specific impairments that they have and implementing a variety of techniques and technologies to optimize quality of life when they do get home," said Barry Muninger, marketing director for Kansas Rehab Hospital.
The approach includes a team of doctors and nurses, plus speech, occupational and physical therapies. Since it's in-patient, Diana meets with members of her team several times a day, rather than a few visits a week.
"It's just a wide variety (of activities), and so, with breaking it up into the different sessions throughout the day, we can focus on one task at a time versus trying to fit it all in," said Jamie Pfannenstiel, CPTA, a physical therapist who's been working with Diana.
The constant contact also allows staff to get a better overall picture of their patients' strengths and weaknesses.
"It provides us with a lot of opportunities to see different impairments with the patient that might not otherwise be detected," Muninger said.
Diana's made great strides and is almost ready to take the next step - going home to enjoy her husband and their family.
"I'm so grateful for what I've got and what I've regained," she said. "They helped me put it all together."
The new guidelines also recommend formal education for patients and families on preventing falls at home.

Influence of Aerobic Training and Combinations of Interventions on Cognition and Neuroplasticity after Stroke

Still no fucking protocols being written up. I suppose we are supposed to listen to these pallative words and magically get better.
http://journal.frontiersin.org/article/10.3389/fnagi.2016.00164/full?
  • 1Aix-Marseille Université, CNRS, ISM, UMR 7287, Marseille, France
  • 2Université Nice Sophia Antipolis, LAMHESS, UPRES EA 6309, Nice, France
Stroke often aggravated age-related cognitive impairments that strongly affect several aspects of quality of life. However, few studies are, to date, focused on rehabilitation strategies that could improve cognition. Among possible interventions, aerobic training is well known to enhance cardiovascular and motor functions but may also induce beneficial effects on cognitive functions. To assess the effectiveness of aerobic training on cognition, it seems necessary to know whether training promotes the neuroplasticity in brain areas involved in cognitive functions. In the present review, we first explore in both human and animal how aerobic training could improve cognition after stroke by highlighting the neuroplasticity mechanisms. Then, we address the potential effect of combinations between aerobic training with other interventions, including resistance exercises and pharmacological treatments. In addition, we postulate that classic recommendations for aerobic training need to be reconsidered to target both cognition and motor recovery because the current guidelines are only focused on cardiovascular and motor recovery. Finally, methodological limitations of training programs and cognitive function assessment are also developed in this review to clarify their effectiveness in stroke patients.

Introduction

Sedentary older adults are prone to cardiovascular diseases, such as stroke (Bherer et al., 2013), which occurs when blood flow is interrupted to a part of the brain. This trauma leads to severe motor dysfunctions and it may also aggravate cognitive impairments resulting from normal aging (Rafnsson et al., 2007, 2009; Deary et al., 2009; Waldstein and Wendell, 2010). Indeed, stroke survivors have more than twice the risk of subsequently developing dementia compared with people who have never had a stroke (Tatemichi et al., 1992; Patel et al., 2002). For instance, a stroke situated on the left hemisphere might disturb language and comprehension, which reduce the ability to communicate (Karbe et al., 1990; Pirmoradi et al., 2016). When the right hemisphere is affected, the intuitive thinking, reasoning, solving problems as well as the perception, judgment and the visual-spatial functions could be impaired (Tatemichi et al., 1994; Patel et al., 2002; Cumming et al., 2012; Sun et al., 2014b; Harris et al., 2015; Tiozzo et al., 2015; Save-Pédebos et al., 2016). It makes thus difficult for patients to locate objects, walk up or down stairs or get dressed. Consequently, cognitive disorders are one of the strongest predictor of the inability to return to work, that contribute to the socioeconomic burden of stroke (Kauranen et al., 2013). However, stroke-induced cognitive disorders are often underestimated relative to motor impairments because they are confused with pre-existing symptoms of age-related mild cognitive impairments or Alzheimer’s Disease (AD; Figure 1; Sun et al., 2014b; Corriveau et al., 2016). Furthermore, cognitive impairments are frequently associated with poor motor recovery (Patel et al., 2002; Leśniak et al., 2008; Rand et al., 2010). It suggests that stroke-induced cognitive dysfunctions and brain plasticity might also affect the stability, flexibility and learning of complex movements (e.g., locomotion, unimanual aiming, bimanual coordination), in which cognitive resources are highly involved as it was already observed in older adults (Temprado et al., 1999, 2013; Sleimen-Malkoun et al., 2012, 2013; Cohen et al., 2016).

Still no fuclkiMore at link.
 

Relief for Stroke Survivors with Shoulder Pain

I had shoulder pain for a couple of weeks, did nothing to address it, it went away.
http://nationalpainreport.com/relief-for-stroke-survivors-with-shoulder-pain-8831250.html
Up to 85% of stroke survivors suffer from chronic shoulder pain and that pain often stops them from continuing their efforts to rehabilitate after their stroke.
When a stroke survivor can no longer move his or her arm, the muscles will atrophy. The shoulder will essentially separate and the pain from the shoulder will often cause them to drop out of rehabilitation.
Choices like opioids, short term joint injections and immobilization might help relieve the pain in the short-term but they don’t address the cause—how to settle down the axillary nerve.
Doctors are having some success with a recently FDA cleared device that treats chronic pain of a peripheral nerve origin. In fact, it was the first implantable neuromodulation device cleared for peripheral nerve pain.
The StimRouter was developed by Bioness, a southern California company that was founded by the legendary Al Mann, the entrepreneur and philanthropist who founded companies that focused on cardiac pacemakers, insulin pumps, spinal cord stimulators and cochlear implants.  Mann passed away earlier this year.
“The goal is to get the stroke patient back into rehab,” said Mark Geiger, Global Director of Marketing Implantables for Bioness. “By targeting the pain at its origin, we believe we have an answer for the chronic shoulder pain that plagues stroke survivors.
Bioness_stimrouter_Set3_073015_implant
The StimRouter System
(Click to expand image)
The StimRouter is being marketed as a minimally invasive, long-term treatment option. No batteries are implanted. There’s less lead migration which is a big challenge for more invasive treatments.
Many pain physicians like what they see so far.
“This represents a paradigm shift in the management of post-stroke shoulder pain,” said Dr. Michael Sein, a rehabilitation physician at Weill Cornell Medicine in New York. “I like the ease of implementation which can be completed in an ambulatory setting as well as the significant levels of pain reduction that is achievable in patients that have failed to improve with prior therapy.
According to Dr. Sein, the traditional therapy has included physical therapy, medications and corticosteroid injections.
While the device was approved last year, the Company just launched the product in early 2016 and is still training pain and rehabilitation physicians around the country. Currently about 70 physicians are trained.
“That number is increasing by the month,” said Geiger.
The StimRouter is also approved for treatment of upper or lower limbs, entrapment syndromes, intercostal neuralgias and other peripheral injuries or disease.
Dr. Porter McRoberts of Fort Lauderdale, Florida is an interventional pain physician who has also used the device.
“100% of my implanted patients have had dramatic improvements in pain, said Dr. McRoberts. “One patient has even had complete resolution of her symptoms. I’ve been extremely happy.”
The Company hopes that for physical therapists and occupational therapists, the StimRouter may help these professionals successfully rehab more of the 800,000 Americans who suffer a stroke each year.

Cheese consumption and risk of cardiovascular disease: a meta-analysis of prospective studies

No fucking clue what the conclusions and results mean. Insiders talking to insiders, stroke survivors be damned. So they should tell us if this new research invalidates or confirms this one:

Dairy products and the risk of stroke and coronary heart disease: the Rotterdam Study 

The latest here:

Cheese consumption and risk of cardiovascular disease: a meta-analysis of prospective studies

Authors

  • Guo-Chong Chen

    Guo-Chong Chen

    • Department of Nutrition and Food Hygiene, School of Public HealthSoochow University
  • Yan Wang

    Yan Wang

    • Yili Innovation CenterInner Mongolia Yili Industrial Group Co., Ltd.
  • Xing Tong

    Xing Tong

    • Department of Nutrition and Food Hygiene, School of Public HealthSoochow University
  • Ignatius M. Y. Szeto

    Ignatius M. Y. Szeto

    • Yili Innovation CenterInner Mongolia Yili Industrial Group Co., Ltd.
  • Gerrit Smit

    Gerrit Smit

    • Yili R&D Center
  • Zeng-Ning Li

    Zeng-Ning Li

    • Department of NutritionThe First Hospital of Hebei Medical University
  • Li-Qiang Qin

    • Department of Nutrition and Food Hygiene, School of Public HealthSoochow University
Original Contribution
DOI: 10.1007/s00394-016-1292-z
Cite this article as:
Chen, G., Wang, Y., Tong, X. et al. Eur J Nutr (2016). doi:10.1007/s00394-016-1292-z

Abstract

Purpose

Cheese contains a high content of saturated fatty acids but also lists of potentially beneficial nutrients. How long-term cheese consumption affects the development of cardiovascular disease (CVD) is unclear. A meta-analysis of prospective observational studies was conducted to evaluate the risks of total CVD, coronary heart disease (CHD), and stroke associated with cheese consumption.

Methods

Potentially eligible studies were identified by searching PubMed and EMBASE databases and by carefully reviewing the bibliographies of retrieved publications and related reviews. The summary relative risks (RRs) with 95 % confidence intervals (CIs) were calculated using the random-effects model.

Results

The final analyses included 15 prospective studies. Most of the studies excluded prevalent CVD at baseline (14/15) and had a duration >10 years (13/15). The summary RR for high vs. low cheese consumption was 0.90 (95 % CI 0.82–0.99) for total CVD (7 studies, 8076 events), 0.86 (95 % CI 0.77–0.96) for CHD (8 studies, 7631 events), and 0.90 (95 % CI 0.84–0.97) for stroke (7 studies, 10,449 events), respectively. The restricted cubic model indicated evidence of nonlinear relationships between cheese consumption and risks of total CVD (Pnonlinearity < 0.001) and stroke (Pnonlinearity = 0.015), with the largest risk reductions observed at the consumption of approximately 40 g/d.

Conclusions

This meta-analysis of prospective studies suggests a nonlinear inverse association between cheese consumption and risk of CVD.

No one can stop you from being successful, but you.

Wang De Shun from China, age 80.
https://www.facebook.com/fitfiftyplus/videos/1174011932642183/

Stem cell propagation fuels cancer risk in different organs

Be careful out there, stem cells have a lot of proving to do yet before they become a standard therapy.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=167223&CultureCode=en
Experiments reveal the crucial contribution of stem cells to the origins of cancer in different organs.
The idea that stem cells – special cells that divide to repair and generate tissues – might be the major determinant of cancer risk has provoked great debate in the scientific community. Some researchers maintain that environmental carcinogens are more important in defining cancer risk. Now researchers at St. Jude Children’s Research Hospital and the University of Cambridge, England, have confirmed the crucial contribution of stem cells to the origins of cancer in different organs of mice. The results appear online today in the journal Cell.
 “The chance accrual of random mistakes in cell DNA likely plays an important role in generating cancer; but  whether this has to happen in specific cell types, such as stem cells, and precisely how other factors such as environmental carcinogens contribute to cancer is unclear,” said the study’s senior author, Richard Gilbertson, M.D., Ph.D., director of the Cancer Research UK Cancer Center at Cambridge University, England, and former St. Jude scientific and Comprehensive Cancer Center director. “Indeed, an argument has raged across the scientific community for some years now. Some say cancer is ‘bad luck’ because mutations arise by chance in stem cells, while others argue environmental carcinogens are more important. This disagreement has arisen largely from the use of different mathematical models to look at existing human cancer and stem cell data, from which it is extremely difficult to tease out the impact of individual factors. Therefore, we tested these opinions in actual experimental models that looked at the individual components that might drive cancer.”
The researchers used a specific “marker molecule” called Prom1 to map the activity of cells in various organs throughout the life of mice.  In some instances, Prom1+ cells were mature, non-dividing cells that did not repair or regenerate the organs, but in a handful of organs these cells were highly active stem cells. “By following these Prom1+ cells in all the major organs in mice through their lifetime journey, we were able to identify in which organs these cells were actively dividing stem cells,” said Liqin Zhu, Ph.D., a research associate at St. Jude and the study’s first author.
Once they had an organism-wide map of the cells’ function, the researchers introduced DNA mutations into these cells similar to the changes that occur in human cancers. “This approach does away with the need for carcinogens, removing them from the cancer equation and allowing us to test if the generative capacity of stem cells influenced cancer risk,” said Zhu. After a rigorous study lasting more than seven years and comprehensive statistical modeling of the results by Arzu Onar-Thomas, Ph.D., associate member of the St. Jude Biostatistics Department, the clear answer was that only cells with stem cell activity make cancer.
“But that’s not the whole story,” said Gilbertson.  “While we have shown that stem cell function is required to generate cancer, our study also revealed that damage to tissues such as the liver, the kind that can occur in humans, can ‘wake up’ sleeping stem cells, make them divide and massively increase cancer risk. Therefore, we propose that the origin of cancer lies in a ‘perfect storm’ that includes DNA mutations, stem cell function and tissue damage.”
The scientists also showed that stem cells in newborn animals are far less likely to undergo malignant transformation than adult stem cells. This finding suggests that stem cells in the newborn are intrinsically resistant to the formation of tumors. “If this biology were to hold true in humans, then it may explain why cancer rates are many-fold lower in children than adults, despite the fact that childhood cancers accrue significant numbers of mutations that alter proteins, and that the growth rates of organs peak in childhood,” said Zhu.
Many of the new cancer models described in the study bear striking similarities to human diseases and should provide a valuable resource for further biological and therapeutic studies.
The study’s authors are Liqin Zhu, David Finkelstein, Culian Gao, Lei Shi, Yongdong Wang, Stanley Pounds, Geoffrey Neale, David Ellison and Arzu Onar-Thomas of St. Jude. The study’s other authors are Dolores López-Terrada of Baylor College of Medicine, Kasper Wang and Sarah Utley of Children’s Hospital Los Angeles, and Richard James Gilbertson of CRUK Cambridge Institute (formerly at St. Jude).
This research was supported by funding from the National Institutes of Health (P01CA96832, R01 and P30CA021765), Cancer Research UK and ALSAC.
http://www.cell.com/cell/fulltext/S0092-8674(16)30995-3

Attached files

  • Liqin Zhu, Ph.D., a research associate at St. Jude and the study’s first author, with Arzu Onar-Thomas, Ph.D., associate member of the St. Jude Biostatistics Department.

Dedicated Rehabilitation Facilities for Stroke Patients at City Hospital

While this is great, it just proves that the stroke world is a complete failure. We wouldn't need such facilities if we had something better than tPA which only completely works 12% of the time. And if we solved the neuronal cascade of death by these 5 causes in the first week and prevented that damage that there would be much less dead and damaged neurons.
Or you could make neurogenesisis and neuroplasticity truly repeatable on demand. Choose any one of these, they are all extremely difficult to solve. But that is what leaders do, they solve the difficult problems. I bet you aren't a leader because you are just going to stay with the fucking failures of the status quo. 

Dedicated Rehabilitation Facilities for Stroke Patients at City Hospital

Stroke patients across Nottinghamshire are benefitting from a new dedicated rehabilitation unit at one of the region’s largest hospitals.

Nottingham University Hospitals NHS Trust (NUH) is one of the first hospitals in the country to provide separate rehabilitation services for stroke patients alongside acute care in the same setting.
Beeston Ward, a former stroke ward at Nottingham City Hospital, has been converted into a specialist rehabilitation unit, complete with a gym, kitchen and space for group exercise classes.
Patients who are suspected of suffering a stroke are taken by ambulance to Nottingham City Hospital where they are immediately assessed and treated by a specialist team on the hyper-acute ward – Berman 1 Stroke Unit. They are then transferred to one of two stroke wards for ongoing treatment and rehabilitation.

Rachel Tomasevic, Project Lead and Physiotherapist at NUH, said: “Patients used to only undergo their rehabilitation on the stroke wards. This meant that they spent a long time on the ward at what is a very emotional and challenging time.
“Creating a space away from the ward for patients to undergo rehabilitation, in addition to the ward environment, will improve their motivation to maximise functional outcomes. It also creates opportunities to interact with other patients and hospital staff through breakfast clubs and group exercise classes to give them a better inpatient experience.”

Ian Astle from Chilwell was one of the first patients to use the new rehabilitation unit. The 80-year-old former Health and Safety Consultant woke up one morning to realise he had suffered a stroke in the night. His wife called an ambulance and Ian was rushed to Nottingham City Hospital where he underwent lifesaving treatment before moving to a stroke ward (Newell Ward).
He said: “The care I have received has been excellent and the staff can’t do enough for you, but I am in a room on the ward by myself. While it is nice to have the privacy it means that you see less people and don’t get to interact with other patients.
Being able to get away from the ward and meet other people while continuing my recovery is just great. I can’t wait to get home and back on the golf course.
The unit is also home to the Stroke Outreach Team, who supports patients in their own homes following discharge, as well as the Transient Ischaemic Attack (TIA) clinic. A TIA is caused by a temporary fall in the blood and oxygen supply to part of the brain and causes symptoms that are similar to a stroke, but do not last as long. Patients are seen after their TIA and the clinic supports and empowers patients to make positive lifestyle choices following the diagnosis of a TIA.
Stroke survivor and campaigner Dr Ossie Newell MBE officially opened the new unit alongside Caroline Shaw, NUH Chief Operating Officer. He said: “I have long been a fighter for the provision of better rehabilitation service availability for stroke survivors in order to assist in their recovery.

Robot-aided assessment of lower extremity functions: a review

Are your therapists doing ANY objective measurements of your lower limb problems. Or are they using subjective crap like Timed Up and Go (TUG) Test
which doesn't look at quality of walking at all.
Or the various minute walking tests.
Or the Berg Balance Scale which I pretty much failed at in the standing on one leg category. Nothing in there was objective enough to help in your rehabilitation. We never worked on any of the testing categories to try to become better. So the test was totally useless. 
Once again proving that everything in stroke is still a clinical research project of one - YOU, and you never signed any release forms for that testing.

Robot-aided assessment of lower extremity functions: a review 

  • Serena MaggioniEmail authorView ORCID ID profile,
  • Alejandro Melendez-Calderon,
  • Edwin van Asseldonk,
  • Verena Klamroth-Marganska,
  • Lars Lünenburger,
  • Robert Riener and
  • Herman van der Kooij
Journal of NeuroEngineering and Rehabilitation201613:72
DOI: 10.1186/s12984-016-0180-3
Received: 8 January 2016
Accepted: 21 July 2016
Published: 2 August 2016

Abstract

The assessment of sensorimotor functions is extremely important to understand the health status of a patient and its change over time. Assessments are necessary to plan and adjust the therapy in order to maximize the chances of individual recovery. Nowadays, however, assessments are seldom used in clinical practice due to administrative constraints or to inadequate validity, reliability and responsiveness. In clinical trials, more sensitive and reliable measurement scales could unmask changes in physiological variables that would not be visible with existing clinical scores.
In the last decades robotic devices have become available for neurorehabilitation training in clinical centers. Besides training, robotic devices can overcome some of the limitations in traditional clinical assessments by providing more objective, sensitive, reliable and time-efficient measurements. However, it is necessary to understand the clinical needs to be able to develop novel robot-aided assessment methods that can be integrated in clinical practice.
This paper aims at providing researchers and developers in the field of robotic neurorehabilitation with a comprehensive review of assessment methods for the lower extremities. Among the ICF domains, we included those related to lower extremities sensorimotor functions and walking; for each chapter we present and discuss existing assessments used in routine clinical practice and contrast those to state-of-the-art instrumented and robot-aided technologies. Based on the shortcomings of current assessments, on the identified clinical needs and on the opportunities offered by robotic devices, we propose future directions for research in rehabilitation robotics. The review and recommendations provided in this paper aim to guide the design of the next generation of robot-aided functional assessments, their validation and their translation to clinical practice.
 

Thursday, August 25, 2016

Does Increased Arterial Stiffness Herald Cognitive Impairment?

What is your doctor doing to reduce arterial stiffness? ANYTHING AT ALL?
Don't follow my ideas.

Watermelon juice reverses hardening of the arteries

 

Stiff arteries relax like younger blood vessels after taking alagebrium

 

Black Raspberry Extract Increased Circulating Endothelial Progenitor Cells and Improved Arterial Stiffness in Patients with Metabolic Syndrome: A Randomized Controlled Trial 

  

Does Increased Arterial Stiffness Herald Cognitive Impairment?

  1. Tatjana Rundek, MD, PhD
+ Author Affiliations
  1. From the Department of Neurology, Evelyn F. McKnight Brain Institute, University of Miami Miller School of Medicine, FL.
  1. Correspondence to Tatjana Rundek, MD, PhD, 1120 NW 14th St, CRB 1348, Miami, FL 33136. E-mail trundek@med.miami.edu
Key Words:
See related article, p 2256.
Cognitive impairment or dementia is one of the most frequent causes of disability in the elderly. A recent meta-analysis reports global prevalence of dementia from all causes to be between 5% and 7% of adults of age >60 years.1 It doubles every 5 years and reaches >30% at the age of 90 years in the most regions of world.1 Dementia has become a significant economic burden in aging societies worldwide. There is a transitional phase between normal function and dementia. The term mild cognitive impairment (MCI) has been introduced to define such transitional cognitive dysfunction in the clinical and research settings.2 The prevalence of MCI is close to 20% in people aged >70 years.2 Given the fact that elderly patients with MCI have a high risk of developing dementia, identification of early biomarkers of MCI would be a critical step to facilitate construction of measures for prevention of dementia.
Arterial stiffness refers to a reduction in the ability of large arteries to readily accommodate the increase in blood volume ejected from the heart during systole.3 It has been proposed as an indirect measure of brain microcirculation and small-vessel damage.4 Recent evidence has suggested that cerebral small-vessel disease is involved in pathophysiology of cognitive decline, vascular dementia, and Alzheimer disease.5 Therefore, arterial stiffness may be a novel imaging biomarker of MCI and dementia.
In this issue of Stroke, Pase et al6 report a strong association between aortic stiffness, measured by pulse wave velocity, and the development of MCI and incident dementia >10 years of surveillance in a sample of 1101 dementia-free Framingham Offspring Study participants. Higher aortic stiffness was associated with an increased risk of MCI (hazard ratio, 1.40; 95% confidence interval, 1.13–1.73), independent of age, education, APOE 4 status, vascular risk factors, and cardiovascular diseases. Similarly, higher aortic stiffness was associated with an increased risk of dementia (hazard ratio 1.45; 95% confidence interval, 1.13–1.87), independent of age, education, and APOE 4 status, but not independent of vascular risk factors. The authors reported that among individuals without diabetes mellitus, the higher aortic stiffness was associated with an increased risk of incident all-cause dementia (hazard ratio 2.27; 95% confidence interval, 1.28–4.05). This association was not present among individuals with diabetes mellitus. Interestingly, central pulse pressure and prevalent hypertension were not associated with increased risks of MCI, all-cause dementia, or Alzheimer disease.
Although a wealth of evidence in cross-sectional studies shows that increased arterial stiffness is associated with poor cognition,7 data from longitudinal studies are sparse. Several studies have reported an association between the top tertile of pulse wave velocity and greater annual decline in Mini Mental State Examination and specific cognitive domains such as executive function, processing speed, or verbal memory.7 Studies on the long-term temporal relationships between arterial stiffness and MCI are limited and therefore the article by Pase et al6 contributes considerably to filling the knowledge gaps linking a long-term effect of arterial stiffness to increased risk of MCI. The study provides compelling evidence for an important vascular role in the pathogenesis of MCI. Vascular risk factors including hypertension, diabetes mellitus, and adiposity are contributing factors to MCI and dementia.8 However, Pase et al6 show that the effect of aortic stiffness on all-cause dementia is stronger among those without diabetes mellitus, indicating that an association between diabetes mellitus and dementia may not be mediated by vascular changes but rather through metabolic mechanisms. Whether arterial stiffness can be a predictor or biomarker of MCI and dementia independent of vascular and metabolic risk factors deserves further investigation.
The finding of arterial stiffness associated with incident dementia is congruent with some previous results. A large body of evidence has suggested a link between vascular factors and dementia including Alzheimer disease.9 Ischemic brain injury manifested as small-vessel disease is commonly seen in patients with dementia. Although arterial stiffness has been associated with aging, vascular risk factors, cardiovascular diseases, genetic disorders, and autoimmune diseases,4,10 the role of arterial stiffness in MCI and dementia is unclear. The mechanism by which arterial stiffness may affect cognition is, however, plausible. Because the brain microcirculation has low impedance or resistance, small cerebral arteries are more vulnerable to greater blood flow pulsatility transmission in the setting of increased systemic arterial stiffness.11 Elevated pulsatility combined with increased flow volume may lead to endothelial dysfunction and microvascular brain damage. Indeed, arterial stiffness has been related to brain small-vessel pathology such as white matter lesions, lacunar infarcts, and microbleeds,12 as well as to medial temporal lobe atrophy in the elderly with memory disorders.13 Therefore, this study emphasizes the potential contributing role of arterial stiffness to cognitive dysfunction and to overall cognitive health.3
It is important to note several limitations to this study. First, as often the case in observational longitudinal studies, the causality between arterial stiffness and MCI or dementia cannot be determined. Although the study is based on the well-characterized population sampled from the reputable Framingham Heart Study, these results may not be generalizable to other populations, especially to race-ethnic diverse populations.14 These results, therefore, need to be confirmed in other samples. Arterial stiffness can cause brain injury through silent brain infarcts and white mater damage; however, there is no direct evidence of brain injury variables analyzed in this study. And finally, structural brain damage leading to cognitive impairment may be predominately affected by stiffness in brain arteries or in direct brain-supplying arteries rather than by systemic arterial stiffness. Although peripheral pulse wave velocity is considered a gold standard for measuring arterial stiffness, it assumes that stiffness is equally distributed across the arterial tree. However, in the case of regional brain damage, this may not be an appropriate assumption, and therefore local stiffness measured in intracranial arteries may be a better marker of brain structural changes and cognitive decline.
Nevertheless, the finding of an association of arterial stiffness with an increased risk of MCI and incident dementia opens new horizons for the investigation of vascular mechanisms of dementia and the search for a valid and early vascular biomarker for MCI and dementia. Interventions that modify vascular risk factors and arterial stiffness have enormous potential for prevention of cognitive impairment and dementia.

Focused Ultrasound Cuts Hand Tremor in Trial

Would this help for post stroke tremors?
http://www.medpagetoday.com/Neurology/GeneralNeurology/59856?
Focused ultrasound thalamotomy produced short-term improvement in hand tremor in patients with essential tremor, researchers reported.
In a randomized sham-controlled trial, patients who received the therapy had greater improvements in physician-rated hand tremor scores at 3 months (47% improvement versus 0.1% improvement, P<0.001), Jeffrey Elias, MD, of the University of Virginia Health Sciences Center, and colleagues reported in the New England Journal of Medicine.
But editorialist Elan Louis, MD, of Yale, noted that data reported in a supplementary appendix (available only online) showed that overall tremor scores (i.e., not just hand tremor) rose by 23% and physician-rated tremor scores rose by 38% at month 12, relative to their nadir at one month post-treatment.
"Whether this loss of efficacy, which is also seen to some extent with deep-brain stimulation, is due to disease progression or tolerance is not clear," Louis wrote, adding that he considered the former "less likely."
The investigators also noted that the treatment came with sensory and gait disturbances affecting roughly one-third of patients.
The FDA approved the device used in the current study for MRI-guided focused ultrasound thalamotomy in essential tremor last month. The current study was the manufacturer's primary registration trial.
The procedure involves ablating tissue with high-intensity sound waves. Medical therapies for essential tremor include beta blockers -- particularly propranolol -- the antiepileptic drug primidone, and other drugs that enhance GABA transmission.
However, efficacy of these treatments is limited, so some patients try deep brain stimulation, which is the standard surgical procedure for this condition. It was approved by the FDA in 1997 for this indication, but there have been few randomized controlled trials of the technology, so evidence of its efficacy remains scant, Elias and colleagues wrote.
To assess whether focused ultrasound thalamotomy could provide another option for patients with moderate-to-severe essential tremor who don't responded to other medical therapies, the researchers enrolled 76 patients, mean age 71 with a mean disease duration of 17 years, and randomized them in a 3:1 fashion to unilateral focused ultrasound (which, if effective, would improve tremor in only the contralateral hand) or to a sham procedure.
The primary outcome was difference in change from baseline to 3 months in hand tremor, rated on a 32-point scale in which higher scores indicate a more severe tremor.
After 3 months, patients in the sham group were allowed to cross over to the active treatment.
Overall, the researchers found that scores improved more after focused ultrasound than with the sham procedure (from scores of 18.1 to 9.6 versus 16 to 15.8) -- a 47% improvement compared with a 0.1% improvement, and a mean difference of 8.3 points (P<0.001). No significant change in tremor scores for the ipsilateral hand was seen in treated patients.
The improvement in the focused ultrasound group persisted at one year, with a 40% improvement from baseline, they reported (P<0.001).
Patients who crossed over into the treatment group improved by 55% at 3 months and by 52% at 6 months, they found (P<0.001).
In terms of secondary outcomes, those who had focused ultrasound had greater improvements in disability (62% reduction versus 3% reduction, P<0.001) and in quality of life (46% improvement versus 3% improvement, P<0.001) at 3 months.
The researchers did note that higher rates of adverse events in thalamotomy group included gait disturbance (36%) and paresthesias or numbness (38%), and these persisted at one year in 9% and 14% of patients, respectively.
In the accompanying editorial, Louis highlighted "several important concerns." First, the study was limited to 1 year, so the benefits further down the road aren't clear, which requires more studies with longer follow-up, he said.
In addition to the overall tremor scores and physician-reported tremor scores increasing, Louis noted that not all patients benefitted from the procedure, with a percent change below 20% in 9 of 56 patients. Some skulls may be too thick for the procedure to work properly, he added.
Unlike with deep-brain stimulation, he warned, a thalamotomy creates a fixed brain lesion -- and altered sensation remained in 14% of patients at 1 year, he wrote.
"Even with these concerns and caveats, pros and cons, the procedure will take its place among other surgical procedures for medically refractory essential tremor," Louis wrote. "Given the perception that it is less invasive than other approaches because it does not involve burr holes and intracerebral electrodes, as well as the evidence that patients with essential tremor are perhaps particularly harm avoidant, the procedure may allow more patients to avail themselves of a surgical option for the treatment of this often disabling disease."
He also called for a head-to-head comparison with deep-brain stimulation.
  • Reviewed by Robert Jasmer, MD Associate Clinical Professor of Medicine, University of California, San Francisco

Researchers find potential way to reduce effects of TBI with neuron-targeting nanoparticle

Don't worry, NOTHING will be done to follow this up with a stroke clinical trial. We have NO fucking stroke leadership or strategy to help survivors at all. You can look at our fucking failures of stroke associations for what the next hundred years looks like unless they are destroyed and recreated to help survivors.
http://www.news-medical.net/news/20160817/Researchers-find-potential-way-to-reduce-effects-of-TBI-with-neuron-targeting-nanoparticle.aspx
A fall down the stairs, a car crash, a sports injury or an explosive blast can all cause traumatic brain injury (TBI). Patients often recover. But in the days or weeks following the hit, they can develop other serious, chronic conditions, such as depression and thinking and memory problems. Now scientists report in the journal ACS Nano a potential way to reduce these effects with a neuron-targeting nanoparticle, using an animal model of TBI.
When someone suffers from a head injury, the damage doesn't necessarily stop after the initial blow. The jolt can cause a cascade of after-effects -- such as inflammation and ultimately the death of brain cells -- and lead to physical and cognitive conditions that can continue for years. One promising approach to treating these after-effects involves delivering short stretches of RNA that can help shut down this chain reaction. But getting the RNA to the damaged part of the brain is a challenge because of the blood-brain barrier, which separates circulating blood from the fluid around brain cells. Sangeeta N. Bhatia and her colleagues at the Massachusetts Institute of Technology's Institute for Medical Engineering & Science wanted to see if they could rush therapeutic RNA to targeted brain cells soon after an injury while the blood-brain barrier is weakened.
The team, led by postdoctoral researcher Ester Kwon, engineered nanoparticles to target neurons by borrowing a protein from the rabies virus. They also loaded the particles with a strip of RNA designed to inhibit the production of a protein associated with neuronal cell death. When given to mice intravenously within a day of receiving a brain injury, the nanoparticles left the circulation and accumulated in the damaged tissue. Analysis also showed that the levels of the protein that the researchers were trying to reduce dropped by about 80 percent in the injured brain tissue.
Source:
American Chemical Society
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