ISC Session: “What’s Old Is New Again: Neuroprotection for Stroke in 2019”

Until we demand that the milquetoast term 'neuroprotection' be called 'neuronal cascade of death' there will never be any urgency to solving it.  I see nothing here that anyone has taken responsibility for solving all the various parts of that

neuronal cascade of death.  None of these seem to have a specific target they are trying to solve. Everything is general, with NO specifics there will never be success. If you can't describe the complete problem you are trying to solve you will fail.  This is why survivors need to be in charge, they have a single-minded goal, 100% recovery.

ISC Session: “What’s Old Is New Again: Neuroprotection for Stroke in 2019”

International Stroke Conference
February 6–8, 2019
Robert W. Regenhardt, MD, PhD
@rwregen
Moderators: Jean Claude Baron, Andrew Demchuk
The first talk, by Nerses Sanossian, was titled “Neuro-protection in the Pre-hospital Setting.” Sanossian began by introducing the ischemic cascade in which there are rapid changes over minutes to hours (O2 depletion, energy failure, terminal depolarization, ion homeostasis failure), secondary changes over minutes to days (excitotoxicity, SD-like depolarizations, disturbance of ion homeostasis), and delayed changes over days to weeks (inflammation, apoptosis). While no neuro-protective agent has proven successful in phase 3 clinical trials, he asserts that these agents still hold promise. Reconsideration of mechanistic targets is important as there has been a shift in treatment paradigm with thrombectomy now the priority for LVO strokes. As these patients are collected from locations of symptom onset, transported to thrombectomy capable hospitals, and admitted for acute care, when is the best time to offer a neuro-protective agent? Future trials must balance the timing against the cost. An agent could be administered pre-hospital, post-arrival/pre-imaging, post-tPA, pre/during transfer if needed, pre-thrombectomy, or post-thrombectomy. There are unique considerations for each timepoint. In the pre-hospital setting, consent can be difficult, there is no imaging available, agents should be safe in ICH, have no interaction with tPA, easily stored in ambulances, administration should be easy (avoid pumps and compounding), agents should be effective despite fewer patients recanalizing, and have robust experimental data at early time points. In-hospital initiation allows standard consent, imaging is available (could tailor agent to stroke subtype), pharmacies can store and dispense agents, agents can be combined with recanalization (improved delivery to target tissue and opportunity for targeting reperfusion injury and hemorrhagic transformation), and patients can be more carefully selected after imaging for those most likely to benefit.

Indeed, a long criticism of many animal models was that they utilized ischemia followed by reperfusion; in the thrombectomy era, now 80% of LVO patients may achieve reperfusion making the prior model more translatable. Several pre-hospital trials have paved the way for future work, including FAST-MAG testing magnesium (completed 2015), RIGHT 2 testing glyceryl trinitrate (completed 2019), FRONTIER testing NA1 (recruiting until 2020), and PHAST-TSC testing trans-sodium crocetinate (approved to start 2019). FAST-MAG had an average symptom onset to agent administration time of 45 min. The agent to tPA time was 92 min and the agent to thrombectomy time was 230 min, illustrating how much faster these pre-hospital agents can be administered. One of the latest agents, trans-sodium crocetinate (PHAST-TSC), is intended to work by enhancing diffusion of oxygen to hypoxic tissues by altering the structure of water molecules in plasma. Preclinical data suggests there may be a benefit for both ischemic and hemorrhagic stroke, making this an exciting pre-hospital target.
Michael Hill gave the second talk, titled “Expanding the Time Window for Thrombectomy: Neuro-protection in the Era of Endovascular Treatment.” Hill began by reminding us that despite thrombectomy’s enormous efficacy for LVO strokes, 37% of those treated are still disabled and 10% still die. The problem is not solved. One approach may be expanding the time window by administering an agent, perhaps pre-hospital, that can prevent infarct expansion and allow more patients to be candidates for thrombectomy. While time is a convenient “surrogate for physiology,” there is significant variation between individual patients and it is only one variable in the equation for infarct progression. Indeed, imaging characteristics may be more important than time as shown in the DAWN and DEFUSE 3 trials for thrombectomy and the WAKEUP and EXTEND trials for tPA.
Hill asked, “Can we help patients on the way to thrombectomy?” He believes we can as about 1/3 have infarct progression while being transferred for thrombectomy. He favors the approach of in-field delivery of an agent to “suspend” strokes. “Freezing ischemic penumbra evolution” has been shown in a rodent model using NA1. Hill also argued that in the era or thrombectomy our human patients are now better modeled by preclinical rodent monofilament ischemia and reperfusion experiments since humans are now achieving reperfusion. Much of the preclinical work with this model is now more translatable. Hill stated that the ESCAPE- NA1 trial is testing the efficacy of NA1 specifically in patients undergoing thrombectomy (recruiting until 2020). It is recruiting at 50 sites and has over 800 already enrolled. He told the audience to look for the results next year.
“Preventing Reperfusion Injury: Neuro-protection after Acute Stroke Treatment” by Lauren Sansing was the third talk. Sansing outlined reasons for the renewed interest in neuro-protection. Like the previous speaker, she made the point that while thrombectomy is highly effective, there is still room for improvement as only 10% of those treated achieve full recovery with mRS 0. Previous trials of neuro-protective agents may have failed as there were low rates of recanalization. In the thrombectomy era, drug is more likely to be delivered to target tissue after recanalization. In the past, there was less regulation on preclinical design. More recently, both the NIH and most journals have increased the level of rigor expected. There has also been increased interactions between basic scientists and clinicians through efforts of NINDS, Stroke Net, and academic groups.
Sansing believes that inflammation plays a key central role in many underlying mechanisms of ischemic injury. She described that the inflammatory response after stroke can be described as a balance of injurious effects and reparative effects. The injurious effects involve IL-1β, TNF, IL-6, endothelial cell activation, platelet aggregation, recruitment of pro-inflammatory neutrophils, monocytes, T cells, and inflammatory microglia. These processes lead to infarct growth, neuronal loss, and astrogliosis. In contrast, the reparative effects involve TGFβ, IL-10, IL-4, BDNF, alternatively activated microglia and macrophages, and regulatory T and B cells. These processes lead to clearance of debris, resolution of inflammation, angiogenesis, and neurogenesis.
Sansing further discussed thrombo-inflammation and the no-reflow phenomenon, in which there is infarct growth into the penumbra, failure of collateral flow, and tissue infarction despite recanalization of the parent vessel. She described that inflammation may be the underling mechanism, including NFΚB, MMP-9, PAI-1, PAR4, leukocyte margination, and neutrophil-platelet aggregates. Inflammation is also involved in several biologic comorbidities, such as aging, diabetes, and hyperglycemia.
Sansing then outlined several promising immunomodulatory targets in the translational pipeline. IL-6 receptor antagonism is one example; a meta-analysis of 24 studies showed elevated IL-6 is associated with poor outcomes. Tocilizumab (anti-IL-6R) is FDA approved for RA and GCA and has shown promising results in preliminary studies. Another is PAR1 functional selectivity with 3K3A-APC. Multiple preclinical studies in aged mice of both sexes with comorbidities such as hypertension have demonstrated effects. The RHAPSODY trial, a phase 2A dose escalation of 3K3A-APC in conjunction with tPA and/or thrombectomy, showed possibly lower rates of hemorrhagic transformation. Sphingosine 1 phosphate signaling with the use of fingolimod, which is FDA approved for MS, is another target. It modulates several cell types but is best known for inhibiting egress of memory T cells from lymph nodes. A meta-analysis of many preclinical models and early preclinical trials are promising. The FAMTAIS trial is ongoing. Lastly, IL-1 receptor antagonism has been explored in over 25 papers and 76 experiments. The phase 2 trial, SCIL-STROKE, enrolled 80 patients to examine Anakinra. While there was no effect on 90-day outcomes, a mediation analysis with baseline IL-6 showed promise and raised new questions.
Angel Chamorro gave the final talk, titled “Vasculo-protection for Stroke.” He opened by stating “Failure is not the opposite of success. It is part of success.” He summarized major lessons learned in the field, including the importance of studying the whole neurovascular unit and not just neurons. He stated the “ischemic cascade is a mess,” underscoring its complicated, inter-related, and multidirectional mechanisms. Chamorro argued that perhaps the best target is reducing oxidative stress. Recanalization is important and full reperfusion is better than partial reperfusion.
Chamorro believes that the vessels themselves are the next exciting target for vasculo-protection. Endothelial cells produce free radicals, which can lead to tight junction opening with blood brain barrier (BBB) degradation and pericyte contraction with no reflow. This may underlie mechanisms of futile recanalization. Indeed, it appears that neuro-protective agents can act directly on the vessels as agents to suppress ROS are still effective in reducing infarct size even when unable to cross the BBB.
Chamorro then discussed uric acid, the end product of nucleotide metabolism, in depth. By reducing nitrosylation of proteins, it is one of the strongest antioxidants, according to Chamorro. In preclinical models, uric acid has met all the STAIR criteria. Furthermore, it has been studied in both sexes, in hypertensive rats, in hyperglycemic mice, and there is tPA synergism. In human stroke patients, Chamorro has shown that uric acid levels are associated with good functional outcomes at hospital discharge. The URICO-ICTUS phase 2b/3 trial showed a trend for improvement given soon after tPA. Uric acid appears to have the most pronounced effects in patients with hyperglycemia, perhaps by blunting toxic effects of glucose. Chamorro believes this may be particularly important as we now know intensive glucose control is not enough to influence outcomes (SHINE). He showed data that glucose is a treatment modifier of thrombectomy utilizing HERMES data. He concluded by stating that uric acid is ready for definitive validation in a large phase 3 trial, but funding is lacking.
The ensuing discussion involved several interesting questions, but one of the most widely debated was, How should we decide which agent to test next in humans? The NINDS recently launched a model to test up to 6 neuroprotectants in parallel. Perhaps combinations of agents will be more effective. Agents should only be considered if all STAIR criteria are met. Others questioned if we should re-test agents that previously failed in the pre-thrombectomy era given that the human condition of LVO and thrombectomy now includes reperfusion. Drug companies may lack incentive to re-test agents that are past their patents. Furthermore, it may be that patient selection is key. I believe that for any agent, we should learn lessons from the thrombectomy trials; we should select patients that are most likely to benefit from a given agent as to not dilute their effects. Time and target are critical. Considerations of stroke subtypes and white matter vs gray matter injury mechanisms will also likely be important. I agree with the speakers and appreciate their optimism. Neuro-protective strategies have a role in the future, and funding their study is essential.

Alzheimer’s Memory Loss Dramatically Reversed in Mice

So your doctors, stroke hospital and stroke association should followup with human research testing this out. That is the minimum a competent doctor, stroke hospital and stroke association should be doing.  But you already know that nothing will be done unless you do this testing yourself. Hope you don't die. You would be in good company;

10 Scientists Who Experimented on Themselves | Mental Floss

 

Alzheimer’s Memory Loss Dramatically Reversed in Mice

Mouse study reverses memory loss in mice with Alzheimer’s.

Memory loss caused by Alzheimer’s disease has been reversed in mice, reports a new study.
Alzheimer’s disease — the most common form of dementia –results from both genetic and environmental factors, and is currently untreatable.

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Scientists have discovered, though, that the disease interferes with electrical signalling in part of the brain responsible for memory.
Using techniques based on epigenetics, the researchers were able to reverse the memory loss.
Epigenetics involves how instructions contained in DNA are expressed in cells.
Professor Zhen Yan, the study’s first author, said:

“We have not only identified the epigenetic factors that contribute to the memory loss, we also found ways to temporarily reverse them in an animal model of AD.”

The scientists found that Alzheimer’s caused neurons in the frontal cortex to gradually lose glutamate receptors.
By inhibiting an enzyme, they were able to restore memory in mice.
Professor Yan said:

“When we gave the Alzheimer’s animals this enzyme inhibitor, we saw the rescue of cognitive function confirmed through evaluations of recognition memory, spatial memory and working memory.
We were quite surprised to see such dramatic cognitive improvement.
At the same time, we saw the recovery of glutamate receptor expression and function in the frontal cortex.”

While the drug only worked on the mice for one week, it is hoped the method can be refined to make it more powerful.
Epigenetics is powerful because it can target the effects of more than one gene, said Professor Yan:

“An epigenetic approach can correct a network of genes, which will collectively restore cells to their normal state and restore the complex brain function.
We have provided evidence showing that abnormal epigenetic regulation of glutamate receptor expression and function did contribute to cognitive decline in Alzheimer’s disease.
If many of the dysregulated genes in AD are normalized by targeting specific epigenetic enzymes, it will be possible to restore cognitive function and behavior.”

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The study was published in the journal Brain (Yan et al., 2019).

Novel Hemoglobin-Based Oxygen Carrier Bound With Albumin Shows Neuroprotection With Possible Antioxidant Effects

We need followup and we need it NOW! WHOM is going to take responsibility and get that done? Our fucking failures of stroke associations will once again DO NOTHING! Just like they've done nothing with the thousands of pieces of earlier research needing followup. Survivors get screwed, stroke staff sit on their asses doing nothing. I would fire the whole lot of them.

Novel Hemoglobin-Based Oxygen Carrier Bound With Albumin Shows Neuroprotection With Possible Antioxidant Effects

Masayuki Gekka, Takeo Abumiya, Teruyuki Komatsu, Ryosuke Funaki, Kota Kurisu, Daisuke Shimbo, Masato Kawabori, Toshiya Osanai, Naoki Nakayama, Ken Kazumata, Kiyohiro Houkin

Download PDF

https://doi.org/10.1161/STROKEAHA.118.021467

Stroke. 2018;STROKEAHA.118.021467

Originally published July 10, 2018

Abstract

Background and Purpose—A hemoglobin-albumin cluster, 1 core of hemoglobin covalently bound with 3 shell albumins, designated as HemoAct was developed as a hemoglobin-based oxygen carrier. We aim to investigate neuroprotection by HemoAct in transient cerebral ischemia and elucidate its underlying mechanisms.

Methods—Male rats were subjected to 2-hour transient middle cerebral artery occlusion and were then administered HemoAct transarterially at the onset of reperfusion. Neurological and pathological findings were examined after 24 hours of reperfusion to identify neuroprotection by HemoAct. Intermittent measurements of cortical blood flow and oxygen content were performed, and a histopathologic analysis was conducted on rats during the early phase of reperfusion to assess the therapeutic mechanism of HemoAct. In addition, the antioxidant effects of HemoAct were examined in hypoxia/reoxygenation-treated rat brain microvascular endothelial cells.

Results—Neurological deterioration, infarct and edema development, and the activation of MMP-9 (matrix metalloprotease-9) and lipid peroxidation after 24 hours of reperfusion were significantly ameliorated by the HemoAct treatment. Reductions in blood flow and tissue partial oxygen pressure in the cortical penumbra after 6 hours of reperfusion were significantly ameliorated by the HemoAct treatment. The histopathologic analysis of the cortical penumbra revealed that HemoAct in HemoAct-treated rats showed superior microvascular perfusion with the mitigation of microvascular narrowing changes than autologous erythrocytes in nontreated rats. Although HemoAct extravasated into the ischemic core with serum protein, it did not induce an increase in serum extravasation or reactive oxygen species production in the ischemic core. In vitro experiments with rat brain microvascular endothelial cells revealed that HemoAct significantly suppressed cellular reactive oxygen species production in hypoxia/reoxygenation-treated cells, similar to albumin.

Conclusions—HemoAct exerted robust neuroprotection in transient cerebral ischemia. Superior microvascular perfusion with an oxygen delivery capability and possible antioxidant effects appear to be the underlying neuroprotective mechanisms.

• antioxidant
• brain ischemia
• hemoglobin
• neuroprotection
• reperfusion

• Received March 17, 2018.
• Revision received June 4, 2018.
• Accepted June 8, 2018.

• © 2018 American Heart Association, Inc.

Prescription and predictors of post-stroke antidepressant treatment: A population-based study

Well fuck, write up a protocol on this. But why do we care about predicting post-stroke depression? Do we not have consensus that all survivors should get anti-depression drugs because they lead to a better recovery? Is there not one stroke medical professional in the world willing to take responsibility and write stroke protocols?
Antidepressants may help people recover from stroke even if they are not depressed
"Taken together, the available data make a strong case for the prophylactic use and effectiveness of antidepressants post stroke," the researchers said.

Prescription and predictors of post-stroke antidepressant treatment: A population-based study

Scandinavica (Apr 2018)

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

OBJECTIVES Post-stroke depression and pathological crying are common and potentially serious complications after stroke and should be diagnosed and treated accordingly. Diagnosis and treatment probably rely on clinical experience and may pose certain challenges. We aimed to examine prescription and predictors of antidepressant treatment after ischemic stroke in a clinical setting.
MATERIALS AND METHODS In this registry-based follow-up study, consecutive ischemic stroke patients were identified from the Danish Stroke Registry, holding information on antidepressant treatment during admission in Aarhus County from 2003 to 2010. Information on prescription after discharge was obtained from the Danish Prescription Database. Treatment initiation was analyzed using the cumulative incidence method including death as a competing risk. Multiple logistic regression was used to identify potential predictors of treatment.
RESULTS Among 5070 consecutive first-ever ischemic stroke patients without prior antidepressant treatment, the cumulative incidence of antidepressant treatment and prescription over 6 months was 35.2% (95% CI: 33.8-36.6). Overall 16.5% (95% CI: 15.5-17.6) started treatment within 14 days corresponding to 48.1% (95% CI: 45.8-50.5) of all treated patients, and the most widely prescribed group of antidepressants was selective serotonin reuptake inhibitors (86%). Increasing stroke severity was associated with higher odds of initiating treatment.
CONCLUSION Antidepressant treatment in this real-life clinical setting was common and initiated early, in almost half the treated patients within 14 days. Our results suggest that special focus should be given to the severe strokes as they may have a greater risk of requiring treatment.

Treatment of stroke in Europe: the Helsingborg Declaration - from 1995

Notice they don't talk about RESULTS, just 'CARE'. No wonder stroke never gets anywhere. No one ever takes responsibility for solving all the problems in stroke. All they are doing is saying they care., but never do anything useful for survivors. They should all be keel hauled.
https://www.ncbi.nlm.nih.gov/pubmed/9190521

[Article in Dutch]

Limburg M¹.

Author information

Abstract

Late in 1995, the Helsingborg Declaration was adopted, a European consensus text on the basic elements for policy in, and objectives of treatment of strokes. This declaration was prompted by the fact that the differences in incidence in different European countries, and the changes of the incidence in the course of the years suggest a great importance of environmental factors that can be influenced. The organizers of this consensus meeting might have enhanced the value of the document by more exactly indicating the (scientific) strength of the argumentation for each recommendation. Nevertheless, many of the recommendations are based on solid evidence. A plea is made to structure stroke care, measure the quality of care, facilitate early diagnosis and therapy after stroke, improve the possibilities for rehabilitation, and apply appropriate secondary prevention.

PMID:

9190521

Executive dysfunction and balance function post-stroke: A cross-sectional study

With executive dysfunction you wouldn't be able to follow therapist instructions. So what is the protocol to address that dysfunction? Don't just describe the problem, offer a solution.
http://search.naric.com/research/rehab/redesign_record.cfm?search=2&type=all&criteria=J76647&phrase=no&rec=134533&article_source=Rehab&international=0&international_language=&international_location=
Physiotherapy , Volume 102(1) , Pgs. 64-70.

NARIC Accession Number: J76647.  What's this?
ISSN: 0031-9406.
Author(s): Hayes, Sara; Donnellan, Claire; Stokes, Emma.
Publication Year: 2016.
Number of Pages: 7.
Abstract: Study investigated the prevalence of executive dysfunction (ED), demographic, and clinical differences between participants with ED and without ED and, independent association between executive function (EF) and balance post-stroke. One hundred participants were evaluated within 6 months of experiencing a first-ever stroke. Participant age ranged from 31 to 98 years, time since stroke ranged from 4 to 180 days, and the participants reported formal education ranging from 7 to 21 years. The primary outcome measure was balance function; secondary outcomes included EF, stroke severity, depression and global cognition. Descriptive statistics were used to report the prevalence of ED post-stroke. Comparisons of demographic and clinical characteristics were made between participants with ED and without ED using independent t-tests. Hierarchical multiple linear regression analysis determined the association between EF and balance post-stroke. Results indicated that ED was present in 47 percent of the study participants the first six months post-stroke. Participants with ED had more severe strokes, poorer global cognition, and poorer balance than participants without ED. Age, years of education, stroke severity, time since stroke, and EF were independently associated with balance post-stroke. The total variance in balance explained by the model was 72 percent. Findings suggest ED is independently associated with balance post-stroke. Physiotherapists should consider this when developing rehabilitation strategies to improve balance post-stroke.(This last sentence is a fucking joke, abandoning all sense of responsibility for anything researched here.)
Descriptor Terms: CLIENT CHARACTERISTICS, COGNITIVE DISABILITIES, DEMOGRAPHICS, EQUILIBRIUM, PHYSICAL THERAPY, POSTURE, PREVALENCE, STROKE.


Can this document be ordered through NARIC's document delivery service*?: Y.

Citation: Hayes, Sara, Donnellan, Claire, Stokes, Emma. (2016). Executive dysfunction and balance function post-stroke: A cross-sectional study.  Physiotherapy , 102(1), Pgs. 64-70. Retrieved 10/11/2017, from REHABDATA database.

Dendritic spines provide cognitive resilience against Alzheimer's disease

You'll have to DEMAND your doctor provide you protocols that will create new dendritic spines.  And after s/he does that ask for proof that the protocols are working. You have to DEMAND accountability and responsibility from your doctors.
http://onlinelibrary.wiley.com/doi/10.1002/ana.25049/full

Authors

• Accepted manuscript online: 16 September 2017Full publication history
• DOI: 10.1002/ana.25049  View/save citation
• Cited by (CrossRef): 0 articles Last updated 23 September 2017

Abstract

Objective: Neuroimaging and other biomarker assays suggest that the pathological processes of Alzheimer's disease (AD) initiate years prior to clinical dementia onset. However some 30%-50% of older individuals that harbor AD pathology do not become symptomatic in their lifetime. It is hypothesized that such individuals exhibit cognitive resilience that protects against AD dementia. We hypothesized that in cases with AD pathology structural changes in dendritic spines would distinguish individuals that had or did not have clinical dementia.
Methods: We compared dendritic spines within layers II and III pyramidal neuron dendrites in Brodmann Area 46 dorsolateral prefrontal cortex using the Golgi-Cox technique in 12 age-matched pathology-free controls, 8 controls with AD pathology (CAD), and 21 AD cases. We used highly optimized methods to trace impregnated dendrites from brightfield microscopy images which enabled accurate three-dimensional digital reconstruction of dendritic structure for morphologic analyses.
Results: Spine density was similar among control and CAD cases but reduced significantly in AD. Thin and mushroom spines were reduced significantly in AD compared to CAD brains, whereas stubby spine density was decreased significantly in CAD and AD compared to controls. Increased spine extent distinguished CAD cases from controls and AD. Linear regression analysis of all cases indicated that spine density was not associated with neuritic plaque score but did display negative correlation with Braak staging.
Interpretation: These observations provide cellular evidence to support the hypothesis that dendritic spine plasticity is a mechanism of cognitive resilience that protects older individuals with AD pathology from developing dementia. This article is protected by copyright. All rights reserved.

Venom of a deadly spider holds promising therapeutics against stroke.

No text, video only. Whom is going to take responsibility for getting this tested in humans?
Bet nothing gets done since we have NO STROKE LEADERSHIP OR STRATEGY.
https://www.facebook.com/ScienceNaturePage/videos/1091656927633231/ 

Sunderland among worst in the country for stroke services - UK

Totally the wrong thing to be focusing on, care. What are their fucking RESULTS in stroke rehab? That is what you need to be shouting bloody murder on. Arguing about services is a waste of time and the wrong issue to be solving. You need to get on The National Stroke Quality Team and get real performance measures implemented and quality ratings that focus on results. This is going to be difficult work because medical teams do not like to be rated on results. Care means absolutely nothing and should never be in any rating system. It is a way to avoid responsibility.
http://www.sunderlandecho.com/news/sunderland-among-worst-in-the-country-for-stroke-services-1-8249547
Sunderland and Durham are affected by a ‘postcode lottery’ of stroke care services, claims a new report. Statistics released by the Stroke Association show regional variations in the treatment and care people receive in hospital, with the North East lagging behind. We know that the quality of care for stroke patients in South Tyneside and Sunderland needs to be improved and this has been a driver for change in both hospitals Ken Bremner The resesarch looked at five catergories and South Tyneside District Hospital was bottom in three, and in the bottom four in one, while the University Hospitals of North Tees and Hartlepool were bottom in one category and in the bottom ten in another. In one of the categories, the percentage of eligible patients who received thrombolysis within four hours, Sunderland Royal Hospital was sixth from the bottom in the country with 63.9% and the University Hospital of North Durham was seventh from bottom with 64.9%. The Stroke Association released the map of the best and worst to highlight the ‘postcode lottery’ of patient care. There were five indicators studied, from between March 2015 and April 2016. Now, the association is calling on the calling on the Government to give all hospitals the support they need to tackle these regional variations. Juliet Bouverie, chief executive of the Stroke Association, said: “Stroke is a medical emergency, and when swift treatment is not given to those who need it, people’s recoveries are put at risk. “It is unacceptable that your postcode determines whether or not you face treatment delays if you have a stroke.” Ken Bremner, Chief Executive of City Hospitals Sunderland NHS Foundation Trust and South Tyneside NHS Foundation Trust, said: “We know that the quality of care for stroke patients in South Tyneside and Sunderland needs to be improved and this has been a driver for change in both hospitals. “We have already started to make arrangements for a temporary change to the way acute stroke services are delivered as it was recognised the service at South Tyneside District Hospital was vulnerable because of challenges in recruiting a specialist stroke consultant. “Acute stroke care for South Tyneside residents is to be temporarily centralised at Sunderland Royal Hospital and by doing this we will be better placed to achieve key national standards and therefore ensure both organisations are providing the best possible care in order to maximise recovery following a stroke. “By making this temporary change our clinical teams are able to work together to improve the national standings for stroke care for all patients and they are confident the rating will move to at least a B, with the potential to achieve a grade A. “The National Stroke Quality Team, as well as our CCG partners, has supported our planned temporary solution as a method to begin to improve these important quality ratings.” Public consultation on a more permanent solution will be undertaken in early 2017.

Sunderland and Durham are affected by a ‘postcode lottery’ of stroke care services, claims a new report. Statistics released by the Stroke Association show regional variations in the treatment and care people receive in hospital, with the North East lagging behind. We know that the quality of care for stroke patients in South Tyneside and Sunderland needs to be improved and this has been a driver for change in both hospitals Ken Bremner The resesarch looked at five catergories and South Tyneside District Hospital was bottom in three, and in the bottom four in one, while the University Hospitals of North Tees and Hartlepool were bottom in one category and in the bottom ten in another. In one of the categories, the percentage of eligible patients who received thrombolysis within four hours, Sunderland Royal Hospital was sixth from the bottom in the country with 63.9% and the University Hospital of North Durham was seventh from bottom with 64.9%. The Stroke Association released the map of the best and worst to highlight the ‘postcode lottery’ of patient care. There were five indicators studied, from between March 2015 and April 2016. Now, the association is calling on the calling on the Government to give all hospitals the support they need to tackle these regional variations. Juliet Bouverie, chief executive of the Stroke Association, said: “Stroke is a medical emergency, and when swift treatment is not given to those who need it, people’s recoveries are put at risk. “It is unacceptable that your postcode determines whether or not you face treatment delays if you have a stroke.” Ken Bremner, Chief Executive of City Hospitals Sunderland NHS Foundation Trust and South Tyneside NHS Foundation Trust, said: “We know that the quality of care for stroke patients in South Tyneside and Sunderland needs to be improved and this has been a driver for change in both hospitals. “We have already started to make arrangements for a temporary change to the way acute stroke services are delivered as it was recognised the service at South Tyneside District Hospital was vulnerable because of challenges in recruiting a specialist stroke consultant. “Acute stroke care for South Tyneside residents is to be temporarily centralised at Sunderland Royal Hospital and by doing this we will be better placed to achieve key national standards and therefore ensure both organisations are providing the best possible care in order to maximise recovery following a stroke. “By making this temporary change our clinical teams are able to work together to improve the national standings for stroke care for all patients and they are confident the rating will move to at least a B, with the potential to achieve a grade A. “The National Stroke Quality Team, as well as our CCG partners, has supported our planned temporary solution as a method to begin to improve these important quality ratings.” Public consultation on a more permanent solution will be undertaken in early 2017.

Read more at: http://www.sunderlandecho.com/news/sunderland-among-worst-in-the-country-for-stroke-services-1-8249547

Acute Ischemic Stroke: Overcoming Barriers by Improving Systems of Care

Wrong target, it should be improving the results of your emergency department on handling stroke not just processes and care. Damn, no one wants to take responsibility for solving anything in stroke.
A CME for:
Target Audience: The intended audience for the activity is emergency department physicians, nurses, and other health care professionals involved in the treatment of patients with acute ischemic stroke (AIS).
Absolutely nothing in there on stopping the neuronal cascade of death by these 5 causes in the first week. So neurons are dying by the millions and your doctors are doing NOTHING about it. I don't care how big the  BHAGs(Big Hairy Audacious Goals)  is.  
http://www.healio.com/cardiology/education-lab/2015/12_december/acute-ischemic-stroke-overcoming-barriers-by-improving-systems-of-care/cme-information?utm_source=maestro&utm_medium=email&utm_campaign=cardiology%20educationlab

Overview

Author(s)/Faculty: Edward C. Jauch, MD, MS, FAHA, FACEP; Andy S. Jagoda, MD, FACEP; Philip B. Gorelick, MD, MPH, FACP; Lee H. Schwamm, MD, FAHA
Source: Healio - Cardiology Education Lab
Type: Multimedia	Articles/Items: 6
Release Date: 12/11/2015	Expiration Date: 12/11/2016
Credit Type: CME	Number of Credits: 1.5
Cost: Free	Provider:
According to the American Heart Association, strokes are experienced by approximately 795,000 Americans each year and remain the leading cause of disability in North America. It is important for emergency room physicians to identify and treat patients with acute ischemic stroke (AIS) quickly in order to best retain patients’ quality of life. Treatment of AIS is time sensitive, and with the recent updates to the use of endovascular procedures and thrombolytic therapy, physicians need to be prepared for a shift in the treatment paradigm without compromising patient safety. In this activity, leading neurologists and emergency medicine physicians discuss the latest evidence and recommendations on stroke management, including updates to guidelines on thrombolytic use, new data concerning endovascular procedures, and information on how the use of telemedicine and collaboration between stroke systems of care can improve processes and patient outcomes.

Button to take the test at the link

7 things you can do to prevent a stroke from Harvard Medical School

Extremely simplistic and anyone spouting these can just wash their hands of any responsibility about stroke. Never mind all these other prevention tips on stroke risk reduction from these 11 possibilities that actually point to research?
Good for their Conscience laundering though.

7 things you can do to prevent a stroke from Harvard Medical School

1 Lower blood pressure

2 Lose weight

3 Exercise more

4 Drink — in moderation

5 Treat atrial fibrillation

6 Treat diabetes

7 Quit smoking

Non-invasive brain stimulation in early rehabilitation after stroke

I'm sure your doctor, if any good at all, can find something in here to create a protocol on brain stimulation. I really don't want to have all the 10 million yearly stroke survivors  figure out a way to electrically stimulate their brains without frying them to pieces. But I bet you'll have to wait 50 years before this becomes standard practice because we have NO stroke strategy or anyone that has taken on the responsibility to implement one.We are fucking screwed and really no one cares.

Non-invasive brain stimulation in early rehabilitation after stroke

AV Blesneag,^* L Popa,^* and AD Stan^*

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Abstract

The new tendency in rehabilitation involves non-invasive tools that, if applied early after stroke, promote neurorecovery. Repetitive transcranial magnetic stimulation and transcranial direct current stimulation may correct the disruption of cortical excitability and effectively contribute to the restoration of movement and speech. The present paper analyses the results of non-invasive brain stimulation (NIBS) trials, highlighting different aspects related to the repetitive transcranial magnetic stimulation frequency, transcranial direct current stimulation polarity, the period and stimulation places in acute and subacute ischemic strokes. The risk of adverse events, the association with motor or language recovery specific training, and the cumulative positive effect evaluation are also discussed.

Novel techniques of neuromodulation and neurorehabilitation

Transcranial direct current stimulation (tDCS) of the brain is an electrophysiological method which may be used to modulate the neocortical excitability. A direct current generator is connected to two patch electrodes (an active and a reference one) positioned over the scalp, to stimulate the subjacent tissue with low amplitudes currents (0.5 - 2.0 mA) and to modify the threshold for discharge of cortical neurons. The modulation of cortical excitability is polarity-dependent: “anodal stimulation” (increased in network excitability) – when the active electrode generates a positive potential compared to the reference electrode; “cathodal stimulation” (decreased in network excitability) – when the active electrode generates a negative potential [4].

Repetitive transcranial magnetic stimulation (rTMS) is another therapeutic tool that can contribute to the modulation and reconfiguration of different cortical areas. In contrast to tDCS, rTMS results in the induction of action potentials and depolarization of the neuronal membrane. The principle of transcranial magnetic stimulation is to produce a perpendicular magnetic field, by a stimulating coil, which induces an electric field, which, in contact with the cerebral tissue, is transmitted as an electric current, parallel to the generating coil. The depth of the stimulation depends on the type of coil and the intensity of the stimulation. The excitatory or inhibitory effect is correlated with the frequency of rTMS: high frequencies (≥ 5 Hz) are excitatory, while low frequencies (≤ 1 Hz) are inhibitory [4,7].

By modulating cortical excitability with respect to neural plasticity, these two non-invasive brain stimulation (NIBS) techniques represent potential therapeutic tools in recovery after stroke [8,9].

There are two main directions of NIBS treatment in neurorehabilitation: the motor deficit and the speech disorders. The improvement of motor and language performances is based on interhemispheric competition theory [10-14]. This model suggests that the balance between the left and the right hemisphere of stroke patients is altered by an increased interhemispheric inhibition from the unaffected hemisphere to the affected hemisphere. Accordingly, a therapeutic effect may be obtained either by increasing the excitability of the affected hemisphere, or by decreasing the excitability of the unaffected hemisphere [10]. The mechanism of excitability enhancement in the motor cortex underlies the motor learning and the use-dependent plasticity, which are impaired in the affected hemisphere. Other positive effects of the NIBS are the enhancement of neural coupling between the primary and secondary motor areas in the affected hemisphere, the reduction of the hyperactivity in the primary and secondary motor areas in the unaffected hemisphere, and the excitability modulation in both hemispheres [10].

The advantages of inhibitory NIBS over the intact hemisphere are the uniform response and the lower risk of potential epileptic seizures, which are more probably to appear after rTMS in the infarcted area [15]. The major disadvantage is the deterioration of bimanual movement due to the reduction of transcallosal inhibition that controls that kind of movement. This possible consequence may be prevented by applying a low frequency rTMS concomitant with anodal tDCS over the affected hemisphere [16]. The neural modulation induced by NIBS and the improvement of motor and speech deficits can be sustained by subsequent motor training and speech therapies [10,13].

Although it was demonstrated that the early rehabilitation facilitates motor recovery after stroke, the application of NIBS in acute stages is controversial [17,18]. The genetic polymorphism can be involved and may explain the different response of stroke patients to this therapy. BDNF is one of the factors strongly involved in synaptic plasticity of the human motor cortex [9]. The consequence of BDNF val66met, a common single nucleotide polymorphism, is the reduced secretion of BDNF [19]. This is clinically expressed by a poorer retention in short-term motor learning and slower cognitive and motor recovery [9,19]. Therewith, the individual variation in response to rTMS may be explained by the difference in BDNF concentration [20].

The majority of the clinical studies evaluating the role of rTMS in rehabilitation were performed in subacute and chronic stroke patients, few data being available for acute stroke [21]. In this respect, a recent Cochrane meta-analysis evaluated the efficacy and safety of rTMS in recovery after stroke regardless of the duration of illness [22]. Nineteen randomized controlled trials (RCTs) with a total of 588 patients were included. Even if the rTMS treatment was not associated with a significant improvement in activities of daily living, or a significant improvement of motor function, a positive trend was noted, larger and homogeneous RCTs being needed in order to confirm the results [22].

The most encountered adverse events reported in clinical trials evaluating rTMS are transient or mild headache (2.4%), anxiety (0.3%), neurocardiogenic syncope after initial exposure to rTMS (0.6%), exacerbation of pre-existing insomnia (0.3%) and local discomfort at the site of the stimulation [22]. Also, epileptiform discharge on EEG and seizures, can be noted especially after high-frequency rTMS (10 Hz) [11].

Much more at link, including all the references.

Researchers find a copolymer scaffold potentially useful in brain repair after brain injury

When is someone in charge going to take responsibility for pushing stuff like this out to stroke hospitals or create clinical trials to prove this out?  Well shit, we have NO ONE in charge, so this will never occur, our stroke associations will not do this, so survivors are once again screwed.
We have no stroke leaders, get used to it.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=153710&CultureCode=en
After 8 weeks new neurons, glia and blood vessels were found surrounding the scaffold and also inside of the synthetic structure based on a ethyl acrylate (EA) and hydroxyl ethyl acrylate (HEA). This regenerative process did not occur in areas where the scaffold was not present, nor in non-implanted control animals. Professors at the CEU Cardenal Herrera University in Valencia have collaborated in this sudy with researchers from the Universitat Politècnica de València, Universidad Complutense and Hospital Clínico San Carlos, in Madrid.
Professors from the Faculty of Health Sciences of the CEU Cardenal Herrera University (CEU-UCH), in Valencia, José Miguel Soria López and María Ángeles García Esparza, have taken part in a new study in order to evaluate, in vivo, the biocompatibility and cell hosting ability of a copolymer channelled scaffold, after an experimental brain injury. This biomaterial, based on ethyl acrylate (EA) and hydroxyl ethyl acrylate (HEA), was implanted after focal brain damage in rats, allowing cell migration, survival and cell colonization by neurons, glial cells, and endothelial cells, which formed vessel-like neostructures, within the scaffold.
The professors collaborated with researchers from Universitat Politècnica de València, Universidad Complutense and Hospital Clínico San Carlos, in Madrid. The results have been published in Neuroscience Letters.
According to Professor Soria, head of the Research Group on neuro-protection and neuro-repair of the central nervous system, at CEU-UCH, the scaffolds made of this acrylate copolymer were implanted in the site of a previous cryolesion in the brain of Wistar rats: “We evaluated the tissue response to the implanted materials after 8 weeks and we observed that they provoked a minimal scar response by the host tissue and, also, permitted the invasion of neurons and glia inside them.” As Professor Soria adds, “this reparative process did not occur in areas where the scaffold was not present, nor in non-implanted control animals.”
In this study, “our findings indicate that this copolymer may constitute an artificial protective niche for the neural cells produced after injury and migrating from subventricular zone (SVZ) to the site of the lesion. In the absence of it, the area with the lesion is irremediably lost. This fact may be of interest for future clinical applications in the regeneration of injured brain,” says Professor Soria.
Professor García Esparza, member of this research group at CEU-UCH, adds: “This copolymer channelled scaffold proves to offer a suitable environment producing a cellular network potentially useful in brain repair after brain injury. In our group it is of greatest importance to identify types of synthetic materials, as a supporting vehicle or scaffold for the cell population to assist neural regeneration processes and new angiogenesis, after local brain injury."
http://www.ncbi.nlm.nih.gov/pubmed/25980992

Group Support Promotes Self-Care for Stroke Patients - Austria

Once again dumping all the responsibility for recovery on the survivor. YOU really need to push back forcefully against this idea. Our stroke medical professionals need to actually solve the problems in stroke, not just push them under the rug. I expect our professionals to solve the neuronal cascade of death. By solving this cascade the resulting disability would be much less and self-care might be appropriate at that time. But don't let them do this until they have solved the cascade of death problem.
http://www.medscape.com/viewarticle/845824
An innovative group program of rehabilitation and education encouraging self-care for patients who have stroke or transient ischemic attack (TIA) and their carers is boosting patients' confidence to re-engage in life and helping them to make lifestyle changes to lower their risk for a recurrent event.
The Acute stroke, Self-management support, Prevention, Information, Rehabilitation, Exercise (ASPIRE) program has been introduced at Yeovil District General Hospital in Somerset, United Kingdom, and consists of post-discharge group work for 2 hours for 12 weeks. Patients can come with spouses or carers and participate in interactive information sessions and individually tailored goal-orientated exercises.
A key and novel part of the program is the involvement of other stroke patients who have previously participated in the course as volunteers.
Peer-to-Peer Support
Presenting details of the ASPIRE program at the recent 24th European Stroke Conference (ESC), consultant therapist in rehabilitation Deborah Neal said the peer-to-peer support provided by other stroke patients helps the new patients build confidence and change their mindset so they better engage in healthy lifestyle behaviors.
She presented new data from the program showing that patients completing the course had a significant benefit in stroke knowledge and that scores for self-efficacy (confidence) also approached significance.
"Normally we wouldn't expect to see any major changes after just 12 two-hour sessions but because this program appears to bring about a change in mindset, the patients go home and change their behaviours," she commented. "One of the key elements that brings about this mindset change is the fact we have the 'expert' patients present. They act as role models. This is the theory of self-efficacy," she added. "It is a very cost-effective model."
Neal also noted that unlike some other group programs, the ASPIRE course is very inclusive. "We take everyone who has had a stroke — ischemic or hemorrhagic — or a TIA. We have no age or disability limits so we take people in wheelchairs and those who are fully mobile, and the whole spectrum of communication and cognition. They all receive an individually tailored exercise program."
The course is run by a physiotherapist, a nurse, and a rehab assistant, with guest speakers including a pharmacist, dietitian, and occupational therapist. Then the patient volunteers and carers add more support.
"We find friendships build up and patients become empowered by each other to follow healthy behaviors outside the program. For example, they may join a local walking group or gym together," Neal said. "We also run a buddy system, putting new patients in touch with others who have been through the program who may live locally to them. In this way we are setting up a stroke community where good habits are spread by the patients themselves. The social interaction itself also helps enormously."
"Drip, Drip, Drip" Approach
Neal noted that before ASPIRE was established, about half the stroke patients in the area were going home without any rehabilitation or regular follow up. "We found that people were still in shock — many hardly recognized that they had had a stroke, but they were at high risk of having another one if they didn't change their lifestyle. They are told at the hospital about risk factors but most don't remember. But our 12-week 'drip, drip, drip' approach is much more effective at getting the messages across."
The weekly sessions also act as a point of contact for previous patients to "drop in" for further advice. Carers also get the chance for some respite if they prefer not to stay at the sessions.
Neal notes that this approach will be difficult to validate in a randomized trial because the program is very pragmatic and heavily individualized. So they are looking at qualitative data instead.
"The number needed to treat in terms of a benefit on mortality or recurrent stroke will be high but effects on confidence and quality of life will be much more obvious and easier to demonstrate," she said.
The current analysis involved two phases In the first, 10 patients attending the program and 7 carers (all spouses) were interviewed about three major outcomes: confidence in doing important everyday activities, developing knowledge for reducing vascular risk, and the benefits of peer support.
The second phase tested the phase 1 outcomes in 19 patients and 6 carers using relevant standardized validated tools, including the Stroke Knowledge Test, the Stroke Self-Efficacy Questionnaire, the Hospital Anxiety and Depression Scale, and the Caregiver Strain Index.
24th European Stroke Conference (ESC). Presented May 14, 2015.

Memory loss associated with Alzheimer’s reversed for first time

Can your doctor reuse this to apply to your memory problems post-stroke? Ask when they are going to start up that clinical trial. We need proof otherwise your doctor will continue to say 'There are no clinical trials proving memory improvement for stroke'. YOU have to demand some responsibility from your doctor to provide effective stroke protocols. This is only 6 months old so if your doctor hasn't created any memory protocol for this, fire them for incompetence. Do not do this on your own, you know how dangerous this might be if your doctor is not in charge.
http://newsroom.ucla.edu/releases/memory-loss-associated-with-alzheimers-reversed-for-first-time

Patient 1 had two years of progressive memory loss. She was considering quitting her job, which involved analyzing data and writing reports, she got disoriented driving, and she mixed up the names of her pets.
Patient 2 kept forgetting once-familiar faces at work, forgot his gym locker combination and had to have his assistants constantly remind him of his work schedule.
Patient 3’s memory was so bad that she used an iPad to record everything, then forgot her password. Her children noticed she commonly lost her train of thought in mid-sentence, and often asked them if they had carried out the tasks that she mistakenly thought she had asked them to do.
— “Reversal of cognitive decline: A novel therapeutic program,” UCLA/Buck Institute, 2014

Since it was first described over 100 years ago, Alzheimer’s disease has been without an effective treatment.
That may finally be about to change: In the first, small study of a novel, personalized and comprehensive program to reverse memory loss, nine of 10 participants, including those described above, displayed subjective or objective improvement in their memories beginning within three to six months.
Six patients had discontinued working or had been struggling at their jobs at the time they joined the study; all were able to return to their jobs or continue working with improved performance, and their improvements have been sustained. (The patient in treatment the longest has been receiving the therapy for two-and-a-half years.)
Among the 10 were patients with memory loss associated with Alzheimer’s disease, amnestic mild cognitive impairment or subjective cognitive impairment (in which the patient reports cognitive problems). One patient who had been diagnosed with late stage Alzheimer’s did not improve.
The study was conducted Dr. Dale Bredesen of the UCLA Mary S. Easton Center for Alzheimer’s Disease Research and the Buck Institute for Research on Aging. It is the first to suggest that memory loss in patients may be reversed — and improvement sustained — using a complex, 36-point therapeutic program that involves comprehensive diet changes, brain stimulation, exercise, sleep optimization, specific pharmaceuticals and vitamins, and multiple additional steps that affect brain chemistry.
The findings are published in the current online edition of the journal Aging.
Bredesen, UCLA’s Augustus Rose Professor of Neurology, director of the Easton Center and the paper’s author, said the findings are “very encouraging,” but he added that the results are anecdotal, and a more extensive, controlled clinical trial is needed.
No single drug has been found to stop or even slow the progression of Alzheimer’s, and drugs have only had modest effects on symptoms. “In the past decade alone, hundreds of clinical trials have been conducted for Alzheimer’s, without success, at an aggregate cost of over $1 billion,” said Bredesen, who also is a professor at the Buck Institute.
Although other chronic illnesses such as cardiovascular disease, cancer and HIV have been improved through the use of combination therapies, comprehensive combination therapies have not been explored for Alzheimer’s and other memory disorders. However, over the past few decades, genetic and biochemical research has revealed an extensive network of molecular interactions involved in the development of Alzheimer’s.
“That suggested that a broader-based therapeutic approach, rather than a single drug that aims at a single target, may be feasible and potentially more effective for the treatment of cognitive decline due to Alzheimer’s,” Bredesen said.
While extensive preclinical studies in numerous other laboratories have identified single pathogenic targets for potential intervention, in human studies, such single target therapeutic approaches have not borne out. But, said Bredesen, it’s possible that addressing multiple targets within the network underlying Alzheimer’s may be successful even when each target is affected in a relatively modest way. “In other words,” he said, “the effects of the various targets may be additive, or even synergistic.”
The uniform failure of drug trials in Alzheimer’s influenced Bredesen’s desire to better understand the fundamental nature of the disease. His laboratory has found evidence that Alzheimer’s stems from an imbalance in nerve cell signaling. In the normal brain, specific signals foster nerve connections and memory making, while balancing signals support memory loss, allowing irrelevant information to be forgotten. But in people with Alzheimer’s, the balance of these opposing signals is disturbed, nerve connections are suppressed and memories are lost.
That finding is contrary to the popular belief that Alzheimer’s is caused by the accumulation of sticky plaques in the brain. Bredesen believes the amyloid beta peptide, the source of the plaques, has a normal function in the brain, as part of a larger set of molecules that promote signals that cause nerve connections to lapse. Thus, the increase in the peptide that occurs in Alzheimer’s shifts the balance in favor of memory loss.
Bredesen therefore thought that, rather than a single targeted agent, the solution might be a multiple-component system approach, in line with the approach for other chronic illnesses.
“The existing Alzheimer’s drugs affect a single target, but Alzheimer’s disease is more complex. Imagine having a roof with 36 holes in it, and your drug patched one hole very well,” he said. “The drug may have worked, and a single hole may have been fixed, but you still have 35 other leaks, and so the underlying process may not be affected much.”
Bredesen’s approach is personalized to the patient, based on extensive testing to determine what is affecting the brain’s plasticity signaling network. In the case of the patient with the demanding job who was forgetting her way home, her therapy consisted of some, but not all, of the components of Bredesen’s program, including:

• eliminating all simple carbohydrates, gluten and processed food from her diet, and eating more vegetables, fruits and non-farmed fish
• meditating twice a day and beginning yoga to reduce stress
• sleeping seven to eight hours per night, up from four to five
• taking melatonin, methylcobalamin, vitamin D3, fish oil and coenzyme Q10 each day
• optimizing oral hygiene using an electric flosser and electric toothbrush
• reinstating hormone replacement therapy, which had previously been discontinued
• fasting for a minimum of 12 hours between dinner and breakfast, and for a minimum of three hours between dinner and bedtime
• exercising for a minimum of 30 minutes, four to six days per week

Bredesen said the program’s downsides are its complexity and that the burden falls on patients and caregivers to follow it. In the study, none of the patients was able to stick to the entire protocol. Their most common complaints were the diet and lifestyle changes, and having to take multiple pills each day.
The good news, though, said Bredesen, are the side effects: “It is noteworthy that the major side effects of this therapeutic system are improved health and an improved body mass index, a stark contrast to the side effects of many drugs.”
The results suggest that memory loss may be reversed and improvement sustained with the therapeutic program, but Bredesen cautioned that the results need to be replicated.
“The current, anecdotal results require a larger trial, not only to confirm or refute the results reported here, but also to address key questions raised, such as the degree of improvement that can be achieved routinely, how late in the course of cognitive decline reversal can be effected, whether such an approach may be effective in patients with familial Alzheimer’s disease, and last, how long improvement can be sustained,” he said.
Cognitive decline is a major concern of the aging population. Alzheimer’s affects approximately 5.4 million Americans and 30 million people globally. By 2050, without effective prevention and treatment, an estimated 160 million people globally would have the disease, including 13 million Americans, which could potentially bankrupt the Medicare system. Unlike several other chronic illnesses, the incidence of Alzheimer’s is on the rise; recent estimates suggest that it has become the third leading cause of death in the U.S. behind cardiovascular disease and cancer.
Multiple entities provided support for the study, including the National Institutes of Health (AG16570, AG034427 and AG036975). The complete list is included in the paper.

FAmily-Led RehabiliTaTion aftEr Stroke in INDia: the ATTEND pilot study

More f*cking stupidity. Lets just push all the work about recovery onto the survivor and family. This way the doctor and therapists have washed their hands of any responsibility of improving the lot of the survivor. This is giving up on the medical teams part.
http://onlinelibrary.wiley.com/doi/10.1111/ijs.12475/abstract;jsessionid=83A9CC168723235DE87F1FA4A6AAEF3F.f02t02?

1. Jeyaraj D. Pandian^1,*,
2. Cynthia Felix¹,
3. Paramdeep Kaur¹,
4. Deepika Sharma¹,
5. Lizzie Julia¹,
6. Gagan Toor¹,
7. Rajni Arora²,
8. Dorcas B.C. Gandhi²,
9. Shweta J. Verma¹,
10. Craig S. Anderson³,
11. Peter Langhorne⁴,
12. G.V.S. Murthy⁵,
13. Maree L. Hackett^6,7,
14. Pallab K. Maulik^8,9,
15. Mohammed Alim⁸,
16. Lisa A. Harvey¹⁰,
17. Stephen Jan⁴,
18. Marion Walker¹¹,
19. Anne Forster¹² and
20. Richard Lindley⁴

Article first published online: 9 MAR 2015

DOI: 10.1111/ijs.12475

© 2015 World Stroke Organization

Issue

International Journal of Stroke

Early View (Online Version of Record published before inclusion in an issue)

Additional Information(Show All)

How to CiteAuthor InformationPublication HistoryFunding Information

1. Conflict of interest: None declared.
2. Funding: Australian NHMRC program (571281) and project (1045391) grants and The George Institute for Global Health, University of Sydney, Australia.
3. Unique identifier: NCTO2123875.
4. Clinical trial registration URL: http://www.clinicaltrials.gov.

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Keywords:

• caregiver;
• developing countries;
• early supported discharge;
• home-based care;
• quality of life;
• rehabilitation;
• stroke;
• therapy

Background

The aim of this pilot study was to determine the feasibility of a multicenter, randomized, controlled trial in India of a family-led, trained caregiver-delivered, home-based rehabilitation intervention vs. routine care.

Methods

A prospective, randomized (within seven-days of hospital admission), blinded outcome assessor, controlled trial of structured home-based rehabilitation delivered by trained and protocol-guided family caregivers (intervention) vs. routine care alone (control) was conducted in patients with residual disability. Key feasibility measures were recruitment, acceptance and adherence to assessment procedures, and follow-up of participants over six-months. CTRI/2014/10/005133.

Results

A total of 104 patients from the stroke unit at Christian Medical College, Ludhiana were recruited over nine-months. Recruitment was feasible and accepted by patients and their carers. Important observations were made regarding potential unblinding of the participants, contamination of therapy between the randomized groups, organization of home visits, and resources required for a multicenter study.

Conclusion

The pilot study established the feasibility of conducting a large-scale study of family-led, trained caregiver-delivered, home-based stroke rehabilitation in a low resource setting. The main phase of the trial ‘ATTEND’ is currently underway in over 10 centers in India.