Haphazard Aspirin Add-On: Not a Great Risk-Reward Tradeoff for DOAC Users

The real solution is to create a test that identifies EXACTLY which persons are susceptible to bleeding from aspirin rather than these blanket prohibitions. In business you'd be fired for not going directly to and solving the root cause.  But I'm not medically trained so don't listen to me.

Haphazard Aspirin Add-On: Not a Great Risk-Reward Tradeoff for DOAC Users

Group suggests deprescribing aspirin with no clear indication

by Nicole Lou, Staff Writer, MedPage Today April 19, 2021

Direct oral anticoagulant (DOAC) users without a clear indication for aspirin were often prescribed combination therapy only to wind up with a higher risk of bleeding and no reduction in thrombotic events, an observational study showed.

People with atrial fibrillation (Afib) or venous thromboembolism (VTE) -- but no recent MI or history of heart valve replacement -- were treated with concomitant aspirin atop their DOAC in 33.8% of cases, making this a "common" phenomenon, according to Jordan Schaefer, MD, of the University of Michigan in Ann Arbor, and colleagues.

Comparison between 1,047 matched pairs revealed that combination and DOAC monotherapy groups differed in some key outcomes over a median 12 months of follow-up:

• All bleeding: 31.6 vs 26.0 per 100 patient-years (P=0.01)
• Nonmajor bleeding: 26.1 vs 21.7 per 100 person-years (P=0.02)
• Major bleeding: 4.95 vs 3.59 per 100 person-years (P=0.09)
• Thrombotic events: similar at 2.5 vs 2.3 per 100 patient-years (P=0.80)
• Hospitalizations: 9.1 vs 6.5 per 100 patient years (P=0.02)
• Mortality: 3.8 vs 3.4 per 100 patient-years (P=0.76)

"Ultimately, while emerging data seem to suggest that anticoagulant monotherapy alone may be sufficient for some patients, further confirmation of these findings is necessary," Schaefer's group wrote in JAMA Internal Medicine.

"Efforts should be made to help clinicians identify and deprescribe ASA [aspirin] for patients taking a DOAC without an indication for ASA," they maintained.

The group had previously shown excess bleeding with combination aspirin and warfarin therapy in patients lacking a clear indication for aspirin.

"It is important to acknowledge that there are numerous patient subgroups and clinical scenarios where the role of combination therapy compared with that of anticoagulant monotherapy has not been sufficiently studied," Schaefer's group noted, citing examples such as people with vascular stents, myeloproliferative neoplasms, poorly controlled vascular risk factors, and thrombophilias.

"In such scenarios, shared decision-making and individualized care should remain standard," they stated.

The study relied on the Michigan Anticoagulation Quality Improvement Initiative for registry data from four anticoagulation clinics in Michigan.

Participants were 3,280 adults with Afib or VTE without a clear indication for aspirin (51.0% men; mean age 68.2). All had started taking a DOAC -- namely apixaban (Eliquis), dabigatran (Pradaxa), edoxaban (Savaysa), or rivaroxaban (Xarelto) -- in 2015-2019.

Main study results were largely supported by sensitivity analyses such as those that excluded patients with any history of MI, coronary artery disease, or peripheral artery disease; or excluded those who started or stopped aspirin after study enrollment.

Even so, investigators cautioned that the observational nature of the study left room for unmeasured confounding and was unable to capture changes in aspirin use during follow-up. Moreover, the study may not be generalizable to geographic areas outside Michigan.

"Finally, the overall rates of thrombosis and many bleeding subtypes were low. Accordingly, this study is likely underpowered to make conclusions about thrombotic outcomes and outcomes of some bleeding subtypes," according to Schaefer and colleagues.

• 

  Nicole Lou is a reporter for MedPage Today, where she covers cardiology news and other developments in medicine. Follow

Disclosures

The study was funded by Blue Cross Blue Shield of Michigan.

Schaefer disclosed no relevant relationships with industry. Co-authors disclosed multiple relevant relationships with industry.

Primary Source

JAMA Internal Medicine

Source Reference: Schaefer JK, et al "Adverse events associated with the addition of aspirin to direct oral anticoagulant therapy without a clear indication" JAMA Intern Med 2021; DOI: 10.1001/jamainternmed.2021.1197.

 

A Qualitative Study Investigating Stroke Survivors' Perceptions of their Psychosocial Needs Being Met During Rehabilitation

 You wouldn't have to solve this secondary problem if you got the primary problem solved; 100% recovery. Do you not understand how stroke recovery should work? Solve the root cause problem first.

A Qualitative Study Investigating Stroke Survivors' Perceptions of their Psychosocial Needs Being Met During Rehabilitation

Robin A. Wenzel
Midwestern University – USA, rwenzel67@midwestern.edu
Emily A. Zgoda
Midwestern University – USA, ezgoda96@gmail.com
Mia C. St. Clair
Midwestern University – USA, miastclair@gmail.com
Lisa J. Knecht-Sabres
Midwestern University – USA, lknech@midwestern.edu
Follow this and additional works at: https://scholarworks.wmich.edu/ojot
Part of the Mental and Social Health Commons, and the Occupational Therapy Commons
Recommended Citation
Wenzel, R. A., Zgoda, E. A., St. Clair, M. C., & Knecht-Sabres, L. J. (2021). A Qualitative Study Investigating
Stroke Survivors’ Perceptions of their Psychosocial Needs Being Met During Rehabilitation. The Open
Journal of Occupational Therapy, 9(2), 1-16. https://doi.org/10.15453/2168-6408.1691

Abstract

Background: 

Depression and anxiety can negatively impact one’s recovery, outcomes, and quality of life. Even though therapists consider the mental health needs of their clients to be a priority, they are dissatisfied with their ability to completely address these needs. The purpose of this study was to examine the client’s perspective regarding the extent to which health care professionals addressed their psychosocial needs after a stroke.
Method: 

A phenomenological research design was used to collect data from six participants. Interviews and focus group were audiotaped, transcribed verbatim, and thematically analyzed. Member checks, peerreview, multiple coders, triangulation, and expert examination were used to increase trustworthiness of findings.
Results:  

Five themes emerged. People with strokes: (a) experience an array of emotions, (b) are not likely to initiate disclosure of their state of mental health, (c) feel their psychosocial needs are not being addressed by health care professionals, (d) grieve the loss of prior roles post stroke and work hard to establish a new normal routine and purpose in life, and (e) have suggestions for improved care.
Conclusion: 

These findings reinforce the importance of addressing the mental health needs of individuals post stroke and the importance of identifying methods to enhance the ability to effectively address the psychosocial needs of clients post stroke.

A neuromarker of individual general fluid intelligence from the white-matter functional connectome

So is this where we lose 5 cognitive years from the stroke?  

The white matter damage? How EXACTLY is your doctor recovering from that damage? Or is nothing being done? My doctor knew nothing and did nothing for any piece of my recovery. It was all from my excellent OT who supposedly used Bobath/NDT. My ER doctors blew out my clot in 90 minutes so I only lost 171 million neurons, since my PMR doctor did nothing in the first week, that caused another 5.4 billion neurons to die.  I will never forgive him for that, especially since for decades nobody even considered doing any analysis as to why survivors didn't recover.  In programming I would have been fired in no time for not solving the root cause of the problem I was assigned.

A neuromarker of individual general fluid intelligence from the white-matter functional connectome

• Jiao Li,
• Bharat B. Biswal,
• Yao Meng,
• Siqi Yang,
• Xujun Duan,
• Qian Cui,
• Huafu Chen &
• Wei Liao 

Translational Psychiatry volume 10, Article number: 147 (2020) Cite this article

• 295 Accesses
• Metrics details

Abstract

Neuroimaging studies have uncovered the neural roots of individual differences in human general fluid intelligence (Gf). Gf is characterized by the function of specific neural circuits in brain gray-matter; however, the association between Gf and neural function in brain white-matter (WM) remains unclear. Given reliable detection of blood-oxygen-level-dependent functional magnetic resonance imaging (BOLD-fMRI) signals in WM, we used a functional, rather than an anatomical, neuromarker in WM to identify individual Gf. We collected longitudinal BOLD-fMRI data (in total three times, ~11 months between time 1 and time 2, and ~29 months between time 1 and time 3) in normal volunteers at rest, and identified WM functional connectomes that predicted the individual Gf at time 1 (n = 326). From internal validation analyses, we demonstrated that the constructed predictive model at time 1 predicted an individual’s Gf from WM functional connectomes at time 2 (time 1 ∩ time 2: n = 105) and further at time 3 (time 1 ∩ time 3: n = 83). From external validation analyses, we demonstrated that the predictive model from time 1 was generalized to unseen individuals from another center (n = 53). From anatomical aspects, WM functional connectivity showing high predictive power predominantly included the superior longitudinal fasciculus system, deep frontal WM, and ventral frontoparietal tracts. These results thus demonstrated that WM functional connectomes offer a novel applicable neuromarker of Gf and supplement the gray-matter connectomes to explore brain–behavior relationships.

Introduction

Neuroimaging and psychological studies have investigated the neural basis of the cognitive processes that motivate novel insights about brain–behavior relationships¹. An enduring aim of brain and cognitive sciences is to understand individual differences in human intelligence². Human general fluid intelligence (Gf) refers to an ability to think logically and to solve novel problems that do not rely on previously acquired knowledge^3,4. Gf has been broadly quantified using a series psychometric test, which further provides a foundation to process brain–behavior associations^5,6. Given that individual differences are inherent to Gf, it is crucial to identify neural correlates of Gf and corresponding variations in brain structure and function.
The neural correlates of individual differences in Gf may be associated with variations in brain size and connections². A larger brain size (volume) consistently indicates higher intelligence⁷; this concept of “the bigger brain, the better intelligence” may result from the efficiency of information flow among neurons^5,8. Recently, the information flow among certain areas associated with Gf have been quantified by functional connectivity studies. These results showed that the variational relationships of regions engaging in common or related performance (even at rest) may be the basis of individual differences in Gf^9,10,11, and measurements of the activity of the resting-state human brain might carry information about intelligence¹². Furthermore, the rate of information flow among the distributed parietal and frontal areas composing the parieto-frontal integration theory (P-FIT) network are likely to play key roles in intelligence¹³. It is not surprising that a large number of these brain regions and brain functional networks are related to individual Gf^12,14,15, due to the diverse abilities associated with Gf, including understanding of daily tasks and problem solving. Accordingly, whole-brain functional connectivity measures may provide more holistic insight to determine an individual’s Gf, rather than global brain size.
Gf is mainly rooted in the functional connectivity of specific neural circuits within gray-matter (GM); however, little is known regarding the neurofunctional substrates of individual differences in Gf in white-matter (WM)^16,17,18. Recently, a small but increasing number of investigations have demonstrated a reliable detection of blood-oxygen-level-dependent functional magnetic resonance imaging (BOLD-fMRI) signals in WM. These studies indicate that neural activation elicits temporal and spectral profiles of hemodynamic responses in WM that are similar to those measured in GM during different functional tasks^{19,20,21,22,23,24}. In parallel with the detection of task-related activations, BOLD-fMRI can also reflect the neural activity in WM at rest (i.e., absence of task requirement)^25,26. Specifically, we found that, during the resting state, the power of low-frequency BOLD-fMRI fluctuations in WM exhibited a specific rather than a random distribution of noise²⁶, and the WM functional connectome exhibited reliable and stable small-worldness and nonrandom modularity²⁷. Abnormal small-worldness in the WM functional connectome was reported in patients with Parkinson’s disease²⁸. Furthermore, the specific functional connectivity organization of the anatomical bundles was able to be identified by resting-state fMRI^20,21,25,29. These investigations not only provided evidence of neural activity and connectivity, using fMRI, but also established cognitive biomarkers (i.e., for memory function) in WM³⁰.
In the current study, using a cross-validation, data-driven analysis, we present novel findings that the whole-brain WM functional network predicted individual Gf and shed light on the possible neurofunctional correlates of Gf in WM. We first built a network-predicted model between connectivity strength and Gf scores of normal individuals following an initial examination (time 1, n = 326 participants). We demonstrated that the network-predicted model derived from these data could predict an individual’s Gf from his/her WM functional connectivity. This predictive model constructed at time 1 can be generalized to both the second (time 2, n = 105 participants) and the third examinations (time 3, n = 83 participants) using the overlapped individuals, thus, accurately predicting an individual’s Gf score from WM functional connectivity during the time 2 and time 3 scans for internal validation. Finally, to further test the generalizability of the predicted model, we showed that this model could also predict novel independent performance Gf (n = 53 participants) for external validation. These results suggested that the whole-brain functional connectivity of WM was a neuromarker of individual differences in Gf and would generalize to independent data to predict individual Gf.

Association between vitamin D status and cognitive impairment in acute ischemic stroke patients: a prospective cohort study

I see nothing here that suggests that this is being written up as a stroke protocol and distributed worldwide to all stroke hospitals and doctors. Isn't that the minimum needed to 'do no harm'? 

Is this just Vitamin D or D3? Inquiring minds want to know.  Does low vitamin D cause this problem or the underlying reason that initially caused the low levels the real problem? Have you actually identified the root cause?

Vitamin D3 Could Help Prevent, Repair Cardiovascular System Damage

The latest here:

Association between vitamin D status and cognitive impairment in acute ischemic stroke patients: a prospective cohort study

Authors Chen H, Liu Y, Huang G, Zhu J, Feng W, He J
Received 11 September 2018
Accepted for publication 18 November 2018
Published 10 December 2018 Volume 2018:13 Pages 2503—2509
DOI https://doi.org/10.2147/CIA.S187142
Checked for plagiarism Yes
Review by Single-blind
Peer reviewers approved by Dr Andrew Yee
Peer reviewer comments 3
Editor who approved publication: Dr Wu

Huijun Chen,^1,* Yuntao Liu,^1,* Guiqian Huang,^1,* Jie Zhu,² Wenqian Feng,² Jincai He<sup>1

1</sup>Department of Neurology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China; ²Department of Mental Health, Mental Health School, Wenzhou Medical University, Wenzhou 325000, China

*These authors contributed equally to this work

Objective: Previous studies found that low vitamin D levels were modestly associated with risk of stroke and poor functional outcome after stroke. In addition, vitamin D deficiency has been linked with cognitive decline. Our study aimed to explore the potential relationship between vitamin D levels in the short-term acute phase of ischemic stroke and cognitive impairment at 1 month.
Methods: In total, 354 ischemic stroke patients were consecutively enrolled in the study and received 1-month follow-up. The serum levels of vitamin D were measured within 24 hours after admission. Cognitive function was evaluated by the Mini-Mental State Examination (MMSE) at 1 month after acute ischemic stroke. Cognitive impairment was defined according to different education levels.
Results: According to MMSE scores, 114 participants (32.2%) had cognitive impairment at 1 month. Patients with vitamin D deficiency were more likely to have cognitive impairment than those with vitamin D insufficiency and vitamin D sufficiency (P<0.001). After adjusting for potential confounders in our Cox proportional hazards model, vitamin D deficiency was independently associated with the development of cognitive impairment in acute ischemic stroke patients.
Conclusion: Independent of established risk factors, vitamin D deficiency in the short-term phase of ischemic stroke was associated with a higher incidence of 1-month cognitive impairment.

Keywords: vitamin D, cognitive impairment, ischemic stroke, Mini-Mental State Examination

This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution - Non Commercial (unported, v3.0) License. By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms.

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Association Between Early Outpatient Visits and Readmissions After Ischemic Stroke

Go back to the drawing board and figure out exactly what will reduce readmissions. Early outpatient visits mean nothing. Was something done at those visits that reduced readmissions? Solve the damn problem, don't just guess at the answer. I would have been fired in no time if I did that lousy a job at determining root cause of programming problems. 

Association Between Early Outpatient Visits and Readmissions After Ischemic Stroke

Samuel W. Terman

,

Mathew J. Reeves

,

Lesli E. Skolarus

, and

James F. Burke

Originally published13 Apr 2018Circulation: Cardiovascular Quality and Outcomes. 2018;11:e004024

• Correction(s) for this article

Abstract

Background:

Reducing hospital readmission is an important goal to optimize poststroke care and reduce costs. Early outpatient follow-up may represent one important strategy to reduce readmissions. We examined the association between time to first outpatient contact and readmission to inform postdischarge transitions.

Methods and Results:

We performed a retrospective cohort study of all Medicare fee-for-service patients discharged home after an acute ischemic stroke in 2012 identified by the InternationalClassification of Diseases, Ninth Revision, Clinical Modification codes. Our primary predictor variable was whether patients had a primary care or neurology visit within 30 days of discharge. Our primary outcome variable was all-cause 30-day hospital readmission. We used separate multivariable Cox models with primary care and neurology visits specified as time-dependent covariates, adjusted for numerous patient- and systems-level factors. The cohort included 78 345 patients. Sixty-one percent and 16% of patients, respectively, had a primary care and neurology visit within 30 days of discharge. Visits occurred a median (interquartile range) 7 (4–13) and 15 (5–22) days after discharge for primary care and neurology, respectively. Thirty-day readmission occurred in 9.4% of patients. Readmissions occurred a median 14 (interquartile range, 7–21) days after discharge. Patients who had a primary care visit within 30 days of discharge had a slightly lower adjusted hazard of readmission than those who did not (hazard ratio, 0.98; 95% confidence interval, 0.97–0.98). The association was nearly identical for 30-day neurology visits (hazard ratio, 0.98; 95% confidence interval, 0.97–0.98).

Conclusions:

Thirty-day outpatient follow-up was associated with a small reduction in hospital readmission among elderly patients with stroke discharged home. Further work should assess how outpatient care may be improved to further reduce readmissions.

The End Comes as a Wave - death of neurons

How will our stroke researchers use this knowledge to come up with prevention protocols post-stroke? Or will nothing be done because we have NO stroke leadership and they are waiting for SOMEONE ELSE TO SOLVE THE PROBLEM?

Inquiring minds want to know specifically whom is going to solve this problem? Specific names, not just put in a 10 year goal that will never be accomplished. We need to start taking names and firing all the incompetent people in stroke.  My manager used to assign many of the most difficult programming problems to me since I would keep at it until the original cause was found and fixed. Whom is that person in stroke research? Every stroke doctor and stroke hospital should be able to immediately roll that persons name off their tongue.

The End Comes as a Wave

by Sophie Fessl September 26, 2018

Shutterstock[See also video, below story]

Death is a part of life, and while much of life is poorly understood, death is shrouded in mystery. What goes on in our brains before we die?
Neuroscientists in Germany and the US have recently shown that “brain tsunamis,” waves of cell depolarization – massive short-circuits of the neurons – sweep the cortex within ten minutes of cardiac arrest. These waves of spreading depolarization mark the beginning of the end, and trigger a gradual poisoning of neurons. They recorded brain tsunamis not just as people died but also after other critical events, such as a brain hemorrhage. Their findings could have immediate application in ERs and critical-care wards.
Measuring what happens in the brain immediately after a stroke or cardiac arrest is difficult, but Jens Dreier, at the Center for Stroke Research Berlin, and Jed Hartings, at the University of Cincinnati, saw an opportunity in their work in neurocritical care. Their centers monitor the brain activity of patients with certain conditions, such as traumatic brain injury or bleeding after an aneurysm. This neuromonitoring involves putting electrodes either directly onto the surface of the brain or deep into the cerebral cortex. Clinicians can then record electrical activity directly from the cortex.

Some patients suffering from such brain injuries did not respond to treatment. After family discussion and agreement, the doctors withdrew life-sustaining therapy while neuromonitoring continued as the patient died. What the neuroscientists observed was striking, says Jed Hartings.
“Previously, it was thought that the end occurs when the brain stops its electrical activity and goes silent,” he says. “But it doesn’t. We show that the brain remains in a viable state for several minutes after this flatline. And then the final brain tsunami occurs: A wave of depolarization sweeps through the cortex.”
This brain activity reflects what happens to the neurons as the heart stops pumping fresh oxygen to it, explains Jens Dreier. “After cardiac arrest, blood flow to the brain stops. Neurons and astrocytes detect that the oxygens levels drop, even before their own metabolism is affected. The neurons then switch off their function to get into an energy-saving mode: electrical activity stops, the neurons no longer send any signals. This is the flatline.” But while the neurons use less energy in this mode, they don’t use none--they still need some to maintain their internal metabolism.
Normally, ion pumps monitor and maintain a difference in charge between the inside and outside of neurons; this difference is essential for neurons to send their signals. But the pumps need energy, and this is where the system fails, Dreier says. “Eventually, there is no longer enough energy to keep the ion pump going. The ion gradients collapse: Ions from inside the neurons stream out, and those from the outside stream in.” As cells, and neurons in particular, have a carefully balanced chemistry, this change in the concentrations has dramatic consequences.
“A massive depolarization occurs as the ion gradients collapse completely, releasing a great amount of energy,” Dreier says. “The massive depolarization isn’t localized though, waves of depolarization spread into the neighboring regions. This is the brain tsunami, or spreading depolarization.”
First results in humans
Spreading depolarizations, for all their dramatic impact, are nothing new. In 1944, the Brazilian physiologist Aristides Leo first described seeing waves of suppressed function in the cortex of rats after he stimulated the cortex intensely, in what he called “spreading depression.” From the 1980s onwards, medics increasingly accepted that spreading depolarization was relevant to brain injuries. By the 1990s, researchers had proven in animals that brain tsunamis cause the death of brain tissue, but because spreading depolarization is so hard to record, it remained unobserved in humans until this century. Finally, in 2002, neuroscientists demonstrated spreading depolarization in the human brain. Since then, COSBID, a clinical research collaboration of which Dreier and Hartings are members, and others have studied spreading depolarizations in brain injuries in hospitals across Europe and the US.
Notably, spreading depolarization does not mark the onset of cell death, but instead starts the clock counting down to cell death. Leão already showed that spreading depolarization is – in principle – reversible. If blood flow isn’t restored after a certain time, neurons are unable to recover and will die – this is the commitment point. However, even if depolarization is reversed, the neurons don’t necessarily survive, says Dreier.
“After depolarization, there is complete chaos in the cells,” he says. “Calcium levels, for example, increase a thousand-fold. These changes are highly toxic to the neuron. However, when blood flow sets in again and energy is provided to the brain, some cells can re-polarize and may recover their function. But it is fiendish: Although the depolarization is reversed, the neuron might still die from apoptosis.”
The commitment point, the beginning of the end, is elusive. “As spreading depolarization is, in principle, reversible, the commitment point at which neurons start dying and at which there is no going back is hard to define,” Dreier says. “Actually, we can only define this point in retrospect. Death is a process that takes some time.”
For Dreier and others, the findings have a concrete call to action.
“We see that patients live longer after a cardiac arrest if some circulation remains. So resuscitation attempts are very important. Even if the heart doesn’t start pumping again immediately, as long as the blood flow is kept going, the brain is kept in a state in which it is able to survive for longer.”
Clues to hemorrhage mystery
Spreading depolarization could also explain the puzzling clinical course seen in patients with sub-arachnoid hemorrhage (aSAH), or bleeding in the space between the brain and the tissues covering it, another recent study by Dreier and Hartings suggests.
Patients with aneurysmal sub-arachnoid haemorrhage are likely to develop a series of complications about a week after the initial bleeding. “This condition has remained enigmatic, as the causes for delayed deterioration were unknown,” Hartings says. “Previously, not much focus was put on the brain damage that occurs soon after the aneurysm ruptures. This was considered too early to medically intervene. But we found that the aneurysm itself causes a significant amount of brain damage.”
Dreier and Hartings analyzed recordings from 11 patients with aSAH and found that spreading depolarizations occur frequently in the initial days after aSAH. “Just the bleeding in the subarachnoid space itself is a trigger for brain tsunamis in humans, causing brain damage,” Hartings says. “The spreading depolarizations signal that a brain infarct [stroke] is developing.” In these patients, clusters of spreading depolarizations occurred again and again. The spreading depolarizations lasted progressively longer and were a marker of neurons dying.
These results could also change treatment for aSAH, Hartings hopes. “Through neuromonitoring, spreading depolarizations can act as an early warning system for clinicians before brain damage is irreversible,” he says. “Clinicians could, for example, pay close attention to whether the brain receives enough blood flow and oxygen.”
The two papers advanced the field of spreading depolarization significantly, says Bill Shuttleworth, Regent’s Professor of Neurosciences at the University of New Mexico, who is part of the COSBID consortium but not involved in the studies. “Previously, the real impact of spreading depolarizations in humans was questioned, but these studies take the step to real relevance of spreading depolarization in the clinic.”
“Looking at the end of life, the researchers tied together death and spreading depolarization in a very controlled clinical setting with strong data. This is an amazing observation, finding other ways in which spreading depolarizations impact the brain,” Shuttleworth says. “And by looking at subarachnoid hemorrhages, the researchers found the first electrophysiological signature for the events causing brain damage.”
“The spreading depolarization shows that brain cells are dying, and gives a tremendously useful marker in the clinic for when something is really hurting the brain,” he says. This is not just a curiosity, but something actionable in intensive care.”

 Video: A recording of brain electrical activity, played back 44x normal rate, in a patient who experienced a traumatic head injury. The crackling sound is the normal activity of brain cells; the periods of silence are short-circuits of electrical activity caused by brain tsunamis, waves of depolarization that spread across injured areas of the brain, causing a local loss of function. The brain’s electrical activity recovers, but with each brain tsunami, damage to cells may worsen. Video posted to YouTube by Mayfield Brain & Spine 

Study examines the rise of plaque in arteries

Maybe we could finally address the root cause of atherosclerosis rather than taking statins to lower cholesterol levels. But statins are a cash cow for Big Pharma, they won't go lightly even with overwhelming evidence.  Probably won't occur in my lifetime. 

Study examines the rise of plaque in arteries

The accumulation of cholesterol plaques in artery walls can lead to atherosclerosis, or the hardening of arteries that contributes to heart attacks and strokes. In a new study, Yale researchers investigate how plaque cells develop at the molecular level, and their findings could help produce targeted treatments for the disease.

Smooth muscle cells, the dominant type of cell found in artery walls, are known to be involved in plaque build-up, but it has not been clear how this occurs. The research team, led by senior study author Daniel Greif, used mice models and primary human cells to study smooth muscle cells and their contribution to atherosclerotic plaques.

They discovered that a single smooth muscle cell gives rise, through a process of clonal expansion, to the majority of cells found in the plaque. Additionally, they learned that a gene known as integrin beta3 regulates the migration of a single smooth muscle cell progenitor from the artery wall into plaque. Once inside the plaque, the progenitor cell reproduces and changes into other cell types. Further, the researchers determined that the gene's role in plaque development occurs in smooth muscle cells as well as in bone marrow-derived cells.   

Together, the findings shed light on the complex mechanisms behind the progression of atherosclerosis, and suggests potential targets for future therapies, the researchers note.

The study is published in Nature Communications.

Getting on with the rest of your life following stroke: a randomized trial of a complex intervention aimed at enhancing life participation post stroke

So rather than actually solving ANY of the problems in stroke, lets research how to make the secondary problems better. Damn it all, go to the root cause and solve that. Solve the neuronal cascade of death by these 5 causes in the first week, resulting in much less disability.
http://journals.sagepub.com/doi/abs/10.1177/0269215514565396?

Show all authors

Nancy E Mayo, Sharon Anderson, Ruth Barclay, ...

First Published January 27, 2015 Research Article

Download PDF	Article information

Abstract

Objective:

To enhance participation post stroke through a structured, community-based program.

Design:

A controlled trial with random allocation to immediate or four-month delayed entry.

Setting:

Eleven community sites in seven Canadian cities.

Subjects:

Community dwelling persons within five years of stroke onset, cognitively intact, able to toilet independently.

Interventions:

Evidence-based program delivered in three 12-week sessions including exercise and project-based activities, done as individuals and in groups.

Main measures:

Hours spent per week in meaningful activities outside of the home and Reintegration to Normal Living Index; Stroke-Specific Geriatric Depression Scale, Apathy Scale, gait speed, EuroQuol EQ-5D, and Preference-Based Stroke Index. All measures were transformed to a scale from 0 to 100. Assessments prior to randomization, after the first session at three months, six months, 12 months, and 15 months.

Results:

A total of 186 persons were randomized. The between-group analysis showed no disadvantage to waiting and so groups were combined and a within-person analysis was carried out at three time points. There were statistically significant increases in all study outcomes on average over all persons. Over 45% of people met or exceeded the pre-specified target of a three hour per week increase in meaningful activity and this most often took a full year of intervention to achieve. Greatest gains were in satisfaction with community integration (mean 4.78; 95% CI: 2.01 to 7.55) and stroke-specific health-related quality of life (mean 4.14; 95% CI: 2.31 to 5.97).

Conclusions:

Community-based programs targeting participation are feasible and effective, but stroke survivors require time to achieve meaningful gains.

Hand Function After Stroke Is Improved By Electrical Stimulation

Well fuck then just write up a godamned protocol on it and publish it worldwide. But you won't. This is where a lack of a complete database of all research and stroke protocols are failing stroke survivors and no one will do anything about that.

WAITING ONCE AGAIN FOR SOMEONE ELSE TO SOLVE THE PROBLEM.

http://www.doctortipster.com/36881-hand-function-stroke-improved-electrical-stiimulation.html
A new electrical stimulation remedy helped stroke survivors with hand weakness improve hand dexterity greater than an existing stimulation approach, in line with new studies in the American Heart Association’s journal Stroke.
Approximately 800,000 people within the United States of America have strokes every year, according to the American Heart Association. Stroke generally results in some paralysis or partial paralysis on one side of the body that can result in survivors having difficulties in executing function. A common remedy in stroke rehabilitation uses low tiers of electrical current to stimulate the paralyzed muscle groups to open the hand, enhance muscle power and likely repair hand function. Stimulation intensity, cycle timing, and repetitions are set by a therapist.

Electrical Stimulation

In the new experimental therapy discovered by researchers at the MetroHealth System, Case Western Reserve University and the Cleveland Functional Electrical Stimulation Center, sufferers manage the stimulation to their vulnerable hand by wearing a glove with sensors on the opposite, unaffected hand. When the affected person opens their unaffected hand, they receive a corresponding amount of stimulation that opens their susceptible stroke-affected hand. This places the affected person in control of their hand and permits them to participate in therapy with the help of electrical stimulation.
According to Jayme S. Knutson, Ph.D., senior author of the study and an assistant professor of Physical Medicine and Rehabilitation at Case Western Reserve University School of Medicine in Cleveland, Ohio, Based on positive findings from our previous studies, we sought to determine if the new glove-controlled hand stimulation therapy could be more effective than the common therapy in improving hand dexterity in patients who are more than six months past their stroke.
Researchers enrolled 80 stroke survivors. For 12 weeks, half of the survivors received remedy using the new glove, and the remainder received the common remedy. Both groups used an electrical stimulator on their own at home for 10 hours every week, plus three hours per week training hand tasks with an occupational therapist in the lab. Hand feature was measured earlier and after remedy with a standard dexterity test that measured the number of blocks members can pick out up, elevate over a barrier and launch in some other place on a desk within a 60 second duration. They determined that sufferers who acquired the new therapy had extra improvement at the dexterity test (4.6 blocks) than the common institution (1.8 blocks). Patients who had greater improvements in hand dexterity following the new therapy have been much less than two years post-stroke and had at least a few finger movements when they started the study. These sufferers saw a development of 9.6 blocks on the dexterity test, compared to 4.1 blocks in the common group.
Sufferers without a finger movement additionally noticed upgrades in arm movement after the new remedy. At the end of treatment, 97 percent of the subjects who obtained the new therapy agreed that they might use their hand greatly than on the start of the study.
Due to the fact that the therapy is new and this was a single-site study, researchers do not know if similar outcomes may also be seen in other rehab centers. They plan to perform a multi-site study to verify their consequences, as well as measure quality of life enhancements for sufferers. And whilst the researchers speculate that the new remedy can be converting neural connections within the brain that manage hand dexterity, extra research is yet to prove what consequences it is able to have on the central nervous system.
The study additionally demonstrates that stroke sufferers can correctly use technology for self-administered therapy at home. According to Knutson, Home-based therapy is becoming increasingly important to offset increasing healthcare costs and to meet the need for high doses of therapy that are critical for attaining the best outcomes. The more therapy a patient can get the better potential outcome they will get.  Once again not getting to the root cause of these problems. Dead and damaged neurons which would be vastly lessened by stopping the neuronal cascade of death by these 5 causes in the first week.

Training in positivity for stroke? A qualitative study of acceptability of use of Positive Mental Training (PosMT) as a tool to assist stroke survivors with post-stroke psychological problems and in coping with rehabilitation

So rather than finding recovery solutions for survivors we have persons researching coping skills. You wouldn't need so many fucking coping skills if you solved the problems in stroke, like the neuronal cascade of death or how to make neuroplasticity and neurogenesis repeatable processes. Solve the root cause, dead and damaged neurons, not the aftereffects. This is all a stupid result of NO stroke leadership or stroke strategy. People researching this stuff should be laughed out of the profession, survivors don't want coping skills they want recovery you fucking idiots. Use those two neurons in your head.

Training in positivity for stroke? A qualitative study of acceptability of use of Positive Mental Training (PosMT) as a tool to assist stroke survivors with post-stroke psychological problems and in coping with rehabilitation

Citation

Mavaddat, N., Dobbin, A., Ross, S., Williams, K., Graffy, J., & Mant, J. (2016). Training in positivity for stroke? A qualitative study of acceptability of use of Positive Mental Training (PosMT) as a tool to assist stroke survivors with post-stroke psychological problems and in coping with rehabilitation. NeuroRehabilitationhttp://dx.doi.org/10.17863/CAM.1245

Description

This is the author accepted manuscript. It is currently under an indefinite embargo pending publication by IOS Press.

Abstract

BACKGROUND: Post-stroke psychological problems predict poor recovery, while positive affect enables patients to focus on rehabilitation and may improve functional outcomes. Positive Mental Training (PosMT), a guided self-help audio shows promise as a tool in promoting positivity, optimism and resilience. OBJECTIVE: To assess acceptability of training in positivity with PosMT for prevention and management of post-stroke psychological problems and to help with coping with rehabilitation. METHODS: A modified PosMT tool consisted of 12 audio tracks each lasting 18 minutes, one listened to every day for a week. Survivors and carers were asked to listen for 4 weeks, but could volunteer to listen for more. Interviews took place about experiences of the tool after 4 and 12 weeks. Subjects: 10 stroke survivors and 5 carers from Stroke Support Groups in the UK. RESULTS: Three stroke survivors did not engage with the tool. The remainder reported positive physical and psychological benefits including improved relaxation, better sleep and reduced anxiety after four weeks. Survivors who completed the programme gained a positive outlook on the future, increased motivation, confidence and ability to cope with rehabilitation. No adverse effects were reported. CONCLUSIONS:The PosMT shows potential as a tool for coping with rehabilitation and overcoming post-stroke psychological problems including anxiety and depression.

Problem-Solving Therapy During Outpatient Stroke Rehabilitation Improves Coping and Health-Related Quality of Life

So rather than finding recovery solutions for survivors we have persons researching coping skills. You wouldn't need so many fucking coping skills if you solved the problems in stroke, like the neuronal cascade of death or how to make neuroplasticity a repeatable process. Solve the root cause, dead and damaged neurons, not the aftereffects. This is all a stupid result of NO stroke leadership or stroke strategy. 

Problem-Solving Therapy During Outpatient Stroke Rehabilitation Improves Coping and Health-Related Quality of Life

1. Marieke M. Visser, MSc;
2. Majanka H. Heijenbrok-Kal, PhD;
3. Adriaan van‘t Spijker, PhD;
4. Engelien Lannoo, PhD;
5. Jan J.V. Busschbach, PhD;
6. Gerard M. Ribbers, MD, PhD

+ Author Affiliations

1. From the Department of Rehabilitation Medicine (M.M.V., M.H.H.-K., G.M.R.) and Department of Psychiatry, Section Medical Psychology and Psychotherapy (A.v.S., J.J.V.B.), Erasmus University Medical Center, Rotterdam, The Netherlands; Rotterdam Neurorehabilitation Research Department (RoNeRes), Rijndam Rehabilitation Center, Rotterdam, The Netherlands (M.M.V., M.H.H.-K., G.M.R.); and Department of Physical and Rehabilitation Medicine, Ghent University Hospital, Ghent, Belgium (E.L.).

1. Correspondence to Majanka H. Heijenbrok-Kal, PhD, Rotterdam Neurorehabilitation Research (RoNeRes), Rijndam Rehabilitation Center, PO Box 23181, 3001 KD, Rotterdam, The Netherlands. E-mail mheijenbrok@rijndam.nl

Abstract

Background and Purpose—This study investigated whether problem-solving therapy (PST) is an effective group intervention for improving coping strategy and health-related quality of life (HRQoL) in patients with stroke.

Methods—In this multicenter randomized controlled trial, the intervention group received PST as add-on to standard outpatient rehabilitation, the control group received outpatient rehabilitation only. Measurements were performed at baseline, directly after the intervention, and 6 and 12 months later. Data were analyzed using linear-mixed models. Primary outcomes were task-oriented coping as measured by the Coping Inventory for Stressful Situations and psychosocial HRQoL as measured by the Stroke-Specific Quality of Life Scale. Secondary outcomes were the EuroQol EQ-5D-5L utility score, emotion-oriented and avoidant coping as measured by the Coping Inventory for Stressful Situations, problem-solving skills as measured by the Social Problem Solving Inventory-Revised, and depression as measured by the Center for Epidemiological Studies Depression Scale.

Results—Included were 166 patients with stroke, mean age 53.06 years (SD, 10.19), 53% men, median time poststroke 7.29 months (interquartile range, 4.90–10.61 months). Six months post intervention, the PST group showed significant improvement when compared with the control group in task-oriented coping (P=0.008), but not stroke-specific psychosocial HRQoL. Furthermore, avoidant coping (P=0.039) and the utility value for general HRQoL (P=0.034) improved more in the PST group than in the control after 6 months.

Conclusions—PST seems to improve task-oriented coping but not disease-specific psychosocial HRQoL after stroke >6-month follow-up. Furthermore, we found indications that PST may improve generic HRQoL recovery and avoidant coping.

Clinical Trial Registration—URL: http://www.trialregister.nl/trialreg/admin/rctview.asp?TC=2509. Unique identifier: CNTR2509.