Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Monday, November 11, 2019

Seaweed-Based Drug Approved for Alzheimer's in China

What is your doctor and stroke hospital doing to ensure this gets tested for our use? NOTHING? Then have them fired. Or do they prefer you travel to China for medical interventions?  


Your chances of getting dementia.


1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.


2. Then this study came out and seems to have a range from 17-66%. December 2013.


3. A 20% chance in this research.   July 2013.


4. Dementia Risk Doubled in Patients Following Stroke September 2018 


5. Parkinson’s Disease May Have Link to Stroke March 2017

Seaweed-Based Drug Approved for Alzheimer's in China

Oligomannate appears to affect gut microbiota, peripheral inflammation

A school of fish swim through seaweed
A seaweed-derived oligomannate preparation (GV-971) received approval from China's National Medical Products Administration (NMPA) to treat mild to moderate Alzheimer's disease, Shanghai Green Valley Pharmaceuticals announced.
A phase III clinical trial of 818 patients with mild-to-moderate Alzheimer's disease showed that oligomannate improved cognition by week 4, showing a mean difference in ADAS-Cog 12 scores of 2.54 (P< 0.0001) between treatment and placebo arms with sustained efficacy until the end of 9 months of treatment, Green Valley said in a press release. The drug was well tolerated and adverse effects in each arm were comparable, the company added.
Full outcomes of the trial have not yet been published, but preclinical data reported in Cell Research showed that, in mice, sodium oligomannate changed gut microbiota, modulated peripheral and central inflammation, and was tied to changes in behavior and Alzheimer's-related pathology. In a commentary accompanying the preclinical study, David Holtzman, MD, of Washington University in St. Louis, and co-authors noted that "GV-971 decreases Aβ-related pathologies by reconditioning the gut microbiota, providing further evidence that gut-targeted interventions may serve as novel strategies to tackle Alzheimer's disease."
The mechanistic relationship between the microbiome and Alzheimer's remains unclear. Increasingly, researchers are looking at ways other organs may affect brain changes: altered liver enzymes have been linked to Alzheimer's disease and people who have had their appendix removed were shown to have a nearly 20% lower risk of Parkinson's disease.
The NMPA's decision marks the first novel drug approved globally for Alzheimer's disease since 2003, Green Valley said. The approval is conditional and will have monitoring for safety. The company plans a multinational phase III trial next year in the U.S, Europe, and Asia to support regulatory filings in other countries.

Cannabis could help alleviate depression and suicidality among people with PTSD

How is your doctor treating you if you are among the 23% ?

23% chance of stroke survivors getting PTSD

Don't worry, your doctor will never write you a prescription for marijuana or CBD and your state legislature won't update their stupid medical marijuana laws to allow this as an approved option. So, legal state or Canada, but you can't do either, you can't treat yourself unless you are medically trained. And if you are medically trained you can't prescribe marijuana to yourself if you won't prescribe it to others.  Good Catch-22 there,  so you are screwed.  

Image result for why doctors won't prescribe marijuana

Cannabis could help alleviate depression and suicidality among people with PTSD

Cannabis may be helping Canadians cope with the effects of post-traumatic stress disorder (PTSD), new research suggests.
In an analysis of health survey data collected by Statistics Canada from more than 24,000 Canadians, researchers from the BC Centre on Substance Use (BCCSU) and University of British Columbia (UBC) found that people who have PTSD but do not medicate with cannabis are far more likely to suffer from severe depression and have suicidal thoughts than those who reported cannabis use over the past year.
The study, published today in the Journal of Psychopharmacology, is the first to document the relationships between PTSD, cannabis use, and severe mental health outcomes in a sample representative of the population.

Stephanie Lake
“We know that with limited treatment options for PTSD, many patients have taken to medicating with cannabis to alleviate their symptoms,” says lead author Stephanie Lake, a research assistant at the BCCSU and PhD candidate at UBC’s school of population and public health. “However, this is the first time that results from a nationally representative survey have shown the potential benefits of treating the disorder with cannabis.”
Data was obtained from Statistics Canada’s 2012 Canadian Community Health Survey – Mental Health (CCHS-MH), which covers Canadians aged 15 and older. Among 24,089 eligible respondents, 420 reported a current clinical diagnosis of PTSD. In total, 106 people with PTSD, or 28.2 per cent, reported past-year cannabis use, compared to 11.2 per cent of those without PTSD.
The researchers found that PTSD was significantly associated with a recent major depressive episode and suicidal ideation among people who don’t use cannabis. Specifically, cannabis non-users with PTSD were about seven times more likely to have experienced a recent major depressive episode and 4.7 times more likely to have thoughts of suicide compared to cannabis non-users without PTSD, the researchers found.
Among cannabis-using respondents, PTSD was not associated with a recent depressive episode or suicide ideation. Over one-quarter of Canadians with PTSD reported past-year cannabis use, which is remarkably high compared to the prevalence of recent use in the general Canadian population (estimated at 11.4 per cent in the present study).

M-J Milloy
People exposed to trauma, including survivors of acute injury, conflict, violence and disaster, suffer from depression, suicide, and substance use disorders at disproportionately high rates compared to the general population. Canada is estimated to have one of the highest prevalence rates of PTSD worldwide, affecting an estimated 9.2 per cent of the population.
“We’re only just beginning to understand what the therapeutic potential of cannabis may be for a variety of health conditions,” says senior author Dr. M-J Milloy, research scientist at BCCSU and Canopy Growth Professor of Cannabis Science at UBC. “These findings are promising, and merit further study in order to fully understand the benefits of cannabis for people living with PTSD.”

How Blood Sugar Levels Affect Alzheimer’s Disease Risk

Your chances of getting dementia. Your doctor should know about this and do something about it. 

1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.  

2. Then this study came out and seems to have a range from 17-66%. December 2013. 

3. A 20% chance in this research.   July 2013. 

4. Dementia Risk Doubled in Patients Following Stroke September 2018 

5. Parkinson’s Disease May Have Link to Stroke March 2017

Do you prefer your doctor being incompetent in not knowing or not doing? There is no excuse for such incompetency, see the following; You are on your own for prevention.

How Blood Sugar Levels Affect Alzheimer’s Disease Risk                  

A significant number of studies continue to suggest links or connections do exist between diabetes and Alzheimer's disease. They claim people with diabetes, especially type 2 diabetes, are at higher risk
Do you prefer your doctor being incompetent in not knowing or not doing?

of eventually developing Alzheimer's dementia or other dementias.
These links, however, aren't fully understood. Studies also can't determine whether taking steps to prevent or control diabetes might help reduce the risk of cognitive decline, including the risk of developing Alzheimer's.
What’s widely recognized is that diabetes is considered a risk factor for vascular dementia. This type of dementia is often caused by reduced or blocked blood flow to the brain.
Doctors know many people with diabetes have brain changes that are clear indicators of both Alzheimer's disease and vascular dementia. Some think each condition fuels the damage caused by the other, hence the persistent theory of a connection between diabetes and Alzheimer's disease.
Diabetes might also increase the risk of developing mild cognitive impairment (MCI). This is a condition where people experience more thinking (cognitive) and memory problems than are usually present in normal aging.
Now, new research is shedding a brighter light on why diabetes might lead to Alzheimer's. This conundrum was taken up at the recent Society for Neuroscience meeting in Chicago.
Again, it was pointed out there's some kind of link between Alzheimer's and diabetes. It's also known the risk for dementia increases twofold in people who have diabetes or metabolic syndrome. But, again, it's not clear what the connection is.
Dr. Liqin Zhao, Ph.D., an associate professor at the University of Kansas, believes the link might be found in the process that enables brain cells to turn sugar into energy. She said one part of that process is called glycolysis.
She pointed out that glycolysis helps brain cells communicate and get rid of the toxins associated with Alzheimer's. In one of her experiments, she gave mice a substance that she thought might help.
This substance is found in the brains of people with a gene that protects them against Alzheimer's.  Zhao said the substance made brain cells healthier overall.
"All of this together increased the brain's resilience against the onset of Alzheimer's disease," she revealed.
Blood sugar might also contribute to the sleep problems often affecting Alzheimer's patients. Dr. Shannon Lynn Macauley-Rambach, Ph.D., Assistant Professor, Gerontology and Geriatric Medicine from Wake Forest School of Medicine, said studies of mice found the brain changes associated with Alzheimer's can interfere with sleep. But, so can abnormal levels of blood sugar, according to her.
"Whether your blood sugar is high or low, which are both found in diseases like Type 2 diabetes -- that this can actually lead to disrupted sleep," she said.
She believes restoring normal levels of blood sugar in Alzheimer's patients might improve their sleep and might even slow down the disease.

Imagining is not doing but involves specific motor commands: A review of experimental data related to motor inhibition

But all the words you use here are worthless to survivors. NOTHING EVEN CLOSE TO A PROTOCOL. WHEN THE HELL WILL YOU DO SOMETHING USEFUL FOR SURVIVORS?

Oops, I'm not playing by the polite rules of Dale Carnegie,  'How to Win Friends and Influence People'. 
Politeness will never solve anything in stroke.  I call them as I see them. I would have them fired. 

Imagining is not doing but involves specific motor commands: A review of experimental data related to motor inhibition

Aymeric Guillot
1,2
*, Franck Di Rienzo
1
,Tadhg MacIntyre
3
,Aidan Moran
4
and  Christian Collet
1
1
Centre de Recherche et d’Innovation sur le Sport (EA 647), équipe Performance Motrice, Mentale et du Matériel, Université de Lyon, Université Claude Bernard Lyon 1,Villeurbanne, France
2
Institut Universitaire de France, Paris, France
3
Physical Education and Sport Sciences Department, University of Limerick, Limerick, Ireland
4
School of Psychology, University College Dublin, Dublin, Ireland
Edited by:
Joel Pearson,The University of New SouthWale, Australia
Reviewed by:
Stephanie D. Preston, University of Michigan, USAYoshikazu Ugawa, Fukushima Medical Universtiy, Japan
*Correspondence:
Aymeric Guillot, Centre de Recherche et d’Innovation sur le Sport,Université Claude Bernard Lyon 1,27-29 Boulevard du 11 Novembre 1918, 69622Villeurbanne Cedex,France.e-mail:  aymeric.guillot@univ-lyon1.fr
There is now compelling evidence that motor imagery (MI) and actual movement share common neural substrate. However, the question of how MI inhibits the transmission of motor commands into the efferent pathways in order to prevent any movement is largely unresolved. Similarly, little is known about the nature of the electromyographic activity that is apparent during MI. In addressing these gaps in the literature, the present paper argues that MI includes motor execution commands for muscle contractions which are blocked at some level of the motor system by inhibitory mechanisms. We first assemble data from neuroimaging studies that demonstrate that the neural networks mediating MI and motor performance are not totally overlapping, thereby highlighting potential differences between MI and actual motor execution. We then review MI data indicating the presence of subliminal muscular activity reflecting the intrinsic characteristics of the motor command as well as increased corticomotor excitability. The third section not only considers the inhibitory mechanisms involved during MI but also examines how the brain resolves the problem of issuing the motor command for action while supervising motor inhibition when people engage involuntary movement during MI.The last part of the paper draws on imagery research in clinical contexts to suggest that some patients move while imagining an action, although they are not aware of such movements. In particular, experimental data from amputees as well as from patients with Parkinson’s disease are discussed. We also review recent studies based on comparing brain activity in tetraplegic patients with that from healthy matched controls that provide insights into inhibitory processes during MI. We conclude by arguing that based on available evidence, a multifactorial explanation of motor inhibition during MI is warranted.

Incremental Value of Computed Tomography Perfusion for Final Infarct Prediction in Acute Ischemic Cerebellar Stroke

Will you stop the prognostic crapola. Survivors want protocols that deliver 100% recovery, NOT this crap. 

Incremental Value of Computed Tomography Perfusion for Final Infarct Prediction in Acute Ischemic Cerebellar Stroke

Author information

1
Department ot Radiology University Hospital, LMU Munich Munich Germany.
2
Department of Neuroradiology University Hospital LMU Munich Germany.
3
Department of Neurology University Hospital LMU Munich Germany.
4
Department of Neurology University Hospital Heidelberg Germany.
5
German Center for Vertigo and Balance Disorders University Hospital LMU Munich Germany.
6
Institute for Stroke and Dementia Research University Hospital LMU Munich Germany.
7
Institute of Diagnostic and Interventional Radiology Pediatric Radiology and Neuroradiology University Medical Center Rostock Germany.

Abstract

Background 
The diagnosis of ischemic cerebellar stroke is challenging because of nonspecific symptoms and very limited accuracy of commonly applied computed tomography (CT) imaging. Advances in CT perfusion imaging provide increasing value in the detection of posterior circulation stroke, but the prognostic value remains unclear. We aimed to identify imaging parameters that predict morphologic outcome in cerebellar stroke patients using advanced CT including whole-brain CT perfusion (WB-CTP).
Methods and Results 
We selected all subjects with cerebellar WB-CTP perfusion deficits and follow-up-confirmed cerebellar infarction from a consecutive cohort with suspected stroke who underwent WB-CTP. Posterior-circulation-Acute-Stroke-Prognosis-Early-CT-Score (pc-ASPECTS) was determined on noncontrast CT, CT angiography source images, and on parametric WB-CTP maps. Cerebellar perfusion deficit volumes on all maps and the final infarction volume on follow-up imaging were quantified. Uni- and multivariate regression analyses were performed. Sixty patients fulfilled the inclusion criteria. pc-ASPECTS on CT angiography source images (ß, -9.239; 95% CI, -14.220 to -4.259; P<0.001) and cerebral blood flow deficit volume (ß, 0.886; 95% CI, 0.684 to 1.089; P<0.001) were significantly associated with final infarction volume in univariate linear regression analysis. The association of cerebral blood flow deficit volume (ß, 0.830; 95% CI, 0.605-1.055; P<0.001) was confirmed in a multivariate linear regression model adjusted for age, sex, pc-ASPECTS on noncontrast CT, and CT angiography source images and the National Institutes of Health Stroke Scale score on admission. No other clinical or imaging parameters were associated with cerebellar stroke final infarction volume (P>0.05).
Conclusions 
In contrast to noncontrast CT and CT angiography, WB-CTP imaging contains prognostic information for morphologic outcome in patients with acute cerebellar stroke.

KEYWORDS:

CT perfusion imaging; ischemic stroke; perfusion imaging; posterior circulation
PMID:
31631729
DOI:
10.1161/JAHA.119.013069
Free full text

Any amount of running linked to significantly lower risk of death

I bet there is zero chance your doctor and therapists have any protocol to get you running again. But if you are willing to try this dangerous activity on your own I'd suggest the book; 'Teaching Me to Run' by Tommye-K. Mayer. Don't do this without your doctors prescription. 

Any amount of running linked to significantly lower risk of death

MedicalXpress Breaking News-and-Events | November 05, 2019

Any amount of running is linked to a significantly lower risk of death from any cause, finds a pooled analysis of the available evidence, published online in the British Journal of Sports Medicine.

If more people took up running—and they wouldn't have to run far or fast—there would likely be substantial improvements in population health and longevity, conclude the researchers.
It's not clear how good running is for staving off the risk of death from any cause and particularly from cardiovascular disease and cancer, say the researchers.
Nor is it clear how much running a person needs to do to reap these potential benefits, nor whether upping the frequency, duration, and pace—in other words, increasing the 'dose'— might be even more advantageous.
To try and find out, the researchers systematically reviewed relevant published research, conference presentations, and doctoral theses and dissertations in a broad range of academic databases.
They looked for studies on the association between running/jogging and the risk of death from all causes, cardiovascular disease, and cancer.
They found 14 suitable studies, involving 232,149 people, whose health had been tracked for between 5.5 and 35 years. During this time, 25,951 of the study participants died.
When the study data were pooled, any amount of running was associated with a 27% lower risk of death from all causes for both sexes, compared with no running.
And it was associated with a 30% lower risk of death from cardiovascular disease, and a 23% lower risk of death from cancer.
Even small 'doses'—for example, once weekly or less, lasting less than 50 minutes each time, and at a speed below 6 miles (8 km) an hour, still seemed to be associated with significant health/longevity benefits.
So running for 25 minutes less than the recommended weekly duration of vigorous physical activity could reduce the risk of death. This makes running a potentially good option for those whose main obstacle to doing enough exercise is lack of time, suggest the researchers.
But upping 'the dose' wasn't associated with a further lowering of the risk of death from any cause, the analysis showed.
This is an observational study, and as such, can't establish cause. And the researchers caution that the number of included studies was small and their methods varied considerably, which may have influenced the results.
Nevertheless, they suggest that any amount of running is better than none, concluding: "Increased rates of participation in running, regardless of its dose, would probably lead to substantial improvements in population health and longevity."
To read more, click here.

Effect of treadmill exercise training on spatial and temporal gait parameters in subjects with chronic stroke: A preliminary report

With NO stroke protocol created this is completely useless for survivors. You'll have to hope like hell that you doctor can get the protocol for treadmill aerobic exercise (T-EX). It is for chronic so it is likely you are not seeing a doctor much anymore so you will have to contact these researchers yourself. Your stroke association won't have this translated into a readable and understandable writeup, they do nothing that actually helps stroke survivors.  

Effect of treadmill exercise training on spatial and temporal gait parameters in subjects with chronic stroke: A preliminary report

 Shawnna L. Patterson, MD, PhD;
1–2
 Mary M. Rodgers, PhD, PT;
3
 Richard F. Macko, MD;
1–2,4
 Larry W. Forrester, PhD
1,3–4
*
1
 Baltimore Department of Veterans Affairs (VAMC) Medical Center Geriatric Research, Education, and Clinical Cen-ter, Baltimore, MD;
2
 Department of Neurology, Baltimore VAMC, Baltimore, MD; Departments of
3
Physical Therapy and Rehabilitation Science and
4
 Neurology, University of Maryland School of Medicine, Baltimore, MD


Abstract—


The effects of task-repetitive locomotor training on stroke patients’ spatial and temporal gait parameters during unassisted walking are not well understood. This study deter-mined the effects of treadmill aerobic exercise (T-EX) on spatial and temporal gait parameters that underlie changes in over-ground walking function. Thirty-nine subjects with hemiparetic stroke underwent T-EX three times weekly for 6months. We measured the subjects pre- and post training on 30-foot timed walks and 6-minute distance walks with usual assistive devices and on an 8 m instrumented walkway without assistive devices. T-EX improved 30-foot walks by 17% and 6-minute walks by23%. Unassisted walking velocity increased 22%, stride length increased 13%, and cadence increased 7%. Paretic and non- paretic step lengths increased significantly, and respective step times decreased significantly. Interlimb symmetry did not change. This study presents preliminary evidence that changes in spatial and temporal gait parameters contribute to the increased velocity of subjects with stroke after T-EX.

Sunday, November 10, 2019

Theta Burst Stimulation of Human Primary Motor Cortex Degrades Selective Muscle Activation in the Ipsilateral Arm

Good luck trying to decipher this, maybe your doctor will do better. Nothing here is of use to us, testing was done with healthy participants. 

Theta Burst Stimulation of Human Primary Motor Cortex Degrades Selective Muscle Activation in the Ipsilateral Arm

Abstract

This study investigated whether repetitive transcranial magnetic stimulation (TMS) delivered as continuous theta burst stimulation (cTBS) to left M1 degraded selective muscle activation in the contralateral and ipsilateral upper limb in healthy participants. Contralateral motor-evoked potentials (cMEPs) were elicited in left and right biceps brachii (BB) before either elbow flexion or forearm pronation. A neurophysiological index, the excitability ratio (ER), was computed from the relative size of BB cMEPs before each type of movement. Short interval intracortical inhibition (SICI) was assessed in cMEPs of right BB with paired-pulse TMS of left M1. Ipsilateral MEPs (iMEPs) and silent periods (iSPs) were measured in left BB with single-pulse TMS of left M1. Low-intensity cTBS was expected to suppress corticospinal output from left M1. A sham condition was also included. Real but not sham cTBS caused increases in BB ER bilaterally. In the right arm, ER increased because BB cMEPs before flexion were less facilitated, whereas cMEPs in the pronation task were unaffected. This was accompanied by an increase in left M1 SICI. In the left arm, ER increased because BB cMEPs before pronation were facilitated but were unaffected in the flexion task. There was also facilitation of left BB iMEPs. These changes in the left arm are consistent with inappropriate facilitation of left BB α-motoneurons (αMNs) before pronation. This is the first demonstration that cTBS of M1 can alter excitability of neurons controlling ipsilateral proximal musculature and degrade ipsilateral upper limb motor control, providing evidence that ipsilateral and contralateral M1 shape the spatial and temporal characteristics of proximal muscle activation appropriate for the task at hand.

Interaction Between Simultaneously Applied Neuromodulatory Interventions in Humans

I got nothing out of this. Hopefully your doctor has an understanding of how this is going to get you 100% recovered. 

Interaction Between Simultaneously Applied Neuromodulatory Interventions in Humans

Siobhan M. Schabrun a * , 
Lucinda S. Chipchase a, 
Natasha Zipf a, 
Gary W. Thickbroom b, 
Paul W. Hodges a 
 a The University of Queensland, NHMRC Centre of Clinical Research Excellence in Spinal Pain, Injury and Health, School of Health and Rehabilitation Science, St Lucia, Brisbane, Queensland 4072, Australia 
b The University of Western Australia, Australian Neuro-muscular Research Institute, Nedlands, Perth, Western Australia 6009, Australia a r t i n f o Article history: Received 3 May 2012 Received in revised form 24 September 2012 Accepted 24 September 2012 Available online xxx 

ABSTRACT 

Background: Transcranial direct current stimulation (tDCS) is a neuromodulatory technique with the potential to enhance the efficacy of traditional therapies such as neuromuscular electrical stimulation(NMES). Yet, concurrent application of tDCS/NMES may also activate homeostatic mechanisms that block or reverse effects on corticomotor excitability. It is unknown how tDCS and NMES interact in the human primamot(M1) and whet effects are summative (increase corticomotor excitability beyond that of tDCS or NMES applied alone) or competitive (block or reduce corticomotor excitability effects of tDCS or NMES applied alone).
Objective: To investigate corticomotor excitability in response to NMES after concurrent application of tDCS protocols that enhance (anodal tDCS) or suppress (cathodal tDCS) excitability of M1.
Methods: We used transcranial magnetic stimulation (TMS) to examine corticomotor excitability before and after the concurrent application of: i) NMES with anodal tDCS; and ii) NMES with cathodal tDCS. Effects were contrasted to four control conditions: i) NMES alone, ii) anodal tDCS alone, iii) cathodal tDCS alone, and iv) sham stimulation.
Results: Concurrent application of two protocols that enhance excitability when applied alone (NMES and anodal tDCS) failed to induce summative effects on corticomotor excitability, as predicted by homeostatic plasticity mechanisms. Combined cathodal tDCS and NMES suppressed the enhanced excitation induced by NMES, an effect that might be explained by calcium dependent anti-gating models.&NBSP;Conclusions: These novel findings highlight the complex mechanisms involved when two neuro-modulues combined suggest that careful testing of combined interventions is necessary before application in clinical contexts. 

a r t i c l e i n f o
 Article history:
Received 3 May 2012
Received in revised form
24 September 2012
Accepted 24 September 2012
Available online xxx
Keywords:
Homeostatic metaplasticity
Neuromuscular electrical stimulation
Primary motor cortex
Transcranial direct current stimulation


Predictors of quality of life 1 year after minor stroke or TIA: A prospective single-centre cohort study

Oh god, what stupid laziness.  There is not a survivor in the world that gives a shit about predictions. They want EXACT stroke protocols that deliver 100% recovery. WHEN THE HELL WILL YOU DELIVER THAT?

Predictors of quality of life 1 year after minor stroke or TIA: A prospective single-centre cohort study

BMJ OpenLam KH, et al. | November 06, 2019
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In this prospective observational cohort study conducted at a single-center hospital in the Netherlands and involving 120 individuals with transient ischemic attack (TIA) or minor stroke who were discharged without rehabilitation treatment, researchers determined possible predictors of quality of life (QoL) in patients with TIA or minor stroke 1 year poststroke to identify which of these patients would require aftercare. Depression and anxiety at baseline predicted a worse mental component of QoL following 1 year. In addition, depression at baseline—along with age and female sex—predicted a worse physical component of QoL after 1 year. The authors concluded that identification of these predictors might enable more efficient and timely selection of patients with TIA or minor stroke who will require stroke aftercare.(Your tyranny of low expectations on full display here. If stroke is too difficult for you to solve please get out and let better people solve it.)
Read the full article on BMJ Open

Researchers successfully reverse Alzheimer's disease in mouse model

Did your doctor followup on this with researchers to get this tested in humans? If not, incompetence reigns in your stroke hospital, beginning at the top with the stroke president and board of directors. Have them all fired.  Only 20 months old.

Researchers successfully reverse Alzheimer's disease in mouse model

The brain of a 10-month-old mouse with Alzheimer's disease (left) is full of amyloid plaques (red) surrounded by activated microglial cells (green). But these hallmarks of Alzheimer's disease are reversed in animals that have gradually lost the BACE1 enzyme (right). Credit: Hu et al., 2018
A team of researchers from the Cleveland Clinic Lerner Research Institute have found that gradually depleting an enzyme called BACE1 completely reverses the formation of amyloid plaques in the brains of mice with Alzheimer's disease, thereby improving the animals' cognitive function. The study, which will be published February 14 in the Journal of Experimental Medicine, raises hopes that drugs targeting this enzyme will be able to successfully treat Alzheimer's disease in humans.
One of the earliest events in Alzheimer's disease is an abnormal buildup of beta- peptide, which can form large, in the brain and disrupt the function of . Also known as beta-secretase, BACE1 helps produce beta-amyloid peptide by cleaving (APP). Drugs that inhibit BACE1 are therefore being developed as potential Alzheimer's disease treatments but, because BACE1 controls many important processes by cleaving proteins other than APP, these drugs could have serious side effects.
Mice completely lacking BACE1 suffer severe neurodevelopmental defects. To investigate whether inhibiting BACE1 in adults might be less harmful, Riqiang Yan and colleagues generated mice that gradually lose this enzyme as they grow older. These mice developed normally and appeared to remain perfectly healthy over time.
The researchers then bred these rodents with mice that start to develop amyloid plaques and Alzheimer's disease when they are 75 days old. The resulting offspring also formed plaques at this age, even though their BACE1 levels were approximately 50% lower than normal. Remarkably, however, the plaques began to disappear as the mice continued to age and lose BACE1 activity, until, at 10 months old, the mice had no plaques in their brains at all.
"To our knowledge, this is the first observation of such a dramatic reversal of amyloid deposition in any study of Alzheimer's disease mouse models," says Yan, who will be moving to become chair of the department of neuroscience at the University of Connecticut this spring.
Decreasing BACE1 activity also resulted in lower beta-amyloid peptide levels and reversed other hallmarks of Alzheimer's disease, such as the activation of microglial cells and the formation of abnormal neuronal processes.
Loss of BACE1 also improved the learning and memory of with Alzheimer's disease. However, when the researchers made electrophysiological recordings of neurons from these animals, they found that depletion of BACE1 only partially restored synaptic function, suggesting that BACE1 may be required for optimal synaptic activity and cognition.
"Our study provides genetic evidence that preformed can be completely reversed after sequential and increased deletion of BACE1 in the adult," says Yan. "Our data show that BACE1 inhibitors have the potential to treat Alzheimer's disease patients without unwanted toxicity. Future studies should develop strategies to minimize the synaptic impairments arising from significant inhibition of BACE1 to achieve maximal and optimal benefits for Alzheimer's patients."

Explore further
PET tracer gauges effectiveness of promising Alzheimer's treatment

More information: Hu et al., 2018. J. Exp. Med. DOI: 10.1084/jem.20171831
Journal information: Journal of Experimental Medicine


Factors associated with community versus personal care home discharges after inpatient stroke rehabilitation: the need for a pre-admission predictive model

You blithering idiots, we need protocols that deliver 100% recovery, not this crapola of predictions of personal care home discharge. Do you understand NOTHING of what survivors want? Maybe you might want to talk to some survivors and not use your standard nocebo phrasing of how lucky you will be to recover. 

Factors associated with community versus personal care home discharges after inpatient stroke rehabilitation: the need for a pre-admission predictive model

Received 23 Jun 2019, Accepted 11 Oct 2019, Published online: 04 Nov 2019
Background: Improved risk factor management and interventions have both been shown to improve mortality in stroke patients. Although this has been a success for acute care, it has placed a higher burden on stroke rehabilitation resources.
Objectives: This study sought to identify the pre-stroke rehabilitation admission factors that best predict personal care home discharge.
Methods: Using a retrospective case-control, chart review design, 60 patients discharged to personal care homes from inpatient stroke rehabilitation between 2008 and 2017 were included. One hundred and eighty-two patients discharged home over the same time span were randomly selected as controls. Statistical analysis was used to identify patient factors independently associated with discharge destination.
Results: Patients were more often discharged to personal care homes if they were older (OR 1.09; CI [1.05–1.15]), had a lower functional independence measure score (OR 0.95; CI [0.92–0.97]), had cognitive deficits (OR 6.19; CI [2.37–18.06]), lived alone before their stroke (OR 7.77; CI [2.75–24.55]), and whether or not there was excessive truncal instability limiting Berg balance scale measurability (OR 0.17; CI [0.06–0.45] if able to measure). Combined, the predictive value of personal care home discharge using these variables was 91.6%.
Conclusions: A combination of age, admission functional independence measure, cognitive impairment, pre-stroke living situation, and measurability of the Berg balance scale on admission to stroke rehabilitation were highly predictive of eventual personal care home discharge.

Additional information

Acknowledgments

Brenden Dufault, University of Manitoba, Canada – Statistical analysis and guidance for write-up.
Kanisha Cruz-Kan, Medical Student, Faculty of Medicine, University of Manitoba, Canada – Data collection.
Himath Jayasinghe, Medical Student, Faculty of Medicine, University of Manitoba, Canada – Data collection.

Walking speed in stroke patients major determinant of recovery

We don't need another stupid recovery prediction. We need protocols that will increase our walking speed to what is necessary to rejoin the normal world. This absolute stupidity is all because we have NO STROKE LEADERSHIP ENFORCING RESEARCH THAT FOLLOWS THE DEFINED STROKE STRATEGY THAT GETS ALL SURVIVORS TO 100% RECOVERY.  Until this is understood and followed by our stroke medical professionals we will never get to 100% recovery.  My suggestion would be to fire everyone in stroke and start over.

Walking speed in stroke patients major determinant of recovery

A study done by Manchester Metropolitan University has discovered that the speed of a patient’s walk recovering from heart stroke is the best way to gauge if that person can get back to work. Researchers investigating the phenomenon were working with physiotherapists and patients in Wales. The project involves moving rehabilitation centers outdoors like Brecon Beacons to adopt new rehabilitation that are being developed to assist young patients of heart strokes.
Though the average age for stroke in UK is 72 for men and 78 for women but there has been a rise of 40 % stroke cases worldwide among people under 65 years within last decade say researchers. The study looked at 46 patients across Wales region that had a stroke before 65 years and observed that only 3 % of them were able to return to regular work. It also discovered that walking speed of a young adult was a key indicator of the individual’s ability to return back to work.
Researchers calculated that walking speed threshold of 0.93m/s or 3 feet per second was the ideal benchmark for returning back to work. They believe that this is the goal that therapists should set for rehabilitation of stroke patients. At Powys based Talybont-on-Usk, young stroke patients were taken on walks near Brecon Canal and Monmouthshire by research team. They wanted to find out if providing fresh air and setting walking goals can help stroke patients to start leading active lives again in the outdoors.
According to Manchester University’s Hanna Jarvis, stroke rehabilitation is usually focused on older people but young patients have specific needs and they want to live life as completely as possible. She said that most of her institute’s patients want to walk outside in the open air to gain confidence of walking in challenging environment. Dr. Jarvis stated that key aim for all young adults recovering from stroke is to return back to work and their research will help to understand how to help them return back to work.

AI Used To Recreate Human Brain Waves In Real Time

I have no clue, so ask your doctor for clarification on how this is going to work AND what researcher they are working with to get this accomplished. No researcher contacted, call the stroke hospital president and politely ask when competent doctors will be hired.  OR not so politely.  Somehow WE have to remove a massive quantity of dead wood in stroke, start with your doctor and work your way up to the board of directors for not setting correct goals for the hospital staff.  100% recovery is the only goal in stroke. DO NOT ACCEPT THE TYRANNY OF LOW EXPECTATIONS THEY WILL TRY TO PASS OFF AS THE ONLY POSSIBILITY. SCREAMING MAY BE REQUIRED.

AI Used To Recreate Human Brain Waves In Real Time

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AI Used To Recreate Human Brain Waves In Real Time
Recently, a team of researchers created a neural network that is able to recreate human brain waves in real-time. As reported by Futurism, the research team, comprised of researchers from the Moscow Institute of Physics and Technology (MIPT) and the Neurobotics corporation, were able to visualize a  person’s brain waves by translating the waves with a computer vision neural network, rendering them as images.
The results of the study were published in bioRxiv, and a video was posted alongside the research paper, which showed how the network reconstructed images. The MIPT research team hopes that the study will help them create post-stroke rehabilitation systems that are controlled by brain waves. In order to create rehabilitative devices for stroke victims, neurobiologists have to study the processes the brain uses to encode information. A critical part of understanding these processes is studying how people perceive video information. According to ZME Science, the current methods of extracting images from brain waves typically analyze the signals originating from the neurons, through the use of implants, or extract images using functional MRI.
The research team from Neurbiotics and MIPT utilized electroencephalography, or EEG, which logs brain waves collected from electrodes placed on the scalp.  In such situations, people often wear devices that track their neural signals while they watch a video or look at pictures. The analysis of brain activity yielded input features that could be used in a machine learning system. The machine learning system was able to reconstruct the images a person witnessed, rendering the images on a screen in real-time.
The experiment was divided into multiple parts. In the experiment’s first phase, the researchers had the subjects watch 10-second clips of YouTube videos for around 20 minutes. There were five different categories that the video were divided into: motorsports, human faces, abstract shapes, waterfalls and moving mechanisms. These different categories can contain a variety of objects. For example, the motorsports category contained clips of snowmobiles and motorcycles.
The research team analyzed the EEG data that was collected while the participants watched the videos. The EEGs displayed specific patterns for each of the different video clips, and this meant that the team could potentially interpret what content the participants were seeing on videos in more or less real-time.
The second phase of the experiment had three categories selected at random. Two neural networks were created to work with these two categories. The first network generated random images that belonged to one of three categories, creating them out of random noise that was refined into an image. Meanwhile, the other network generated noise based on the EEG scans. The data in both of the networks were compared and the randomly generated images were updated based on the EEG noise data, until the generated images became similar to the images that the test subjects were seeing.
After the system had been designed, the researchers tested the program’s ability to visualize brain waves by showing the test subjects videos they hadn’t yet seen from the same categories. The EEGs generated during the second round of viewings were given to the networks, and the networks were able to generate images that could be easily placed into the right category 90% of the time.
The researchers noted that the results of their experiment were surprising because for a long time it was assumed that there wasn’t sufficient information in an EEG to reconstruct the images observed by people. However, the results of the research team proved that it can be done.
Vladimir Konyshev, the head of the Neurorobotics Lab at MIPT, explained that although the research team is currently focused on creating assistive technologies for those who are disabled, the technology they are working could be used to create neural control devices for the general population at some point. Konyshev explained to TechXplore:
“We’re working on the Assistive Technologies project of Neuronet of the National Technology Initiative, which focuses on the brain-computer interface that enables post-stroke patients to control an exoskeleton arm for neurorehabilitation purposes, or paralyzed patients to drive an electric wheelchair, for example. The ultimate goal is to increase the accuracy of neural control for healthy individuals, too.”