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.

Friday, April 30, 2021

Q&A: Evobrutinib reduces blood neurofilament light levels in patients with MS

 Considering that NFL predicts damage post stroke just maybe you want your hospital to ensure human testing in stroke and creation of protocols. Would it help stroke recovery?

 Earlier research statements: from these:

The is a protein known as neurofilament light (NFL). The protein is abundant in neurons found in the brain. When neurons are injured following a or from other , NFL is released into cerebrospinal fluid that bathes the brain and then into the . The amount of NFL released is indicative of neuron injury in the brain, according to the research team.

 

"We found that higher NFL levels forecast worse functional outcomes and shorter survival time after a stroke. We found this to be the case for ischemic stroke and hemorrhagic strokes. Our study establishes NFL as a promising prognostic biomarker for stroke."

 

When neurons are injured following a stroke or from other neurological diseases, NFL is released into cerebrospinal fluid and then the blood. The amount of NFL released is indicative of neuron injury in the brain, according to the research team

 The latest here:

Q&A: Evobrutinib reduces blood neurofilament light levels in patients with MS

 

Evobrutinib, a Bruton’s tyrosine kinase inhibitor that targets B cells and myeloid cells, significantly decreased blood neurofilament light levels as early as 12 weeks in patients with MS, with sustained reductions through 24 weeks.

The findings showed that evobrutinib has a “beneficial effect” for decreasing neuroaxonal damage in MS, according to the study abstract. Researchers presented the results at the American Academy of Neurology annual meeting, which was held virtually.

The present study was a post hoc analysis of a phase 2, placebo-controlled trial that examined the efficacy of evobrutinib (Merck KGaA) on blood levels of neurofilament light (NfL) chain levels. The trial included four treatment groups: evobrutinib 25 mg once per day, 75 mg once per day, 75 mg twice per day or placebo. Researchers evaluated neurofilament light levels and included patients in the post hoc analysis who had measurements from baseline and at least once between baseline and 24 weeks.

Healio Neurology spoke with Jens Kuhle, MD, PhD, study author and head of the MS center at the University Hospital Basel in Switzerland, to learn more about the study results and the potential role for evobrutinib in MS.

Healio Neurology: What prompted this research?

Kuhle: Only recent developments of highly sensitive detection methods now allow us to reliably measure NfL in blood samples, even in healthy controls. Blood NfL is a biomarker that may allow monitoring of disease activity and treatment response with higher sensitivity than current gold standard of treatment monitoring in MS, clinical examination and MRI. Elevated blood NfL levels are a specific indicator of neuroaxonal injury and predict future brain atrophy and disease worsening in patients with MS.

An important next step is the development of reliable and age-adjusted reference values for NfL measurements in blood to move this biomarker further toward individual application in clinical practice. This is an endeavor recently concluded in more than 10,000 serum samples from more than 5,000 healthy controls in our laboratory.

Healio Neurology: Have researchers tried to treat MS with Bruton’s tyrosine kinase inhibitors before?

Kuhle: Treating patients with MS with Bruton’s tyrosine kinase (BTK) inhibitors is currently being studied. So far, there are no BTK inhibitors approved for the treatment of MS, but preclinical and clinical data suggest that evobrutinib has the potential to inhibit MS mechanisms involved in disease activity and progression. The results on blood NfL, coupled with the previously published and presented attributes of central nervous system penetration as well as very high BTK occupancy, show that there is a strong potential for evobrutinib and BTK inhibition to play an important role in the treatment of people living with MS.

Healio Neurology: Can you provide a brief overview of the study results?

Kuhle: The data presented at AAN provide key insights into the role evobrutinib may play in modulating the clinical course of MS and further suggest that BTK inhibition with evobrutinib may reduce tissue damage associated with MS. In a post hoc analysis of the phase 2 placebo-controlled trial of evobrutinib in patients with relapsing MS (RMS), we evaluated 166 patients, with NfL values taken at baseline and at least one NfL value post-baseline.

The largest relative reductions of NfL levels were observed with evobrutinib 75 mg taken twice per day at weeks 12 and 24 compared with placebo. As elevated NfL is associated with clinical disability and brain atrophy in MS, these results, combined with the previous clinical trial data that demonstrated a reduction in T1 gadolinium-enhancing lesions and annualized relapse rates, further support the hypothesis that BTK inhibition with evobrutinib may impact both inflammatory and progressive aspects of MS within the CNS. Evobrutinib is the first BTK inhibitor to demonstrate reduction of NfL in patients with MS.

Healio Neurology: Did the study result in any surprising or unexpected findings?

Kuhle: We were hoping and expecting to find that evobrutinib was able to significantly reduce blood NfL levels, which predicts future brain atrophy and may have implications also for developing disease progression in patients with RMS. The findings from this analysis are encouraging and show a strong potential for evobrutinib in the treatment of people living with MS.

Healio Neurology also spoke with Davorka Tomic, executive medical director of global clinical development in neurology for Merck KGaA, regarding the next steps for evobrutinib. She described the new phase 3 studies of evobrutinib.

Healio Neurology: What are the next steps for this agent?

Tomic: Evobrutinib is currently being evaluated in phase 3 trials following the positive results of the phase 2 clinical trial, which was previously published in The New England Journal of Medicine. The two new trials, EVOLUTION RMS 1 and 2, are multicenter, randomized, parallel-group, double-blind, double-dummy, active-controlled studies of evobrutinib vs. teriflunomide, in participants with RMS. Each trial’s primary endpoint is annualized relapse rate over 96 weeks of treatment. Secondary endpoints include confirmed disability progression as measured by the Expanded Disability Status Scale, Patient-Reported Outcomes Measurement Information System related to physical function and fatigue and number of lesions on brain MRI.

Reference:

Kuhle J. The effect of evobrutinib, a BTK inhibitor, on blood neurofilament light chain levels in relapsing multiple sclerosis. Presented at: American Academy of Neurology Annual Meeting; April 17-22, 2021 (virtual meeting).

 

Thursday, April 29, 2021

Doctors Explain How to Improve Your Circulation for Healthier Blood Flow

 What was your doctors' prescription to improve your blood flow? ANYTHING AT ALL?

So ask your doctor for EXACT PROTOCOLS to increase blood flow.  These posts contain my writings and ideas on increasing blood flow.  DO NOT FOLLOW THEM, I'M NOT MEDICALLY TRAINED. Your doctor supposedly is, so ask him/her. 

Or is it more important to deliver more oxygen to you brain?

Possible solutions: Obviously not vetted coming from me. Don't do them. 

Normobaric oxygen (10)

How to Improve Your Brain Function with An Oxygen Concentrator April 2018 

Or is it more important to increase the loading ability of red blood cells to carry more oxygen? 

Like this?

University of Glasgow Study Demonstrates the Ability of Oxycyte® to Supply Oxygen to Critical Penumbral Tissue in Acute Ischemic Stroke  August 2012

Or like this?

chronic cannabis users have higher cerebral blood flow and extract more oxygen from brain blood flow than nonusers. August 2017  

The latest here:

 

Doctors Explain How to Improve Your Circulation for Healthier Blood Flow

Krissy Brady
·8 min read
Photo credit: Дмитрий Ларичев - Getty Images
Photo credit: Дмитрий Ларичев - Getty Images


“Hearst Magazines and Verizon Media may earn commission or revenue on some items through the links below.”

You might not think about it as much as you do eating healthy, exercising, and getting enough sleep, but maintaining good circulation is one of the most important building blocks to keeping your health on the rails.

“The circulatory system of the body delivers vital oxygen and nutrients to all of our muscles and organs,” says Vincent Varghese, D.O., a cardiac interventionist at Deborah Heart and Lung Center in New Jersey. “When plaque or arterial blockages develop, normal blood flow is hindered and can lead to devastating effects, such as heart attack, stroke, or even leg amputation [in severe cases].”

The process of plaque build-up is a slow one and usually takes decades, he adds, yet studies have shown the precursors of plaque developing as early as our twenties. A sedentary lifestyle, unhealthy eating, high blood pressure, diabetes, smoking, and a family history of early heart or vascular disease can all contribute to poor circulation.

“The most common symptom of impaired circulation to the legs is claudication,” says Caitlin W. Hicks, M.D., a board-certified vascular surgeon and associate professor of surgery at Johns Hopkins Hospital in Baltimore. “It’s a condition where you may experience pain in the buttocks or calves when walking that goes away with rest.”

Cold extremities, leg swelling, and foot wounds that take a while to heal, especially if you have a family history, are all signs you should check in with a vascular specialist.

1. Go on regular walks.

Walking can benefit both the arteries and veins. “Contraction of the calf muscles causes venous blood to be pushed back up to the heart,” says Misty Humphries, M.D., a board-certified vascular surgeon and associate professor of vascular surgery in Sacramento, CA. “The arteries dilate when patients walk and improve blood flow all throughout the body.” Aim for a minimum of 30 minutes of walking three times per week.

But if walking’s not your thing, any type of sweat session can improve circulation. “When you exercise, your muscles need greater blood flow, which supplies oxygen and other nutrients,” says Nachiket Patel, M.D., a board-certified interventional cardiologist and clinical assistant professor of medicine at the University of Arizona College of Medicine in Phoenix.

Shoot for 20 minutes of heart-pumping cardio (think: cycling, elliptical, HIIT) four to five times per week. (Note: If it’s been a while since your last workout, you may want to consider checking in with your doc before starting a new routine).

2. Take more work breaks.

The perks of taking more work breaks is two-fold: It helps you get into the habit of alternating between sitting, standing, and walking, so there’s less demand on the circulatory system (blood flow slows down while you’re sitting and can cause blood to pool in your legs, resulting in muscle pain and fatigue); and it can keep your stress levels from getting out of whack.

“By keeping stress levels down, you’re less likely to binge eat or smoke,” says Dr. Humphries. “Both of these habits can lead to atherosclerosis (plaque buildup) in the arteries that results in a narrowing of the vessels.” Do your best to take stretch breaks every 15 to 20 minutes, and get-up-and-go breaks from sitting every hour—even if it’s just a power walk around your home.

3. Eat more fruits and veggies.

Besides reducing your sugar and fatty food intake to steer clear of high blood pressure, plaque formation, and diabetes, adding more fruits and veggies to your repertoire leads to more nitrates and other compounds in your diet, says Dr. Patel, which your body then uses to create nitric oxide—a chemical compound we exhale that boosts blood flow by relaxing blood vessels.

Foods that are high in nitric oxide converters include leafy green vegetables (spinach, kale, swiss chard, bok choy, arugula), beets, cauliflower, carrots, broccoli, citrus fruits, watermelon, and pomegranates. The more colorful your plate looks, the better off you will be.

Photo credit: tenkende - Getty Images
Photo credit: tenkende - Getty Images

4. Stay hydrated.

“Your blood is about half water, so staying well-hydrated will help keep it moving,” says Dr. Patel. When you’re dehydrated, not only does the amount of blood circulating through your body decrease, but your blood retains more sodium, causing it to thicken and making it that much harder for your circulatory system to do its thing.

The easiest way to make sure you’re getting enough fluids is to check your pee: Straw-colored or clear means you’re hydrated—anything darker than that means you need to up your H20 intake.

5. Quit smoking.

Smoking causes a build-up of plaque in your arteries that can ultimately lead to peripheral artery disease (PAD). “Symptoms of PAD can range from leg pain with walking (claudication) to pain at rest to gangrene (tissue death caused by a lack of blood flow),” says Dr. Hicks.

Quitting smoking slows the process of plaque formation and vessel damage. The process of quitting is different for everyone, but there is medication available through your doctor if you find yourself struggling.

6. Manage your blood pressure.

High blood pressure messes with your circulation by making your heart and blood vessels worker harder and less efficiently. This creates itty bitty tears in the artery walls, which is what gives plaque (from bad cholesterol) the chance to make itself at home. “A cholesterol blockage can occur in any type of artery, including heart and peripheral arteries,” says Dr. Patel.

Exercising, cutting back on sodium, and reducing stress are some of the lifestyle factors that can help lower your blood pressure and improve your circulation in the process. Aim for a blood pressure less than 120/80mmHg.

7. Control your blood sugar.

Elevated glucose levels can cause damage to the lining of your small blood vessels and this can mess with your circulation. Diabetes also promotes the formation of plaque in the body, increasing your risk of PAD. The fatty deposits narrow the blood vessels (especially in your legs and feet).

“Aim for a hemoglobin A1C less than 6.5% if you have diabetes,” says Dr. Varghese. Your diet plays a big role here, and loading up on foods that can help lower your blood sugar naturally, such as leafy greens, whole grains, lean proteins, and legumes, can make a big difference.

8. Wear compression socks.

“Wearing compression socks adds a layer of support to your veins,” says Dr. Humphries. “It helps to prevent the superficial veins that aren’t wrapped in muscle from dilating.” As veins dilate from standing or sitting over long periods of time, they can become varicose veins (twisted, enlarged veins) that cause pain and swelling.

Wear compression socks from morning to evening to steadily squeeze your legs so your veins can move blood more efficiently. They’re available through pharmacies and medical supply stores and even online—prescription-strength are also available if your varicose veins are causing symptoms.

9. Elevate your legs.

Elevating your legs (at or above heart level) improves blood flow to the rest of your body by keeping the blood from pooling in your lower legs. “When you elevate your legs it helps take the pressure off your veins, since they don’t have to work against gravity to get blood back to the heart,” says Dr. Patel.

The most convenient time to elevate your legs would be when you’re watching TV or having a nap—lie down and prop your legs above heart level (a leg elevation pillow can help you comfortably hold the position) for 15 minutes or more at a time.

Photo credit: Deagreez - Getty Images
Photo credit: Deagreez - Getty Images

10. Drink green tea.

Green tea contains catechins, which are compounds that help to improve blood vessel function. “Catechins have been shown to inhibit oxidation (an imbalance of free radicals and antioxidants in the body), decrease blood vessel inflammation, as well as arterial plaque buildup,” says Dr. Patel. It’s thought green tea relaxes blood vessels so the body can pump blood more easily, but more research is needed to understand its full impact.

11. Take it easy on the booze.

“Alcohol consumption at levels above one to two drinks per day is associated with high blood pressure,” says Dr. Patel. When you sip those cocktails, your body has to work harder to pump blood and puts additional stress on your veins.

Spread out your alcohol intake as much as possible—and when you do indulge, stay within the recommended daily intake for alcohol, which is two drinks or less for men and one drink or less for women.

12. Finally, have a family meeting.

“If there’s a family history of early heart or vascular disease, before the age of 55 in men and 65 in women, you should see a specialist at least 10 years before you reach that age,” says Dr. Varghese. “Even without classic risk factors, your genetics and family history play a key role in plaque development.”

 

Evidence of Amyloid Reduction With Blood-Brain Barrier Opening With Focused Ultrasound

 How is your doctor measuring your amyloid burden post stroke and what protocols are in place to remove that? 

Is your doctor 6 years out-of-date already?

Alzheimer’s breakthrough uses ultrasound technology March 2015

Your doctor's reasons for having nothing? There is absolutely no excuse for doing nothing.

Laziness? Incompetence? Or just don't care? No leadership? No strategy? Not my job?

Evidence of Amyloid Reduction With Blood-Brain Barrier Opening With Focused Ultrasound

By Erika Powers

VIRTUAL -- April 27, 2021 -- Hippocampal blood-brain barrier opening with focused ultrasound shows promise as a potential treatment for Alzheimer’s disease, according to a study presented at the Virtual 2021 Annual Meeting of the American Academy of Neurology (AAN).

“Progressive amyloid deposition and cognitive decline characterise Alzheimer’s disease,” said Vibhor Krishna, MD, The Ohio State University, Columbus, Ohio. “Blood-brain barrier opening with focused ultrasound is safe and feasible in patients with Alzheimer’s disease, and there is initial evidence of amyloid reduction.”

For the study, the researchers screened 10 individuals with probable Alzheimer’s disease with mild to moderate dementia symptoms. A total of 6 patients were enrolled, and 5 were treated.

At 3 timepoints, 2 weeks apart, blood-brain barrier was opened in 5 different locations with a high amyloid burden, defined by a standardised uptake value 25% greater than the cerebellum using amyloid positron emission tomography (PET). The targeted brain regions included the hippocampus, entorhinal cortex, thalamus, frontal cortex, and parietal cortex.

The primary outcome variable was the absence of cognitive decline, haemorrhage, new onset of seizures, or neurological deficits. The researchers also assessed blood-brain barrier opening (with dynamic contrast imaging) and postoperative PET amyloid levels.

“No haemorrhage and cerebral oedema were observed,” said Dr. Krishna. “Blood-brain barrier opening was focal, immediate, and no contrast enhancement was observed 1 day postoperative.”

The amyloid reduction varied between 1% to 15% from baseline without significant differences between different tissue types (gray vs white matter).

No serious adverse events were recorded, and the most common adverse event was confusion. One patient reported worsening in cognition at day, and another patient reported worsening cognition 5 weeks after treatment.

“This strategy needs further testing in a larger cohort as a potential therapeutic for Alzheimer’s disease,” said Dr. Krishna.

[Presentation title: Safety of Hippocampal Blood-Brain Barrier Opening With Focused Ultrasound in Alzheimer’s Disease]

Depressive-, Cognitive- or Stroke-Related Risk Factors of Post-Stroke Depression: Which One Could Better Help Clinicians and Patients?

Are you that fucking stupid that you missed the reason for depression? Lack of EXACT PROTOCOLS LEADING TO 100% RECOVERY. 

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. Yes, I'm a bomb thrower and proud of it. Someday a stroke 'leader' will ream me out for making them look bad by being truthful , I look forward to that day.

 The latest here:

Depressive-, Cognitive- or Stroke-Related Risk Factors of Post-Stroke Depression: Which One Could Better Help Clinicians and Patients?

Authors Perrain R, Calvet D, Guiraud V, Mekaoui L, Mas JL, Gorwood P

Received 30 November 2020

Accepted for publication 5 March 2021

Published 29 April 2021 Volume 2021:17 Pages 1243—1251

DOI https://doi.org/10.2147/NDT.S294722

Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 2

Editor who approved publication: Dr Roger Pinder

Download Article [PDF] 

Rebecca Perrain,1,2 David Calvet,3– 5 Vincent Guiraud,3– 5 Lila Mekaoui,1 Jean-Louis Mas,3– 5 Philip Gorwood1,2,5

1GHU Paris Psychiatrie et Neurosciences, CMME, Hôpital Sainte-Anne, Paris, France; 2University of Paris, Paris, France; 3GHU Paris Psychiatrie et Neurosciences, Department of Neurology, Hôpital Sainte-Anne, Paris, France; 4University of Paris, FHU Neurovasc, Paris, France; 5Institute of Psychiatry and Neuroscience of Paris, INSERMU1266, Paris, France

Correspondence: Rebecca Perrain
Clinique des Maladies Mentales et de l’Encéphale, Sainte-Anne Hospital, GHU Paris– Psychiatrie & Neurosciences, 100 rue de la Santé 75674 Paris Cedex 14, Paris, France
Tel +33 1 45 65 83 64
Fax +33 1 45 65 76 56
Email r.perrain@ghu-paris.fr

Purpose: Post-stroke depression (PSD) affects one third of stroke survivors, with multiple severe negative consequences. We aim to assess the weight of four different types of clinical risk factors for PSD.
Patients and Methods: We conducted a prospective cohort study in a stroke centre. After stroke, patients were assessed for cognitive performances, psychiatric standardized questionnaires and socio-demographic features. They were called three months after and assessed for major depressive episode using DSM criteria.
Results: PSD was diagnosed in 8 of the 59 (13.6%) patients enrolled in the study. After multivariate analysis, only “previous history of depressive episode” remained a significant predictive factor for PSD, the model explaining 19% of the total variance (OR=18.0; p=0.002). Patients with a previous history of depression had a 10-fold increased risk for PSD.
Conclusion: Previous history of depression is confirmed as a strong risk factor for PDS and allow the identification of an at-risk sub-group of patients.

Keywords: post-stroke depression, depression, stroke, risk factors, prevention, cohort

Introduction

Worldwide, strokes are the second leading cause of death, after cardiovascular diseases.1 In France, strokes are the first leading cause of acquired disability in adults,2 leading to more quality of life issues when compared to other vascular diseases, such as myocardial infarction.3 Post-stroke depression (PSD) is affecting one third of stroke survivors, with negative consequences such as higher mortality4 and poor recovery.5 The recent “Stroke early management guideline” from the American Heart Association and American Stroke Association, briefly mentioned PSD, with no specific recommendation regarding efficient screening tools, recommended ways to detect the diagnosis or appropriate treatment strategies.

Several reviews identified a set of PSD risk factors, stressing the role of mood-related factors such as previous history of mood disorder, pathological crying at stroke onset, or family history of depression.4,6–9 Socio–demographic factors and global medical factors were also analysed with some of them being identified as PSD predictors. However, results are still discordant.7–9

Cognitive status, at the interface between neurologic damages and psychiatric symptoms, was analysed as well. Post–stroke cognitive impairment has been already associated with PSD.4,10–12

Cognitive impairment is also observed independently during major depressive episodes,13 and could be ongoing afterwards. Delayed memory,14 executive functions and attentional skills15 have been shown to be impaired even after reaching clinical remission.16

Executive and attentional dysfunctions are often coupled. Recent findings have shown that attentional dysfunction could be the primum movens of all depression-related cognitive impairment.17 Other studies suggested that psychomotor retardation could reflect the « burden » of past depression as being correlated with the number of previous depressive episodes.17,18

To our knowledge, there is a lack of studies comparing these different risk factors, and among them neurocognitive impairments, assessing their weight in PSD outcome. Some results suggested that depressive-related symptoms were the most predictive item, but cognitive impairment was always assessed in a global way.8

We therefore assessed the weight of four different types of risk factors for PSD. We distinguished those related to psychiatric and mood-related morbidity, those depending on non-psychiatric co-morbidities and stroke-related features, the ones related to specific cognitive impairment – at the interface between neurologic damages and psychiatric symptoms – and lastly the generic ones such as socio-demographic features.

Patients and Methods

We conducted a prospective cohort study with consecutive inclusions in a stroke unit, at Sainte-Anne hospital, Paris.

Inclusion and Exclusion Criteria

  • Inclusion criteria were (1) age over 18, (2) ischemic or haemorrhagic stroke within 14 days of stroke onset confirmed by magnetic resonance imaging or computed tomography scan.
  • Exclusion criteria were (1) poor global medical condition precluding an hour participation in assessments, including hemiparesia (N=35, 10.9%), (2) an impossible follow-up, (3) not a fluent French speaker, (4) aphasia with a language National Institute of Health Stroke Score (NIHSS) item ≥2 or a Boston Diagnostic Aphasia Examination <8, (5) hemineglect according to the bells test, (6) antidepressant taken at the stroke onset (as studies showed a preventive effect and then a lower rate of PSD with preventive antidepressant treatment),19 (7) major depressive episode present at the stroke onset (8) adults under legal protection and pregnancy or breastfeeding. (9) subdural haematoma, subarachnoid haemorrhage, thrombophlebitis and post-chirurgical stroke.

Estimated Sample Size

We used the 2.19 odds ratio published in our recent meta-analysis on risk factors associated with PSD regarding “previous history of depression” (the most informative marker),8 and a PSD prevalence of 17.7% for PSD according to another recent meta-analysis7 to compute estimated sample size. We estimated that 76 patients were needed to detect a significant role of such risk factors at the end of the cohort, with a risk of 5% and a power of 90%. As the tests demand different skills, we estimated on a preliminary test sample that one patient out of four would roughly be able to be finally tested, raising the number of patients to be included to 304.

Demographic Data

The following demographic data were assessed: age, gender, profession, school level, marital status.

Clinical Assessment

Data collection and clinical assessment occurred within 14 days of stroke onset, from patient bedside.

  1. Stroke characteristics: were assessed including lesion side (right, left, bilateral, median) and stroke severity with the NIHSS.20
  2. Cognitive tasks: were performed directly from patient bedside, and included the d2 test (sustained and selective attention),21 the Dubois’s 5 words test (verbal memory),22 the clock drawing test (executive functions, spatial organisation),23 and the digit span trial (working memory, verbal memory).24 The test description is available in Supplemental Materials.
  3. Psychiatric assessment: included the screening of actual and past depressive episodes with a semi-structured interview (Mini International Neuropsychiatric Interview, MINI-depression, Fifth edition), depressive symptoms being assessed with the Beck Depression Inventory.25 Patients were asked for other past psychiatric history (psychiatric care, treatments). Patients also filled-in the Clinical Global Impression and the Standardised Assessment of Personality Abbreviated Scale (SAPAS), a questionnaire of 8 questions to detect personality disorder. Score ≥3 indicate a personality disorder.26 Alcohol Use Disorders Identification Test (AUDIT-C) was completed: the threshold value is 5 for men and 4 for women.27 Heavy Smoking Index was completed to detect tobacco use disorder (threshold value of 2).28

Three months after the first visit, all patients were called by a psychiatrist and assessed for depression using DSM criteria with MINI-depression. The single assessment of depression after 3 months is based on a previous work, showing that 85% of PSD occurred in the three months following stroke.29

This study was conducted in accordance with the Declaration of Helsinki and was approved by the French National Ethics Committee called “Comité de Protection des Personnes Sud-Méditerranée II” which reference number is 217 R15. The identification number of the protocol was 2017-A00339-44. All patients gave written informed consent prior to participation. All data were recorded anonymously. This study was registered on clinicaltrials.gov (NTC04008719).

Statistical Analyses

Student t-test was used to compare continuous variables and χ2 test to compare categorical variables. Fisher’s exact test was used when minimum expected count was not obtained. Initial data were analysed to study correlation between variables: Pearson correlation was used. When variables were not normally distributed, Spearman test was used. Logistic regression was performed to detect in a multivariate way which parameters were predictive of PSD. For all tests, the threshold of significance was set at p≤0.05.

Positive Predictive Value (PPV) and Negative Predictive Value (NPV) of the confirmed predictive factors were calculated. Positive predictive value (PPV) is the proportion of patients with positive predictors that will have PSD (PPV = True Positives/[True Positives + False Positive]), and the negative predictive value (NPV) is the proportion of patients with negative predictors that will not have PSD (NPV = True Negatives/[True Negatives + False Negatives]).

All statistical analyses were performed with IBM SPSS Statistics for windows, version 23.0. Armonk, NY:IBM Corp.

Results

Among 321 consecutive stroke patients screened between May 2017 and October 2017, 59 were finally included (Figure 1).

Figure 1 Flow-chart of the study.

Comparison Between Included and Excluded Patients

There was no difference between the recruited population compared to the others regarding gender. However, the included patients were younger (p<0.001) with a lower level of severity considering NIHSS (p<0.001).

Sample Characteristics at Baseline

Fifty-three (89.8%) ischaemic strokes were detected, the other being haemorrhagic. Our sample included 21 (35.6%) women, mean age was 61.9 (SD18.5).

Clinical, imaging characteristics and cognitive tests (Table 1) were not independent, as the NIHSS, working memory, verbal memory and age were correlated with some parameters of the d2 Test, and the number of past depressive episode was correlated with the percentage of d2 mistakes.

Table 1 Sample Characteristics of 59 Patients Hospitalized for a Stroke. There Was No Missing Value

Prevalence of PSD, Univariate and Multivariate Analyses

Three months later, two patients could not be assessed. One died (stroke recurrence) and one was lost to follow-up.

PSD was diagnosed in 8 patients (13.6% of total sample), all of them being men.

Univariate analysis (Table 2) identified four variables associated with PSD: previous history of depression, previous history of hypertension, tobacco use disorder and male gender, but none of the cognitive test results. We then analysed the associated variables in a logistic regression analysis (Table 3) apart from gender because of the absence of contrast (100% of PSD being males). Only “previous history of depressive episode” remained a significant predictive factor, the model explaining 19% of the total variance (OR=18.0; p=0.002). When considering only male patients, the model explained 33% of the total variance (OR=42.0; p=0.001).

Table 2 Univariate Approach of Factors Describing a Sample of 59 Patients with Stroke, According to the Development (or Not) of a Post-Stroke Depression 3 Months Later

Table 3 Logistic Regression

Calculated PPV and NPV were, respectively, 46% and 95% for previous history of depression. When considering only male patients, we obtained PPV 75% and NPV 93%.

Discussion

In a study analysing 59 consecutive patients hospitalized in a neurological department specialized in stroke, 14% developed a PSD three months later. A past history of depression assessed at inclusion was the only predictive factor of future PSD when using a multivariate approach, with a positive predictive value of 46% and a negative predictive value of 95%. Patients with a previous history of depression had indeed a 10-fold increased risk for PSD. Contrary to our initial hypothesis, no cognitive test performed at the acute period of the stroke was predictive of later PSD.

Patients included in our study were significantly younger and clinically less severe (considering NIHSS) than the rest of the sample. This is explainable as aphasia and hemiparesia were exclusion criteria and are distinct NIHSS items. We assume that it is a selection bias, limiting the generalisation of our results and narrowing its predictive value to patients that are questionable.

In our sample, depression prevalence three months after stroke is 14%, contrasting with the 30% described in previous studies,4,29 but close to a recent meta-analysis that found a pooled prevalence of PSD of 17.7%.7 Our strict DSM assessment avoided over-estimation, but our method excluded aphasic and clinically instable patients, leading indeed to younger, more professionally active patients; therefore, to patients with a lower risk of developing PSD. Moreover, we chose a single assessment of PSD after 3 months whereas other studies frequently rely on a follow-up of 6 months.6

We aimed at identifying predictive factors for PSD and after logistic regression, only the item “previous history of depression” remained relevant. The fact that no cognitive test was associated with PSD, could be due to the small sample size leading to a lack of statistical power as an association between cognitive impairment and PSD has been already detected.4 On the other hand, these studies assessed cognitive functions in a global way that did not allow specific predictive features.30,31

Previous history of depression is a simple feature and can be accurately assessed with brief semi-structured interview, such as the MINI. Our results stress the need of a systematic interview of patients with stroke, at the acute phase, to screen and detect unnoticed past depressive episodes. Previous history of depressive episode is a well-known risk factor for depressive recurrence.32 Genetic factors as polymorphisms of serotonin transporters confer vulnerability to depression and have been identified as risk factors for post-stroke depression.4,33 Stroke could be considered as a biopsychosocial stress leading to recurrence. Another hypothesis of possible mechanism of the impact of previous history of depressive episode on PSD, is that previous depressive episodes have consequences like a possible cognitive scar that could lead to recurrence.15

Some limits should be stressed in the present study. First, the recruitment was monocentric and hospital-based, limiting results generalizability. However, this approach allows a complete recruitment of all stroke patients comparing with other studies in rehabilitation units and a relatively low attrition rate was observed in our sample. Second, we excluded patients with severe stroke, therefore all patients with significant aphasia, which creates a bias and explains the high drop-out between patients screening and inclusion. However, as language is needed to obtain patients’ agreement and is required to understand the different cognitive tests, such bias is difficult to avoid. Anyhow, it means that the conclusions drawn from this study have to be limited to patients able to communicate and to perform cognitive tests. Third, the sample size remains relatively small and may have lowered statistical power. Finally, all depressed patients were men, which constitutes a sample bias and is strikingly not in line with previous reviews.

Conclusion

We confirm the strength of mood-related risk factors for PSD and allow the identification of an at-risk sub-group of patients for whom a specific follow-up monitoring their mood is needed. Further placebo-controlled trials are needed to recommend preventive antidepressant for this sub-group. Many studies are involved in identifying new complex biomarkers, but the fact that a simple clinical factor, such as past depressive episode, is driving the majority of predictive factor in the present study could be considered as a positive result, such factor being relatively easy, quick and costless to assess.

Acknowledgment

The authors thank neurologists, nurses, neuropsychologist, speech-therapist of the neuro-vascular unit, Sainte-Anne Hospital. Thanks to Amandine Petit, research nurse at the CMME. Thanks to Alexis Dorra for statistical advice. Raw data are available on request by mailing the corresponding author.

 

Meningeal lymphatics affect microglia responses and anti-Aβ(amyloid beta) immunotherapy

Since this is in mice your doctor and hospital will need to ensure human testing and creation of protocols that prevent the amyloid beta from accumulating. You need this because of this risk.

Dementia Risk Doubled in Patients Following Stroke September 2018

Maybe you want to see if this research also delivers VEGF-C  to the brain or you could ask your doctor about it:

Calcium carbonate nanoparticle delivering vascular endothelial growth factor-C siRNA effectively inhibits lymphangiogenesis and growth of gastric cancer in vivo

Your doctor should easily be able to get the protocol that delivered the VEGF-C to the mice and translate it to human delivery.

The latest here:

Meningeal lymphatics affect microglia responses and anti-Aβ(amyloid beta) immunotherapy

Abstract

Alzheimer’s disease (AD) is the most prevalent cause of dementia1. Although there is no effective treatment for AD, passive immunotherapy with monoclonal antibodies against amyloid beta (Aβ) is a promising therapeutic strategy2,3. Meningeal lymphatic drainage has an important role in the accumulation of Aβ in the brain4, but it is not known whether modulation of meningeal lymphatic function can influence the outcome of immunotherapy in AD. Here we show that ablation of meningeal lymphatic vessels in 5xFAD mice (a mouse model of amyloid deposition that expresses five mutations found in familial AD) worsened the outcome of mice treated with anti-Aβ passive immunotherapy by exacerbating the deposition of Aβ, microgliosis, neurovascular dysfunction, and behavioural deficits. By contrast, therapeutic delivery of vascular endothelial growth factor C improved clearance of Aβ by monoclonal antibodies. Notably, there was a substantial overlap between the gene signature of microglia from 5xFAD mice with impaired meningeal lymphatic function and the transcriptional profile of activated microglia from the brains of individuals with AD. Overall, our data demonstrate that impaired meningeal lymphatic drainage exacerbates the microglial inflammatory response in AD and that enhancement of meningeal lymphatic function combined with immunotherapies could lead to better clinical outcomes.

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Abstract submission: 13th World Stroke Congress, October28-29, 2021

 Very obviously they care nothing about survivors, there is no way to get submitted without joining the WSO. And since they do nothing for survivors why bother listening to them at their conference.

This just proves once again what Amy Farber has to say. For the past five years Farber has been battling not only her own disease but also the wall of resistance erected by those who believe that a patient can make about as much of a meaningful contribution to the process of scientific discovery as a laboratory rat.

Abstract submission:WSC2021

My email to them.

How does a person become a patient voice presenter at the World Stroke Congress? Just maybe you want to listen to me; author of Deans' Stroke Musings. There is a lot wrong in stroke and you're not addressing any of it.
Dean Reinke 


Vagus nerve stimulation and rehab to restore hand and arm function after stroke

 

You mean you didn't know about all this earlier research on vagus nerve stimulation? How do we get our stoke hospital to implement this? What technique will force our hospitals to GET THERE?

 

Utilization and Availability of Advanced Imaging in Patients With Acute Ischemic Stroke

 Why are you continuing to promote such slow methods to diagnose stroke?

Maybe these?

Maybe you want these much faster objective diagnosis options.

Hats off to Helmet of Hope - stroke diagnosis in 30 seconds; February 2017

 

Microwave Imaging for Brain Stroke Detection and Monitoring using High Performance Computing in 94 seconds March 2017

 

New Device Quickly Assesses Brain Bleeding in Head Injuries - 5-10 minutes April 2017

Ski-Mask Design AIR Coil Offers Whole-Brain Imaging Without Claustrophobia

The latest here:

Utilization and Availability of Advanced Imaging in Patients With Acute Ischemic Stroke

Originally publishedhttps://doi.org/10.1161/CIRCOUTCOMES.120.006989Circulation: Cardiovascular Quality and Outcomes. 2021;14:e006989

Background:

Recent clinical trials have established the efficacy of endovascular stroke therapy and intravenous thrombolysis using advanced imaging, particularly computed tomography perfusion (CTP). The availability and utilization of CTP for patients and hospitals that treat acute ischemic stroke (AIS), however, is uncertain.

Methods:

We performed a retrospective cross-sectional analysis using 2 complementary Medicare datasets, full sample Texas and 5% national fee-for-service data from 2014 to 2017. AIS cases were identified using International Classification of Diseases, NinthRevision and International Classification of Diseases, Tenth Revision coding criteria. Imaging utilization performed in the initial evaluation of patients with AIS was derived using Current Procedural Terminology codes from professional claims. Primary outcomes were utilization of imaging in AIS cases and the change in utilization over time. Hospitals were defined as imaging modality–performing if they submitted at least 1 claim for that modality per calendar year. The National Medicare dataset was used to validate state-level findings, and a local hospital-level cohort was used to validate the claims-based approach.

Results:

Among 50 797 AIS cases in the Texas Medicare fee-for-service cohort, 64% were evaluated with noncontrast head CT, 17% with CT angiography, 3% with CTP, and 33% with magnetic resonance imaging. CTP utilization was greater in patients treated with endovascular stroke therapy (17%) and intravenous thrombolysis (9%). CT angiography (4%/y) and CTP (1%/y) utilization increased over the study period. These findings were validated in the National dataset. Among hospitals in the Texas cohort, 100% were noncontrast head CT–performing, 77% CT angiography–performing, and 14% CTP-performing in 2017. Most AIS cases (69%) were evaluated at non-CTP–performing hospitals. CTP-performing hospitals were clustered in urban areas, whereas large regions of the state lacked immediate access.

Conclusions:

In state-wide and national Medicare fee-for-service cohorts, CTP utilization in patients with AIS was low, and most patients were evaluated at non-CTP–performing hospitals. These findings support the need for alternative means of screening for AIS recanalization therapies.

Footnotes

The Data Supplement is available at https://www.ahajournals.org/doi/suppl/10.1161/CIRCOUTCOMES.120.006989.

Sunil A. Sheth, MD, Department of Neurology, UTHealth McGovern Medical School, 6431 Fannin St, MSB 7.210. Email

Editorial Utilization of Advanced Imaging for Acute Ischemic Stroke The Ongoing Quest for Optimized Stroke Systems of Care

You're normalizing failure. Anything less than 100% recovery is failure, maybe you want to talk to survivors sometimes who will disabuse you of your fucking tyranny of low expectations. You have the wrong definition of the holy grail of stroke. It is 100% RECOVERY FOR ALL!


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