The Broad Concept of “Spasticity-Plus Syndrome” in Multiple Sclerosis: A Possible New Concept in the Management of Multiple Sclerosis Symptoms

I would think your doctor would immediately prescribe Nabiximols for your spasticity. Since 30% of survivors that have it and there is absolutely nothing else for treating spasticity(botox does not cure spasticity).

This has been out there for years;
Nabiximols is an oromucosal spray formulated in a 1:1 ratio of tetrahydrocannabinol and cannabidiol and approved in several countries for treatment-resistant spasticity in patients with MS.(How fucking incompetent is your doctor in not using it?)

The Broad Concept of “Spasticity-Plus Syndrome” in Multiple Sclerosis: A Possible New Concept in the Management of Multiple Sclerosis Symptoms

Óscar Fernández^1*, Lucienne Costa-Frossard², Marisa Martínez-Ginés³, Paloma Montero⁴, José Maria Prieto⁵ and Lluis Ramió⁶

• ¹Biomedical Research Institute of Malaga, University of Málaga, Málaga, Spain
• ²Department of Neurology, Ramón y Cajal University Hospital, Madrid, Spain
• ³Department of Neurology, Gregorio Marañón Hospital, Madrid, Spain
• ⁴Servicio de Neurología, Hospital Clínico San Carlos, Madrid, Spain
• ⁵Servicio de Neurologia, Complejo Hospitalario Universitario de Santiago, Santiago de Compostela, Spain
• ⁶Servicio de Neurologia, Hospital Universitari de Girona Doctor Josep Trueta, Girona, Spain

Multiple sclerosis (MS) pathology progressively affects multiple central nervous system (CNS) areas. Due to this fact, MS produces a wide array of symptoms. Symptomatic therapy of one MS symptom can cause or worsen other unwanted symptoms (anticholinergics used for bladder dysfunction produce impairment of cognition, many MS drugs produce erectile dysfunction, etc.). Appropriate symptomatic therapy is an unmet need. Several important functions/symptoms (muscle tone, sleep, bladder, pain) are mediated, in great part, in the brainstem. Cannabinoid receptors are distributed throughout the CNS irregularly: There is an accumulation of CB₁ and CB₂ receptors in the brainstem. Nabiximols (a combination of THC and CBD oromucosal spray) interact with both CB₁ and CB₂ receptors. In several clinical trials with Nabiximols for MS spasticity, the investigators report improvement not only in spasticity itself, but also in several functions/symptoms mentioned before (spasms, cramps, pain, gait, sleep, bladder function, fatigue, and possibly tremor). We can conceptualize and, therefore, hypothesize, through this indirect information, that it could be considered the existence of a broad “Spasticity-Plus Syndrome” that involves, a cluster of symptoms apart from spasticity itself, the rest of the mentioned functions/symptoms, probably because they are interlinked after the increase of muscle tone and mediated, at least in part, in the same or close areas of the brainstem. If this holds true, there exists the possibility to treat several spasticity-related symptoms induced by MS pathology with a single therapy, which would permit to avoid the unnecessary adverse effects produced by polytherapy. This would result in an important advance in the symptomatic management of MS.

In the last two decades, the availability of new disease-modifying therapies has radically changed the management of multiple sclerosis (MS) and relapsing–remitting MS in particular (1), resulting in a longer life expectancy for patients with the disease (2). Nevertheless, MS currently remains incurable and, in most patients, disability will eventually progress and they must live with the very many symptoms associated with the disease. These symptoms can have a major impact on patient's quality of life (3) and their management is considered important, although traditionally, this area has received far less attention than disease-modifying therapies (4).

A wide range of treatments are available to manage each of the MS symptoms (5–7). Given that different agents are used for different symptoms and a patient may have several symptoms present at the same time, many MS patients are multi-medicated, particularly as most patients will also be receiving disease-modifying therapies. This article will assess the current fragmented approaches to pharmacological management of spasticity muscle tone increase-related symptoms and their shortcomings. Given that the treatment of MS-associated muscle spasticity has been associated in a good number of clinical trials and also observational studies with the improvement of several other functions/symptoms present in MS (8), we will conceptualize, and subsequently hypothesize, about the clinical interest of introducing the more broad concept of “Spasticity-Plus Syndrome” to provide a unified framework for managing all these seemingly related functions/symptoms. By applying such a concept, it would be possible to simplify the management of symptoms associated with MS and reduce importantly the interactions and adverse effects associated with poly-medication.

Playing Mahjong for 12 Weeks Improved Executive Function in Elderly People With Mild Cognitive Impairment: A Study of Implications for TBI-Induced Cognitive Deficits

What will it take to get this into all stroke hospitals and used with all stroke patients? 

We 5 lost cognitive years from the stroke, we need something to recover that.

Do we need to whap upside the head all the boards of directors of stroke hospitals with a 2x4 to get them to see the light? 

Playing Mahjong for 12 Weeks Improved Executive Function in Elderly People With Mild Cognitive Impairment: A Study of Implications for TBI-Induced Cognitive Deficits

Han Zhang¹, Yi Peng¹, Chunliu Li¹, Hong Lan¹, Guoqiang Xing^2*, Zhu Chen¹ and Bo Zhang¹

• ¹Department of Medical Rehabilitation, The Affiliated Hospital and the Second Clinical Medical College of North Sichuan Medical University, Nanchong Central Hospital, Nanchong, China
• ²The Affiliated Hospital and the Second Clinical Medical College of North Sichuan Medical University, Nanchong, China

Background: Mild cognitive impairment (MCI) is common among elderly people. So far, effective treatment that can stabilize or reverse the cognitive decline associated with MCI is lacking. Recent studies suggest that playing mahjong may improve attention and memory in elderly people. However, its effect on executive function remains unknown.

Methods: 56 elderly people (74.3 ± 4.3 years of age) with MCI from the First Social Welfare the First Nursing Home of Nanchong were randomized into mahjong and control groups (N = 28, each group). Subjects in the mahjong group played mahjong three times a week for 12 weeks, while people in the control group assumed normal daily activity. Executive function was evaluated using the Montreal Cognitive Assessment—Beijing (MoCA-B), the Shape Trail Test (STT), and the Functional Activities Questionnaire (FAQ) before the study and then at 6 and 12 weeks after mahjong administration.

Results: There were no baseline differences in MoCA-B, STT, and FAQ scoring between the two groups. The MoCA-B, STT, and FAQ scores, however, improved significantly in the mahjong group but not in the control group after the 12-week mahjong administration. Significant correlations were also found between STT and FAQ scores.

Conclusions: Playing Mahjong for 12 weeks improved the executive function of elderly people with MCI. Because Mahjong is a simple, low-cost entertainment activity, it could be widely applied to slow down or reverse the progression of cognitive decline in people with MCI, including those with traumatic brain injury.

Coronary Calcium Score for the Prediction of Asymptomatic Coronary Artery Disease in Patients With Ischemic Stroke

The first question to ask your stroke hospital. Do they have anyone in charge of research analysis and creation of stroke interventions from such research? IF NOT, THEY ARE COMPLETELY INCOMPETENT AND HAVE NO BUSINESS BEING A STROKE HOSPITAL.

Coronary Calcium Score for the Prediction of Asymptomatic Coronary Artery Disease in Patients With Ischemic Stroke

Hye-Yeon Choi¹, Soo Jeong Shin², Joonsang Yoo^2,3, Kijeong Lee⁴, Dongbeom Song², Young Dae Kim², Hyo Suk Nam², Kyung Yul Lee², Hye Sun Lee⁵, Dong Joon Kim⁶ and Ji Hoe Heo^2,7*

• ¹Department of Neurology, Kyung Hee University College of Medicine, Kyung Hee University Hospital at Gangdong, Seoul, South Korea
• ²Department of Neurology, Yonsei University College of Medicine, Seoul, South Korea
• ³Department of Neurology, Keimyung University School of Medicine, Daegu, South Korea
• ⁴Department of Neurology, College of Medicine, Eunpyeong St. Mary Hospital, Catholic University of Korea, Seoul, South Korea
• ⁵Biostatistics Collaboration Unit, Yonsei University College of Medicine, Seoul, South Korea
• ⁶Department of Radiology, Yonsei University College of Medicine, Seoul, South Korea
• ⁷Integrative Research Center for Cerebrovascular and Cardiovascular Diseases, Yonsei University College of Medicine, Yonsei University Health System, Seoul, South Korea

Purpose: 

Many patients with ischemic stroke have concomitant coronary artery disease (CAD). However, it remains unclear which stroke patients should undergo evaluation for asymptomatic CAD, and which screening tools are appropriate. We investigated the role of coronary artery calcium (CAC) score as a screening tool for asymptomatic but severe CAD in acute stroke patients. We determined the selection criteria for CAC screening based on risk factors and cerebral atherosclerosis.

Materials and Methods: 

The present study included consecutive patients with acute stroke who had undergone cerebral angiography and multi-detector computed tomography coronary angiography. Severe CAD was defined as left main artery disease or three-vessel disease. Enrolled patients were randomly assigned to two sets; a set for developing selection criteria and a set for validation. To develop selection criteria, we identified associated factors with severe CAD regarding clinical factors and cerebral atherosclerosis. CAD predictability of selection criteria with the CAC score was calculated.

Results: 

Overall, 2,658 patients were included. Severe CAD was present in 360 patients (13.5%). CAC score was associated with CAD severity (P < 0.001). In the development set (N = 1,860), severe CAD was associated with age >65 years [odds ratio (95% confidence interval), 2.62 (1.93–3.55)], male sex (1.81 [1.33–2.46]), dyslipidemia (1.77 [1.25–2.61]), peripheral artery disease (2.64 [1.37–5.06]) and stenosis in the cervicocephalic branches, including the internal carotid (2.79 [2.06–3.78]) and vertebrobasilar arteries (2.08 [1.57–2.76]). We determined the combination of clinical and arterial factors as the selection criteria for CAC evaluation. The cut-off criterion was two or more elements of the selection criteria. The area under the curve (AUC) of the selection criteria was 0.701. The AUC significantly improved to 0.836 when the CAC score was added (P < 0.001). In the validation set (N = 798), the AUC of the selection criteria only was 0.661, and that of the CAC score was 0.833. The AUC of the selection criteria + CAC score significantly improved to 0.861(P < 0.001).

Conclusion: 

The necessity for CAC evaluation could be determined based on the presence of risk factors and significant stenosis of the cervicocephalic arteries. CAC evaluation may be useful for screening for severe CAD in stroke patients.

Introduction

Ischemic heart disease is the leading cause of long-term mortality in patients with stroke (1). The annual risk of myocardial infarction in patients with ischemic stroke is ~2.2% (1, 2). The presence and extent of asymptomatic stenosis in coronary angiography is strongly predictive of major cardiovascular events. Previous studies identified significant (≥50%) stenosis of the coronary artery in 20–41% of patients with stroke via autopsy, coronary angiography, or multi-detector computed tomography angiography (MDCTA) (3–7). Therefore, coronary screening may be necessary for stroke patients at high risk of coronary artery disease (CAD). However, it still remains uncertain which group of patients with stroke should undergo evaluation for asymptomatic CAD, and which evaluation tools are most appropriate for coronary screening in such patients.

Atherosclerosis is a systemic disease and CAD shares several risk factors with cerebral atherosclerosis (8). In fact, previous studies have demonstrated a significant association between CAD and atherosclerosis of the cervicocephalic arteries including the vertebrobasilar artery (VBA) and carotid arteries (4, 6, 9, 10). These findings suggest that CAD may be predicted to some extent by the presence of cerebral atherosclerosis and vascular risk factors.

Previous studies have indicated that coronary artery calcium (CAC) is superior to risk factor-based prediction of CAD and coronary events (11–14). Additionally, other studies reported that CAC scores are associated with the severity of CAD (15). In a large prospective population cohort registry, the risk of coronary events increased as the CAC score increased (12). This study aimed to investigate the role of the CAC score as a screening tool for the diagnosis of asymptomatic but severe CAD in patients with acute stroke. We also sought to determine the selection criteria for CAC screening in patients with stroke based on the presence of risk factors and cerebral atherosclerosis.

More at link. 

Getting Closer to a Blood Test for Alzheimer’s Disease? Dr. Francis Collins, NIH director

You'll want this so you can use the Alzheimer prevention protocols your doctor has.

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

 

You can't use mine, I'm not medically trained, your doctors are much better; vetted and clinically tested. 

Dementia prevention 19 ways per Dean

The latest here:

Getting Closer to a Blood Test for Alzheimer’s Disease? Dr. Francis Collins, NIH director

As research on Alzheimer’s disease (AD) advances, a desperate need remains for an easy blood test to help diagnose the condition as early as possible. Ideally, such a test could also distinguish AD from other forms of dementia that produce similar symptoms. As published recently in Nature Medicine, an NIH-funded research team has designed a simple blood test that is on course to meet these criteria [1].
The latest work builds on a large body of work showing that one secret to predicting a person’s cognitive decline and treatment response in AD lies in a protein called tau. Using the powerful, but expensive, approach of PET scan imaging, we know that tau builds up in the brain as Alzheimer’s disease progresses. We also know that some tau spills from the brain into the bloodstream.
The trouble is that the circulating tau protein breaks down far too quickly for a blood test to offer a reliable measure of what’s happening in a person’s brain. A few years ago, researchers discovered a possible solution: test for blood levels of a slightly different and more stable version of the protein called pTau181 [2]. (The “p” in its name comes from the addition of phosphorus in a particular part of the protein’s structure.)
In the latest study, researchers in the lab of Adam Boxer, University of California, San Francisco, followed up further on this compelling lead. Boxer’s team measured pTau181 levels in blood samples from 362 people between the ages of 58 and 70. Those samples included 56 people with an Alzheimer’s diagnosis, along with 47 people with mild cognitive impairment and 69 healthy controls.
The researchers also included another 190 people diagnosed with frontotemporal lobar degeneration (FTLD). It is a relatively rare form of dementia that leads to a gradual decline in behavior, language, and movement, often in connection with a buildup of tau in the brain.
The study found that levels of pTau181 were roughly 3.5-times higher in the blood of people with AD compared to people without AD. Those with mild cognitive impairment due to underlying AD also showed an intermediate increase in blood levels of pTau181.
Importantly, people with FLTD had normal blood levels of pTau181. As a result, the blood test could reliably distinguish between a person with AD and a person with FLTD. That’s important because, while FLTD is a relatively rare condition, its prevalence is similar to AD in people under the age of 65. But both conditions have similar symptoms, making it often challenging to distinguish them.
The findings add to evidence that the new blood test can help in diagnosing AD and in distinguishing it from other neurodegenerative conditions. In fact, it does so with an accuracy that often rivals more expensive PET scans and more invasive cerebrospinal fluid tests, which are now the only reliable ways to measure tau.
There’s still plenty of work to do before this blood test is ready for a doctor’s office. But these initial findings are very promising in helping to simplify the diagnosis of this devastating condition that now affects an estimated 5.5 million Americans [3].
References:
[1] Diagnostic value of plasma phosphorylated tau181 in Alzheimer’s disease and frontotemporal lobar degeneration. Thijssen EH, La Joie R, Wolf A, Strom A, Wang P, Iaccarino L, Bourakova V, Cobigo Y, Heuer H, Spina S, VandeVrede L, Chai X, Proctor NK, Airey DC, Shcherbinin S, Duggan Evans C, Sims JR, Zetterberg H, Blennow K, Karydas AM, Teunissen CE, Kramer JH, Grinberg LT, Seeley WW, Rosen H, Boeve BF, Miller BL, Rabinovici GD, Dage JL, Rojas JC, Boxer AL; Advancing Research and Treatment for Frontotemporal Lobar Degeneration (ARTFL) investigators. Nat Med. 2020 Mar 2.
[2] Plasma phospho-tau181 increases with Alzheimer’s disease clinical severity and is associated with tau- and amyloid-positron emission tomography. Mielke MM, Hagen CE, Xu J, Chai X, Vemuri P, Lowe VJ, Airey DC, Knopman DS, Roberts RO, Machulda MM, Jack CR Jr, Petersen RC, Dage JL. Alzheimers Dement. 2018 Aug;14(8):989-997.
[3] Alzheimer’s Disease Fact Sheet. National Institute on Aging, May 22, 2019.

An Association Between Hyperchloremia and Acute Kidney Injury in Patients With Acute Ischemic Stroke

Is your doctor testing for this? Does your hospital have a protocol for this? I had to read up on this to find out what it was.

Hyperchloremia is an electrolyte disturbance in which there is an elevated level of the chloride ions in the blood. The normal serum range for chloride is 96 to 106 mEq/L, therefore chloride levels at or above 110 mEq/L usually indicate kidney dysfunction as it is a regulator of chloride concentration. 

An Association Between Hyperchloremia and Acute Kidney Injury in Patients With Acute Ischemic Stroke

Show all authors

J. Tyler Haller, PharmD, BCCCP, Keaton Smetana, PharmD, BCCCP, Michael J. Erdman, PharmD, BCPS, ...

First Published March 25, 2020 Research Article

https://doi.org/10.1177/1941874420913715

Article information

Abstract

Background and Purpose:

While an association between hyperchloremia and worse outcomes, such as acute kidney injury and increased mortality, has been demonstrated in hemorrhagic stroke, it is unclear whether the same relationship exists after acute ischemic stroke. This study aims to determine the relationship between moderate hyperchloremia (serum chloride ≥115 mmol/L) and acute kidney injury in patients with ischemic stroke.

Methods:

This is a multicenter, retrospective, propensity-matched cohort study of adults admitted for acute ischemic stroke. The primary objective was to determine the relationship between moderate hyperchloremia and acute kidney injury, as defined by the Acute Kidney Injury Network criteria. Secondary objectives included mortality and hospital length of stay.

Results:

A total of 407 patients were included in the unmatched cohort (332 nonhyperchloremia and 75 hyperchloremia) and 114 patients (57 in each group) were matched based upon propensity scores. In the matched cohort, hyperchloremia was associated with an increased risk of acute kidney injury (relative risk 1.91 [95% confidence interval 1.01-3.59]) and a longer hospital length of stay (16 vs 12 days; P = .03). Mortality was higher in the hyperchloremia group (19.3% vs 10.5%, P = .19), but this did not reach statistical significance.

Conclusions:

In this study, hyperchloremia after ischemic stroke was associated with increased rates of acute kidney injury and longer hospital length of stay. Further research is needed to determine which interventions may increase chloride levels in patients with acute ischemic stroke and the association between hyperchloremia and clinical outcomes.

Keywords ischemic stroke, acute kidney injury, hyperchloremia, critical care, fluids and electrolytes

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The effects of perceived enjoyment of activities on cognition in late-life

Did your doctor get you recovered enough to enjoy the activities you want to do?  Remember, IT IS YOUR DOCTOR'S RESPONSIBILITY TO GET YOU 100% RECOVERED. Don't let them weasel their way out by suggesting it is YOUR RESPONSIBILITY.  Mine didn't, I can't ride a two wheel bike, I can't do whitewater canoeing. 

The effects of perceived enjoyment of activities on cognition in late-life

Clinical Gerontologist — Gardner HD, Strong JV, Mast BT, et al. | March 30, 2020

Via performing a cross-sectional study, researchers determined the connection between both frequency and perceived enjoyment of leisure activities and cognitive scores. Self-reported frequency and perceived pleasure of leisure activities were obtained from 58 healthy, community-dwelling older adults who were administered a battery of cognitive tests that assessed all major domains: verbal memory, executive functioning, attention, language, and visuospatial ability. Perceived pleasantness or enjoyment of Socializing and Being Effective were predictive of higher scores on attention tests, processing speed, and language. In Being Effective and Doing subscales, frequency of activity participation predicted lower scores on executive functioning tasks. Overall, frequency and perceived enjoyment of some activities appear to be associated with cognition in later life.

• See Also: Sleep-disordered breathing tied to dementia-related brain changes

Read the full article on Clinical Gerontologist

 

13 Things Every Stroke Survivor Wished You Knew

Well it is missing the most important point. You are completely on your own trying to recover. Your doctors and therapists KNOW NOTHING SPECIFIC TO GET YOU RECOVERED.  As proven by their having no protocols and using the craptastic saying: 'All strokes are different, all stroke recoveries are different.'

13 Things Every Stroke Survivor Wished You Knew

Potential neurological symptoms of COVID-19

Be careful out there. 

Potential neurological symptoms of COVID-19

Show all authors

Hai-Yang Wang, Xue-Lin Li, Zhong-Rui Yan, ...

First Published March 28, 2020 Letter

https://doi.org/10.1177/1756286420917830

Article information

Dear Editor,
The coronavirus disease 2019 (COVID-19) outbreak in Wuhan, China has spread rapidly, with confirmed cases currently appearing in multiple countries. Although many details, such as the source of the virus and its ability to spread between individuals, remain unknown, an increasing number of cases have been confirmed to have been caused by human-to-human transmission.^1,2 The primary symptoms of COVID-19 include fever, dry cough, and fatigue.² However, some physicians in affected areas have found that some patients diagnosed with COVID-19 have not shown typical respiratory symptoms, such as fever and coughing, at the time of diagnosis; rather, some infected patients have exhibited only neurological symptoms as the initial symptoms, such as the following: (1) headache, languidness, unstable walking, and malaise, which may be due to non-specific manifestations caused by COVID-19 (the proportion of non-specific manifestations as the first symptoms needs to be further explored); (2) cerebral hemorrhage; (3) cerebral infarction; and (4) other neurological diseases. In a recent study of 214 patients with COVID-19, 78 (36.4%) patients had neurological manifestations, such as headache, dizziness, acute cerebrovascular diseases, and impaired consciousness.³ Of these 214 patients, 40 (18.7%) patients required intensive care unit (ICU) interventions for their severe neurological involvement.³ Currently, although there have been many cases of patients with COVID-19 complicated by cerebral hemorrhages, relevant studies on this association are lacking. Hence, the physiological relationship between COVID-19 and the incidence of cerebral hemorrhage remains unclear. Based on several lines of evidence, we hypothesize that COVID-19 may involve cranial hemorrhage. First, recent studies have shown that this novel severe acute respiratory syndrome (SARS) coronavirus, SARS-CoV-2, invades human respiratory epithelial cells mediated by its S-proteins and angiotensin-converting enzyme 2 (ACE2) receptors on human cell surfaces,⁴ as ACE2 is required for SARS-CoV-2 to infect cells.^5,6 ACE2 signaling lowers blood pressure. Since the expression of ACE2 is reduced in patients with hypertension, the ability of ACE2 to lower blood pressure is concomitantly reduced in these patients. Following SARS-CoV-2 infection, the expression and function of ACE2 proteins are reduced. Since the expression of ACE2 in patients with hypertension is already low, SARS-CoV-2 infection is more likely to induce cerebral hemorrhage in such patients. As a second line of evidence suggesting that SARS-CoV-2 infection may induce cerebral hemorrhage, patients with COVID-19 often suffer from coagulopathy and prolonged prothrombin time,^7,8 both of which are also contributing factors to secondary cerebral hemorrhage. In contrast, no cases of secondary cerebral infarctions have been reported in patients with COVID-19. However, COVID-19 may cause an increase in D-dimers,⁷ which lead easily to thrombotic vascular events. Previous studies have reported cases of secondary cerebral infarction in SARS. Hence, we speculate that COVID-19 also has the potential to induce cerebral venous and/or arterial infarctions. Finally, few studies have reported any cases of neurological damage associated with COVID-19. However, a previous study has shown that RNA sequences of the novel human-infectious coronavirus, HCoV-OC43, were detected in the cerebrospinal fluid of a 15-year-old child with acute demyelinating encephalomyelitis.⁹ SARS-CoV has also been detected in the sera and cerebrospinal fluids of two patients with persistent epilepsy and SARS.¹⁰ A recent report firstly shows that SARS-CoV-2 can also attack and damage the nervous system, with detection of SARS-CoV-2 RNA in the cerebrospinal fluid.¹¹ With the outbreak of COVID-19, we should be vigilant for the presence of neurological symptoms similar to those reported for infections by these previous human infectious coronaviruses.
Due to a lack of clear and specific clinical symptoms in the patients mentioned above, diagnosis of COVID-19 is especially challenging, which may lead to missed or erroneous diagnoses that may increase the chance of transmitting the infection. In addition, due to the absence of fever and respiratory symptoms, such patients with COVID-19 may ignore or be unaware of their illness. Since infected patients are contagious during the incubation period, these patients with atypical presentations represent an important hidden source of the spread of the virus. Therefore, medical staff should inquire about the medical history of each patient in more detail. For such atypical cases, timely routine blood tests, respiratory-tract pathogen tests, and chest computed tomographies should be conducted. Furthermore, protective measures should be taken to avoid the risk of exposure to medical staff and other patients.

Conflict of interest statement
The authors declare that there is no conflict of interest.Ethic statement
This article does not contain any studies involving human participants performed by any of the authors.Funding
The authors received no financial support for the research, authorship, and/or publication of this article.ORCID iDs
Hai-Yang Wang https://orcid.org/0000-0001-6148-4924
Xue-Lin Li https://orcid.org/0000-0002-6724-6932

Right side car entry

Drove in my car down to Florida in Feb. with a friend.  This meant that I got to ride passenger at times. That right side car entry brings a whole different set of problems, none of which were even practised in the car in the therapy department. Lifting the left leg in is not a problem but the left arm/hand stays to the left side of the left leg, Which then slides under my left butt cheek as I try to get my right leg in. My compensating solution is to sit on the seat, making sure my left arm is in my lap as I pivot and bring both legs in. This works for cars but while in Florida our hosts had a Chevy Silverado pickup which means grabbing the handle on the door post to lift myself up, get my left butt cheek on the seat, grab my left arm while trying not to fall out of the pickup, put it in my lap and swing both legs in. Nothing in this was ever mentioned, modeled or tried in therapy. I'm assuming car entry is an ADL and thus should have EXACT PROTOCOLS on how to do that.

Or the left side problems described here:

Drivers side car door closing

The surprising link between coffee and bone health

With our vastly increased risks of falls and thus broken bones another reason for your stroke hospital to have a 24 hour coffee station. It will never occur, your stroke hospital has no employee whose only job is to evaluate research on stroke and implement into hospital procedures.  I'm assuming my great quantity of coffee, 12 cups a day, is why I haven't yet broken my left hip after falling on it numerous times, on concrete, on ice.

The surprising link between coffee and bone health

Melissa Sammy, MDLinx | February 27, 2020

Ah, coffee—the beverage that makes the world go ‘round. This simple brew has been shown to not only increase longevity and enhance exercise performance, but also reduce the risk of type 2 diabetes and fight cancer. Now, we can add increased bone strength to the list of coffee’s many health benefits—thanks to new research published in The Journal of Clinical Endocrinology & Metabolism (JCEM).

Researchers have found that people who regularly drink coffee tend to have stronger bones than those who don't.

Researchers from the University of Hong Kong found that coffee lovers tend to have stronger bones than their non-coffee drinking peers. Specifically, they found a robust association between habitual coffee consumption and the prevention of bone fractures in later life. The results are both surprising and significant because they run counter to decades of prior findings on the subject of coffee and bone health.
Some researchers have argued that coffee may adversely affect bone density and lead to osteoporosis, given the negative effect of caffeine on calcium absorption. But many of these studies have remained inconclusive, with researchers often reporting conflicting results.
“Inconsistent associations between coffee consumption and bone mineral density (BMD) have been observed in epidemiological studies,” wrote the authors of the JCEM report. “Moreover, the relationship of bioactive components in coffee with BMD has not been studied.”

• See Also: 6 surprising benefits of caffeine

This inconsistency in the literature led researchers of the current study “to identify coffee-associated metabolites and evaluate their association with BMD.” To that end, they assessed 564 healthy community-dwelling Chinese adults previously enrolled in the Hong Kong Osteoporosis Study—a large prospective cohort that began in 1995 to investigate the incidence of osteoporosis. The researchers separated self-identified coffee drinkers from abstainers, and asked participants to record the frequency of their coffee consumption.
They compared the BMD of those who reported drinking coffee regularly with those who didn't, and found that daily coffee drinkers had significantly higher BMD. Specifically, the researchers identified 12 serum metabolites that were much more highly concentrated among regular coffee consumers.
“Three metabolites, in particular, were associated with an increase in bone density in the population, and also, a decrease in the risk of fracture,” said Cleveland Clinic’s Chad Deal, MD, who did not take part in the study.
The metabolite 5-acetylamino-6-formylamino-3-methyluracil (AFMU; β = 0.012, SE = 0.005; P = 0.013) was significantly correlated with BMD at the lumbar spine, while 3-hydroxyhippurate (β = 0.007, SE = 0.003, P = 0.027) and trigonelline (β = 0.007, SE = 0.004; P = 0.043) were significantly associated with BMD at the femoral neck.
“Among these [12] metabolites, 11 known metabolites were previously identified to be associated with coffee intake and 6 of them were related to caffeine metabolism. Habitual coffee intake was positively and significantly associated with BMD at the lumbar spine and femoral neck,” the authors wrote.

• See Also: Does caffeine have an effect on your sex life?

Although the study was relatively small and largely based on self-reported data, some health experts, including Dr. Deal, have suggested that it offers sufficiently robust evidence in spite of its limitations. He noted that a potential benefit from this research comes from the identification of specific metabolites in coffee that are good for bone health—a discovery that could translate to the development of new drugs to help protect bone health in the future.
“For all those folks who drink lots of coffee and are concerned about the health effects of coffee, this is good news,” he said. “It appears to show that coffee is, in general, probably good for bone health.”
That said, Dr. Deal also advised heavy coffee drinkers with known low bone mass to test for calcium excretion levels, as caffeine is known to naturally increase the excretion of calcium through urine.
Furthermore, a final word of caution: Despite coffee’s host of positive health effects, the popular beverage does have its downsides. In addition to causing “the jitters” and restlessness in some folks, drinking coffee can raise cholesterol levels in select populations, as well as increase the risk of bladder cancer in males and non-smokers with high coffee consumption.
So, before you pick up that next cup o’ joe, be sure to carefully weigh the pros and cons, and remember—everything in moderation.

Spices in a high-saturated-fat, high-carbohydrate meal reduce postprandial proinflammatory cytokine secretion in men with overweight or obesity: A 3-period, crossover, randomized controlled trial

Since cytokines are implicated in chronic fatigue syndrome would administration of this help? WHOM DO WE ASK THAT SIMPLE QUESTION?

I would suggest this for sensation recovery.

The Szechuan pepper that sends the equivalent of 50 light taps to the brain per second. 

Don't expect your doctor to do anything with this, they not only know nothing, they do nothing. To prove that ask how many decades since they installed an intervention from stroke research. I bet the answer is 1996 when tPA was approved. 

 

Spices in a high-saturated-fat, high-carbohydrate meal reduce postprandial proinflammatory cytokine secretion in men with overweight or obesity: A 3-period, crossover, randomized controlled trial

The Journal of Nutrition — Oh ES, et al. | March 26, 2020

Researchers undertook a 3-period crossover study with nonsmoking men (40–65 y old) with overweight/obesity (25 ≤ BMI ≤ 35 kg/m²), elevated waist circumference (≥ 94 cm), and ≥ 1 cardiovascular disease risk factor, to determine the postprandial influence of a blend of spices in a high-saturated-fat, high-carbohydrate meal (HFCM) on inflammatory cytokine responses. The participants were randomly assigned to consume the following: a HFCM (∼1000 kcal, 33% kcal from saturated fat and 36% kcal from carbohydrate), a HFCM comprising 2 g spice blend, or an HFCM comprising 6 g spice blend. Basil, bay leaf, black pepper, cinnamon, coriander, cumin, ginger, oregano, parsley, red pepper, rosemary, thyme, and turmeric were included in the spice blend. Experts collected blood samples prior to, and hourly for 4 h following the HFCM. They noted a significant spice-by-time interaction on IL-1β, IL-8, and TNF-α secretion from LPS-stimulated peripheral blood mononuclear cells. Among men with overweight/obesity, the attenuation of HFCM-induced postprandial IL-1β secretion by a HFCM containing 6 g spice blend was revealed in this study.

• See Also: The latest global ‘pandemic’ isn’t coronavirus

Read the full article on The Journal of Nutrition

Walking in the woods

A 124 acre natural area is next to my apartment complex with unmaintained trails. It is very wet and the drainage takes forever to dissipate.  I have two pair of high(14 inches) waterproof boots. Tho old pair has flex cracks 7 inches up, vinyl and rubber patches did not stick.  The new pair had the heels separate from the soles which led me to wondering why I had ice cold water inside my boots when I was walking thru 2 inches of water. So now I still wear the old boots and try to not go above 7 inches. Last night it rained and the pools over the trails swelled even farther. This led me to bushwack around one of the largest ones. Deer trails are not the greatest to follow, they can easily squeeze under trees 3-4 feet off the ground. I can't do that very well any more.  Now when you meet someone coming toward you where an actual trail exists, they turn around and walk back. I assume to not get within 6 feet of you.  

I have given up on the 10,000 steps a day, it was hard to get it in and do all the social events I had in the evening when we still had social events. Now I do an hour which gets me about 5-6,000 steps, except when I am wading through pools or bushwacking. It took me 4 hours to do this and only got in 8846 steps, normally I would do this in 2 hours.

Bushwacking looking backward

Bushwacking looking forward

This is the trail, some of the trees in the distance have orange paint dots on them signifying the route.

Evaluation of a staff behaviour change intervention to increase the use of ward-based practice books and active practice during inpatient stroke rehabilitation: a phase-1 pre–post observational study

Useless for two reasons;

1. I bet these are guidelines in the books, NOT PROTOCOLS.

2. You need to be measuring survivor recovery, survivors don't give a shit about staff changes unless they lead to recovery. MEASURE WHAT IS IMPORTANT. 

Evaluation of a staff behaviour change intervention to increase the use of ward-based practice books and active practice during inpatient stroke rehabilitation: a phase-1 pre–post observational study

Show all authors

Claire Stewart, Emma Power, Annie McCluskey, ...

First Published March 23, 2020 Research Article

https://doi.org/10.1177/0269215520911420

Article information

Abstract

Objective:

The aim of this study was to evaluate a staff behaviour change intervention to increase the use of ward-based practice books and active practice by stroke inpatients.

Design:

This is a pre–post observational study.

Setting:

This study was conducted in a inpatient rehabilitation unit in Australia.

Subjects:

Stroke inpatients participated in the study.

Intervention:

A staff behaviour change intervention was designed to support staff to implement practice books. The intervention included staff training on motivation and coaching, and weekly audit and feedback for six months. The environment was restructured to bring staff together weekly at the bedside to review audit data and share skills.

Main measures:

Medical record audit and behavioural mapping were used to compare the number of stroke participants with/using a practice book pre- and post-intervention. Pre- and post-intervention, the percentage of observations where a stroke participant was actively practising, repetitions of practice recorded and type of supervision were compared.

Results:

A total of 24 participants were observed (n = 12 pre, n = 12 post). Post-intervention, the number of participants with practice books increased from one to six (OR = 11, 95% CI = (0.9, 550.7)), but this change was not statistically significant (P = 0.069). Five participants recorded repetitions in their practice books post-intervention, three were observed using practice books. There was no change in median repetitions recorded (r_pbs = 0.00, 95% CI = (−0.4, 0.4), P = 1.000) or observed active practice (r_pbs = –0.02, 95% CI = (−0.4, 0.4), P = 0.933). Active practice was often fully supervised by a therapist.

Conclusion:

A staff behaviour change intervention has the potential to increase the number of stroke survivors receiving ward-based practice books but did not increase active practice. (Precisely because these were not protocols with EXACT INSTRUCTIONS AND NUMBER OF REPETITIONS TO ACCOMPLISH RESULTS. The whole point of stroke research is 100% recovery. This got us nowhere closer to that.)

Michael Pollan Explains Caffeine Cravings (And Why You Don't Have To Quit) on Fresh Air

I have no intention of quitting. I don't know the quantity or timeline required for dementia and Parkinson's prevention. 

How coffee protects against Parkinson’s Aug. 2014 

 Coffee May Lower Your Risk of Dementia Feb. 2013 

And this: Coffee's Phenylindanes Fight Alzheimer's Plaque  

This also: Two Compounds in Coffee May Team Up to Fight Parkinson's  

The latest here:

Michael Pollan Explains Caffeine Cravings (And Why You Don't Have To Quit) on Fresh Air

Association of magnesium intake with type 2 diabetes and total stroke: An updated systematic review and meta-analysis

Is your doctor testing your magnesium levels and prescribing AN EXACT PROTOCOL to get these risk reductions? If not, call the hospital president and ask when competence will be required in the hospital.   Yes, this is for those with diabetes but we have to guess at related help since our fucking failures of stroke associations never do any followup research that might help survivors.  You presidents of stroke associations can contact me and prove me wrong.

Association of magnesium intake with type 2 diabetes and total stroke: An updated systematic review and meta-analysis

BMJ Open — Zhao B, Zeng L, Zhao J, et al. | March 23, 2020

To update the detailed links between T2D and total stroke and magnesium consumption as well as the dose–response trend, researchers undertook systematic review and meta-analyses including prospective cohort investigations assessing these two diseases. The included 41 eligible studies with 53 cohorts were identified from PubMed, Embase, Cochrane Library, Web of Science and ClinicalTrials.gov, via a search from inception to 15 March 2019. On comparing the highest magnesium intake to the lowest, a significant reduction in the magnitude of the risk by 22%, 11%, and 12% was observed for T2D, for total stroke, and for ischaemic stroke, respectively. In subgroup analyses, a significant reduction in the risk for total and ischaemic stroke was noted among females, participants with ≥25 mg/m² body mass index and those with ≥12-year follow-up. Overall, findings revealed significantly inverse links of magnesium consumption with T2D and total stroke in a dose-dependent manner. According to the findings, feasible magnesium-rich dietary patterns may be highly advantageous for particular groups and could be highlighted in the primary T2D and total stroke prevention strategies disseminated to the public.

• See Also: New sleep method strengthens brain's ability to retain memories

Read the full article on BMJ Open

Flavonoid intake and MRI markers of brain health in the Framingham Offspring cohort

Notice that this doesn't apply to us and our fucking failures of stroke associations

won't do the necessary studies to see how this might help stroke survivors. Don't do anything with this unless your doctor prescribes it. And since quartiles are not explained here your doctor needs to get the full clinical research so you know exactly how many bottles of red wine you should be consuming. My doctor told me I had a bunch of white matter hyperintensities but never showed me them on any scan, so I don't know the size or any intervention needed, because my doctor knew nothing.

The main dietary sources of flavonoids include tea, citrus fruit, citrus fruit juices, berries, red wine, apples, and legumes. Individual flavonoid intakes may vary considerably depending on whether tea, red wine, soy products, or fruit and vegetables are commonly consumed.

Flavonoid intake and MRI markers of brain health in the Framingham Offspring cohort

The Journal of Nutrition — Shishtar E, et al. | March 26, 2020

Researchers assessed MRI measures of brain health, including total brain tissue volume, white matter hyperintensities volume (WMHV), and hippocampal volume, in correlation with the intake of dietary flavonoid. Participants included members of the Framingham Heart Study Offspring Cohort who were free of stroke at exam 7 and had at least 1 valid food frequency questionnaire from exams 5, 6, or 7 (n = 2,086; mean age at exam 7, 60.6 y). Flavonoid intakes were grouped according to quartiles categories of consumption. In the highest quartile category of flavan-3-ols and flavonoid polymers intake vs in the lowest quartile category, the mean (95% CI) of the WMHV of participants was found to be significantly smaller after accounting for crucial demographic, lifestyle, and clinical factors. For flavan-3-ols and flavonoid polymers as well as for total flavonoids, inverse trend links with WMHV were also noted. The findings revealed a likely impact of higher flavonoid intakes on the risk of Alzheimer disease and related dementias (ADRD) in middle-aged and older adults, by causing a decrease in WMHV, a marker strongly related to ADRD. These findings contribute to the literature on flavonoids and ADRD.

Read the full article on The Journal of Nutrition