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.

Tuesday, February 28, 2017

Proportional Motor Recovery After Stroke Implications for Trial Design

Yes, novel interventions are needed. Solve the 5 causes of the neuronal cascade of death in the first week. Using Fugl-Meyer for comparison seems useless since it is totally subjective and has limited discrimination.
http://stroke.ahajournals.org/content/48/3/795?etoc=
Cathy M. Stinear, Winston D. Byblow, Suzanne J. Ackerley, Marie-Claire Smith, Victor M. Borges, P. Alan Barber
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Abstract

Background and Purpose—Recovery of upper-limb motor impairment after first-ever ischemic stroke is proportional to the degree of initial impairment in patients with a functional corticospinal tract (CST). This study aimed to investigate whether proportional recovery occurs in a more clinically relevant sample including patients with intracerebral hemorrhage and previous stroke.
Methods—Patients with upper-limb weakness were assessed 3 days and 3 months poststroke with the Fugl–Meyer scale. Transcranial magnetic stimulation was used to test CST function, and patients were dichotomized according to the presence of motor evoked potentials in the paretic wrist extensors. Linear regression modeling of Δ Fugl–Meyer score between 3 days and 3 months was performed, with predictors including initial impairment (66 − baseline Fugl–Meyer score), age, sex, stroke type, previous stroke, comorbidities, and upper-limb therapy dose.
Results—One hundred ninety-two patients were recruited, and 157 completed 3-month follow-up. Patients with a functional CST made a proportional recovery of 63% (95% confidence interval, 55%–70%) of initial motor impairment. The recovery of patients without a functional CST was not proportional to initial impairment and was reduced by greater CST damage.
Conclusions—Recovery of motor impairment in patients with intact CST is proportional to initial impairment and unaffected by previous stroke, type of stroke, or upper-limb therapy dose. Novel interventions that interact with the neurobiological mechanisms of recovery are needed. The generalizability of proportional recovery is such that patients with intracerebral hemorrhage and previous stroke may usefully be included in interventional rehabilitation trials.
Clinical Trial Registration—URL: http://www.anzctr.org.au. Unique identifier: ANZCTR12611000755932.

Defining the Role of the Stroke Physician During Endovascular Therapy of Acute Ischemic Stroke

Well fuck, this is so simple, you need to write up a protocol not a guideline. Does anyone even have two neurons to rub together and create a spark of knowledge?

http://stroke.ahajournals.org/content/48/3/805?etoc=
Grant Stotts, Alexandre Y. Poppe, Daniel Roy, Tudor G. Jovin, Cheemun Lum, David Williams, John Thornton, Blaise W. Baxter, Thomas Devlin, Donald F. Frei, Chris Fanale, Ashfaq Shuaib, Jeremy L. Rempel, Bijoy K. Menon, Andrew M. Demchuk, Mayank Goyal, Michael D. Hill
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Introduction

Six recent trials and a patient-level meta-analysis have demonstrated the superiority of endovascular therapy (EVT) compared with standard care (including intravenous alteplase) among patients with large-artery anterior circulation strokes.17 The absolute benefit of EVT was substantial in these trials, and EVT now requires careful implementation and optimization in real-world settings to provide all eligible patients with this new standard of care. Parallel rather than serial workflow, with team members having well-defined roles, is a crucial element in providing rapid and effective delivery of acute stroke care.8
There is little or no literature on the division of labor or the expected role for each individual in this setting, and existing stroke guidelines do not elaborate on this issue. Although each system may require customization, it is clear is that there must be physician leadership outside of the angiography suite, a physician in addition to the neurointerventionalist (who is most commonly a radiologist, but who may be a neurosurgeon or neurologist) in the angiography suite, and a physician to coordinate care between the other stroke team members throughout the periprocedural period. We suggest that it is necessary to designate a physician to fulfill these roles during the EVT process, and we have termed herein the individual fulfilling this role the stroke physician.
The stroke physician must work in close collaboration with the neurointerventionalist to optimize the speed, efficiency, and safety of EVT, elements which are critical to enhancing patient outcomes. A proposed division of physician roles is shown in Table, with emphasis on parallel rather than serial workflow. The administration of intravenous alteplase is ideally performed under the guidance of a stroke physician with specialized training in stroke care. This is most often a neurologist but may also be an emergency physician, geriatrician, internist, or family physician, …
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Vessel Wall Enhancement and Blood–Cerebrospinal Fluid Barrier Disruption After Mechanical Thrombectomy in Acute Ischemic Stroke

Are you people that

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http://stroke.ahajournals.org/content/48/3/651?etoc=
Arturo Renú, Carlos Laredo, Antonio Lopez-Rueda, Laura Llull, Raúl Tudela, Luis San-Roman, Xabier Urra, Jordi Blasco, Juan Macho, Laura Oleaga, Angel Chamorro, Sergio Amaro

form below to view the article. Access to this article can also be purchased.


Abstract

Background and Purpose—Less than half of acute ischemic stroke patients treated with mechanical thrombectomy obtain permanent clinical benefits. Consequently, there is an urgent need to identify mechanisms implicated in the limited efficacy of early reperfusion. We evaluated the predictors and prognostic significance of vessel wall permeability impairment and its association with blood–cerebrospinal fluid barrier (BCSFB) disruption after acute stroke treated with thrombectomy.
Methods—A prospective cohort of acute stroke patients treated with stent retrievers was analyzed. Vessel wall permeability impairment was identified as gadolinium vessel wall enhancement (GVE) in a 24- to 48-hour follow-up contrast-enhanced magnetic resonance imaging, and severe BCSFB disruption was defined as subarachnoid hemorrhage or gadolinium sulcal enhancement (present across >10 slices). Infarct volume was evaluated in follow-up magnetic resonance imaging, and clinical outcome was evaluated with the modified Rankin Scale at day 90.
Results—A total of 60 patients (median National Institutes of Health Stroke Scale score, 18) were analyzed, of whom 28 (47%) received intravenous alteplase before mechanical thrombectomy. Overall, 34 (57%) patients had GVE and 27 (45%) had severe BCSFB disruption. GVE was significantly associated with alteplase use before thrombectomy and with more stent retriever passes, along with the presence of severe BCSFB disruption. GVE was associated with poor clinical outcome, and both GVE and severe BCSFB disruption were associated with increased final infarct volume.
Conclusions—These findings may support the clinical relevance of direct vessel damage and BCSFB disruption after acute stroke and reinforce the need for further improvements in reperfusion strategies. Further validation in larger cohorts of patients is warranted.

Monday, February 27, 2017

Use of a 3-Item Short-Form Version of the Barthel Index for Use in Stroke

This research is pretty useless with the Barthel scales also being subjective. Isn't anyone ever going to start using objective 3d scans of damage and location to determine stroke severity and recovery possibilities?
http://stroke.ahajournals.org/content/48/3/618?etoc=

Rachael L. MacIsaac, Myzoon Ali, Martin Taylor-Rowan, Helen Rodgers, Kennedy R. Lees, Terence J. Quinn
and on behalf of the VISTA Collaborators
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Abstract

Background and Purpose—There may be a potential to reduce the number of items assessed in the Barthel Index (BI), and shortened versions of the BI have been described. We sought to collate all existing short-form BI (SF-BI) and perform a comparative validation using clinical trial data.
Methods—We performed a systematic review across multidisciplinary electronic databases to find all published SF-BI. Our validation used the VISTA (Virtual International Stroke Trials Archive) resource. We describe concurrent validity (agreement of each SF-BI with BI), convergent and divergent validity (agreement of each SF-BI with other outcome measures available in the data set), predictive validity (association of prognostic factors with SF-BI outcomes), and content validity (item correlation and exploratory factor analyses).
Results—From 3546 titles, we found 8 articles describing 6 differing SF-BI. Using acute trial data (n=8852), internal reliability suggested redundancy in BI (Cronbach α, 0.96). Each SF-BI demonstrated a strong correlation with BI, modified Rankin Scale, National Institutes of Health Stroke Scale (all ρ≥0.83; P<0.001). Using rehabilitation trial data (n=332), SF-BI demonstrated modest correlation with quality of life measures Stroke Impact Scale and 5 domain EuroQOL (ρ≥0.50, P<0.001). Prespecified prognostic factors were associated with SF-BI outcomes (all P<0.001). Our factor analysis described a 3 factor structure, and item reduction suggested an optimal 3-item SF-BI comprising bladder control, transfer, and mobility items in keeping with 1 of the 3-item SF-BI previously described in the literature.
Conclusions—There is redundancy in the original BI; we have demonstrated internal and external validity of a 3-item SF-BI that should be simple to use.

Lifestyle Factors and Early Clinical Outcome in Patients With Acute Stroke

This told me nothing useful. No clue what describes a severe stroke.
http://stroke.ahajournals.org/content/48/3/611?etoc=
Annette Ingeman, Grethe Andersen, Reimar W. Thomsen, Heidi H. Hundborg, Henrik H. Rasmussen, Søren P. Johnsen
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Abstract

Background and Purpose—We examined the associations of individual and combined lifestyle factors with early adverse stroke outcomes.
Methods—A total of 82 597 patients were identified from nationwide registries. Lifestyle factors at the time of stroke admission included body mass index (kg/m2), smoking habits, and alcohol intake, which were grouped (healthy, moderately healthy, moderately unhealthy, and unhealthy). The associations between lifestyle and outcomes were examined using multivariable regression.
Results—A total of 18.3% had a severe stroke, 7.8% pneumonia, 12.5% urinary tract infection, and 9.9% died within 30 days. The association between lifestyle, stroke severity, and mortality, respectively, differed according to sex. Unhealthy lifestyle was associated with lower risk of severe stroke (adjusted odds ratio [OR], 0.73; 95% confidence interval [CI], 0.63–0.84) and 30-day mortality among men (adjusted OR, 0.71; 95% CI, 0.58–0.87), but not among women (severe stroke: adjusted OR, 1.14; 95% CI, 0.85–1.55, and mortality: adjusted OR, 1.34; 95% CI, 0.90–1.99). No sex differences were found for pneumonia and urinary tract infection. Unhealthy lifestyle was not associated with a statistically significant increased risk of developing in-hospital pneumonia (adjusted OR, 1.30; 95% CI, 0.98–1.73) or urinary tract infection (adjusted OR, 0.98; 95% CI, 0.72–1.33). Underweight was associated with a higher 30-day mortality (men: adjusted OR, 1.71; 95% CI, 1.50–1.96, and women: adjusted OR, 1.46; 95% CI, 1.34–1.60).
Conclusions—Healthy lifestyle was not associated with a lower risk of adverse stroke outcomes, in particularly among men. However, underweight may be a particular concern being associated with an increased risk of adverse outcomes among both sexes.

EMG driven musculoskeletal model for robot assisted stroke rehabilitation system

This is an engineering student so I guess going down the failed rehab route was to be expected. You want to have better recoveries and less need for rehab? Then the solution is to stop these 5 causes of the neuronal cascade of death in the first week. 
https://figshare.com/articles/EMG_driven_musculoskeletal_model_for_robot_assisted_stroke_rehabilitation_system/4697485
byJauw, Veronica Lestari
Neuro-rehabilitation is a medical process aimed at restoring the sensory and motor functions of the nervous system via repetitive learning and training process. The success of neuro-rehabilitation is simply measured by how fast the patients can recover from the disability. However, the continuous growth of the number of disabled patients and the lack of resources and rehabilitation facilities has then questioned the justification of its success in the future. There are questions about whether the present approaches of neuro-rehabilitation are still efficient to keep up with the future growth of the disabled patients which is growing exponentially. Hence, there is a need for constant advancement in neuro-rehabilitation engineering to improve the efficiency of automated rehabilitation. By doing this, the recovery rate of the patients can be increased, allowing more patients to be rehabilitated even with the lack of resources and rehabilitation facilities. The current study explores the utilization of 9 different upper limb’s muscles to find the best correlation between the electromyography (EMG) signals of the muscles and the individual torque of the upper joints via mathematical models. The EMG signals are acquired in real time and processed by rectification and filtration to eliminate the interference of the signal. These processed signals are then used as the input variables in GA; training the optimized correlation coefficients to minimize the discrepancy between the actual and simulated torque. The best correlation will be used as a control model in the rehabilitative robot’s controller as a decision making. Should the patient require assistance; this model will calculate the amount of assistive force required and supply it to the patient through the servo to complete the rehabilitation cycle. A comparative study, supported by the quantitative data of the simulation results, indicates that the individual torque of the upper limb’s joints is best modeled as the inverse logarithm of the EMG signals of the upper limb muscles with a constant. The estimated torque calculated from this model is the closest to the actual torque among the other mathematical models and thus, it has the lowest discrepancy. The average of 32% discrepancy is calculated throughout 100 generations in ±34 minutes. However, this figure is not attainable upon the integration of the inverse logarithm mathematical model into the controller mainly due to the communication rate between the DAQ system and the server. There is a discrepancy of approximately 10% between the experimental and simulated results which deems to be quite significant.

Alzheimer’s Linked To Too Much of This In Your Diet - Sugar

More reason for your doctor to finally get a diet protocol written. Or are you going to have to do your doctors work and figure out what your diet protocol should be?
Article explaining it here:

Alzheimer’s Linked To Too Much of This In Your Diet - Sugar

Research that the article was written from:

Macrophage Migration Inhibitory Factor is subjected to glucose modification and oxidation in Alzheimer’s Disease

Your choice as to which one to read, or you could ask your doctor to summarize it.

Increase in noncalcified plaque associated with testosterone treatment in older men

Well your doctor has a lot of studying to do. 

Testosterone Improves Woman’s Brain Functions

FDA Concludes Testosterone Use May Increase Risk of Cardiovascular Events

 

FDA warns about blood clot risk with testosterone products


Testosterone increases neurotoxicity of glutamate in vitro and ischemia-reperfusion injury in an animal model

 

Thinking with your gonads: testosterone and cognition

 

Effect of testosterone on functional recovery in a castrate male rat stroke model

 

Lower Testosterone Levels Predict Incident Stroke and Transient Ischemic Attack in Older Men

 

Could androgens maintain specific domains of mental health in aging men by preserving hippocampal neurogenesis?


Single-Dose Testosterone Administration Impairs Cognitive Reflection in Men

The latest here:

Increase in noncalcified plaque associated with testosterone treatment in older men

Testosterone treatment in older men was linked to a significantly greater increase in coronary artery noncalcified plaque volume, according to a new study in JAMA.
“Although testosterone replacement is increasingly being used clinically, the [CV] benefits and risk of testosterone administration to older men with age-related decline in testosterone levels remain uncertain,” Matthew J. Budoff, MD, professor of medicine at David Geffen School of Medicine at UCLA and program director and director of cardiac CT at Harbor-UCLA Medical Center, and colleagues wrote. “Several observational studies show an inverse association between serum testosterone concentration and adverse [CV] outcomes, the metabolic syndrome, diabetes, and mortality, independent of traditional [CV] risk factors.”
In a double blind, placebo-controlled trial, Budoff and colleagues analyzed 170 men aged 65 years or older with an average of two serum testosterone levels lower than 275 ng/dL and symptoms suggestive of hypogonadism. Participants were enrolled between June 2010 and June 2014 and were randomly assigned testosterone gel (n = 82) or placebo gel (n = 88) for 12 months.
Matt Budoff
Matthew J. Budoff
Of those enrolled, data were available for 138 participants (73 receiving intervention, 65 receiving placebo; mean age, 71 years; 81% white). At baseline, 50.7% participants (n = 70) had a coronary artery calcification (CAC) score higher than 300 Agatston units.
The primary outcome was noncalcified plaque volume and was determined by coronary CTA.
From baseline to 12 months, participants in the testosterone arm had a significantly greater increase in noncalcified plaque volume (from median value 204 mm3 to 232 mm3) compared with placebo (from median value 317 mm3 to 325 mm3) with an estimated difference of 41 mm3 (95% CI, 14-67; P = .003).
The median total plaque volume increased in the testosterone group from 272 mm3 to 318 mm3, compared with 499 mm3 to 541 mm3 for placebo (estimated difference, 47 mm3; 95% CI, 13-80; P = .006). The median CAC score decreased in in the testosterone group (from 255 to 244 Agatston units) and increased in the placebo group (from 494 to 503 Agatston units) from baseline to 12 months (estimated difference, –27 Agatston units; 95% CI, –80 to 26 Agatston units), according to the researchers.
No one in either group had a major adverse CV event.
“The increase in coronary artery noncalcified and total plaque volumes in men treated with testosterone is concerning because any limitation of the vascular lumen could be considered deleterious,” Budoff and colleagues wrote. “The clinical significance of these increases could depend on the differential effects of testosterone on the individual components of noncalcified plaque.”
The researchers concluded that larger studies are needed to understand the clinical implications. – by Cassie Homer

E-cigarettes associated with CV risk factors

How is your doctor getting you the benefits of nicotine post-stroke? Assuming that your doctor knows anything about using nicotine for stroke recovery.

Nicotine Holds Promise for Stronger Stroke Recovery

 

Nicotine Patch Appears To Help Mild Cognitive Loss

 

Can nicotine protect the aging brain?


http://www.healio.com/cardiology/chd-prevention/news/online/%7B074547e8-f19d-4fc1-9f33-fd2cba02df23%7D/e-cigarettes-associated-with-cv-risk-factors
Habitual electronic cigarette use was associated with a shift in cardiac autonomic balance toward sympathetic predominance and increased oxidative stress, both indicators of CV risk, according to recently published findings.
“Although tobacco cigarettes are widely recognized as the most common preventable cause of [CVD] in the world, virtually nothing is known about the [CV] risks of e-cigarettes,” Holly R. Middlekauff, MD, of the David Geffen School of Medicine at the University of California, Los Angeles, and colleagues wrote. “Rather than wait decades for epidemiological data in habitual e-cigarette users to become available, we reasoned that investigations into several of the known mechanisms by which tobacco cigarettes increase [CV] risk would provide insights in the health risk of e-cigarettes.”
Habitual e-cigarette users (n = 23) and nonuser controls (n = 19) aged 21 to 45 years, with no current tobacco smoking and no known health problems or prescription medications, were studied. The participants (35% women; 35% white; mean age, 27.6 years) were measured for heart rate variability components and oxidative stress.
The high-frequency component (0.15-0.4 Hz), an indicator of vagal activity, was decreased in e-cigarette users compared with nonusers (mean, 46.5 normalized units [nu] vs. 57.8 nu, P = .04). The low-frequency component (0.04-0.15 Hz), a mixture of both vagal and sympathetic activity, was increased in the e-cigarette users vs. nonusers (mean, 52 nu vs. 39.9 nu; P = .03). The ratio of low frequency to high frequency, reflecting the cardiac sympathovagal balance, also was increased for e-cigarette users (mean, 1.37 vs. 0.85; P = .05).
E-cigarette users had increased oxidative stress as the LDL oxidizability was increased compared with nonusers (mean, 3,801 U vs. 2,413.3 U; P = .01). No significant associations were found between e-cigarette users and high-density antioxidant/anti-inflammatory capacity and paraoxonase-1 activity.
“Although data from e-cigarette users were not compared with those from smokers of combustible cigarettes, the results of Moheimani et al demonstrate that the use of e-cigarettes is not without consequence and might impose CV harm and increase CVD risk,” Aruni Bhatnagar, PhD, director of The Diabetes and Obesity Center at the University of Louisville School of Medicine, wrote in an accompanying editorial. “Nevertheless, changes in [heart rate variability] and [LDL] oxidizability are indirect indices of [CV] injury, and it remains unclear to what extent these changes represent an increase in CVD risk.”
In a press release, Joep Perk, MD, cardiovascular prevention spokesman for the European Society of Cardiology, said: “E-cigarettes are one of the tools we have in nicotine replacement therapy, but as clinicians we should be cautious of putting people on large amounts of central nervous system stimulant drugs. Other smoking cessation schemes, such as chewing gum or patches, always include the decision to taper off use and eventually stop. This is not, in general, the case with e-cigarettes, which tend to be seen as a replacement and not a weaning off nicotine addiction. ... This is an area where we need more knowledge. The more data we collect, the more it seems that nicotine replacement strategies that taper off and ultimately end nicotine use are the way to go.” – by Cassie Homer

Caffeine cannot prevent memory deficits linked to alcohol consumption, study finds

But did they consider that they might not be correctly accounting for the positive effects of alcohol? 

But all this other research. I'm using it for social connections for prevention of dementia thus I'm ignoring the cons because I think the benefits exceed the cons. But I'm not medically trained so don't listen to me. 

Alcohol for these 12 reasons.


 

How you react to coffee might hold major clues to your metabolism.

The latest here:

Caffeine cannot prevent memory deficits linked to alcohol consumption, study finds


Recent study challenges the view that the negative side effects of these drugs can be cancelled out when they are taken together.
French novelist Honore de Balzac described coffee’s effect as: “Ideas begin to move like the battalions of the Grand Army on the battlefield, and the battle takes place. Things remembered arrive at full gallop, ensign to the wind.” Indeed, caffeine is a brain stimulant used by many to overcome fatigue and increase productivity. Highly caffeinated drinks are now commonly consumed together with alcohol, and this work explores a very current concern: does this counteract the negative effect of alcohol on memory?
A study recently published in Frontiers in Behavioral Neuroscience indicates that despite its impact on alertness and concentration, caffeine cannot counteract the memory deficits that result from alcohol consumption.
“Our results in mice show that even at low doses that do not change social behavior, alcohol causes amnesic effects. This, in turn, was found to not be counteracted by caffeine consumption,” says Dr Laura López-Cruz, first author of the study undertaken at Universitat Jaume I (Spain) and currently researcher in the Psychology Department of the University of Cambridge.
“Caffeine and alcohol are known to have common mechanisms in the brain. However, this finding forces us to question what we do not know about their biochemistry,” summarizes Lopez-Cruz.
The results draw into question what we know about a key brain chemical system: the adenosine system. This system regulates sleep, social interaction and social memory. Consuming alcohol increases the amount of adenosine present in the brain, inducing sleepiness and impairing long-term social memory. In contrast, caffeine blocks the activity of adenosine, increasing alertness and anxiety levels.
Due to opposing physiological and behavioral effects of alcohol and caffeine, it was expected that caffeine would counteract a key negative side effect of ethanol ingestion: namely issues with social memory.
People frequently face difficulty with remembering conversations and other behaviors that have taken place during alcohol consumption, an affect not reserved to heavy drinkers. Understanding these amnesic episodes, which pose a risk to personal safety, and if they can be prevented is therefore of great importance.
The researchers investigated memory in mice through a social recognition task, based on the tendency of healthy rodents to prefer exploring and interacting with other animals from the same species upon a novel encounter.
Each test animal was initially given either caffeine, alcohol or a combination, then placed in a chamber with another mouse, stranger to the test animal on one side, and an object on the other side, for the test animal to explore during 10 minutes. A day later, when any effects of the drugs should have worn off, the mice were placed back in the chamber, but another novel mouse now replaced the object. Hence the experimental mice were given the choice of interacting with a familiar mouse from the previous day, or a novel mouse.
“We used the amount of time sniffing each mouse as an index of social recognition,” Lopez-Cruz explains. “If the mouse remembers the previous day’s encounter, they should spend more time sniffing the novel mouse.”
When treated with caffeine, mice spent more time exploring a novel conspecific. In contrast, when a mouse had been treated with alcohol, they spent equal amounts of time with novel and familiar mice, suggesting that the drug had impaired their memory. Most notable was the finding that mice who had been injected with a combination of alcohol and caffeine also did not differentiate between the novel and familiar mouse, demonstrating impaired social memory.
Previous research had found that low doses of caffeine did improve ethanol induced memory impairment. This led Lopez-Cruz and colleagues to suggest that high doses of caffeine may have more widespread effects that are not yet fully understood.
As the popularity of highly caffeinated drinks continues to rise, with 68% of adolescents consuming them according to the European Food Safety Authority (2011), these results provide an insight into how they cannot be relied on to balance out the negative effects of alcohol.

Chronic Stroke Survivors Improve Reaching Accuracy by Reducing Movement Variability at the Trained Movement Speed

No mention of objective measurement of spasticity preventing completion of the reaching task. All I can conclude from that is that these survivors were cherry picked and fairly high functioning already.
http://journals.sagepub.com/doi/abs/10.1177/1545968317693112
First Published February 1, 2017 research-article


Background. Recovery from stroke is often said to have “plateaued” after 6 to 12 months. Yet training can still improve performance even in the chronic phase. Here we investigate the biomechanics of accuracy improvements during a reaching task and test whether they are affected by the speed at which movements are practiced.  
Method. We trained 36 chronic stroke survivors (57.5 years, SD ± 11.5; 10 females) over 4 consecutive days to improve endpoint accuracy in an arm-reaching task (420 repetitions/day). Half of the group trained using fast movements and the other half slow movements. The trunk was constrained allowing only shoulder and elbow movement for task performance.  
Results. Before training, movements were variable, tended to undershoot the target, and terminated in contralateral workspace (flexion bias). Both groups improved movement accuracy by reducing trial-to-trial variability; however, change in endpoint bias (systematic error) was not significant. Improvements were greatest at the trained movement speed and generalized to other speeds in the fast training group. Small but significant improvements were observed in clinical measures in the fast training group.
 Conclusions. The reduction in trial-to-trial variability without an alteration to endpoint bias suggests that improvements are achieved by better control over motor commands within the existing repertoire. Thus, 4 days’ training allows stroke survivors to improve movements that they can already make. Whether new movement patterns can be acquired in the chronic phase will need to be tested in longer term studies. We recommend that training needs to be performed at slow and fast movement speeds to enhance generalization.

Stroke Lesions in a Large Upper Limb Rehabilitation Trial Cohort Rarely Match Lesions in Common Preclinical Models

Only 86 references of which I'm sure your doctor has not read a single one.  No clue what use this will be in your stroke rehab protocols.

http://journals.sagepub.com/doi/abs/10.1177/1545968316688799
First Published January 1, 2017 research-article
Background. Stroke patients with mild-moderate upper extremity motor impairments and minimal sensory and cognitive deficits provide a useful model to study recovery and improve rehabilitation. Laboratory-based investigators use lesioning techniques for similar goals.  
Objective. To determine whether stroke lesions in an upper extremity rehabilitation trial cohort match lesions from the preclinical stroke recovery models used to drive translational research. Methods. Clinical neuroimages from 297 participants enrolled in the Interdisciplinary Comprehensive Arm Rehabilitation Evaluation (ICARE) study were reviewed. Images were characterized based on lesion type (ischemic or hemorrhagic), volume, vascular territory, depth (cortical gray matter, cortical white matter, subcortical), old strokes, and leukoaraiosis. Lesions were compared with those of preclinical stroke models commonly used to study upper limb recovery. Results. Among the ischemic stroke participants, median infarct volume was 1.8 mL, with most lesions confined to subcortical structures (61%) including the anterior choroidal artery territory (30%) and the pons (23%). Of ICARE participants, <1% had lesions resembling proximal middle cerebral artery or surface vessel occlusion models. Preclinical models of subcortical white matter injury best resembled the ICARE population (33%). Intracranial hemorrhage participants had small (median 12.5 mL) lesions that best matched the capsular hematoma preclinical model.  
Conclusions. ICARE subjects are not representative of all stroke patients, but they represent a clinically and scientifically important subgroup. Compared with lesions in general stroke populations and widely studied animal models of recovery, ICARE participants had smaller, more subcortically based strokes. Improved preclinical-clinical translational efforts may require better alignment of lesions between preclinical and human stroke recovery models.

Fatigue after stroke: a major but neglected issue.

16 years and still a neglected issue. No one in stroke has any leadership capability. Leaders tackle the difficult problems, they don't ignore them.
https://www.ncbi.nlm.nih.gov/pubmed?Db=pubmed&Cmd=ShowDetailView&TermToSearch=11490100
2001 Aug;12(2):75-81.

Abstract

Subjective fatigue, defined as a feeling of early exhaustion developing during mental activity, with weariness, lack of energy and aversion to effort, remains virtually unstudied in patients with stroke, bur recent surveys suggest that it is a major, commonly overlooked, stroke sequela. While the few existing series did not show significant correlations between fatigue and stroke severity, lesion location, cognitive and neurological impairment and depression, recent neurobehavioral studies have highlighted an association between fatigue and brainstem and thalamic lesions. This suggests that fatigue may be linked to the interruption of neural networks involved in tonic attention, such as the reticular activating system. In fact, several subtypes of fatigue may develop after stroke, in connection with cognitive sequelae, neurological impairment, psychological factors and sleep disorders. A challenge is to identify and delineate these different subtypes and to distinguish them from mood disorders, which frequently coexist. We emphasize the concept of 'primary' poststroke fatigue, which may develop in the absence of depression or a significant cognitive sequela, and which may be linked to attentional deficits resulting from specific damage to the reticular formation and related structures involved in the subcortical attentional network. In the patients with excellent neurological and neuropsychological recovery, poststroke fatigue may be the only persisting sequela, which may severely limit their return to previous activities. The recognition of poststroke fatigue may be critical during recovery and rehabilitation after stroke.
PMID:
11490100
DOI:
47685

The Assessment of Motor Fatigability in Persons With Multiple Sclerosis

Obviously we have no similar research for stroke. Because we have NO stroke leadership and NO stroke strategy.
In one study, two years after their stroke 10 per cent of stroke survivors said they were always tired and 30 per cent said they were sometimes tired. In another study, at least 12 months after their stroke, 50 per cent of stroke survivors said tiredness was their main problem. 

The Assessment of Motor Fatigability in Persons With Multiple Sclerosis

A Systematic Review

First Published January 1, 2017 review-article




Background. Persons with multiple sclerosis (PwMS) are often characterized by increased motor fatigability, which is a performance change on an objectively measured criterion after any type of voluntary muscle contractions. This review summarizes the existing literature to determine which protocols and outcome measures are best to detect or study motor fatigability and the underlying mechanisms in MS.  
Methods. Two electronic databases, PubMed and Web of Science, were searched for relevant articles published until August 2016 with a combination of multiple sclerosis, fatigability, muscle fatigue, and motor fatigue.  
Results. A total of 48 articles were retained for data extraction. A variety of fatigability protocols were reported; protocols showed differences in type (isometric vs concentric), duration (15 to 180 s), and number of contractions (fixed or until exhaustion). Also, 12 articles reported motor fatigability during functional movements, predominantly assessed by changes in walking speed; 11 studies evaluated the mechanisms underlying motor fatigability, using additional electrical nerve or transcranial magnetic stimulation. Three articles reported psychometrics of the outcomes. Conclusions. The disparity of protocols and outcome measures to study different aspects of motor fatigability in PwMS impedes direct comparison between data. Most protocols use maximal single-joint isometric contractions, with the advantage of high standardization. Because there is no head-to-head comparison of the different protocols and only limited information on psychometric properties of outcomes, there is currently no gold standard to assess motor fatigability. The disability level, disease phenotype, and studied limb may influence the assessment of motor fatigability in PwMS.

Nutrition and healthy eating from Mayo Clinic

A year old, has your doctor done one damn thing about this? Even this is pretty much useless, guidelines, not protocols.
http://www.mayoclinic.org/healthy-lifestyle/nutrition-and-healthy-eating/expert-blog/brain-healthy-foods/bgp-20191732/?

Nutrition-wise blog

Feed your mind

By Katherine Zeratsky, R.D., L.D. March 3, 2016
Did you know that what you eat can affect your brain's function? The Mediterranean diet and the DASH diet, both known to reduce heart disease, have also been shown to slow cognitive decline.
To look more closely at this association, scientists designed a study called the Mediterranean-DASH diet intervention for neurodegenerative delay (MIND).
As the name suggests, the MIND diet is styled after the Mediterranean and DASH diets but with modifications based on previous research on diet and dementia.
For example, the MIND diet recommends higher levels of vegetables, especially leafy greens, because they appear to have a positive association with slowing cognitive decline. On the other hand, fruits, except for berries, are not associated with slowing cognitive decline.
The MIND diet includes 10 brain-healthy foods:
  • Green leafy vegetables
  • Vegetables
  • Nuts
  • Berries
  • Beans
  • Whole grains
  • Seafood
  • Poultry
  • Olive oil
  • Wine
The MIND diet categorizes five foods as unhealthy:
  • Red meat
  • Butter and stick margarine
  • Cheese
  • Pastries and sweets
  • Fried and fast foods
In this observational study, the MIND diet was strongly associated with slower cognitive decline and had greater estimated effects than either the Mediterranean diet or the DASH diet. Of course, future studies are needed to evaluate whether this diet can prevent dementia.
This news provides yet one more reason to eat your vegetables, especially the green and leafy ones. But what about fruit?
Fruit is a low-calorie, nutrient- and fiber-rich food that has long been a part of a healthy eating pattern. There are still good reasons to include it in your diet. For your brain's sake, consider adding more fresh or frozen berries.
Additionally, let's not rule out all things on the "unhealthy" list. Both the Mediterranean and DASH diets included limited quantities of meat and cheese.
What do you think of this research? What brain-healthy foods will make it on your plate?