Incidence and prevalence of dementia associated with transient ischaemic attack and stroke: analysis of the population-based Oxford Vascular Study

So if you have a severe stroke, NIHSS score >10, then your doctor needs to have a dementia prevention protocol with an incredibly high efficacy rating. NOT guidelines, A PROTOCOL! I have no clue what my NIHSS score was, but taking it myself was probably a 9 or 10. So you have described a problem. What the hell is the solution to that problem? Survivors expect solutions. Are you a doctor or just an automaton that parrots useless answers?

Incidence and prevalence of dementia associated with transient ischaemic attack and stroke: analysis of the population-based Oxford Vascular Study

Summary

Background

Risk of dementia after stroke is a major concern for patients and carers. Reliable data for risk of dementia, particularly after transient ischaemic attack or minor stroke, are scarce. We studied the risks of, and risk factors for, dementia before and after transient ischaemic attack and stroke.

Methods

The Oxford Vascular Study is a prospective incidence study of all vascular events in a population of 92 728 people residing in Oxfordshire, UK. Patients with transient ischaemic attack or stroke occurring between April 1, 2002, and March 31, 2012, were ascertained with multiple methods, including assessment in a dedicated daily emergency clinic and daily review of all hospital admissions. Pre-event and post-event (incident) dementia were diagnosed at initial assessment and during 5-years' follow-up on the basis of cognitive testing supplemented by data obtained from hand searches of all hospital and primary care records. We assessed the association between post-event dementia and stroke severity (as measured with the US National Institutes of Health Stroke Scale [NIHSS] score), location (ie, dysphasia), previous events, markers of susceptibility or reserve (age, low education, pre-morbid dependency, leucoaraiosis), baseline cognition, and vascular risk factors with Cox regression models adjusted for age, sex, and education. We compared incidence and prevalence of dementia in our population with published UK population age-matched and sex-matched rates.

Findings

Among 2305 patients (mean age 74·4 years [SD 13·0]), 688 (30%) had transient ischaemic attacks and 1617 (70%) had strokes. Pre-event dementia was diagnosed in 225 patients; prevalence was highest in severe stroke (ie, NIHSS >10) and lowest in transient ischaemic attack. Of 2080 patients without pre-event dementia, 1982 (95%) were followed up to the end of study or death. Post-event dementia occurred in 432 of 2080 patients during 5 years of follow-up. The incidence of post-event dementia at 1 year was 34·4% (95% CI 29·7–41·5) in patients with severe stroke (NIHSS score >10), 8·2% (6·2–10·2) in those with minor stroke (NIHSS score <3), and 5·2% (3·4–7·0) in those with transient ischaemic attack. Compared with the UK age-matched and sex-matched population, the 1-year standardised morbidity ratio for the incidence of dementia was 47·3 (95% CI 35·9–61·2), 5·8 (4·4–7·5), and 3·5 (2·5–4·8), respectively. Consequently, prevalence of dementia in 1-year survivors was brought forward by approximately 25 years in those who had severe strokes, 4 years in those who had minor strokes, and 2 years in those who had transient ischaemic attacks. 5-year risk of dementia was associated with age, event severity, previous stroke, dysphasia, baseline cognition, low education, pre-morbid dependency, leucoaraiosis, and diabetes (p<0·0001 for all comparisons, except for previous stroke [p=0·006]).

Interpretation

The incidence of dementia in patients who have had a transient ischaemic attack or stroke varies substantially depending on clinical characteristics including lesion burden and susceptibility factors. Incidence of dementia is nearly 50 times higher in the year after a major stroke compared with that in the general population, but excess risk is substantially lower after transient ischaemic attack and minor stroke.

Funding

Wellcome Trust, Wolfson Foundation, British Heart Foundation, National Institute for Health Research, and the National Institute for Health Research Oxford Biomedical Research Centre.

• View related content for this article

Introduction

Reliable estimates of the incidence of dementia after transient ischaemic attack and stroke are required to counsel patients and families and to inform prevention trials. However, most available data are from cross-sectional studies and hospital-based cohorts of major stroke, which are subject to selection biases and were done before the advent of robust secondary prevention.

¹

^, 

²

Stroke has been estimated to bring forward the onset of dementia by about 10 years,

³

but there are few data on the effect of event severity, particularly the risk after transient ischaemic attacks or minor stroke, which make up around 70% of all acute cerebrovascular events and often result in anxiety in patients and families about future risks.

⁴

Anxiety could be compounded by the reportedly high rates of cognitive impairment after transient ischaemic attack,

⁵

^, 

⁶

and by public education suggesting high incidence of dementia.

⁷

The frequency of progression of cognitive impairment to dementia after transient ischaemic attack and minor stroke is unclear, as is the extent to which the prevalence and incidence of dementia are higher among those who have had transient ischaemic attacks or minor strokes than those expected among the age-matched general population.

Loss of muscle and weight associated with disability after stroke

Don't just describe a problem, survivors need solutions. GET THERE!

Loss of muscle and weight associated with disability after stroke

25 Jan 2019

Topic(s):

Cardiovascular Rehabilitation

Stroke

Berlin, Germany – 25 January 2019: Loss of muscle and body weight is associated with disability after stroke, reports a study presented today  at Heart & Stroke 2019, a meeting of the European Society of Cardiology (ESC) Council on Stroke, and published in the Journal of Cachexia, Sarcopenia and Muscle.¹

Study author Dr Nadja Scherbakov, of the Centre for Stroke Research Berlin and Charité University Hospital, Berlin, Germany, said: “Body wasting in the course of a disease – called cachexia – is observed in cancer and chronic diseases like heart failure, chronic obstructive pulmonary disease and kidney disease. To the best of our knowledge, our study is the first to prospectively investigate the development of cachexia in patients after acute stroke.”
“Stroke is the main cause of adult disability and it is common understanding that this is all due to brain injury and impaired innervation,” she continued. “Our findings show that the amount of skeletal muscle throughout the body declines after stroke. This opens the door for treatment options such as dietary supplementation and exercise training to prevent muscle wasting after stroke.”

The study examined changes in body weight and composition during the year after an ischaemic stroke and their association with disability. The researchers found that 21% of patients had developed cachexia one year later, meaning they had lost at least 5% of their body weight. This included the loss of 19% of their body fat and 6.5% of their muscle mass. Notably, this body wasting occurred equally in patients with and without limb paresis.
Patients with cachexia had significantly lower functional capacity and significantly lower handgrip strength than those without cachexia.
Dr Scherbakov said: “The disability caused by stroke is usually attributed to brain damage, with little attention paid to the effector organ, which is the skeletal muscle. Exercise training is the most promising way to delay or prevent progression of muscle wasting and may be a therapy option. Treatment of cachexia includes dietary supplementation with protein, vitamins and minerals, and might also prevent muscle wasting after stroke.”
She added: “Older patients with moderately severe stroke were particularly prone to developing cachexia after stroke, so it is very important to monitor their body weight, appetite and nutritional status.”
Patients with cachexia had significantly higher levels of inflammation in the body, as measured by C-reactive protein (CRP) in the blood, than those without cachexia. Patients with systemic inflammation had a fivefold greater risk of muscle wasting, 11% higher risk of weight loss, 30% greater chance of reduced appetite, and 6% higher likelihood of low handgrip strength.
Dr Scherbakov said: “This suggests that systemic inflammation may contribute to tissue wasting and the development of cachexia.”
The study was conducted in the Stroke Unit, Department of Neurology, Charité Campus Virchow Clinic, Berlin, in 150 patients with mild to moderate ischaemic stroke recruited within 48 hours after stroke. Baseline measurements included body weight; body composition by dual-x-ray absorptiometry; functional status by the National Institutes of Health Stroke Scale (NIHSS), modified Rankin scale, and Barthel index; and muscle strength by handgrip and quadriceps tests. The measurements were repeated one year later.

 

A modified standardized nine hole peg test for valid and reliable kinematic assessment of dexterity post-stroke

I never had this test. Probably because after spasticity set in, it was impossible to pick up the pegs and even more impossible to release them. So what the fuck is your solution to those that are that badly impaired? I expect a solution, not knowing one is medical malpractice. 

A modified standardized nine hole peg test for valid and reliable kinematic assessment of dexterity post-stroke

• Gudrun M JohanssonEmail author and
• Charlotte K Häger

Journal of NeuroEngineering and Rehabilitation201916:8

https://doi.org/10.1186/s12984-019-0479-y

©  The Author(s). 2019

• Received: 31 May 2018
• Accepted: 2 January 2019
• Published: 14 January 2019

Abstract

Background

Impairments in dexterity after stroke are commonly assessed by the Nine Hole Peg Test (NHPT), where the only outcome variable is the time taken to complete the test. We aimed to kinematically quantify and to compare the motor performance of the NHPT in persons post-stroke and controls (discriminant validity), to compare kinematics to clinical assessments of upper extremity function (convergent validity), and to establish the within-session reliability.

Methods

The NHPT was modified and standardized (S-NHPT) by 1) replacing the original peg container with an additional identical nine hole pegboard, 2) adding a specific order of which peg to pick, and 3) specifying to insert the peg taken from the original pegboard into the corresponding hole of the target pegboard. Eight optical cameras registered upper body kinematics of 30 persons post-stroke and 41 controls during the S-NHPT. Four sequential phases of the task were identified and analyzed for kinematic group differences. Clinical assessments were performed.

Results

The stroke group performed the S-NHPT slower (total movement time; mean diff 9.8 s, SE diff 1.4), less smoothly (number of movement units; mean diff 0.4, SE diff 0.1) and less efficiently (path ratio; mean diff 0.05, SE diff 0.02), and used increased scapular/trunk movements (acromion displacement; mean diff 15.7 mm, SE diff 3.5) than controls (P < 0.000, r ≥ 0.32), indicating discriminant validity. The stroke group also spent a significantly longer time grasping and releasing pegs relative to the transfer phases of the task compared to controls. Within the stroke group, kinematics correlated with time to complete the S-NHPT and the Fugl-Meyer Assessment (r_s 0.38–0.70), suggesting convergent validity. Within-session reliability for the S-NHPT was generally high to very high for both groups (ICCs 0.71–0.94).

Conclusions

The S-NHPT shows adequate discriminant validity, convergent validity and within-session reliability. Standardization of the test facilitates kinematic analysis of movement performance, which in turn enables identification of differences in movement control between persons post-stroke and controls that may otherwise not be captured through the traditional time-based NHPT. Future research should ascertain further psychometric properties, e.g. sensitivity, of the S-NHPT.

Slower Reorientation of Trunk for Reactive Turning while Walking in Hemiparesis Stroke Patients

Don't just describe a problem. Provide a solution to that problem. You now have left research hanging that will never be followed up on.  We need to have a serious discussion on the point of stroke research with these mentors and senior researchers. SOLUTIONS and PROTOCOLS needed!

Slower Reorientation of Trunk for Reactive Turning while Walking in Hemiparesis Stroke Patients

Takahito Nakamura, Takahiro Higuchi, Toyo Kikumoto, Takanori Takeda, Hideyuki Tashiro & Fumihiko Hoshi

Received 10 Jul 2018, Accepted 02 Nov 2018, Published online: 02 Jan 2019

• Download citation
• https://doi.org/10.1080/00222895.2018.1547894

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Abstract

We examined the behavioral characteristics of reactive turning in hemiplegic stroke patients when they were informed of the turning direction just before turning was required at an unpredictable time. Eleven stroke patients and 20 healthy elderly control people were asked to initiate a turn as soon as a visual cue to inform them of the turning direction was activated unpredictably using a foot switch. Both the segmental reorientation and stepping type when turning 90° while walking were measured. The results indicated preserved segmental reorientation of the head and pelvis in stroke patients. Stroke patients showed delays in pelvic turning but not in head turning. Their delayed pelvic movement might be due to motor dysfunction and the time taken to ensure stability when deciding when to turn.

Keywords: Stroke, turning, reactive, segmental reorientation, step

Additional information

Funding

This study was supported by Grants-in-Aid for Scientific Research (KAKENHI) under Grant 26350622.

Researchers map how Alzheimer’s pathology spreads across brain networks

You are likely going to need a solution to this. So what the fuck followup is being done by your doctor and stroke hospital? Or are they twiddling their thumbs again waiting for SOMEONE ELSE TO SOLVE THE PROBLEM? ?

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.

 

Researchers map how Alzheimer’s pathology spreads across brain networks 

Alzheimer's DiseaseNeuroscience

Capitalizing on recent advances in neuroimaging and genetic biomarker research, scientists have been able to identify specific pathways by which tau and beta-amyloid, two proteins that are hallmarks of Alzheimer’s disease, accumulate in the brain over time. The NIA-supported researchers also found that the patterns of tau and beta-amyloid accumulation were related to specific genetic profiles, providing better understanding of Alzheimer’s disease risk and possible new avenues for diagnosis and monitoring of the disease.
Improved technology makes possible for intensive, side-by-side comparisons of how tau and beta-amyloid spread in the brain in distinctive patterns. Using this technology, researchers were able to reveal nuances into how, even in disease, the brain follows a dynamic and complex network of circuits and connections. The results were reported in the Oct. 29 issue of Nature Medicine.
The study was led by Dr. Jorge Sepulcre and Dr. Keith Johnson of The Gordon Center for Medical Imaging at Massachusetts General Hospital and Harvard Medical School, and Dr. Reisa Sperling, director of the Center for Alzheimer Research and Treatment at the Brigham and Women's Hospital and professor of Neurology at Harvard Medical School. The team used data from the Harvard Aging Brain Study and the Allen Human Brain Atlas.

Patterns of pathology progression in the human brain using network-based PET imaging. (Image courtesy of Dr. Jorge Sepulcre.)

In a brain with Alzheimer’s disease, abnormal deposits of tau and beta-amyloid do not randomly appear, but instead show unique spatial patterns that follow the brain’s existing connected neural networks. To better understand how tau and beta-amyloid interact with and influence each other, the researchers looked closely at 3-D brain network and gene maps and found that both tau and beta-amyloid were associated with genes devoted to lipid metabolism, and that the APOE E4 gene – a risk factor for Alzheimer’s disease – played a central role in the relationships of these genetic networks.
The scientists found common genetic background for the malfunction of both proteins. The findings showed that in addition to APOE, other variations in genetic pathways shared by tau and beta-amyloid could trigger their accumulation. The study also found that tau propagation was associated with an axon-related (parts of neurons that pass messages away from the cell body) genetic profile, while beta-amyloid’s spread was connected with a dendrite-related (parts of neurons that receive messages from other cells) genetic profile.
The researchers hope this new understanding of tau and beta-amyloid’s propagation patterns can be combined with a person’s genetic profile to help develop precision medicine approaches for improved diagnosis, monitoring and therapies for Alzheimer’s disease in the brain.
This research was funded in part by NIH grants K23EB019023, T32EB013180, R01HL137230, R01-AG027435-S1, P50-AG00513421, R01AG046396, P01-AG036694 and 1RF1AG052653-01A1.
Reference: Sepulcre J et al. Neurogenetic contributions to amyloid beta and tau spreading in the human cortex. Nature Medicine. 2018 Oct 29 doi: 10.1038/s41591-018-0206-4. [Epub ahead of print]

Post Stroke Fatigue; Point Prevalence, Characterization, Associations and Radiological Correlation in a Rehabilitation Hospital

Yes, we know post stroke fatigue exists in 40-70% of stroke cases. What the fuck is your solution? Stop researching doing observational models and come up with solutions. Are you that blitheringly stupid that you don't understand the needs of stroke survivors?
http://www.lenus.ie/hse/bitstream/10147/622705/1/art5.html
A Khan, M Delargy
National Rehabilitation Hospital, Rochestown Avenue, Dún Laoghaire, Co. Dublin

Abstract

Post stroke fatigue (PSF) is a frequently reported symptom by stroke survivors undergoing rehabilitation. This cross sectional observational study was undertaken in a rehabilitation facility to look at its prevalence and relationship with various variables like personal factors, type of stroke, social context, hemispheric involvement on CT scan and mobility status. The results showed that PSF was present in 83% (25 out of 30) of the patients included in the study. No clear association could be established between PSF, social, radiological and functional characteristics.

Introduction
Post stroke fatigue is a common yet under diagnosed phenomenon among stroke patients. Relatively little is known about how it is experienced and how mobility deficits, social supports and radiological associations relate to it. On the other hand, fatigue is a well-researched symptom in multiple sclerosis with number of scales used for evaluation and various treatment modalities in place including medications and nonpharmacological strategies. This study aimed to determine the point prevalence of post stroke fatigue in a rehabilitation hospital, its relationship to sociodemographic, clinical and radiological factors.

Methods
Cross sectional observational study. All the stroke inpatients with age >18 years in the National Rehabilitation Hospital Jan- Feb 2015 admitted for rehabilitation who had a stroke in the last 6 months of admission were interviewed using a structured questionnaire and review of medical record. Patients with profound aphasia, cognitive impairments, who refused to participate, with background liver and renal dysfunction were excluded from the study. Post stroke fatigue was assessed by using the Fatigue severity scale and the Fatigue severity visual analogue scale. The level of functioning was assessed by the disability rating scale.

Results
A total of 30 (21 males, 9 females) patients fulfilled the inclusion criteria, out of which n=25 reported fatigue at the time of interview with a mean age of 47.4. Five patients with mean age of 55 denied the symptom. Sample included 21 patients with ischemic stroke and 9 with haemorrhagic stroke. Out of the 25 who reported fatigue, n=17 had sustained an ischemic stroke. Mean time since injury was four months in the fatigued and three months in the non-fatigued group. N=12 were employed, n=8 lived alone, n=10 were moderately dependent out of the 25 individuals who reported fatigue. There were 17 smokers and 7 alcohol dependant individuals in the fatigue group. Past medical history of depression was present in four (16 %) and hypothyroidism in two (8 %) patients who reported fatigue. No significant past medical history was seen in the non-fatigue group. There was right sided involvement on the CT scan in n=9 (36 %), and n=2 (40 %) in fatigued and non-fatigued group respectively. Sixteen (64 %) patients had left sided involvement in the fatigued group versus three (60%) in the nonfatigued patients. Out of 25, 16 patients in the fatigue group were mobile with or without aid and all 5 out of 5 were mobile in the nonfatigued group.

Overall, fatigue was more prevalent in the male smoker population who had sustained an ischemic stroke in the last four months more so with left sided radiological involvement. Demographics, socioeconomic and clinical characteristics of both these groups included in the analysis are enlisted in table 1. The differences between fatigued and not fatigued patients were assessed by chi-square test. Data was analysed using SPSS v. 17.

This survey shows that post stroke fatigue is a prevalent symptom n= 25 (83.3 %) in patients undergoing rehabilitation post stroke in the NRH. The limitation of the study is its small sample size. No clear correlation could be concluded between fatigue, psychosocial, clinical or radiological variables. No association was established between fatigue, level of functioning and mobility. However, the survey does suggest necessity of formal assessment of fatigue in stroke rehabilitation. It would be interesting to look at the effect of fatigue on multidisciplinary therapies.

Discussion
Persistent fatigue is a common and debilitating consequence of stroke. Prevalence rates of post stroke fatigue (PSF) are substantial, varying between 38 and 73%¹. It has been hypothesized that fatigue after stroke results from a combination of organic brain lesion and psychosocial stress related to adjustment to a new life situation. It interferes with the rehabilitation process and impairs the patient’s ability to regain functions lost because of the stroke². Besides being frequent, PSF was judged by between 23% and 59.5% of stroke patients to be one of their worst symptoms. Nevertheless, the level of awareness of this condition among relatives, work colleagues and medical staff remains low³. Risk factors for post stroke fatigue include older age and female sex, activities of daily living impairment, living alone or in an institution, anxiety, pre stroke depression, leukoaraiosis, myocardial infarction, diabetes mellitus, pain and sleeping disturbances^4,5.

There is no uniform definition of PSF and it is generally defined as “a subjective experience of extreme and persistent tiredness, weakness, or exhaustion after stroke, which can present itself mentally, physically or both and which is unrelated to previous exertion levels”. Since this definition is intrinsically subjective and no derivative assessment tools have been specifically constructed for patients with stroke, a large variety of fatigue rating scales have been used in research and clinical practice. Some of these tools assess the dimension of fatigue severity, such as Visual Analogue Scales others, such as the Fatigue Severity Scale, measure the impact of fatigue in daily life¹. A better understanding of PSF will enable healthcare professionals to recognize this ‘invisible handicap’ more frequently and explain it clearly to the patients³.  Further research is required to operationalize and validate fatigue assessment tools and to identify specific interventions that may alleviate fatigue post brain injury⁶.

Conflict of Interest
None declared.

Correspondence:
Dr. Aaisha Khan, Specialist Registrar in Rehabilitation Medicine, National Rehabilitation Hospital, Dun Laoghaire, Dublin
Email: aaishakhan678@gmail.com

Stroke rates higher in asymptomatic vs. symptomatic AF

Pretty much useless since nothing is presented on how to find  asymptomatic AF. Don't just describe a problem. Suggest a solution, otherwise this research is almost completely useless.
https://www.healio.com/cardiology/arrhythmia-disorders/news/online/%7B4f08a315-afbe-4605-9b90-8fbef54d60f0%7D/stroke-rates-higher-in-asymptomatic-vs-symptomatic-af?utm_source=selligent&utm_medium=email&utm_campaign=cardiology%20news&m_bt=592835816269
Previous stroke rates were higher among patients with newly diagnosed atrial fibrillation compared with those who experienced prior symptoms, according to results from the GLORIA-AF registry, presented at EHRA Europace-Cardiostim 2017.
According to the presentation from Steffen P. Christow, MD, cardiologist at Hospital Ingolstadt GmbH in Germany, AF has a significant effect on morbidity and mortality in patients because of a fivefold risk for stroke.

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“Patients with nonvalvular [AF] have a fivefold increased risk of stroke compared to those without [AF]. Strokes in patients with nonvalvular [AF] tend to be particularly severe and disabling, with about half of patients dying within 1 year,” Christow said in a press release from the European Society of Cardiology. “When patients are unaware of their [AF], they remain untreated and unprotected from stroke.”
The multinational, prospective GLORIA-AF registry enrolled 6,011 patients aged 18 years or older who were newly diagnosed with nonvalvular AF and had a high risk for stroke.
According to Christow and colleagues, the aims of the study were to investigate patient characteristics that influenced choice of antithrombotic treatment of newly diagnosed patients with nonvalvular AF at risk for stroke, describe antithrombotic treatment patterns and collect safety and efficacy data on antithrombotic treatments.
At the time of diagnosis, approximately two-thirds of the patients included in the study were asymptomatic and one-third of patients were symptomatic.
The results of the study showed that asymptomatic patients were twice as likely to have permanent AF (OR = 0.49; 95% CI, 0.4-0.59), more than twice as likely to have had a previous stroke (OR = 0.37; 95% CI, 0.3-0.46) and twice as likely to have had a previous stroke or transient ischemic attack (OR = 0.47; 95% CI, 0.4-0.56) vs. patients who were symptomatic.
Symptomatic patients were more likely to have had CAD (OR = 1.28; 95% CI, 1.1-1.48) or congestive HF (OR = 2.79; 95% CI, 2.45-3.18) than asymptomatic patients, Christow and colleagues found.
“The finding of a higher rate of previous stroke in the asymptomatic patients despite no differences in the number of stroke risk factors may be explained by a longer but undiagnosed history of [AF],” Christow said in the release. “These results underline the urgent need for public programs to detect [AF] in the general population.” – by Dave Quaile
Reference:
Christow SP, et al. Abstract 1669. Presented at: EHRA Europace – Cardiostim 2017; June 18-21, 2017; Vienna.

Admission Brain Cortical Volume An Independent Determinant of Poststroke Cognitive Vulnerability

So you have identified a problem. What the fuck is your suggested solution?
http://stroke.ahajournals.org/content/48/8/2113?etoc=

Sharmila Sagnier, Gwenaëlle Catheline, Bixente Dilharreguy, Fanny Munsch, Antoine Bigourdan, Mathilde Poli, Sabrina Debruxelles, Stéphane Olindo, Pauline Renou, François Rouanet, Vincent Dousset, Thomas Tourdias, Igor Sibon

https://doi.org/10.1161/STROKEAHA.117.017646

Stroke. 2017;48:2113-2120

Originally published June 16, 2017

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Abstract

Background and Purpose—Several markers of poststroke cognitive impairment have been reported. The role of brain cortical volume remains uncertain. The aim of this study was to evaluate the influence of brain cortical volume on cognitive outcomes using a voxel-based morphometry approach in subjects without prestroke dementia.

Methods—Ischemic stroke patients were prospectively recruited 24 to 72 hours post stroke (M0). Cognition was evaluated at M0, 3 months, and 1 year (M12) using the Montreal Cognitive Assessment, the Isaacs set test, and the Zazzo’s cancellation task. A 3-T brain magnetic resonance imaging was performed at M0. Grey matter (GM) was segmented using Statistical Parametric Mapping 12 software. Association between global GM volume and cognitive score slopes between M0 and M12 was evaluated using a linear mixed model. Correlations between focal GM volumes and changes in cognitive performance were evaluated using Statistical Parametric Mapping 12.

Results—Two-hundred forty-eight patients were included (mean age 65±SD 14 years old, 66% men). Global GM volume was significantly associated with changes in Montreal Cognitive Assessment scores (β=0.01; P=0.04) and in the number of errors on the Zazzo’s cancellation task (β=−0.02; P=0.04) independently of other clinical/radiological confounders. Subjects with lower GM volumes in the left fronto-temporo-insular cortex were more vulnerable to transient Montreal Cognitive Assessment and Isaacs set test impairment. Subjects with lower GM volumes in right temporo-insular cortex, together with basal ganglia, were more vulnerable to transient cognitive impairment on the Zazzo’s cancellation task.

Conclusions—Smaller cortical volumes in fronto-temporo-insular areas measured 24 to 72 hours post stroke are associated with cognitive vulnerability in the subacute stroke phase.

Association between total-Tau and brain atrophy one year after first-ever stroke

So what the fuck is the solution? I don't care how well you describe the problem, it is totally useless without a solution. Once again more followup needed which will never occur. Maybe some of these might help which your doctor knows nothing about. How fucking incompetent is your doctor and stroke hospital? Don't do these on your own

From June, 2013;

Low Diastolic Pressure Linked to Brain Atrophy

And this from November, 2012:

Relationship between Physical Activity and Brain Atrophy Progression.

And from September, 2014: 

Lack of sleep may shrink your brain

From June, 2013:

Preventing Alzheimer’s disease-related gray matter atrophy by B-vitamin treatment

 

Brain atrophy in cognitively impaired elderly: the importance of long-chain ω-3 fatty acids and B vitamin status in a randomized controlled trial

Study shows that IVIG could prevent brain atrophy, delay onset of Alzheimer's disease Oct. 2015

The latest here:
Association between total-Tau and brain atrophy one year after first-ever stroke

• Hege Ihle-HansenEmail author,
• Guri Hagberg,
• Brynjar Fure,
• Bente Thommessen,
• Morten W. Fagerland,
• Anne R. Øksengård,
• Knut Engedal and
• Per Selnes

BMC NeurologyBMC series – open, inclusive and trusted201717:107

DOI: 10.1186/s12883-017-0890-6

©  The Author(s). 2017

Received: 31 January 2017

Accepted: 29 May 2017

Published: 5 June 2017

Open Peer Review reports

Abstract

Background

Although the most serious consequence of neuronal ischemia is acute neuronal death, mounting evidence suggests similarities between stroke and neurodegenerative disease. Brain atrophy visualized on structural MRI and pathological cerebrospinal fluid (CSF) concentrations of microtubule-associated protein tau (T-tau) and phosphorylated microtubule-associated protein tau indicate neurofibrillary degeneration. We aimed to explore the association between CSF T-tau and brain atrophy 1 year post-stroke.

Methods

We included 210 patients with first-ever ischemic stroke or transitory ischemic attack without pre-existing cognitive impairment. After 12 months, subjects underwent MRI, and CSF biomarkers were assessed. Using SIENAX (part of FSL), ventricular CSF volume and total brain volume were estimated and normalized for subject head size. The association between T-tau as explanatory variable and ventricular and total brain volume as outcome variables were studied using linear regression.

Results

One hundred eighty-two patients completed the follow-up. Forty-four had a lumbar puncture. Of these, 31 had their MRI with identical scan parameters. Mean age was 70.2 years (SD 11.7). Ventricular volume on MRI was significantly associated with age, but not with gender. In the multiple regression model, there was a significant association between T-tau and both ventricular (beta 0.44, 95% CI 376.3, 394.9, p = 0.021) and global brain volume (beta −0.50, 95% CI −565.9, −78.3, p = 0.011). There was no significant association between CSF T-tau 1 year post-stroke and baseline volumes.

Conclusion

T-tau measured 1 year post-stroke is associated with measures of brain atrophy. The findings indicate that acute stroke may enhance or trigger tau-linked neurodegeneration with loss of neurons.

Trial registration

Clinicaltrials.gov NCT00506818, July 23, 2007.

Inclusion from February 2007, randomization and intervention from May 2007 and trial registration in July 2007.

Higher Levels of Biomarker Linked to Increased Stroke Risk for Women

So fucking what? No solution is proposed if women have this biomarker other than further studies needed. Problems should never be described without at least a proposed solution.
http://dgnews.docguide.com/higher-levels-biomarker-linked-increased-stroke-risk-women?

MINNEAPOLIS, Minn -- May 10, 2017 -- Women with elevated levels of beta-2 microglobulin may be at a higher risk of ischaemic stroke, according to a study published in the May 10, 2017, online issue of Neurology.
“Recent studies have found associations between beta-2 microglobulin and heart disease,” said Pamela Rist, Brigham and Women’s Hospital, and Harvard Medical School, Boston, Massachusetts. “However, less is known about the association between beta-2 microglobulin and ischaemic stroke.”
The researchers looked at women with a mean age of 61 years enrolled in the Nurses’ Health Study who provided blood samples between 1989 and 1990 and who had no history of stroke or cancer. Participants were asked to complete questionnaires about their lifestyle and medical history every 2 years.
To learn more about beta-2 microglobulin and any possible link to stroke, the researchers measured the protein levels in 473 study participants who later had an ischaemic stroke as well as 473 participants of the same age who did not have a stroke. They were also matched based on other factors that could affect stroke risk, such as whether they smoked or used hormone treatments. The strokes occurred an average of 9 years after the start of the study.
Results showed that participants who later had an ischaemic stroke had higher levels of beta-2 microglobulin than those who did not have a stroke. The average level of the protein was 1.86 mg/L in those who had ischaemic strokes, compared with 1.80 mg/L in those who did not have a stroke.
The researchers divided the participants into 4 groups based on their levels of the protein. Those in the highest quarter of beta-2 microglobulin levels were 56% more likely to have a stroke than those in the bottom quarter. In the top quarter, 163 of the 283 women had strokes, compared with 106 of the 227 women in the bottom quarter.
The results were adjusted for other factors that could affect stroke risk, such as physical activity, high blood pressure and diabetes.
Rist said that limitations of the study are that it was conducted mainly among white women and that it could not examine any changes in protein levels.
“Given the high rate of disability from stroke, it is important to identify people who may be at higher risk of this disease,” she said. “This protein could be a marker that might help us in the fight against stroke. Further studies are needed to determine if beta-2 microglobulin levels can be modified through lifestyle changes.”
SOURCE: American Academy of Neurology

Relation of Urinary Retention and Functional Recovery in Stroke Patients During Rehabilitation Program

So you have explained a problem, What the fuck is your suggested solution? Catheterization is not the answer.
https://synapse.koreamed.org/search.php?where=aview&id=10.5535/arm.2017.41.2.204&code=1041ARM&vmode=FULL

Seok Beom Son, MD, Seong Yun Chung, MD, Seok Kang, MD and Joon Shik Yoon, MD, PhD

Department of Physical Medicine and Rehabilitation, Korea University Guro Hospital, Seoul, Korea.

Corresponding author: Joon Shik Yoon. Department of Physical Medicine and Rehabilitation, Korea University Guro Hospital, 148 Gurodong-ro, Guro-gu, Seoul 08308, Korea. Tel: +82-2-2626-1500, Fax: +82-2-2626-1513, Email: rehab46@korea.ac.kr

Received June 13, 2016; Accepted September 02, 2016.

This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted noncommercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Go to: Abstract

Objective To investigate the relationship between urinary retention and short-term functional recovery in subacute stage after stroke. Methods The medical records of 94 patients admitted to the rehabilitation unit of Korea University Guro Hospital were reviewed retrospectively. The postvoid residual urine (PVR) was measured at least once a day using a bladder scan, and urinary retention (UR) was defined when the daily PVR volume consistently checked more than 100 mL. Clinical data and functional outcomes of patients in the rehabilitation ward were collected. Functional outcomes were measured using the Mini-Mental State Examination (MMSE), Berg Balance Scale (BBS), Functional Ambulation Category (FAC) level, Fugl-Meyer Assessment (FMA), and Modified Barthel Index (MBI) at admission (or transfer) and discharge. The data of patients with and without urinary retention were compared and analyzed. Results Of the 94 participants, 25 patients were classified to the UR group and 69 were classified to the non-UR group. At the initial stage of rehabilitation, the scores of MMSE, BBS, FAC, MBI were significantly worse in the UR group (p<0.05). Both groups showed significant improvements of all functional outcomes after rehabilitation (p<0.05). The non-UR group showed more prominent recovery of BBS, FAC, MBI scores (p<0.05). Conclusion Urinary retention in post-stroke patients is significantly related to the poor functional status at initial stage of rehabilitation, and also to poor recovery after rehabilitation.

Neural Markers Associated with the Temporal Deployment of Attention: A Systematic Review of Non-motor Psychophysical Measures Post-stroke

The focus of this research was not to come up with a solution to this problem but to describe the problem of attention. Thus this is totally useless for survivors.
This is where a great stroke association president would keep the research focus on solving all the problems in stroke, not just describing them.
http://journal.frontiersin.org/article/10.3389/fnhum.2017.00031/full?

Essie Low, Robin Laycock^† and Sheila Crewther^*

• Department of Psychology and Counselling, La Trobe University, Melbourne, VIC, Australia

In recent years, evidence has emerged to suggest abnormal temporal dynamics of attentional processing in stroke patients, especially those presenting with neglect symptoms. However, there has been little profiling of the nature and extent of such temporal anomalies. In addition, many paradigms currently used to measure the time required to deploy visual attention in stroke require a psychomotor response, and may therefore confound performance outcomes. Thus, the aim of this systematic review was to identify and evaluate studies that have employed non-motor psychophysical paradigms to characterize the temporal deployment of visual attention in space. A total of 13 non-motor psychophysical studies were identified, in which stimulus exposure times were manipulated to measure the time course of attentional deployment. Findings suggest that prolonged attentional deployment thresholds are more likely to occur with lesions within more ventral areas of the fronto-parietal network, irrespective of whether patients presented with neglect. Furthermore, this deficit was greater following right-hemispheric lesions, suggesting a dominant role for the right-hemisphere in facilitating efficient deployment of attention. These findings indicate that area and hemisphere of lesion may serve as putative markers of attentional deployment efficiency. In addition, findings also provide support for using non-motor psychophysical paradigms as a more rigorous approach to measuring and understanding the temporal dynamics of attention.

Study Aims

The focus of this systematic review was two-fold. Firstly, this review was aimed at investigating the degree to which temporal deployment of visual attention (i.e., the time course of attentional deployment) may be compromised post-stroke, and the neural markers associated with it. This aim would be addressed by exploring how performance on tasks were differentially affected by the following factors: (1) between patients with and without neglect; (2) between patients with lesions to different cerebral regions; and (3) between patients with lesions to different hemispheres, i.e., right-hemisphere damage (RHD) and left-hemisphere damage (LHD) patients.

In addition, this review aimed to identify studies that have employed non-motor psychophysical paradigms to characterize temporal deployment of attention following stroke. Identification of these studies was expected to provide knowledge of the extent to which non-motor contributions to performance are important in explaining temporal processing impairments. A list of common non-motor psychophysical paradigms and their associated methodologies is summarized in Table 1.

Low Circulating Acute Brain-Derived Neurotrophic Factor Levels Are Associated With Poor Long-Term Functional Outcome After Ischemic Stroke

I absolutely hate crapola like this, describes a problem but offers no solution.  I have 101 posts on BDNF if you want your doctor to devise a solution for you and hope that your doctor is the smartest in the world and has a correct solution.
http://stroke.ahajournals.org/content/47/7/1943

Tara M. Stanne, N. David Åberg, Staffan Nilsson, Katarina Jood, Christian Blomstrand, Ulf Andreasson, Kaj Blennow, Henrik Zetterberg, Jörgen Isgaard, Johan Svensson, Christina Jern

https://doi.org/10.1161/STROKEAHA.115.012383

Stroke. 2016;47:1943-1945

Originally published June 14, 2016

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Abstract

Background and Purpose—Brain-derived neurotrophic factor (BDNF) plays important roles in brain plasticity and repair, and it influences stroke outcomes in animal models. Circulating BDNF concentrations are lowered in patients with traumatic brain injury, and low BDNF predicts poor recovery after this injury. We sought to investigate whether circulating concentrations of BDNF are altered in the acute phase of ischemic stroke and whether they are associated with short- or long-term functional outcome.

Methods—Serum concentrations of BDNF were measured in the Sahlgrenska Academy Study on Ischemic Stroke. The main outcomes were modified Rankin Scale (mRS) good (mRS score of 0–2) versus poor (mRS score of 3–6) at 3 months and 2 years after stroke, and good (mRS score of 0–2) versus poor (mRS score of 3–5) at 7 years after stroke.

Results—Acute concentrations of BDNF were significantly lower in ischemic stroke cases (n=491) compared with controls (n=513). BDNF concentrations were not significantly associated with 3-month outcome. However, patients with BDNF in the lowest tertile had an increased risk of experiencing a poor outcome both at 2-year and 7-year follow-up, and these associations were independent of vascular risk factors and stroke severity (odds ratio, 2.6; confidence intervals, 1.4–4.9; P=0.002 and odds ratio, 2.1; confidence intervals, 1.1–3.9; P=0.028, respectively).

Conclusions—Circulating concentrations of BDNF protein are lowered in the acute phase of ischemic stroke, and low levels are associated with poor long-term functional outcome. Further studies are necessary to confirm these associations and to determine the predictive value of BDNF in stroke outcomes.

Clinical Utility of Mindfulness Training in the Treatment of Fatigue After Stroke, Traumatic Brain Injury and Multiple Sclerosis: A Systematic Literature Review and Meta-analysis

Well we still know nothing about stroke fatigue and mindfulness training just seems like dealing with the symptoms, not the causes. A good placebo, but not the actual solution.
http://journal.frontiersin.org/article/10.3389/fpsyg.2016.00912/full?

Kristine M. Ulrichsen^1*, Tobias Kaufmann², Erlend S. Dørum^1,2,3, Knut K. Kolskår^1,2,3, Geneviève Richard^1,2,3, Dag Alnæs², Tone J. Arneberg⁴, Lars T. Westlye^2,3* and Jan E. Nordvik¹

• ¹Sunnaas Rehabilitation Hospital HT, Nesodden, Norway
• ²KG Jebsen Centre for Psychosis Research, Division of Mental Health and Addiction, NORMENT: Norwegian Centre for Mental Disorders Research, Oslo University Hospital and Institute of Clinical Medicine, University of Oslo, Oslo, Norway
• ³Department of Psychology, University of Oslo, Oslo, Norway
• ⁴Department of Behavioural Sciences, Oslo and Akershus University College of Applied Sciences, Oslo, Norway

Background: Fatigue is a common symptom following neurological illnesses and injuries, and is rated as one of the most debilitating sequela in conditions such as stroke, traumatic brain injury (TBI), and multiple sclerosis (MS). Yet effective treatments are lacking, suggesting a pressing need for a better understanding of its etiology and mechanisms that may alleviate the symptoms. Recently mindfulness-based interventions have demonstrated promising results for fatigue symptom relief.
Objective: Investigate the efficacy of mindfulness-based interventions for fatigue across neurological conditions and acquired brain injuries.
Materials and Methods: Systematic literature searches were conducted in PubMed, Medline, Web of Science, and PsycINFO. We included randomized controlled trials applying mindfulness-based interventions in patients with neurological conditions or acquired brain injuries. Four studies (N = 257) were retained for meta-analysis. The studies included patients diagnosed with MS, TBI, and stroke.
Results: The estimated effect size for the total sample was -0.37 (95% CI: -0.58, -0.17).
Conclusion: The results indicate that mindfulness-based interventions may relieve fatigue in neurological conditions such as stroke, TBI, and MS. However, the effect size is moderate, and further research is needed in order to determine the effect and improve our understanding of how mindfulness-based interventions affect fatigue symptom perception in patients with neurological conditions.

Introduction

Fatigue is a prevalent condition associated with a number of diseases (Hofman et al., 2007; Kluger et al., 2013). Curative pharmacologic or non-pharmacologic treatments have not yet been identified (Lee et al., 2008; Cantor et al., 2014; Wu et al., 2015). In some cases, like cancer-related fatigue, mindfulness-based interventions have resulted in significant reduction of fatigue symptoms (Pachman et al., 2014). However, the mechanisms of fatigue are poorly understood (Kutlubaev et al., 2012; Wu et al., 2015). Neurological diseases cause harm to the central nervous system, and fatigue associated with these kinds of diagnoses may have another etiology and respond differently to treatment than other types of fatigue. The objective of this systematic review is to investigate the effect of mindfulness-based interventions on fatigue symptoms following neurological conditions and acquired brain injuries.

Fatigue and increased fatigability are reported in a range of neurological conditions, like Parkinson’s, traumatic brain injury (TBI), myasthenia gravis, stroke, and multiple sclerosis (MS; Chaudhuri and Behan, 2004; DeLuca, 2005; Colle et al., 2006; Barker-Collo et al., 2007; Cantor et al., 2008; Friedman et al., 2011; Kluger et al., 2013). Often manifested as a mental and physical lack of energy, increased tiredness and reduced initiative (Glader et al., 2002; Choi-Kwon and Kim, 2011), fatigue can be persistent (Duncan et al., 2012; Ponsford et al., 2014) and pose a serious barrier to rehabilitation (Michael, 2002). Moreover, fatigue is associated with negative outcomes such as lower levels of functioning (Juengst et al., 2013), reduced quality of life, increased institutionalization and mortality (Glader et al., 2002; Lerdal et al., 2009).

Self-reports confirm fatigue as a distressing condition, and it is rated as the worst or one of the worst symptoms by 55, 50, and 40% of MS, TBI, and stroke patients, respectively (Fisk et al., 1994; LaChapelle and Finlayson, 1998; Ingles et al., 1999). Adding to the impact of the symptoms, nearly half of the stroke patients suffering from fatigue felt that they were offered insufficient help managing the fatigue (McKevitt et al., 2010). Due to the debilitating consequences, and incomplete understanding of the mechanisms and treatments of fatigue, the topic was listed among the top ten research priorities in a consensus report from UK stroke survivors, caregivers, and health professionals (Pollock et al., 2014). Such reports are in line with the literature on fatigue in other neurological conditions, often emphasizing the substantial limitations in our comprehension and treatment of this symptom (Chaudhuri and Behan, 2004).

Agreeing on a universally accepted definition of fatigue has proven problematic (Chaudhuri and Behan, 2004; Immink, 2014). Although the search for biological correlates of fatigue is ongoing, the experience of fatigue is fundamentally subjective (Chaudhuri and Behan, 2004; Dittner et al., 2004), and common not only to ill health but also in draining physical activities. The feeling of fatigue is thus both intimate, yet universal, and the experience has proven difficult to quantify and measure objectively (Dittner et al., 2004; Belmont et al., 2006; Mollayeva et al., 2013). However, it is generally accepted to differentiate “normal” fatigue from “pathological” fatigue (de Groot et al., 2003). While normal fatigue is considered to reflect a state of weariness associated with strain that can be lessened by rest, serving a protective and restorative function (Choi-Kwon and Kim, 2011), the pathological fatigue seen in many patients with acquired brain injury and MS tends to be more persistent, less related to strain, abnormal, excessive, and problematic (de Groot et al., 2003).

Fatigue is frequently measured by self-report questionnaires (Belmont et al., 2006; Lerdal et al., 2009). A multitude of scales are available [see Krupp et al., 1989, Fatigue Severity Scale (FSS); Schwartz et al., 1993, Fatigue Assessment Instrument (FAI); Smets et al., 1995, Modified Fatigue Impact Scale (MFIS)], and the same tools are often used across conditions (Dittner et al., 2004). Besides self-report measures, performance-based tests are sometimes also applied (Lerdal et al., 2009), presumably measuring more objective aspects of fatigue, but no objective “gold standard” or litmus test is currently available (Dittner et al., 2004).

Why some people develop fatigue in the face of neurological injury or disease, whereas others do not, is yet to be answered. Several factors have been found to be associated with or predict post-stroke fatigue (PSF), including functional impairment severity, depression, pain, sleep disturbances, cognitive impairments, physical deconditioning, pre-stroke fatigue, sedative medications, coronary heart disease, and increasing age (Mead et al., 2011; Wang et al., 2014). The variety of predictors suggests a complex etiology, further complicating treatment and diagnostic assessments. As fatigue is a pivotal part of both depression and sleep disturbances, these conditions have been posed as alternative or supplementing explanations (Kos et al., 2007). There are, however, many patients experiencing fatigue without reporting depression (van der Werf et al., 2001; Glader et al., 2002), and some studies fail to find associations between fatigue and sleep problems (Schepers et al., 2006). Findings like this may indicate that fatigue can be a partly independent symptom, and neurological fatigue in the absence of conditions such as depression or sleep problems has been referred to as “primary fatigue” (Forwell et al., 2008).

Owing to the multidimensionality of fatigue, the construct is often conceptualized as reflecting different subcategories. An applicable categorization is the division between peripheral (predominantly physical/muscular) and brain-derived central (more psychologically rooted, the sense of complete exhaustion) fatigue (Chaudhuri and Behan, 2000, 2004), in which mental fatigue constitutes an important dimension of the latter (Chaudhuri and Behan, 2000, 2004). The coping hypothesis offers one explanation for this experience, stating that increased fatigue is rooted in the continuous effort needed in order to compensate for cognitive impairments caused by the brain injury (Van Zomeren et al., 1984). Indeed, a few studies have reported that individuals with TBI and MS are showing increased brain activation compared to healthy controls while performing cognitive tasks (McAllister et al., 1999, 2001; DeLuca et al., 2008; Kohl et al., 2009) possibly indicating increased mental effort, while yet other studies have identified reduced sustained attention (McAvinue et al., 2005), selective attention deficits (Ziino and Ponsford, 2006), and a tendency to stimulus over-selectivity (McHugh and Wood, 2013) in patients with TBI. These findings are in line with the hypothesis of a central, brain-derived fatigue in neurological conditions, which might be associated with disruptions in circuits involving basal ganglia, frontal cortex thalamus (Chaudhuri and Behan, 2000). As pointed out by Chaudhuri and Behan (2004), (central) fatigue is “consistently seen with lesions in pathways associated with arousal and attention, reticular and limbic systems and basal ganglia” (pp. 979–980).

The models, hypotheses and correlates reviewed above are by no means offering an exhaustive account of the mechanisms of fatigue in neurological conditions. Still, by highlighting relevant aspects of the condition, such accounts may provide clues about potentially effective treatment strategies. Attentional impairments seem to be a recurrent and relevant aspect. Thus, in order to improve attentional regulation and control, a treatment procedure that has been suggested, among others, is mindfulness-based training (Chen et al., 2011; McHugh and Wood, 2013).

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