Low gait speed is associated with low physical activity and high sedentary time following stroke

Fucking useless, describes a problem, offers NO SOLUTION.  Even the famous Julie Bernhardt is implicated in crapola like this. That shows you how far the dead wood exists in stroke. 

Low gait speed is associated with low physical activity and high sedentary time following stroke

Natalie A. Fini, Julie Bernhardt & Anne E. Holland

Pages 2001-2008 | Received 15 May 2019, Accepted 06 Nov 2019, Published online: 22 Nov 2019

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• https://doi.org/10.1080/09638288.2019.1691273
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Abstract

Purpose

This study describes physical activity levels and factors associated with physical activity at the end of stroke rehabilitation.

Methods

Primary stroke survivors were assessed at completion of physical rehabilitation. Outcomes included physical activity (e.g. step count, moderate-vigorous physical activity duration) and sedentary time measured with the Sensewear Armband, gait speed, and cognition. The number of participants meeting physical activity recommendations was calculated. Differences in physical activity were examined between household ambulators (gait speed <0.4 m/s), limited community ambulators (0.4–0.8 m/s), and unlimited community ambulators (>0.8 m/s). The influence of age, cognition, and gait speed on physical activity was determined by multiple regression.

Results

Seventy-nine stroke survivors participated. Twenty-one participants achieved 30 min/day of moderate-vigorous physical activity accumulated in 10 min bouts. Unlimited community ambulators took more steps/day (median 4975 vs. 469 limited, 355 household, p < 0.001), had higher moderate-vigorous physical activity (median 74 min/day vs. 22 limited, 31 household, p < 0.001) and lower sedentary time (mean 1105 vs. 1239 limited, 1232 household minutes/day, p < 0.001). Age, gait speed, and cognition predicted 21.3% of the variance in moderate-vigorous physical activity (p = 0.001); adding employment status to the model predicted 57.3% of the variance in step count (p < 0.001).

Conclusions

Physical activity is low following stroke and should be a target for treatment, particularly in those with gait speeds ≤0.8 m/s.

• Implications for rehabilitation

• Seventy-three percent of stroke survivors performed ≥30 minutes of moderate to vigorous physical activity throughout the day.

• Twenty-seven percent of stroke survivors accumulated ≥30 minutes of moderate to vigorous physical activity in 10 minute bouts.

• Despite relatively good physical ability, daily step count was low in this sample.

• Those with gait speeds ≤0.8 m/s had lower physical activity levels and higher sedentary time.

 

The Role of The Gut Microbiome in Parkinson’s Disease

 

You'll want your doctor to have protocols to verify and possibly correct your gut microbiota.  First of all for your stroke rehab, then for preventing your chances of Parkinsons. 

• gut bacteria (27 posts to December 2012)

• Gut Microbes (6 posts to May2015)

• gut microbiome (13 posts to March 2016)

• gut microbiota (14 posts to June 2016)

• gut-brain axis (12 posts to March 2017)

• gut-brain connection (1 post to December 2017)

 

Your risk of Parkinsons here:

Parkinson’s Disease May Have Link to Stroke March 2017 

The latest here:

The Role of The Gut Microbiome in Parkinson’s Disease

Show all authors

Amy Gallop, MD, James Weagley, BS, Saif-ur-Rahman Paracha, MD, ...

First Published July 5, 2021 Review Article 

https://doi.org/10.1177/08919887211018268

Article information

Abstract

The gut microbiota is known to play a role in various disease states through inflammatory, immune and endocrinologic response. Parkinson’s Disease is of particular interest as gastrointestinal involvement is one of the earlier features seen in this disease. This paper examines the relationship between gut microbiota and Parkinson’s Disease, which has a growing body of literature. Inflammation caused by gut dysbiosis is thought to increase a-synuclein aggregation and worsen motor and neurologic symptoms of Parkinson’s disease. We discuss potential treatment and supplementation to modify the microbiota. Some of these treatments require further research before recommendations can be made, such as cord blood transplant, antibiotic use, immunomodulation and fecal microbiota transplant. Other interventions, such as increasing dietary fiber, polyphenol and fermented food intake, can be made with few risks and may have some benefit for symptom relief and speed of disease progression.

Keywords

Parkinson’s disease, microbiome, inflammation, neuro-degeneration, gut-brain axis

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Self-Reported and Objective Sleep Measures in Stroke Survivors With Incomplete Motor Recovery at the Chronic Stage

So you described a problem, offered NO SOLUTION. Useless.

Self-Reported and Objective Sleep Measures in Stroke Survivors With Incomplete Motor Recovery at the Chronic Stage

Show all authors

Melanie K. Fleming, PhD, Tom Smejka, MSc, David Henderson Slater, MRCP,

First Published July 1, 2021 Research Article 

https://doi.org/10.1177/15459683211029889

Article information

Abstract

Background. 

 Stroke survivors commonly complain of difficulty sleeping. Poor sleep is associated with reduced quality of life and more understanding of long-term consequences of stroke on sleep is needed.  

Objective. The primary aims were to (1) compare sleep measures between chronic stroke survivors and healthy controls and (2) test for a relationship between motor impairment, time since stroke and sleep. Secondary aims were to explore mood and inactivity as potential correlates of sleep and test the correlation between self-reported and objective sleep measures.  

Methods. Cross-sectional sleep measures were obtained for 69 chronic stroke survivors (mean 65 months post-stroke, 63 years old, 24 female) and 63 healthy controls (mean 61 years old, 27 female). Self-reported sleep was assessed with the sleep condition indicator (SCI) and sleep diary ratings, objective sleep with 7-nights actigraphy and mood with the Hospital Anxiety and Depression Scale. Upper extremity motor impairment was assessed with the Fugl-Meyer assessment.  

Results. Stroke survivors had significantly poorer SCI score (P < .001) and higher wake after sleep onset (P = .005) than controls. Neither motor impairment, nor time since stroke, explained significant variance in sleep measures for the stroke group. For all participants together, greater depression was associated with poorer SCI score (R²_adj = .197, P < .001) and higher age with more fragmented sleep (R²_adj = .108, P < .001). There were weak correlations between nightly sleep ratings and actigraphy sleep measures (r_s = .15–.24).  

Conclusions. Sleep disturbance is present long-term after stroke. Depressive symptoms may present a modifiable factor which should be investigated alongside techniques to improve sleep in this population.

Keywords

actigraphy, self-report, motor impairment, sleep disruption, mood

Introduction

Many stroke survivors report a major change in their sleeping habits since having a stroke.¹ Although there is some evidence for improvements in sleep parameters from the acute to the chronic stage of stroke,^2,3 systematic reviews report a high prevalence of sleep disorders, such as insomnia and sleep disordered breathing, after stroke.^4,5 Sleep disorders are reported to be more common in stroke survivors compared to normative values or to healthy control groups.⁶ Increases in estimated sleep time (per 24 hour period) from pre-stroke to post-stroke have been found to correlate negatively with the ability to engage in activities of daily living at the chronic stage² and reduced quality of life has also been demonstrated for stroke survivors reporting insomnia.⁷

Although some research on sleep after stroke focuses on diagnosable sleep disorders, such as sleep disordered breathing, restless leg syndrome and primary insomnia,^5,8 there is also research directly comparing between people with chronic stroke and age-matched controls with sleep measures as a continuum rather than categorising participants as having a sleep disorder or not. This is important, as alongside other post-stroke complications, sub-clinical sleep disruption has the potential for debilitating long-term consequences. Recently, evidence has begun to emerge that treatments, such as cognitive behavioural therapy for insomnia, may also be useful for people with sub-clinical insomnia symptoms.⁹ The studies that have analysed sleep measures as a continuum report longer sleep latency, greater wake after sleep onset (WASO) and more fragmented sleep, as well as lower subjective sleep quality for stroke survivors compared to controls.^10-13 However, these studies typically have modest sample sizes (20–35 per group). Therefore, confirmation of these findings with a larger sample size is desirable to enable us to further understand this long-term condition.

There is some indication that sleep quality may relate to stroke outcomes, using broad measures of independence in activities of daily living¹⁴ or disability.^15,16 We previously demonstrated that sleep disruption during inpatient rehabilitation from stroke and brain injury is associated with poorer motor outcomes¹⁷ and hypothesise that this may be, at least in part, due to impaired consolidation of motor learning underlying motor recovery.¹⁸ If this is the case, and if sleep disruption persists long-term, then recovery after discharge from rehabilitation may also be limited. Additionally, factors that accompany motor impairment, such as spasticity and pain, may directly affect ability to initiate and maintain sleep. Finally, limitations in movement of the upper or lower limb can affect mobility and therefore physical activity which may indirectly affect sleep. These factors may, to some extent, depend on how long the person has been living with motor impairment. Alternatively, relationships between motor impairment and sleep quality might be expected due to effects of the stroke on cortico-subcortical circuits involved both in the control of sleep and in the control of movement. For example, Gottlieb et al¹⁹ demonstrated that stroke survivors with poor sleep efficiency had altered brain volume in the thalamus, hippocampus and caudate in comparison with controls with normal sleep efficiency. However, to our knowledge, there are no studies at the chronic stage to consider the relationship between motor impairment and sleep quality specifically.

Mood disorders are also common post-stroke complications.^20,21 Depression and anxiety have been found to relate to poor self-reported sleep in stroke survivors and older adults without stroke,^16,22-25 with greater insomnia symptoms present in stroke survivors with depression or anxiety than without.⁴ However, to our knowledge, there are few studies examining whether depression and anxiety relate to objective measures of sleep in this population. Pajediene et al²⁶ found a correlation between polysomnography variables reflecting poor sleep and more depressed mood (from the Hospital Anxiety and Depression Scale) in a sample of 13 acute stroke patients, though the magnitude of this correlation is not reported. In contrast, Bakken et al²⁷ found no significant correlation between the Beck depression Inventory Score and actigraphy variables WASO or number of awakenings. Further research is therefore needed to elucidate whether relationships between self-report measures of mood and sleep are also seen when sleep is measured with actigraphy.

It is currently unknown whether subjective reports of sleep quality are reflective of objective measures of sleep in this population. Ouellet and Morin²⁸ reported that people with traumatic brain injury subjectively reported worse sleep than control participants, but that this was not detected using polysomnography (PSG) suggesting a mismatch between objective and subjective sleep quality. In stroke survivors, 6 months post-stroke, Bakken et al³ report some correspondence between Pittsburgh Sleep Quality Index (PSQI) ratings and time spent asleep, but no meaningful correlations between PSQI and measures of sleep disruption from actigraphy. It is important to understand the relationship between self-reported and objective measures of sleep problems in this population, in order to best tailor interventions aimed at improving aspects of sleep quality.

The primary aims of this study were therefore to compare both objective and self-reported sleep measures between community dwelling chronic stroke survivors and age- and sex-matched healthy controls and to investigate whether variance in sleep measures in stroke survivors could be explained by variance in upper limb motor impairment or time since stroke. Additionally, we sought to explore potential correlates of sleep measures across both groups. We were particularly interested in the chronic stage of stroke, as this is the time when intensive rehabilitation efforts are likely to have completed and the long-term impact of stroke can be understood.

We hypothesised that stroke survivors would demonstrate poorer self-reported sleep, more fragmented sleep and longer time awake overnight than healthy controls. We also hypothesised that stroke survivors with a poorer motor outcome (worse upper limb impairment) would have more sleep disruption than those with good functional outcomes.

Finally, we aimed to test for differences in the agreement across subjective and objective sleep quality measures between stroke survivors and controls. We anticipated that there would be less correspondence between objective and subjective sleep measures for stroke survivors.

More at link.

 

The Strength of the Corticospinal Tract Not the Reticulospinal Tract Determines Upper-Limb Impairment Level and Capacity for Skill-Acquisition in the Sub-Acute Post-Stroke Period

 

Absolutely nothing here is of any use at all. NOTHING ON INCREASING THE STRENGTH OF THE CORTICOSPINAL TRACT!  Useless. What the fuck was the point of this research? I'd fire you immediately for even suggesting this crapola. And until we get survivors in charge stroke survivors will be screwed.

The Strength of the Corticospinal Tract Not the Reticulospinal Tract Determines Upper-Limb Impairment Level and Capacity for Skill-Acquisition in the Sub-Acute Post-Stroke Period

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Ulrike Hammerbeck, PhD, Sarah F. Tyson, PhD, Prawin Samraj, MS, ...

First Published July 4, 2021 Research Article 

https://doi.org/10.1177/15459683211028243

Article information

Abstract

Background. 

Upper-limb impairment in patients with chronic stroke appears to be partly attributable to an upregulated reticulospinal tract (RST). Here, we assessed whether the impact of corticospinal (CST) and RST connectivity on motor impairment and skill-acquisition differs in sub-acute stroke, using transcranial magnetic stimulation (TMS)–based proxy measures.  

Methods. 

Thirty-eight stroke survivors were randomized to either reach training 3-6 weeks post-stroke (plus usual care) or usual care only. At 3, 6 and 12 weeks post-stroke, we measured ipsilesional and contralesional cortical connectivity (surrogates for CST and RST connectivity, respectively) to weak pre-activated triceps and deltoid muscles with single pulse TMS, accuracy of planar reaching movements, muscle strength (Motricity Index) and synergies (Fugl-Meyer upper-limb score).  

Results. Strength and presence of synergies were associated with ipsilesional (CST) connectivity to the paretic upper-limb at 3 and 12 weeks. Training led to planar reaching skill beyond that expected from spontaneous recovery and occurred for both weak and strong ipsilesional tract integrity. Reaching ability, presence of synergies, skill-acquisition and strength were not affected by either the presence or absence of contralesional (RST) connectivity.  

Conclusion. 

The degree of ipsilesional CST connectivity is the main determinant of proximal dexterity, upper-limb strength and synergy expression in sub-acute stroke. In contrast, there is no evidence for enhanced contralesional RST connectivity contributing to any of these components of impairment. In the sub-acute post-stroke period, the balance of activity between CST and RST may matter more for the paretic phenotype than RST upregulation per se.

Keywords

stroke, upper limb, motor impairment, skill learning, corticospinal tract, reticulospinal tract

Introduction

Motor impairment after stroke is closely associated with ipsilesional corticospinal tract (CST) damage.^1-4 In addition, recent data suggest that arm flexor synergies, finger enslaving on the paretic side and mirror movements on the non-paretic hand after stroke are all attributable to an increased influence of the reticulospinal tract (RST) after damage to the CST.^5-11 Studies in primates have shown that 6 months after a lesion in the pyramidal tract,¹² there is upregulation of the RST. In patients with chronic stroke, the incidence of contralesional connectivity to the ipsilateral paretic limb is increased, particularly in patients with moderate to severe paresis,^13,14 suggesting a similar upregulation of RST activity during recovery.¹⁵ An unanswered question is the impact of this RST upregulation after the initial plegic stage³; does it contribute to, or impede recovery, or is it an epiphenomenon of recovery, neither good nor bad.⁷ Furthermore, it is unclear whether unwanted muscle synergies result from actual upregulation of pre-existing cortico-reticulospinal descending pathways or can be attributed instead to a relative imbalance between them (in the absence of upregulation) and the CST.⁶

Using transcranial magnetic stimulation (TMS), we sought to determine the degree of ipsilesional and contralesional cortical connectivity to paretic arm muscles in a group of patients with moderate to severe stroke in the early sub-acute period. TMS of the human motor cortex in one hemisphere can evoke responses in ipsilateral muscles with characteristics compatible with activation of oligosynaptic cortico-bulbospinal pathways,¹⁶ most likely representing cortico-reticulo-spinal connection.^13,14,17-19 This provides an indirect method of assessing the excitability of the RST in stroke survivors.^11,20-22 We further investigated the effect of these two forms of connectivity on strength, synergies, planar reaching accuracy and capacity for skill-acquisition. We examined inputs to proximal muscles involved in planar reaching movements since these are thought to receive greater reticulospinal inputs than distal arm muscles.^16,23

More at link.

Does the Prevention of Complications Explain the Survival Benefit of Organized Inpatient (Stroke Unit) Care?

I consider stroke units to still be a failure. They aren't even measuring 100% recovery. Survival IS NOT THE GOAL. 100% recovery  is the only goal in stroke. 

Does the Prevention of Complications Explain the Survival Benefit of Organized Inpatient (Stroke Unit) Care?

Further Analysis of a Systematic Review

Lindsay Govan

,

Peter Langhorne

,

Christopher J. Weir

and for the Stroke Unit Trialists Collaboration

Originally published9 Aug 2007https://doi.org/10.1161/STROKEAHA.106.478842Stroke. 2007;38:2536–2540

• Other version(s) of this article

Abstract

Background and Purpose— Systematic reviews have shown that organized inpatient (stroke unit) care reduces the risk of death after stroke. However, it is unclear how this is achieved. We tested whether stroke unit care could reduce deaths by preventing complications.

Methods— We updated a collaborative systematic review of 31 controlled clinical trials (6936 participants) to include reported interventions and complications during early hospital care plus the certified cause of death during follow up. Each secondary analysis used data from between 7 and 17 studies (1652 to 3327 participants). Complications were grouped as physiological, neurological, cardiovascular, complications of immobility, and others. Bayesian hierarchical models were used to estimate odds ratios for features occurring in stroke units versus conventional care.

Results— Based on the data of 17 trials (3327 participants), organized (stroke unit) care reduced case fatality during scheduled follow up (OR: 0.75; 95% credible intervals: 0.59 to 0.92), in particular deaths certified as attributable to complications of immobility (0.59; 0.41 to 0.86). Stroke unit care was associated with statistically significant increases in the reported use of oxygen (2.39; 1.39 to 4.66), measures to prevent aspiration (2.42; 1.36 to 4.36), and paracetamol (2.80; 1.14 to 4.83) plus a nonsignificant reduction in the use of urinary catheterization. Stroke units were associated with statistically significant reductions in stroke progression/recurrence (0.66; 0.46 to 0.95) and in some complications of immobility: chest infections (0.60; 0.42 to 0.87), other infections (0.56; 0.40 to 0.84), and pressure sores (0.44; 0.22 to 0.85). There were no significant differences in cardiovascular, physiological, or other complications.

Conclusions— Organized inpatient (stroke unit) care appears to reduce the risk of death after stroke through the prevention and treatment of complications, in particular infections.

 

AI That Detects Post-Stroke Depression Type Can Help Stroke Survivors Get Right Treatment

 Why aren't we preventing depression by having EXACT STROKE REHAB PROTOCOLS LEADING TO 100% RECOVERY? This sounds impressive but it is not.

AI That Detects Post-Stroke Depression Type Can Help Stroke Survivors Get Right Treatment

Summary: New AI technology can detect a patient’s stroke depression type, and improve treatment options.

Source: Hiroshima University

An AI developed by Japanese researchers might soon help stroke survivors get the right treatment by detecting a patient’s post-stroke depression (PSD) type, a frequently seen but often overlooked neuropsychiatric manifestation after a stroke that could impair functional recovery.

The AI was developed by Hiroshima University (HU) researchers using a probabilistic artificial neural network called log-linearized Gaussian mixture network. The neural network was trained to distinguish between depression, apathy, or anxiety based on 36 evaluation indices obtained from functional, physical, and cognitive tests on 274 patients.

Details about their research that analyzed the relationship between PSD and activities of daily living independence, degree of paralysis, stress awareness, and higher brain function using machine learning are published in Scientific Reports.

Early PSD detection

The researchers said each PSD type might have different underlying neuroanatomic mechanisms which could have a distinct impact on a patient’s functional recovery. And its early detection is crucial to give the appropriate treatment needed by the patient.

“Depression is a highly comorbid neuropsychiatric symptom during the acute and subacute phase after a stroke and has been reported to negatively influence functional and cognitive recovery. Thus, early diagnosis and intervention are crucial for post-stroke depression,” study author Seiji Hama, a research associate at HU’s Graduate School of Biomedical and Health Science, said.

“However, PSD is multifactorial, and associated neurological symptoms may hinder the detection process. This study is the first step in aiming to accurately diagnose PSD using data obtained in routine practice without any special equipment.”

The researchers tested the AI’s diagnostic accuracy through the receiver operating characteristic curve which visually evaluates the performance of a machine learning algorithm by giving it an area under the curve (AUC) score. An AUC score of 1.0 means a perfect performance. The PSD detection AI scored above 0.85.

Stress threshold hypothesis

Various post-stroke physical disorders, cognitive dysfunction, and mood disorders associated with stress responses are intricately intertwined, making it difficult to understand the cause of PSD and, therefore, making its diagnosis challenging.

 

 

Favorable Venous Outflow Linked to Reperfusion Success After Thrombectomy

I'm 100% positive your definition of success doesn't correspond to any survivors.  I'm sure you're using the tyranny of low expectations to claim success when none exists.

Favorable Venous Outflow Linked to Reperfusion Success After Thrombectomy

A favorable venous outflow (VO), determined by the cortical vein opacification score (COVES), is associated with reperfusion success and good functional outcomes in patients who undergo endovascular thrombectomy for acute ischemic stroke due to large vessel occlusion (AIS-LVO), according to study findings published in Neurology.

This retrospective study included 565 consecutive patients with AIS-LVO who were treated by endovascular thrombectomy at 2 comprehensive stroke centers in Germany and the United States. Study investigators used baseline CTA to evaluate collateral status (Tan scale) and VO with the COVES. They defined a favorable VR by a COVES between 3 and 6, and an unfavorable one by a COVES between 0 and 2.

The primary study outcome was excellent reperfusion status (defined by the modified Thrombolysis on Cerebral Infarction 2c/3), while the secondary outcome was good functional outcomes 90 days post-treatment.

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Patients with favorable VO (VO+) were significantly younger (median, 72 years vs 76.5 years, respectively; P <.001), more likely to have received intravenous tPA (70% vs 40.9%, respectively; P <.001), and had less severe symptoms at presentation (P <.001) compared with patients with unfavorable VO.

Excellent vessel reperfusion during thrombectomy was associated with favorable VO in a multivariable logistic regression analysis (odds ratio [OR], 2.10; 95% CI, 1.39-3.16; P <.001).

A secondary outcome multivariable binary logistic regression analysis found independent associations between favorable clinical outcomes and both favorable VO+ profiles (OR, 8.9; 95% CI, 5.3-14.9; P <.001) and excellent post-thrombectomy vessel reperfusion status (OR, 2.7; 95% CI, 1.7-4.4; P <.001).

Limitations of this study included its retrospective design as well as the inclusion of only patients from 2 comprehensive stroke centers, which may limit the generalizability of the findings.

The study investigators concluded that the assessment of the venous microvascular system, among other alternative blood flow pathways, could “be an additional useful vascular biomarker associated with endovascular treatment success and good functional outcomes” in patients with AIS-LVO.

Disclosure: Several study authors declared affiliations with the pharmaceutical industry. Please see the original reference for a full list of authors’ disclosures.

Reference

Faizy TD, Kabiri R, Christensen S, et al. Association of venous outflow profiles and successful vessel reperfusion after thrombectomy. Published online May 5, 2021. Neurology. doi:10.1212/WNL.0000000000012106

 

A Primary Care Agenda for Brain Health: A Scientific Statement From the American Heart Association

But is this enough to recover your  5 lost years of brain cognition due to your stroke?

A Primary Care Agenda for Brain Health: A Scientific Statement From the American Heart Association

Ronald M. Lazar

,

Virginia J. Howard

,

Walter N. Kernan

,

Hugo J. Aparicio

,

Deborah A. Levine

,

Anthony J. Viera

,

Lori C. Jordan

,

David L. Nyenhuis

,

Katherine L. Possin

,

Farzaneh A. Sorond

, … See all authors

Originally published15 Mar 2021https://doi.org/10.1161/STR.0000000000000367Stroke. 2021;52:e295–e308

Abstract

A healthy brain is critical for living a longer and fuller life. The projected aging of the population, however, raises new challenges in maintaining quality of life. As we age, there is increasing compromise of neuronal activity that affects functions such as cognition, also making the brain vulnerable to disease. Once pathology-induced decline begins, few therapeutic options are available. Prevention is therefore paramount, and primary care can play a critical role. The purpose of this American Heart Association scientific statement is to provide an up-to-date summary for primary care providers in the assessment and modification of risk factors at the individual level that maintain brain health and prevent cognitive impairment. Building on the 2017 American Heart Association/American Stroke Association presidential advisory on defining brain health that included “Life’s Simple 7,” we describe here modifiable risk factors for cognitive decline, including depression, hypertension, physical inactivity, diabetes, obesity, hyperlipidemia, poor diet, smoking, social isolation, excessive alcohol use, sleep disorders, and hearing loss. These risk factors include behaviors, conditions, and lifestyles that can emerge before adulthood and can be routinely identified and managed by primary care clinicians.

The brain, through its capacity for cognition, is the organ that functions to register and record experiences. In youth, sound cognition is expected, but with aging, the increasingly vulnerable brain acquires injuries, and cognitive decline becomes more prevalent. As the average age of the US population grows, this age effect becomes of greater concern as the number of individuals with or at risk for mild cognitive impairment (MCI) and dementia grows.¹ As of now, 1 in 5 Americans ≥65 years of age has MCI, and 1 in 7 has dementia²; by 2050, however, the number of Americans with dementia will triple.³ The importance of cognition was affirmed by the Affordable Care Act, which mandated coverage of an assessment of cognitive function as part of the annual wellness benefit for Medicare beneficiaries.⁴ The question arises, however, about what the health care community can do proactively to mitigate or forestall the onset of decline before it happens. Primary care is well suited to emphasize brain health as part of the goal of many preventive interventions. The purpose of this document is to summarize information that will help primary care providers optimize their effectiveness in maintaining brain health.

For clinicians and scientists, brain health can be approached along many structural, physiological, and epidemiological dimensions. Clinically, optimal brain health is the absence of cognitive impairment/dementia, stroke, and other brain diseases. Pathologically, optimal brain health is the absence of neurodegenerative, cerebrovascular, and comorbid diseases that interfere with everyday physical and cognitive functioning. Pragmatically, it is the preservation of neuronal function to meet the demands of everyday life, operationally defined in terms of the capacity to function adaptively in one’s environment. With aging come increasingly compromised neuronal activity and greater vulnerability to disease.⁵ The ability to think, solve problems, remember, perceive, and communicate is crucial to successful living; their loss can lead to helplessness and dependency. Once pathologically based decline begins, however, there are few therapeutic options to halt or slow the downward course.

Because of their central role in patient care and management, primary care providers are in a strategic position to identify and manage risk factors for cognitive decline. The goal is to identify and modify risk factors leading to brain injury before it happens. People with dementia experience lower quality of life,⁶ and caregivers, typically family members, experience high rates of psychological stress and physical ill health.⁷ Dementia is among the costliest medical conditions, shown to be more expensive in both direct and indirect costs than heart disease or cancer,⁸ with worldwide costs estimated at $818 billion in 2015.⁹ Delaying cognitive decline through primary care provider–instigated risk factor modification for even a small percentage of individuals would enable many more people to reach end of life without dementia and would have substantial benefits for patients, caregivers, and society.¹⁰

In 2017, the American Heart Association (AHA)/American Stroke Association issued a presidential advisory on defining brain health that included “Life’s Simple 7”¹¹ as a follow-up to an earlier statement on the promotion of cardiovascular health¹² (Figure). (now Essential 8) The goal of that document was to provide a model for operationally defining brain health in highly quantifiable terms and to suggest specific therapeutic targets for preventive intervention that included risk factor management and lifestyle changes. The purpose of the current statement is to update the evidence supporting that strategy and to emphasize the importance of dissemination and surveillance in the primary care setting. We acknowledge that the notion of brain health encompasses other functions such as mobility and emotional status, but they are interdependent with systems and conditions outside the brain. We chose cognition because it is uniquely dependent on the brain.

• Download figure
• Download PowerPoint

Figure. The American Heart Association’s Life’s Simple 7, as described by Lloyd-Jones et al¹² and later Gorelick et al.¹¹

 

Direct thrombectomy, bridging therapy confer similar functional outcomes in stroke

 So both are complete failures in getting to 100% recovery? No measurement of that has to mean complete failure at that.

Direct thrombectomy, bridging therapy confer similar functional outcomes in stroke

Results of a meta-analysis published in Neurology determined there was no difference in functional outcomes between direct thrombectomy and combination with bridging IV thrombolysis among Asian patients with large vessel occlusion stroke.

“The safety and efficacy of intravenous thrombolysis (IVT) for patients with large vessel occlusion (LVO) who are also eligible for endovascular stroke treatment has been questioned,” Aristeidis Katsanos, MD, a neurologist and stroke fellow at McMaster University and the Population Health Research Institute, and colleagues wrote. “Direct endovascular thrombectomy (dEVT), bypassing the administration of any intravenous thrombolytic agent, has been suggested as an alternative therapeutic approach to the combination of IVT followed by endovascular treatment for acute ischemic stroke (AIS) patients who are eligible for both treatment modalities and present at a site that can offer prompt endovascular treatment. The hypothesis that dEVT is a non-inferior option to the current standard of care combination of IVT and endovascular thrombectomy, referred also as bridging therapy (BT), has been evaluated in the setting of multiple observational studies and recently published randomized-controlled clinical trials (RCTs).”

Researchers detected no difference in functional outcomes between direct thrombectomy and combination with bridging IV thrombolysis among Asian patients with large vessel occlusion stroke. Source: Adobe Stock

Katsanos and colleagues conducted a systematic review and meta-analysis to assess the current evidence on the relative efficacy and safety of dEVT compared with BT in Asian patients with AIS. They noted a median age of 70 years in the overall study population; 44% were women.

The study included patients with LVO AIS who were eligible for both therapeutic options presenting within 4.5 hours from stroke onset. Through searching Medline and Scopus, investigators identified three randomized controlled trials that included a total of 1,092 patients. The probability of a modified Rankin scale (mRS) score of 0-2 at 3 months served as the primary outcome.

Investigators observed no different between dEVT and BT with regard to outcomes of mRS 0-2 (OR = 1.08; 95% CI, 0.85-1.38; adjusted OR = 1.11; 95% CI, 0.76-1.63), mRS 0-1 (OR = 1.10; 95% CI, 0.84-1.43; adjusted OR = 1.16; 95% CI, 0.84-1.61) and functional improvement at 3 months (common OR = 1.08; 95% CI, 0.88-1.34; adjusted common OR = 1.09; 95% CI, 0.86-1.37). Katsanos and colleagues noted patients who received dEVT compared with BT had a significantly poorer chance of successful recanalization prior to the endovascular procedure (OR = 0.37; 95% CI, 0.18-0.77).

According to researchers, although patients who received dEVT compared with BT had reduced intracranial bleeding rates (OR = 0.67; 95% CI, 0.49-0.92), there was no significant difference in the likelihood of symptomatic intracranial hemorrhage. They also reported no differences between the groups regarding all-cause mortality, serious adverse events or procedural complications.

“Effect estimates from available RCTs, presented in the current systematic review and meta-analysis, when compared to those provided by observational studies, raise concerns for heterogeneity in inclusion criteria and the possibility for selection bias within published cohorts,” Katsanos and colleagues wrote. “… The issue of generalizability of the evidence from individual RCTs and the results from the current meta-analysis beyond the Asian population deserves particular attention.”

 

WSO PRESIDENT'S AWARD FOR SERVICES TO STROKE: THE STROKE UNIT STORY World Stroke Academy. Langhorne P. 10/24/14; 63647

 Behind the paywall, so useless to survivors. You'll never be able to tell if your stroke unit is following proper protocols.

WSO PRESIDENT'S AWARD FOR SERVICES TO STROKE: THE STROKE UNIT STORY

World Stroke Academy. Langhorne P. 10/24/14; 63647 

Prof. Peter Langhorne

All contributions

Biography

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