10 superfoods to boost a healthy diet

Still pretty much totally useless. NO protocols, NO daily amounts. But it does wonders for conscience laundering making Harvard feel like they are helping the planet.

10 superfoods to boost a healthy diet

Posted August 29, 2018, 10:30 am

Katherine D. McManus, MS, RD, LDN
Contributor

No single food — not even a superfood — can offer all the nutrition, health benefits, and energy we need to nourish ourselves. The 2015–2020 US Dietary Guidelines recommend healthy eating patterns, “combining healthy choices from across all food groups — while paying attention to calorie limits.”
Over the years, research has shown that healthy dietary patterns can reduce risk of high blood pressure, heart disease, diabetes, and certain cancers. Dietary patterns such as the DASH (Dietary Approaches to Stop Hypertension) diet and the Mediterranean diet, which are mostly plant-based, have demonstrated significant health benefits and reduction of chronic disease.
However, there are a few foods that can be singled out for special recognition. These “superfoods” offer some very important nutrients that can power-pack your meals and snacks, and further enhance a healthy eating pattern.

Superfoods list

Berries. High in fiber, berries are naturally sweet, and their rich colors mean they are high in antioxidants and disease-fighting nutrients.
How to include them: When berries are not in season, it is just as healthy to buy them frozen. Add to yogurt, cereals, and smoothies, or eat plain for a snack.
Fish. Fish can be a good source of protein and omega-3 fatty acids, which help prevent heart disease.
How to include it: Buy fresh, frozen, or canned fish. Fish with the highest omega-3 content are salmon, tuna steaks, mackerel, herring, trout, anchovies, and sardines.
Leafy greens. Dark, leafy greens are a good source of vitamin A, vitamin C, and calcium, as well as several phytochemicals (chemicals made by plants that have a positive effect on your health). They also add fiber into the diet.
How to include them: Try varieties such as spinach, swiss chard, kale, collard greens, or mustard greens. Throw them into salads or sauté them in a little olive oil. You can also add greens to soups and stews.
Nuts. Hazelnuts, walnuts, almonds, pecans — nuts are a good source of plant protein. They also contain monounsaturated fats, which may be a factor in reducing the risk of heart disease.
How to include them: Add a handful to oatmeal or yogurt, or have as a snack. But remember they are calorically dense, so limit to a small handful. Try the various types of nut butters such as peanut (technically a legume), almond, or cashew. Nuts are also a great accompaniment to cooked veggies or salads.
Olive oil. Olive oil is a good source of vitamin E, polyphenols, and monounsaturated fatty acids, all which help reduce the risk of heart disease.
How to include it: Use in place of butter or margarine in pasta or rice dishes. Drizzle over vegetables, use as a dressing, or when sautéing.
Whole grains. A good source of both soluble and insoluble fiber, whole grains also contain several B vitamins, minerals, and phytonutrients. They have been shown to lower cholesterol and protect against heart disease and diabetes.
How to include them: Try having a bowl of oatmeal for breakfast. Substitute bulgur, quinoa, wheat berries, or brown rice for your usual baked potato. When buying breads at the supermarket, look to see that the first ingredient is “100% whole wheat flour.”
Yogurt. A good source of calcium and protein, yogurt also contains live cultures called probiotics. These “good bacteria” can protect the body from other, more harmful bacteria.
How to include it: Try eating more yogurt, but watch out for fruited or flavored yogurts, which contain a lot of added sugar. Buy plain yogurt and add your own fruit. Look for yogurts that have “live active cultures” such as Lactobacillus, L. acidophilus, L. bulgaricus, and S. thermophilus. You can use yogurt in place of mayonnaise or sour cream in dips or sauces.
Cruciferous vegetables. These include broccoli, Brussels sprouts, cabbage, cauliflower, collard greens, kale, kohlrabi, mustard greens, radishes, and turnips. They are an excellent source of fiber, vitamins, and phytochemicals including indoles, thiocyanates, and nitriles, which may prevent against some types of cancer.
How to include them: Steam or stir-fry, adding healthy oils and herbs and seasonings for flavor. Try adding a frozen cruciferous vegetable medley to soups, casseroles, and pasta dishes.
Legumes. This broad category includes kidney, black, red, and garbanzo beans, as well as soybeans and peas. Legumes are an excellent source of fiber, folate, and plant-based protein. Studies show they can help reduce the risk of heart disease.
How to include them: Add to salads, soups, and casseroles. Make a chili or a bean- based spread such as hummus.
Tomatoes. These are high in vitamin C and lycopene, which has been shown to reduce the risk of prostate cancer.
How to include them: Try tomatoes in a salad or as a tomato sauce over your pasta. You can also put them in stews, soups, or chili. Lycopene becomes more available for your body to use when tomatoes are prepared and heated in a healthy fat such as olive oil.

Quantitative EEG as Biomarkers for the Monitoring of Post-Stroke Motor Recovery in BCI and tDCS Rehabilitation

Survivors don't care one whit about biomarkers and recovery prediction. Do something useful, create stroke rehab protocols that get survivors 100% recovered. That is the only stroke goal. NOT these fucking lazy prediction and biomarker researches.  This is all because we have NO STROKE LEADERSHIP.

Quantitative EEG as Biomarkers for the Monitoring of Post-Stroke Motor Recovery in BCI and tDCS Rehabilitation

Ravikiran Mane, Effie Chew, Kok Soon Phua, Kai Keng Ang, A. P. Vinod, Cuntai Guan

Quantitative EEG as Biomarkers for the Monitoring of Post-Stroke

Motor Recovery in BCI and tDCS Rehabilitation

Ravikiran Mane, Effie Chew, Kok Soon Phua, Kai Keng Ang, A. P. Vinod, Cuntai Guan

Abstract

— This study investigates the neurological changes in the brain activity of chronic stroke patients undergoing different types of motor rehabilitative interventions and their relationship with the clinical recovery using the Quantitative Electroencephalography (QEEG) features. Over a period of

two weeks, 19 hemiplegic chronic stroke patients underwent 10 sessions of upper extremity motor rehabilitation using a brain computer interface paradigm (BCI group, n= 9) and transcranial direct current stimulation coupled BCI paradigm (tDCS group, n=10). The pre- and post-treatment brain activations, as well as the intervention-induced changes in the neuronal activity, were quantified using 11 QEEG features and their relationship with clinical motor improvement was investigated.

Significant treatment-induced change in the relative theta power was observed in the BCI group and the change was significantly correlated with the clinical improvements. Also, in the BCI group, the relative theta power and interactions between the theta, alpha, and beta power were identified as monitory biomarkers of motor recovery. On the contrary, the tDCS group was characterized by the significant change in brain asymmetry.

Furthermore, we observed significant intergroup differences in the predictive capabilities of post-intervention QEEG features between the BCI and tDCS group. Based on the intergroup

differences observed in this study and convergent results from the other neuroimaging analysis performed on the same cohort, we suggest that distinctly different mechanisms of neuronal

recovery were facilitated by tDCS and BCI interventions and these treatment specific mechanisms can be encapsulated using QEEG.

Shoals Hospital Acute Rehab Stroke Program was recently recertified by the Joint Commission.

How fucking stupid do you think we are when you present 'care'  as the best you can do? Come back with your results and then we can see how good you are.  Joint Commission certification tells us nothing about quality results delivered. These are all non-negotiable or get out of the stroke business.

1. tPA full recovery better than 12%?
2. Full stroke recovery better than 10%?
3.  30 day stroke deaths better than your competitors?

https://www.courierjournal.net/news/article_e5cfcf96-aa36-11e8-bde3-dfd499ce90a9.html

MUSCLE SHOALS – Officials at Shoals Hospital announced last week that the Shoals Hospital Acute Rehab Stroke Program was recently recertified by the Joint Commission. A Joint Commission reviewer recently carried out an onsite certification survey. The favorable results and recertification reflect the organization’s commitment to providing safe and effective patient care to individuals recovering from stroke. The survey also verifies J.W. Sommer’s compliance with national stroke-specific care standards. The reviewer noted many positive attributes about the program including:
• The staff is fully engaged and works collaboratively as a team
• The staff promotes a culture of clinical excellence centered around patient safety
• Excellent patient education documentation is distributed by all disciplines
• “Our focus in the J.W. Sommer Rehabilitation Unit is to provide the best care for the rehabilitation patients we are privileged to serve,” said Shoals Hospital CEO, Kidada Hawkins. “We are honored to have this endorsement from the Joint Commission.”
Studies indicate that sixty percent of stroke survivors can benefit from comprehensive rehabilitation. Eighty percent of patients receiving this level of therapy return to their homes, work, active retirement or etc., according to the National Rehabilitation Caucus. The Joint Commission acknowledgment of J.W. Sommer’s continuum of care for stroke offers patients and families peace of mind in knowing they are getting quality stroke care for maximized results.
J.W. Sommer remains the area’s only Certified Stroke Rehabilitation Unit,” Hawkins added. “Congratulations to the leadership of this effort including Medical Director Steve Howell, MD, Unit Administrator Pamela Moore, Stroke Program Coordinator Lauren Carpenter, and Director of Therapeutic Services April Allen.

Poststroke Depression Biomarkers: A Narrative Review

If you got survivors 100% recovered you wouldn't have to tackle this secondary problem of depression. Focus on the primary problem and you wouldn't have all these secondary problems to deal with. That is where exact stroke protocols tied to specific objective damage diagnosis comes in. If your doctor and stroke hospital can't see that they need to be fired.
https://www.frontiersin.org/articles/10.3389/fneur.2018.00577/full?

Oleg A. Levada^* and Alexandra S. Troyan

• State Institution “Zaporizhzhia Medical Academy of Postgraduate Education Ministry of Health of Ukraine, ” Zaporizhzhia, Ukraine

Poststroke depression (PSD) is the most prevalent psychiatric disorder after stroke, which is independently correlated with negative clinical outcome. The identification of specific biomarkers could help to increase the sensitivity of PSD diagnosis and elucidate its pathophysiological mechanisms. The aim of current study was to review and summarize literature exploring potential biomarkers for PSD diagnosis. The PubMed database was searched for papers published in English from October 1977 to December 2017, 90 of which met inclusion criteria for clinical studies related to PSD biomarkers. PSD biomarkers were subdivided into neuroimaging, molecular, and neurophysiological. Some of them could be recommended to support PSD diagnosing. According to the data, lesions affecting the frontal-subcortical circles of mood regulation (prefrontal cortex, basal nuclei, and thalamus) predominantly in the left hemisphere can be considered as neuroimaging markers and predictors for PSD for at least 1 year after stroke. Additional pontine and lobar cerebral microbleeds in acute stroke patients, as well as severe microvascular lesions of the brain, increase the likelihood of PSD. The following molecular candidates can help to differentiate PSD patients from non-depressed stroke subjects: decreased serum BDNF concentrations; increased early markers of inflammation (high-sensitivity C-reactive protein, ferritin, neopterin, and glutamate), serum pro-inflammatory cytokines (TNF-α, IL-1β, IL-6, IL-18, IFN-γ), as well as pro-inflammatory/anti-inflammatory ratios (TNF-α/IL-10, IL-1β/IL-10, IL-6/IL-10, IL-18/IL-10, IFN-γ/IL-10); lowered complement expression; decreased serum vitamin D levels; hypercortisolemia and blunted cortisol awakening response; S/S 5-HTTLPR, STin2 9/12, and 12/12 genotypes of the serotonin transporter gene SLC6A4, 5-HTR2a 1438 A/A, and BDNF met/met genotypes; higher SLC6A4 promoter and BDNF promoter methylation status. Neurophysiological markers of PSD, that reflect a violation of perception and cognitive processing, are the elongation of the latency of N200, P300, and N400, as well as the decrease in the P300 and N400 amplitude of the event-related potentials. The selected panel of biomarkers may be useful for paraclinical underpinning of PSD diagnosis, clarifying various aspects of its multifactorial pathogenesis, optimizing therapeutic interventions, and assessing treatment effectiveness.

Introduction

Poststroke depression (PSD) is the most prevalent psychiatric disorder after stroke, which affects nearly one-third of the survivors during first 5 years after disease onset (1–3). The diagnosis of PSD includes the following characteristics: (1) presence of major/minor depressive episode according to DSM-III-IV-5 or other valid approaches; (2) evidence of stroke from history, physical examination, and/or neuroimaging data; and (3) onset of PSD is temporally related to the stroke (3). Several epidemiological findings have demonstrated that PSD is independently linked to negative clinical outcomes, such as significantly longer hospitalization; more severe functional disability (3–6); profound diminutions in physical, psycho-social, cognitive, and eco-social domains of quality of life (3, 7); unsatisfactory results of poststroke rehabilitation (8); elevated rates of mortality (3, 9–11); higher risks of recurrent stroke at 1 year (12); as well as considerable strain for caregivers (13). Data mentioned above highlight the importance of identifying PSD among stroke survivors.

The detection of depressive symptoms at early stroke stages and recognition subjects at risk for PSD diagnosis remains challenging. Clinical measures currently used to assess PSD, especially in the acute poststroke patients, may lack the specificity necessary to detect symptoms (14, 15). From this point of view, the identification of specific biomarkers might help to increase the sensitivity of PSD diagnosis. Moreover, it could be helpful for elucidating the pathophysiological mechanisms of PSD and ultimately lead to choosing specific targeted treatment (16).

Thus, we aimed to review and summarize the literature exploring potential biomarkers for PSD diagnosis.

Feasibility of Cognitive Functions Screened With the Montreal Cognitive Assessment in Determining ADL Dependence Early After Stroke

Will you stop with the assessments and recovery predictions and just deliver stroke rehab protocols. Survivors want 100% recovery. Why are you doing these wastes of time? 

Feasibility of Cognitive Functions Screened With the Montreal Cognitive Assessment in Determining ADL Dependence Early After Stroke

Tamar Abzhandadze^1,2*, Lena Rafsten^1,2, Åsa Lundgren-Nilsson^1,3 and Katharina S. Sunnerhagen^1,3

• ¹Institute of Neuroscience and Physiology, Rehabilitation medicine, University of Gothenburg, Gothenburg, Sweden
• ²Department of Occupational Therapy and Physiotherapy, Sahlgrenska University Hospital, Gothenburg, Sweden
• ³Centre for Person-Centred Care (GPCC), University of Gothenburg, Gothenburg, Sweden

Objective: To investigate the feasibility of assessing cognitive function using the Montreal Cognitive Assessment (MoCA) given 36–48 h post stroke to explain dependence in activities of daily living (ADL).

Methods: This is a cross-sectional, exploratory study. Cognitive function and basic ADL were assessed with the MoCA and the Barthel Index (BI), respectively, within 36–48 h of admission. Neurological functions were assessed with the National Institute of Health Stroke Scale (NIHSS) upon admittance to the hospital. Binary logistic regression analyses were performed to assess the feasibility of the MoCA in explaining ADL dependence.

Results: Data were available for 550 patients (42% females, mean age 69 years). Moderate correlations (r_s > +0.30, p < 0.001) were found between the total score on the BI, MoCA, and visuospatial/executive functions. The regression analysis model including only MoCA as an independent variable had a high sensitivity for explaining ADL dependence. However, the model with independent variables of MoCA, NIHSS, and age had the best area under the curve value (0.74).

Conclusions: Cognitive functions assessed with the MoCA partly explain ADL dependence 36–48 h post stroke. Stroke-related neurological deficits and age should be additional considerations.

Introduction

Cognitive functions play an important role in patients' rehabilitation setting management (1) and safe discharge. Few studies have investigated the utility of assessing patients' cognitive functions during the early stages of stroke onset to explain activity-related outcomes. As even mild stroke can lead to cognitive impairments and influence patients' everyday functioning (2), it is important to identify these difficulties.

The Montreal Cognitive Assessment (MoCA) is a recommended tool for assessing cognitive functions in patients with acute stroke (3, 4). Good validity and reliability were reported for those with mild to moderate stroke (4). Studies performed on a subacute stroke population showed a positive association between impaired cognitive function assessed with the MoCA and a high level of global disability (5). Poor executive and memory functions were positively associated with dependence in activities of daily living (ADL) (6). However, explanatory factors for favorable ADL outcomes 3 to 12 month post stroke were stroke localization (7), younger age, less severity of neurological deficits, and good function in the upper extremities (7, 8).

The length of stay after the stroke has decreased substantially and particularly, the patients with very mild to mild neurological deficits, face very short hospital stay (9). The clinicians often have only couple of days to identify stroke related difficulties. Thus, there is increased need of very early assessments of cognitive functions. The MoCA and basic ADL with the Barthel Index (BI) are both commonly used instruments for this, in order to plan discharge. Whether cognitive functions assessed by the MoCA can explain patients' ADL ability at the early stage of stroke onset remains unknown. The aim of this study was therefore to investigate the feasibility of the MoCA to explain ADL dependence 36–48 h post stroke.

Electromyography Assessment During Gait in a Robotic Exoskeleton for Acute Stroke

I got absolutely nothing out of this that would've helped at any time for my gait rehab.
https://www.frontiersin.org/articles/10.3389/fneur.2018.00630/full?

Ghaith J. Androwis^1,2, Rakesh Pilkar^1,3, Arvind Ramanujam¹ and Karen J. Nolan^1,2,3*

• ¹Human Performance and Engineering Research, Kessler Foundation, West Orange, NJ, United States
• ²Children's Specialized Hospital, Mountainside, NJ, United States
• ³Department of Physical Medicine and Rehabilitation, Rutgers–New Jersey Medical School, Newark, NJ, United States

Background: Robotic exoskeleton (RE) based gait training involves repetitive task-oriented movements and weight shifts to promote functional recovery. To effectively understand the neuromuscular alterations occurring due to hemiplegia as well as due to the utilization of RE in acute stroke, there is a need for electromyography (EMG) techniques that not only quantify the intensity of muscle activations but also quantify and compare activation timings in different gait training environments.

Purpose: To examine the applicability of a novel EMG analysis technique, Burst Duration Similarity Index (BDSI) during a single session of inpatient gait training in RE and during traditional overground gait training for individuals with acute stroke.

Methods: Surface EMG was collected bilaterally with and without the RE device for five participants with acute stroke during the normalized gait cycle to measure lower limb muscle activations. EMG outcomes included integrated EMG (iEMG) calculated from the root-mean-square profiles, and a novel measure, BDSI derived from activation timing comparisons.

Results: EMG data demonstrated volitional although varied levels of muscle activations on the affected and unaffected limbs, during gait with and without the RE. During the stance phase mean iEMG of the soleus (p = 0.019) and rectus femoris (RF) (p = 0.017) on the affected side significantly decreased with RE, as compared to without the RE. The differences in mean BDSI scores on the affected side with RE were significantly higher than without RE for the vastus lateralis (VL) (p = 0.010) and RF (p = 0.019).

Conclusions: A traditional amplitude analysis (iEMG) and a novel timing analysis (BDSI) techniques were presented to assess the neuromuscular adaptations resulting in lower extremities muscles during RE assisted hemiplegic gait post acute stroke. The RE gait training environment allowed participants with hemiplegia post acute stroke to preserve their volitional neuromuscular activations during gait iEMG and BDSI analyses showed that the neuromuscular changes occurring in the RE environment were characterized by correctly timed amplitude and temporal adaptations. As a result of these adaptations, VL and RF on the affected side closely matched the activation patterns of healthy gait. Preliminary EMG data suggests that the RE provides an effective gait training environment for in acute stroke rehabilitation.

Introduction

Recovery of function post stroke is based on neural adaptation, and progressive task specific repetitive training based on the principles of neuroplasticity (1, 2). While major advances have been made in early intervention for the treatment of patients post stroke, the majority of survivors have residual mobility challenges and hemiplegia (3, 4). Hemiplegia typically manifests in pronounced asymmetrical deficits and is one of the most common disabling impairments resulting from stroke (5). Asymmetrical gait can be associated with muscle weakness, leading to inefficient ambulation, balance control challenges and risk of musculoskeletal injury to the non-paretic limb (6, 7). Task-oriented, high-repetition movements can improve muscular strength, motor control and movement coordination in patients post stroke (2). The task-specific training pertains to the training driven to achieve a functional task such as walking rather than focusing on minimizing an impairment (8, 9). In acute phase, traditional gait rehabilitation administered by a physical therapist is strenuous, inconsistent (in terms of movements generated) and less intense (in terms of number of steps). Integrating robotic exoskeleton (RE) technology into standard of care programs during the critical acute phase when the injured nervous system is highly plastic could maximize repetitive practice (9, 10), improve functional outcome measurements and provide quality gait training (10, 11). Programmable RE technology can also be used to advance progression during treatment and under the guidance of a physical therapist can emulate some features of manual assistance in a consistent and reproducible manner (2). The RE based training involves repetitive task-oriented (gait) movements and weight shifts to promote functional recovery. RE gait training may lead to changes in muscle activation as it provides task-specific movements to the lower limbs, increased step dosing and may provide a more symmetrical gait pattern (12).

An additional challenge in acute stroke is that many patients have a difficult time producing volitional movements that can be practiced repeatedly especially during the acute stage. In order to recover from physiological and functional lower extremity deficits, the task-related activities should include contributions from appropriate muscle groups during practice of these movements (13). Using an RE during gait rehabilitation in the acute phase may allow volitional muscle activation and improved phasic coordination (activation timing) during walking. However, the accuracy of these muscle contributions should be tracked. Surface electromyography (EMG) is one of the most effective, non-invasive tools which provides easy access to underlying neuromuscular processes that cause muscles to generate force, produce movement and achieve any functional task (14). During gait, EMG data reveals characteristic patterns of activation associated with each involved muscle in terms of onset timings, burst durations and levels of activations (15). These characteristic patterns significantly differ between healthy and pathological gait and this information can be used to assess the levels of improvement in muscle function, motor control, and neuromuscular adaptations post rehabilitation interventions. Bilateral EMG recordings of lower extremities can be further utilized to compare changes on the paretic side with respect to non-paretic side to assess inter-limb synchronization post RE intervention in individuals with stroke related hemiplegia.

To effectively understand the alterations occurring due to the RE, there is a need for EMG techniques that not only quantify the intensity of muscle activations but also quantify and compare activation timings for a single muscle during different gait training environments (e.g., overground or RE assisted). Although EMG amplitude is one of the most common variables reported in the literature (14, 16, 17), it does not distinctively provide temporal information (on–off timings). Particularly, in a cyclic activity such as gait, it is not only important for lower extremity muscles to produce activations but also activate them at the accurate time, especially for individuals with neurological disability such as acute stroke (16). In the post-stroke gait rehabilitation setting, the need to assess temporal information is even more apparent as muscle activation timing may be altered due to, (1) hemiplegia secondary to stroke and (2) the presence of a RE. The temporal features extracted from EMG data can allow the assessment of accuracy of participant's volitional contributions during training but also assess the modifications that the RE guided gait training may have. Several techniques have been used to extract the temporal information of muscle activations; however, their applicability in the domain of RE based gait training in acute stroke is limited.

The purpose of this investigation was to examine the applicability of a novel EMG analysis technique, Burst Duration Similarity Index (BDSI) during a single session of inpatient gait training in a RE and during traditional over ground gait training for individuals with acute stroke. EMG outcomes included standard measures of integrated EMG (iEMG) calculated from the root-mean-square (RMS) profiles, and a novel measure, BDSI (18) which quantifies the similarity between the two muscle activations by measuring co-excitation (common active regions) and co-inhibition (common inactive regions) during gait. Using iEMG and BDSI EMG analyses techniques, we hypothesized that the RE gait training environment will preserve the volitional neuromuscular activations in acute stroke. Volitional neuromuscular activations represent the residual post stroke muscle function during walking in the lower limbs. Our secondary hypothesis is that the RE gait training environment will change the activation timing of lower extremity muscles, measured by applying the BDSI technique, to match established normative healthy gait muscle activation timing patterns (15).

Clinical Outcome of Isolated Cerebellar Stroke—A Prospective Observational Study

If this is so much better than NIHSS scoring then write it up as a stroke protocol and get it distributed worldwide. Or are you lazy AND incompetent? 

Clinical Outcome of Isolated Cerebellar Stroke—A Prospective Observational Study

https://www.frontiersin.org/articles/10.3389/fneur.2018.00580/full?

Alina Nickel^1*, Bastian Cheng¹, Hans Pinnschmidt², Emine Arpa¹, Christos Ganos³, Christian Gerloff¹ and Götz Thomalla¹

• ¹Department of Neurology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany
• ²Institute of Medical Biometry and Epidemiology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany
• ³Department of Neurology, Charité, University of Medicine Berlin, Berlin, Germany

Background: The aim of this prospective study was to investigate clinical deficits of patients with isolated cerebellar stroke applying a dedicated clinical score, the modified International Cooperative Ataxia Rating Scale (MICARS) and identifying factors that influence recovery.

Methods: Fifteen patients with acute isolated cerebellar stroke received a standard stroke MRI on the day of admission and were clinically assessed using the mRS, NIHSS and the modified International Cooperative Ataxia Rating Scale (MICARS) on day 1, 3, 7, 30, and 90. A generalized linear model for repeated measures was employed to analyze the effect of stroke lesion location, volume, days after stroke, patient age, and MICARS score at admission on the total MICARS score.

Results: Median patient age was 54 years, lesion location in most cases was right (87%) and in the PICA territory (11/15). Median lesion volume was 3.2 ml. Median NIHSS was 1. The median MICARS decreased from on day 1 with 23–4 at day 90. The generalized linear model identified MICARS score at day 1, lesion location, days after admission and the interaction of the last two on the total MICARS score, whereas there was no significant effect of stroke volume or patient age.

Conclusions: Isolated cerebellar stroke can present with low NIHSS while more specific scales like the MICARS indicate a severe deficit. Patient age at onset of stroke and lesion volume had no significant effect on recovery from cerebellar symptoms as opposed to severity of symptoms at admission and lesion location.

Introduction

Acute cerebellar stroke is a relatively rare subtype of acute stroke representing approximately 3% of all ischemic and hemorrhagic strokes (1, 2). Clinical symptoms of cerebellar stroke are manifold and can be subtle so that they are often not recognized at hospital admission (2). Symptoms are frequently underestimated or missed by standard clinical stroke scores such as the National Institutes of Health Stroke Scale (NIHSS). Dedicated clinical scales such as the MICARS are available (3) but not widely used in routine stroke diagnostic and treatment.

Imaging of cerebellar stroke also may be challenging. Whereas small ischemic lesions in the cerebellum are detectable by magnetic resonance diffusion weighed imaging (DWI), identification may be difficult or impossible on computed tomography (CT) (4). Missed diagnosis of cerebellar stroke is not only detrimental to the diagnostic work up of stroke etiology of individual patients but can also lead to serious complications (4).

Studies addressing the clinical course and functional outcome of patients with isolated cerebellar stroke are scarce, and little is known about factors that influence recovery from isolated cerebellar stroke. Therefore, we aimed to investigate the clinical course and prognostic factors of clinical deficits caused by isolated ischemic cerebellar stroke confirmed by Magnetic resonance imaging (MRI) in a prospective study applying a dedicated cerebellar symptom rating scale.

Application of Machine Learning to Automated Analysis of Cerebral Edema in Large Cohorts of Ischemic Stroke Patients

I would rather have Dr. Watson analyze this big data, s/he has already been doing this for other medical applications. If your stroke hospital can't see that this could be much better that all of their stroke doctors combined they need to stop being a stroke hospital.

Other uses by Dr. Watson:

VA partners with IBM to use supercomputer Watson to treat cancer

MD Anderson Cancer Center to Use IBM Watson

IBM Watson, Boston Children’s team on rare pediatric diseases

Multiple Sclerosis @Point of Care app with Dr. Watson

Fighting Diabetes with Watson: Medtronic & IBM Watson Health

IBM Watson Makes a Treatment Plan for Brain-Cancer Patient in 10 Minutes; Doctors Take 160 Hours

The latest here:

Application of Machine Learning to Automated Analysis of Cerebral Edema in Large Cohorts of Ischemic Stroke Patients

Rajat Dhar^1*†, Yasheng Chen^2†, Hongyu An³ and Jin-Moo Lee²

• ¹Division of Neurocritical Care, Department of Neurology, Washington University in St. Louis, St. Louis, MO, United States
• ²Division of Cerebrovascular Diseases, Department of Neurology, Washington University in St. Louis, St. Louis, MO, United States
• ³Department of Radiology, Washington University in St. Louis, St. Louis, MO, United States

Cerebral edema contributes to neurological deterioration and death after hemispheric stroke but there remains no effective means of preventing or accurately predicting its occurrence. Big data approaches may provide insights into the biologic variability and genetic contributions to severity and time course of cerebral edema. These methods require quantitative analyses of edema severity across large cohorts of stroke patients. We have proposed that changes in cerebrospinal fluid (CSF) volume over time may represent a sensitive and dynamic marker of edema progression that can be measured from routinely available CT scans. To facilitate and scale up such approaches we have created a machine learning algorithm capable of segmenting and measuring CSF volume from serial CT scans of stroke patients. We now present results of our preliminary processing pipeline that was able to efficiently extract CSF volumetrics from an initial cohort of 155 subjects enrolled in a prospective longitudinal stroke study. We demonstrate a high degree of reproducibility in total cranial volume registration between scans (R = 0.982) as well as a strong correlation of baseline CSF volume and patient age (as a surrogate of brain atrophy, R = 0.725). Reduction in CSF volume from baseline to final CT was correlated with infarct volume (R = 0.715) and degree of midline shift (quadratic model, p < 2.2 × 10⁻¹⁶). We utilized generalized estimating equations (GEE) to model CSF volumes over time (using linear and quadratic terms), adjusting for age. This model demonstrated that CSF volume decreases over time (p lt; 2.2 × 10⁻¹³) and is lower in those with cerebral edema (p = 0.0004). We are now fully automating this pipeline to allow rapid analysis of even larger cohorts of stroke patients from multiple sites using an XNAT (eXtensible Neuroimaging Archive Toolkit) platform. Data on kinetics of edema across thousands of patients will facilitate precision approaches to prediction of malignant edema as well as modeling of variability and further understanding of genetic variants that influence edema severity.

Introduction

Over 10 million persons suffer a stroke each year worldwide (1). Most of these patients have at least one brain imaging study performed during their acute hospitalization, primarily for diagnostic purposes on presentation (2). Follow-up scans are often obtained to evaluate the size of infarction, degree of cerebral edema, as well as exclude the development of hemorrhagic transformation (3). Computed tomography (CT) is the most frequently employed modality for acute stroke imaging due to its widespread availability, lower cost, and greater speed of scanning, especially important in acutely unstable patients where “time is brain” (4). Although conventional CT does not have the ability of magnetic resonance imaging (MRI) to detect hyper-acute stroke, its ability to track progression of infarction and edema after stroke are comparable while affording greater temporal resolution with serial imaging (5). This practice means that there is a massive global imaging dataset of stroke patients with information on stroke location, infarct size, development of edema, and hemorrhagic transformation. While these parameters can be assessed by human raters, such evaluation is not scalable when leveraging imaging data from thousands of patients.

Cerebral edema develops around regions of brain infarction within the first week after stroke. This pathologic increase in brain water and hemispheric volume can lead to mass effect and is the major cause of death and neurological worsening after stroke (6). Development of edema is usually heralded by abrupt mental status worsening 2 days or more after admission, when herniation and midline shift have already developed (7). However, this process actually begins in the first hours after stroke and evolves continually and progressively over the first few days. At first decreases in blood and cerebrospinal fluid (CSF) compartments within the cranial compartment compensate for this increase in brain volume. However, once this has been exhausted, decompensation with worsening rapidly follows. Current measures of edema such as midline shift (MLS) or neurological deterioration capture only this decompensated state and not the critical early stages of edema before worsening. Further, assessing edema utilizing only MLS neglects the full spectrum of edema, including those with increased brain volume who never develop MLS. Measures of lesion volume either requires MRI (not feasible in all stroke patients) or can be estimated using CT; however, hypodensity on CT may be subtle early on and represents a variable combination of infarct plus edema. It is only the latter component that contributes to swelling and risk of herniation, and so lesion volume (even on MRI) only partially predicts risk of herniation (8).

We have proposed a sensitive quantitative metric of edema severity that can be extracted from CT imaging at variable time points after stroke (9). This leverages the reciprocal biologic relationship between increase in brain volume due to swelling and proportional decrease in CSF volume as compensation. CSF is pushed out of hemispheric sulci, cerebral ventricles, and the basal cisterns as edema develops in the hours and days after stroke. The reduction in CSF volume precedes the development of midline shift and clinical worsening due to edema. We demonstrated that the volume of CSF displaced up to the time of maximal edema closely correlated with extent of midline shift.

We have also developed an automated algorithm to segment CSF from CT scans of stroke patients (10). This critical step employed random forest-based machine learning (ML) trained on manually delineated scans. Features integrated into the ML platform include Haar-like patterns of pixels. This supervised learning approach was able to rapidly and reliably measure CSF volume on serial CT scans from two sites in our preliminary testing, performing significantly better than simple threshold-based models for CSF segmentation which were confounded by density of infarction mimicking CSF. Correlations of automated CSF volumes to ground-truth values exceeded 0.95, with volumes that closely approximated actual CSF values after active contour refinement. This automated approach facilitates the translation of this metric to studies evaluating edema in large numbers of stroke patients. Exploring the variability in quantifiable edema severity between patients will not only unlock opportunities for precise prediction of malignant edema at earlier time points but also provide the basis for understanding the genetic basis of cerebral edema. Such studies require thousands of stroke patients with serial imaging to undergo CSF-based edema measurement. We now present a proof-of-principle application of a processing algorithm capable of handling large datasets of CT scans and extracting CSF volumes for such analyses.

Rosuvastatin Reduces Neuroinflammation in the Hemorrhagic Transformation After rt-PA Treatment in a Mouse Model of Experimental Stroke

Is this just a followup to these much earlier research articles which I bet your stroke hospital never did anything with? If my doctor had been following stroke research at all he could have asked me if I wanted to try statin therapy even though it had only been tested in rats. My stroke was May 2006 so my doctor had been incompetent for three years already.
Statins:
tested in rats from 2003
http://oc1dean.blogspot.com/2011/09/statins-induce-angiogenesis.html 
tested in humans, March, 2011
http://www.medwirenews.com/39/91658/Stroke/Acute_statin_therapy_improves_survival_after_ischemic_stroke.html 

Rosuvastatin Reduces Neuroinflammation in the Hemorrhagic Transformation After rt-PA Treatment in a Mouse Model of Experimental Stroke

Dan Lu^1,2†, Yanfang Liu^1,2†, Hongcheng Mai^1,2, Jiankun Zang^1,2, Lingling Shen^1,2, Yusheng Zhang^1* and Anding Xu^1,2*

• ¹Department of Neurology and Stroke Center, The First Affiliated Hospital, Jinan University, Guangzhou, China
• ²Clinical Neuroscience Institute of Jinan University, Guangzhou, China

Hemorrhagic transformation (HT) is a serious complication that stimulates inflammation during reperfusion therapy after acute ischemic stroke. Rosuvastatin, a 3-hydroxymethyl-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, might improve the outcome of HT by inhibiting neuroinflammation. This study aimed to explore the protective effects of rosuvastatin against HT after recombinant tissue plasminogen activator (rt-PA) treatment in mice with experimental stroke via the attenuation of inflammation. A total of one hundred sixty-nine male BALB/c mice were used in the experiment. HT was successfully established in 70 mice that were subjected to 3 h of middle cerebral artery occlusion (MCAO) followed by a 10 mg/kg rt-PA injection over 10 min and reperfusion for 24 h. The mice were then administered rosuvastatin (1 mg/kg, 5 mg/kg) or saline (vehicle). The brain water content and neurological deficits (wire hang and adhesive removal somatosensory tests) were assessed at 24 h after rt-PA reperfusion following MCAO surgery. The morphology, blood-brain barrier (BBB) permeability and number of astrocytes and microglia were assessed by immunohistochemistry, electron microscopy and western blotting at 24 h after rt-PA reperfusion following MCAO surgery. Rosuvastatin protected against impaired neurological function and reversed the BBB leakage observed in the HT group. The increased activation of astrocytes and microglia and secretion of inflammatory factors caused by HT damage were significantly attenuated by high-dose rosuvastatin treatment vs. normal-dose rosuvastatin treatment. Related inflammatory pathways, such as the nuclear factor kappa B (NF-κB) and mitogen-activated protein kinase (MAPK) pathways, were downregulated in the rosuvastatin-treated groups compared with the HT group. In conclusion, our results indicate that rosuvastatin is a promising therapeutic agent for HT after rt-PA reperfusion following MCAO surgery in mice, as it attenuates neuroinflammation. Additionally, high-dose rosuvastatin treatment could have a greater anti-inflammatory effect on HT than normal-dose rosuvastatin treatment.

Introduction

Hemorrhagic transformation (HT) is a serious complication that occurs after acute ischemic stroke (Álvarez-Sabin et al., 2013; Wang et al., 2015). In clinical practice, after the administration of intravenous recombinant tissue plasminogen activator (IV-rt-PA) within the therapeutic window, the rate of type two parenchymal hemorrhage within 7 days is 6.8%, with a 90-day mortality rate as high as 17.9% (Emberson et al., 2014). Studies have shown that disturbances in the blood-brain barrier (BBB), which is composed mainly of endothelial cells, pericytes and astrocytes, occur throughout the process of HT (Kelly et al., 2006; Mishiro et al., 2012; Ozkul-Wermester et al., 2014). Emerging data have shown that the oxidative stress and overexpression and release of proinflammatory cytokines caused by rt-PA reperfusion are associated with BBB disruption (Wang et al., 2015). Furthermore, increasing studies in the literature have shown that inflammation related to the interaction between microglia and astrocytes but not astrocytes alone contributes to ischemia-induced HT and oedema (del Zoppo et al., 2012).

Statins, also known as 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors, are well known for having beneficial effects on vascular events by lowering cholesterol levels (Postmus et al., 2014) and are used as neuroprotectants in experimental brain ischemia (Spence, 2014). In vivo studies have shown that statins induce time- and concentration-dependent reductions in Aβ production, and the reduced production of Aβ has been attributed to reductions in neuroinflammation (Hosaka et al., 2013). One study has suggested that reduced chronic neuroinflammation might be a key mechanism underlying statin-induced neuroprotection (McFarland et al., 2014). Furthermore, statins play a protective role against neurodegenerative conditions, including vascular dementia, Alzheimer’s disease (AD) and Parkinson’s disease (PD; Mandas et al., 2014). However, whether statins protect against HT and the related mechanisms in mice have not been determined.

Rats who were treated with rosuvastatin (a synthetically derived statin) immediately post-spinal cord injury demonstrated reduced inflammatory cell infiltration, tumor necrosis factor alpha (TNF-α) expression, myeloperoxidase activity, nitric oxide levels and caspase-3 activity in caudal spinal cord tissue (Kahveci et al., 2014). Pretreatment with rosuvastatin significantly reduced lipopolysaccharide (LPS)-induced interleukin 1 beta (IL-1β) and TNF-α release (Kahveci et al., 2014). Because the protective effect of rosuvastatin relies on the modulation of several signaling transduction pathways, including the nuclear factor kappa B (NF-κB), phosphatidylinositol 3-kinase and protein kinase B (PI3K/Akt) and c-Jun N-terminal kinase (JNK) pathways (Li et al., 2015; Liu et al., 2017), determining the potential role played by rosuvastatin in neuroinflammation-related diseases is critical.

In this study, experiments were performed to demonstrate our hypothesis that rosuvastatin protects against HT in middle cerebral artery occlusion (MCAO) mice by attenuating inflammation.

Inhibition of Notch1 Signaling at the Subacute Stage of Stroke Promotes Endogenous Neurogenesis and Motor Recovery After Stroke

Sounds interesting. Now we just need to update the stroke strategy and followup with human clinical trials.  But that will never occur with our fucking failures of stroke associations along with NO stroke leadership and NO stroke strategy. Survivors are completely and totally fucking screwed until whatever passes for stroke leadership is replaced by stroke survivors.
https://www.frontiersin.org/articles/10.3389/fncel.2018.00245/full?

Xiao-Zhu Hao^1†, Le-Kang Yin^2†, Jia-Qi Tian¹, Chan-Chan Li¹, Xiao-Yuan Feng¹, Zhen-Wei Yao¹, Min Jiang³ and Yan-Mei Yang^1*

• ¹Department of Radiology, Huashan Hospital, Fudan University, Shanghai, China
• ²Department of Radiology, Shanghai Chest Hospital, Shanghai Jiaotong University, Shanghai, China
• ³Institutes of Brain Science and State Key Laboratory of Medical Neurobiology, Fudan University, Shanghai, China

Background and Purpose: It is still not clear whether Notch1 signaling inhibition can promote functional outcomes after stroke, given that it plays time-dependent roles in the sequential process of endogenous neurogenesis. The purpose of this study was to identify the appropriate time frame for Notch1 signaling inhibition according to the temporal evolution of Notch1 signaling activation and the responses of neural stem cells (NSCs), in order to target it for therapeutic intervention and stimulate neurorestorative strategies after stroke.

Methods: Sprague-Dawley (SD) rats were subjected to 90-min of middle cerebral artery occlusion (MCAO). Rats were sacrificed before, and at day 1, day 2, day 3, day 4, and day 7 after ischemia for immunohistochemical analysis of the Notch intracellular domain (NICD), Nestin and doublecortin (Dcx). Next, MCAO rats were treated with the γ-secretase inhibitor N-[N-(3,5-di uorophenacetyl)-1-alanyl]-S-phenylglycine t-butylester (DAPT) or with saline at day 4 after ischemia, and subsequently evaluated with behavioral test analysis and magnetic resonance imaging (MRI). The rat brains were then harvested for immunohistochemical analysis of Dcx, NeuN and myelin basic protein (MBP) at 2, 3, 4, and 8 weeks.

Results: Notch1 signaling was maximally activated at day 3 after ischemia in parallel with the temporal evolution of NSCs. Inhibiting Notch1 signaling at day 4 after reperfusion with DAPT further promoted recovery of MRI parameters of the corticospinal tract (CST) and the functional outcomes, concomitantly with an increase in neuroblasts, their migration to the ischemic boundary, and potential differentiation to mature neurons, as well as the amelioration of axonal bundle integrity.

Conclusion: Inhibition of Notch1 signaling at the subacute stage of stroke could maximally promote endogenous neurogenesis and axonal reorganization.

Introduction

Stroke is one of the leading causes of death and serious long-term disability (Stinear et al., 2007; Smajlović, 2015). Importantly, a large number of stroke patients are permanently disabled in that only a minority of patients can benefit from thrombolysis given its limited therapeutic time window. Novel neurorestorative therapies with a wider therapeutic window that can promote brain repair, are thus, urgently needed to enhance functional neurological recovery following stroke (Barone, 2010; Zhan et al., 2011). Previous studies have demonstrated that cerebral ischemia induces proliferation of NSCs in the SVZ, which migrate into the damaged brain regions, differentiate into mature neurons and ultimately integrate into local as well as remote neural circuits (Arvidsson et al., 2002; Zhang et al., 2008; Wang L. et al., 2009; Sun et al., 2013), suggesting that endogenous neurogenesis could be a target for rehabilitative therapy in stroke patients.

In recent years, Notch1 signaling, which is critical for endogenous neurogenesis, has been regarded as a potential therapeutic target for promoting functional recovery after stroke (Wei et al., 2011). Notch1 is expressed in NSCs and neuroblasts and its activity is fundamental for neural development as well as neural specification by controlling maintenance, proliferation and differentiation of NSCs in young and aged brain in normal or pathological conditions (Zhang et al., 2008; Wang X. et al., 2009; Sun et al., 2013). Interestingly, while some studies have found that Notch1 signaling activation could promote neurogenesis (Oya et al., 2009; Wang X. et al., 2009), others support the idea that Notch1 signaling negatively regulates neurogenesis (Li et al., 2012). Notably, preventing Notch1 cleavage into the Notch intracellular domain (NICD) with the γ-secretase inhibitor N-[N-(3,5-diuorophenacetyl)-1-alanyl]-S-phenylglycine t-butylester (DAPT), subsequently improves functional outcomes following stroke (Li et al., 2012). Except for differences in animal strain and stroke models, the most plausible explanation for the conflicting results cited above is the spatio-temporal regulation of Notch activity (Zhao et al., 2012); in other words, Notch-1 signaling playing space and time-dependent roles in the sequential process of neurogenesis (Chambers et al., 2001). Moreover, several studies have found that Notch-1 signaling was activated in the acute stage of stroke to promote NSCs proliferation and was attenuated in the subacute stage to promote neuronal differentiation (Oya et al., 2009; Wang L. et al., 2009). Based on this standpoint, the detection of the temporal evolution of Notch1 signaling activation following cerebral ischemia and attempts to timely control its activation are required to augment the neural progenitor pool and promote neural differentiation to attain morphological and functional maturity in the adult brain.

Furthermore, it appears unreasonable and insufficient to define the beneficial or detrimental effects of therapeutic interventions of the Notch1 pathway based on in vitro pathological examinations. Thus, it is important to develop non-invasive methods to monitor modifications of brain tissue and predict long-term motor outcomes, which is essential to promote clinical applications of emerging neurorestorative therapies. Cross-sectional studies have demonstrated that diffusion tensor imaging (DTI) could provide unparalleled insights into the microstructural properties of central nervous system (CNS) tissue (Nucifora et al., 2007; Budde and Frank, 2012). For instance, diffusion parameter changes in the CST have been established as surrogate makers of motor deficit after stroke (Thomalla et al., 2005; Stinear et al., 2007; Lindenberg et al., 2012; Feng et al., 2015).

In this study, firstly, we aimed to detect the temporal evolution of Notch1 signaling activation and NSCs responses after stroke. Based on our results, we then attempted to find the appropriate therapeutic time frame for DAPT treatment. More importantly, for the first time, we measured the comprehensive microstructure changes in the CNS with a set of MR parameters, combined with the post mortem immunohistochemical analysis of neurogenesis and remyelination of the CST, and ultimately demonstrated the neurorestorative effects of DAPT treatment at the subacute stage after stroke.

A novel robotic assistive device for hand stroke-rehabilitation

Well shit there are already robotic hands already out there, this is just a design. Hope you weren't hoping for kudos. Are you considering those like myself that have dead neurons in the hand control area?

Your doctor and stroke hospital can look at the intersection of these sets to see what they already should have been testing.

• hand (205)

• robotics (184)

A novel robotic assistive device for hand stroke-rehabilitation

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Author(s)

Alistair McConnell ; Xianwen Kong ; Patricia A Vargas

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Abstract:

This paper proposes a novel design of a robotic hand exoskeleton device (PMHand) for the purpose of aiding post stroke rehabilitation. The main effects of a stroke on the human hand and the current rehabilitation methods and their limitations are briefly reviewed. The design process and fabrication of a full hand exoskeleton, control system and preliminary experimental results are presented in detail.

Published in: The 23rd IEEE International Symposium on Robot and Human Interactive Communication

Date of Conference: 25-29 Aug. 2014

Date Added to IEEE Xplore: 20 October 2014

ISBN Information:

ISSN Information:

INSPEC Accession Number: 14695134

DOI: 10.1109/ROMAN.2014.6926370

Publisher: IEEE

Conference Location: Edinburgh, UK

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I. Introduction

The purpose of this work is to create a robot rehabilitation device that can be used to aid the recovery of stroke patients. The device aims to help patients recover normal patterns of motion in their hand after a stroke, and also to aid physiotherapists in tracking how the rehabilitation is progressing. The total number of stroke survivors in the UK at present is approximately 1.2 million, with more than half of these survivors suffering disabilities that affect their daily lives [1]. Every year an estimated 152,000 people in the UK have a stroke. Most of the rehabilitation available comes in the form of exercise with a physiotherapist; this requires either regular home visits from the physiotherapist, or the patient traveling to a hospital once a week for treatment. Once with the physiotherapist, several different exercises will be given to the patient. These will first be done with the aid of the physiotherapist, to ensure they are being performed correctly, and then the patient will be instructed to continue practicing on their own. This can lead to the problem of the patient not performing the exercises in the correct way, the recommended amount or potentially not at all. The other method of stroke rehabilitation is the use of specifically designed physiotherapy machines which are normally performed at the hospital or a clinic where the patient is supervised. This paper proposes a device that will both aid the patients rehabilitation and improve the way a physiotherapist interacts with them. The device will be of a light weight design, low cost, aesthetically friendly and it will ensure the exercises are performed correctly and the progress of each patient is recorded for the physiotherapist to analyse at a later data.

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Post-stroke rehabilitation training with cytoflavin: a clinical and neuropsychological study

Whatever the hell evoked potential is? 

Post-stroke rehabilitation training with cytoflavin: a clinical and neuropsychological study

(PMID:30132452)

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Shukin IA ¹ , 

Lebedeva AV ¹ , 

Soldatov MA ² , 

Fidler MC ²  

Affiliations

Zhurnal Nevrologii i Psikhiatrii Imeni S.S. Korsakova [01 Jan 2018, 118(7):25-29]

Type: Journal Article, English Abstract (lang: rus)
DOI: 10.17116/jnevro20181187125

Abstract

To evaluate the efficacy of cytoflavin in the treatment of patients with chronic cerebral ischemia and mild cognitive impairment predominantly of vascular origin.Treatment results of 140 patients, aged 60-74, with chronic cerebral ischemia were analyzed. The main group included 77 patients (35 men and 42 women of average age 66.38±4.64 years) who received cytoflavin throughout the observation period: 2 tablets twice a day 30 minutes before meals. The comparison group included 63 patients (26 men and 37 women of average age 67.48±5.22 years) who during the whole period of observation received ethyl methyl hydroxypyridine succinate: 2 tablets (250 mg) twice a day, according to the same scheme as in the main group. Treatment efficacy was assessed by neuropsychological testing and P300 evoked potentials.During treatment, there was an improvement in neurophysiological parameters in both groups, which was more pronounced in patients treated with cytoflavin: their P300 amplitude increased by1.3 times in the left hemisphere (from 9.21 (8.36, 10.11) to 12.41 (10.23, 13.37 μV) and 1,7 times in the right hemisphere (from 6.48 (5.26, 7.35) to 11.04 (9.29, 12.18) μV). Our study confirms the advisability of using drugs that have complex cytoprotective and energy-correcting mechanism in patients with cognitive impairment. Cytoflavin has shown the high efficacy and safety and can be recommended as part of complex therapy for cognitive disorders. Using simple and inexpensive instrumental methods (assessment of cognitive P300 evoked potential) along with diagnostic scales in patients with cognitive impairment can significantly objectify the assessment of treatment dynamics.

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Aerobic Training in Canadian Stroke Rehabilitation Programs

There is nothing here that suggests anything resembling a protocol for this. So a complete waste of time writing this up. Once again expecting stroke survivors to figure out their own rehabilitation therapy. Isn't that what your doctors and therapists are being paid for? Wrong, your doctors and therapists are being paid for meetings NOT RESULTS.  You as a survivor will continue to be screwed until we get survivor led leadership and a strategy.
https://europepmc.org/abstract/med/30138234

(PMID:30138234)

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Nathoo C ¹ , 

Buren S , 

El-Haddad R , 

Feldman K , 

Schroeder E , 

Brooks D , 

Inness EL , 

Marzolini S  

Affiliations

Journal of Neurologic Physical Therapy : JNPT [22 Aug 2018]

Type: Journal Article
DOI: 10.1097/NPT.0000000000000237

Abstract

Aerobic training (AT) is recommended for people after stroke, yet uptake and operationalization of AT in clinical practice in Canada have not been measured. We surveyed inclusion of structured AT and barriers to implementation in public inpatient/outpatient stroke rehabilitation programs across Canada.A Web-based questionnaire was sent to 89 stroke rehabilitation program leads.Forty-six programs from 7 of 9 eligible Canadian provinces/territories completed the questionnaire. Seventy-eight percent of programs reported including AT, with most (75%) excluding participants with severe physical impairments, and 28% excluding those with coexisting cardiac conditions. A greater proportion of dedicated stroke rehabilitation programs prescribed AT, compared to nondedicated stroke units (68.8% vs 31.3%, P = 0.02). The top 2 challenges for programs that included and did not include AT were "insufficient time within therapy sessions" and "length of stay in rehabilitation." Programs that did not include AT ranked "not a goal of most patients" and "not an organizational/program priority" as third and fourth, whereas they were ranked eighth and thirteenth by programs with AT. Best practice recommendations(Useless, this is not a protocol.) were inconsistently followed for conducting preparticipation exercise testing (36.1%) and for monitoring patients from higher-risk populations, specifically people with diabetes at risk for hypoglycemia (78.8%) and hypertension (36.6%). Of programs conducting preparticipation exercise testing, 91% did not monitor electrocardiography.Most stroke rehabilitation programs across Canada include AT. People with severe physical impairment and those with cardiac, metabolic, and hemodynamic comorbidities may be excluded or not appropriately monitored during exercise. More detailed guidelines and training practices are needed to address these challenges.Video Abstract available for more insights from the authors (see Video, Supplemental Digital Content 1, available at: http://links.lww.com/JNPT/A233).

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