Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Sunday, June 25, 2017

Markerless motion capture systems as training device in neurological rehabilitation: a systematic review of their use, application, target population and efficacy

It is impossible to even attempt to figure out any stroke rehab if you don't even have an objective measurement of what is wrong and can objectively see improvements. This is long overdue. Your therapists and doctors have been flying completely blind about stroke rehab since forever.

Markerless motion capture systems as training device in neurological rehabilitation: a systematic review of their use, application, target population and efficacy

  • Els KnippenbergEmail author,
  • Jonas Verbrugghe,
  • Ilse Lamers,
  • Steven Palmaers,
  • Annick Timmermans and
  • Annemie Spooren
Journal of NeuroEngineering and Rehabilitation201714:61
DOI: 10.1186/s12984-017-0270-x
Received: 26 August 2016
Accepted: 5 June 2017
Published: 24 June 2017



Abstract

Background

Client-centred task-oriented training is important in neurological rehabilitation but is time consuming and costly in clinical practice. The use of technology, especially motion capture systems (MCS) which are low cost and easy to apply in clinical practice, may be used to support this kind of training, but knowledge and evidence of their use for training is scarce. The present review aims to investigate 1) which motion capture systems are used as training devices in neurological rehabilitation, 2) how they are applied, 3) in which target population, 4) what the content of the training and 5) efficacy of training with MCS is.

Methods

A computerised systematic literature review was conducted in four databases (PubMed, Cinahl, Cochrane Database and IEEE). The following MeSH terms and key words were used: Motion, Movement, Detection, Capture, Kinect, Rehabilitation, Nervous System Diseases, Multiple Sclerosis, Stroke, Spinal Cord, Parkinson Disease, Cerebral Palsy and Traumatic Brain Injury. The Van Tulder’s Quality assessment was used to score the methodological quality of the selected studies. The descriptive analysis is reported by MCS, target population, training parameters and training efficacy.

Results

Eighteen studies were selected (mean Van Tulder score = 8.06 ± 3.67). Based on methodological quality, six studies were selected for analysis of training efficacy. Most commonly used MCS was Microsoft Kinect, training was mostly conducted in upper limb stroke rehabilitation. Training programs varied in intensity, frequency and content. None of the studies reported an individualised training program based on client-centred approach.

Conclusion

Motion capture systems are training devices with potential in neurological rehabilitation to increase the motivation during training and may assist improvement on one or more International Classification of Functioning, Disability and Health (ICF) levels. Although client-centred task-oriented training is important in neurological rehabilitation, the client-centred approach was not included. Future technological developments should take up the challenge to combine MCS with the principles of a client-centred task-oriented approach and prove efficacy using randomised controlled trials with long-term follow-up.

Trial registration

Prospero registration number 42016035582.

The Diagnosis and Management of Mild Cognitive Impairment

You will need this for your doctor to baseline your cognition.
http://jamanetwork.com/journals/jama/article-abstract/2040164

A Clinical Review

JAMA. 2014;312(23):2551-2561. doi:10.1001/jama.2014.13806
Importance  Cognitive decline is a common and feared aspect of aging. Mild cognitive impairment (MCI) is defined as the symptomatic predementia stage on the continuum of cognitive decline, characterized by objective impairment in cognition that is not severe enough to require help with usual activities of daily living.
Objective  To present evidence on the diagnosis, treatment, and prognosis of MCI and to provide physicians with an evidence-based framework for caring for older patients with MCI and their caregivers.
Evidence Acquisition  We searched PubMed for English-language articles in peer-reviewed journals and the Cochrane Library database from inception through July 2014. Relevant references from retrieved articles were also evaluated.
Findings  The prevalence of MCI in adults aged 65 years and older is 10% to 20%; risk increases with age and men appear to be at higher risk than women. In older patients with MCI, clinicians should consider depression, polypharmacy, and uncontrolled cardiovascular risk factors, all of which may increase risk for cognitive impairment and other negative outcomes. Currently, no medications have proven effective for MCI; treatments and interventions should be aimed at reducing cardiovascular risk factors and prevention of stroke. Aerobic exercise, mental activity, and social engagement may help decrease risk of further cognitive decline. Although patients with MCI are at greater risk for developing dementia compared with the general population, there is currently substantial variation in risk estimates (from <5% to 20% annual conversion rates), depending on the population studied. Current research targets improving early detection and treatment of MCI, particularly in patients at high risk for progression to dementia.
Conclusions and Relevance  Cognitive decline and MCI have important implications for patients and their families and will require that primary care clinicians be skilled in identifying and managing this common disorder as the number of older adults increases in coming decades. Current evidence supports aerobic exercise, mental activity, and cardiovascular risk factor control in patients with MCI.

Multivariate Analyses of Peripheral Blood Leukocyte Transcripts Distinguish Alzheimer’s, Parkinson’s, Control and Those at Risk for Developing Alzheimer’s

You'll want your doctor to follow this up with for your risk of getting dementia/Alzheimers
http://www.neurobiologyofaging.org/article/S0197-4580(17)30167-7/fulltext



Highlights

  • Peripheral blood leukocyte transcripts can be used as a prognostic marker of progression to the clinical stages of Alzheimer’s disease in unimpaired older adults.
  • Peripheral blood leukocyte transcripts distinguish Parkinson’s disease from Alzheimer’s disease.
  • Peripheral blood leukocyte transcripts distinguish cognitively resilient apoe4 homozygotes.
  • The same peripheral blood leukocyte transcripts used to distinguish probable Alzheimer’s disease in blood samples were also able to distinguish neuropathologically confirmed Alzheimer’s disease in brain samples.

Abstract

The need for a reliable, simple and inexpensive blood test for Alzheimer’s disease (AD) suitable for use in a primary care setting is widely recognized. This has led to a large number of publications describing blood tests for AD, which have, for the most part, not been replicable. We have chosen to examine transcripts expressed by the cellular, leukocyte compartment of blood. We have used hypothesis based cDNA arrays and quantitative PCR to quantify expression of selected sets of genes followed by multivariate analyses in multiple independent samples. Rather than one study with no replicates we chose an experimental design in which there were multiple replicates using different platforms and different sample populations. We have divided 177 blood and 27 brain samples into multiple replicates to demonstrate the ability to distinguish early clinical AD (CDR 0.5), Parkinson’s disease (PD), and cognitively unimpaired APOE4 homozygotes, as well as to determine persons at risk for future cognitive impairment with significant accuracy. We assess our methods in a training/test set and also show that the variables we use distinguish AD, PD and control brain. Importantly, we describe variability of the weights assigned to individual transcripts in multivariate analyses in repeated studies and suggest that the variability we describe may be the cause of inability to repeat many prior studies. Our data constitute a proof of principle that multivariate analysis of the transcriptome related to cell stress and inflammation of peripheral blood leukocytes has significant potential as a minimally invasive and inexpensive diagnostic tool for diagnosis and early detection of risk for AD.

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Designing for diversity: Atablet-based ePRO system to assist stroke rehabilitation

 Hopefully you can track this down yourself. 

Designing for diversity: Atablet-based ePRO system to assist stroke rehabilitation

Factors predicting falls and mobility outcomes in patients with stroke returning home after rehabilitation who are at risk of falling

It would be much better to come up with fall prevention protocols than this piece of laziness. 
http://www.archives-pmr.org/article/S0003-9993(17)30408-2/abstract
DOI:

Abstract





Objective

To identify factors predicting falls and limited mobility in people with stroke at 12 months after returning home from rehabilitation.




Design

Observational cohort study with 12 month follow-up.




Setting

Community.




Participants

People with stroke (n=144) and increased falls risk discharged home from rehabilitation.




Interventions

Not applicable.




Main Outcome Measures

Falls were measured using monthly calendars completed by participants, and mobility was assessed using gait speed over five metres (high mobility (>0.8m/s) versus low mobility (≤0.8m/s). Both measures were assessed at 12 months post-discharge. Demographics and functional measures including balance, strength, visual or spatial deficits, disability, physical activity level, executive function, functional independence and falls risk were analysed to determine factors significantly predicting falls and mobility levels after 12 months.




Results

Those assessed as being at high falls risk (Falls Risk for Older People in the Community (FROP-Com) score ≥19) were 4.5 times more likely to fall by 12 months (OR:4.506, 95% CI:1.71-11.86, p-value:0.002). Factors significantly associated with lower usual gait speed (<0.8m/s) at 12 months in the multivariable analysis were age (OR:1.07, 95% CI=1.01–1.14, p-value=0.033), physical activity (OR:1.09, 95% CI =1.03-1.17, p-value=0.007) and functional mobility (OR:0.83, 95% CI =0.75-0.93, p-value=0.001).




Conclusion

Several factors predicted falls and limited mobility for patients with stroke 12 months after rehabilitation discharge. These results suggest that clinicians should include assessment of falls risk (FROP-Com), physical activity, and dual task Timed Up and Go during rehabilitation to identify those most at risk of falling and experiencing limited mobility outcomes at 12 months, and target these areas during in-patient and out-patient rehabilitation to optimise long term outcomes.

Neuroplasticity and functional recovery after intensive language therapy in chronic post stroke aphasia: Which factors are relevant?

Maybe you can get something out of this since no one seems to want to  make this useable to stroke survivors that need it.  On your own once again.
http://journal.frontiersin.org/article/10.3389/fnhum.2017.00332/full
  • 1Department of Psychiatry, Campus Benjamin Franklin, Charite University Medical School, Germany
The relevance of neuroscience-based treatment for post stroke aphasia

Neuroscience-based interventions for aphasia are among the most promising approaches towards successful language rehabilitation. Associated therapeutic techniques are highly effective in reducing cognitive-behavioural difficulties resulting from brain damage and can induce neuroplasticity (Taub et al., 2002; Berthier & Pulvermüller, 2011). However, it is still not clear how language recovery and reorganisation of language is reflected by functional changes manifest in human brain activity. In aphasia research, previous studies addressed the role of the left (LH) and right (RH) hemisphere across the entire recovery phase. It has been suggested that brain reorganization in aphasia is a dynamic process, in which the involvement of perilesional LH regions and RH areas (e.g. Broca-homologue or RH superior temporal cortex, Musso et al., 1999) is dependent on the specific phase of language recovery (Saur et al., 2006). These data highlight the importance to control for time post stroke when investigating treatment-related changes to avoid the influence of spontaneous remission.
To date, only few studies have addressed therapy-induced neuroplasticity in patients with post stroke aphasia (PSA), and findings are rather inconsistent. The reasons for the heterogeneity of previous results may be attributed to patient-specific variables such as lesion size and site, symptom severity, etc. (Crosson et al., 2005). While patient-specific variables seem to influence functional recovery, the specific impact of non-patient factors (e.g. neuroimaging method, language task, therapy method, - intensity, - amount and – duration) has rarely been addressed. However, to maximize therapy outcome, it is important to systematically investigate all possible factors and to identify neurophysiological predictors of recovery. Focussing on intensive, clinically effective, and short-term interventions and on suitable language tasks seems promising to achieve this goal.

Understanding the neuronal mechanisms underlying language recovery by studying treatment-induced changes

Measuring neuronal correlates of good (or poor) language recovery could help to identify patients who might benefit (or not) from a specific therapeutic method and can contribute to the development of effective neuroscience-based neurorehabilitation techniques. The study of therapy-induced neuroplasticity in PSA offers the possibility to systematically control for potentially confounding variables while at the same time measuring behavioural and neuronal changes following speech and language therapy (SLT) within a reasonable time frame. Previous findings do not allow to determine whether any behavioural or neurophysiological changes were caused by a specific therapeutic technique or by other factors. This differentiation is only possible by randomized controlled trials (RCTs) with chronic patients (> 1 year post stroke), for whom spontaneous remission effects can be excluded. Only RCTs with at least two active treatment groups and a no-treatment waiting-list group will ultimately allow to determine the specificity and amount of therapy-induced changes. Additionally, multiple pre-, and post-therapy scanning sessions will help to control for repeated scanning effects (Fridriksson et al., 2006). Although none of the clinical RCTs conducted in chronic aphasia comprised measurement of brain correlates before and after therapy, a promising heuristic is provided by efficient intensive interventions in chronic PSA patients. In fact, some intensive interventions have proved to lead to significant and consistent improvements of language performance (Brady et al., 2016; Breitenstein et al., 2017) and may therefore be good candidates to study neuroplasticity.

Neuroplasticity after intensive aphasia treatment methods

Within a short period of time (for example < 4 weeks), spontaneous, non-therapy-related neuronal changes are highly unlikely in chronic patients, therefore, one can interpret any changes in behaviour and brain activity across short-term intervals as treatment-induced. While intensive training can lead to such changes already within days or weeks (see Berthier & Pulvermüller, 2011), these effects are unlikely for non-intensive methods. In fact, several RCTs demonstrated higher efficacy of intensive SLT compared to non-intensive treatment (Brady et al., 2016). Although it is not entirely clear yet, which treatment intensity and duration is required to induce optimal recovery, meta-analyses suggest a minimum of 1-2 hours a day over a period of 2-4 weeks (Bhogal et al., 2003). This therapy frequency might be regarded as intensive treatment.
The efficacy of intensive therapies can be explained by neuroscientific principles of learning and memory: high intensity and massed practice facilitates and enhances learning and cortical plasticity by correlated neuronal activity and by strengthening of synaptic contacts between neurons (Berthier and Pulvermüller, 2011). From this perspective, any intensive cognitive-behavioural intervention can maximize the effects of training-induced brain plasticity, which is ultimately a consequence of effective learning. Similarly, multiple repetitions of stimuli or tasks applied during language training, as well as the imitation of language skills modelled by language therapists will enhance learning and re-structuring of residual language networks. However, it should be noted that intensity, repetition, or inter-individual patient characteristics are not the only factors impacting on learning and language recovery. For example, a recent cross-over RCT demonstrated a significant influence of the therapy method used: Communicative-pragmatic and behaviourally relevant language training in social interactions resulted in significantly better recovery than equally intensive conventional exercises such as naming and describing pictures (Stahl et al., 2016). The importance of behavioural relevance and effective neurorehabilitation techniques for functional outcome has also been suggested in the context of motor deficits caused by stroke (e.g. Taub et al., 2002). Behaviourally relevant therapeutic methods delivered at high intensity could provide an avenue towards effective treatment in chronic PSA and may help to increase motivation, engagement and compliance of patients.

Neuroplastic changes in the left and right hemisphere following intensive short-term aphasia therapy

A recent review (Crinion & Leff, 2015) of neuroplastic changes following therapy in PSA patients, reported consistent treatment-related brain activation changes in LH perilesional fronto-temporal regions and/or in the inferior frontal gyrus in the RH. Unfortunately, due to the heterogeneity of patient and non-patient variables in these intervention studies, it is difficult to draw any concise conclusions about the neuronal mechanisms underlying language recovery. Several factors might explain this variability of previous findings and could be relevant for interpreting treatment-related data and for identifying predictors of recovery. These factors include the phase of PSA (see Saur et al., 2006), symptom severity (Lazar et al., 2010), or education and cognitive reserve (Hillis & Tippett, 2014). Also, the degree of premorbid functional lateralization of language could influence functional recovery (Knecht et al., 2002), as well the type of aphasia. Interestingly, language recovery does not seem to be driven by lesion size (Mattioli et al., 2014), but more likely by lesion location and load: For example, the structural integrity of subcortical white matter tracts (i.e. the arcuate fasciculus, Marchina et al., 2011) and specific left hemispheric cortical regions have been identified to influence recovery (Fridriksson, 2010; Bonilha et al., 2016). Moreover, non-patient related factors (e.g. therapy method, intensity, and language task used during neuroimaging) may strongly influence recovery. By focusing on intensive and effective interventions with chronic patients, the number of potential confounds of previous research might be diminished. To date, very few studies on neuroplastic changes following intensive, successful SLT have been published. These studies will be focused on now: Intensive aphasia therapy (a minimum of 1-2h/d, for at least two weeks, Bhogal et al., 2003) combined with functional or structural neuroimaging in chronic PSA patients has been reported for three different methods. The first method, Constraint-Induced Aphasia Therapy (CIAT, Pulvermüller et al., 2001), also called Intensive Language Action Therapy (ILAT, Difrancesco et al., 2012) is one of the most researched SLTs and its clinical effectiveness has been demonstrated in several RCTs (Pulvermüller et al., 2001; Meinzer et al., 2005; Berthier et al., 2009; Stahl et al., 2016). The other two intensive therapy regimes, anomia treatment (Bonilha et al., 2016) and melodic intonation therapy (MIT, Schlaug et al., 2009) have shown to be effective, as evidenced by group studies or case series.
CIAT/ILAT-induced changes in brain activation following two weeks of intensive training (3h/d) were observed using various neuroimaging methods and language tasks. A significant body of data was obtained with EEG and MEG and language tasks applied comprised lexical decisions (Pulvermüller et al., 2005), passive reading of words (Barbancho et al., 2015) and an auditory passive listening mismatch negativity (MMN, Näätänen et al., 1997) design (Mohr et al., 2016; Lucchese et al., 2016). The source estimates performed on EEG lexical decision data suggested activation changes in right-frontal and left-temporoparietal areas correlating with clinical language improvements (Pulvermüller et al., 2005). In an fMRI study, pre-post-therapy changes in neurometabolic brain activation brought about by ILAT were reported in RH frontotemporal areas when patients were auditorily processing complex and semantically ambiguous sentences (Mohr et al., 2014). A previous fMRI study (Meinzer et al., 2008) found ILAT-induced metabolic changes in LH perilesional areas during an overt naming task. Similarly, in an MEG study, ILAT led to enhancement of LH perilesional neuromagnetic activity evoked by words presented in a passive auditory MMN paradigm and which correlated with clinical improvements (Mohr et al., 2016).
Although these intensive short-term studies were not RCTs, the results of several of them can be interpreted, because significant correlations between clinical language improvement and brain activation changes were found. As this therapy method uses communicative-pragmatic language training, involvement of residual language regions and neuroplasticity in both hemispheres can be assumed. Still, the diversity of results across studies of ILAT shows that the language task and stimulus type might be important factors that could influence the topography of neuroplastic changes.
While bi-hemispheric neural recruitment and improvements of naming had previously been reported in short-term, intensive anomia treatment for trained items only (Fridriksson et al., 2006), recent studies found improved naming, and thus generalization effects, also for untrained items (Fridriksson et al., 2012). However, as this treatment method specifically focuses on naming, changes in other language domains were not reported. Neuroplastic changes following anomia treatment showed an increase of brain activation during picture naming which was observed in fronto-temporal LH perilesional areas with fMRI (Fridriksson et al., 2012). These activity changes across the two weeks of intensive training (also 3h/d) correlated with improvements in naming performance, which were associated with intact functional connections between preserved cortical areas of the language network that were responsive to therapy (Bonhila et al, 2016). Anomia therapy involves training of overt naming of concrete objects depicted on cards by using either semantic or phonological cueing and thus, focuses on one specific aspect of aphasia, namely anomia and linguistic naming excercises, but does not emphasise behavioural relevance or communicative use of language. Consequently, training-induced neuroplasticity may specifically tap into left-hemispheric residual language networks associated with the abilitiy to name objects.
Using structural DTI before and after intensive melodic intonation therapy (MIT), an increase in fibre density and volume of the arcuate fasciculus in the RH was reported (Schlaug et al., 2009). However, as no correlation was found between language improvement and structural brain changes after therapy, it is difficult to interpret these structural data. Interestingly, in another study by this group, improvements in speech production after MIT correlated with structural changes in right hemisphere inferior frontal gyrus in patients with Broca’s aphasia (Wan et al., 2014). Language improvement in spontaneous speech and re-structuring of the language system in the RH after MIT could be driven by aspects of this therapy method which possibly involve right-hemisphere dominant cognitive and motor functions such as melodic intonation, rhythm, and left hand tapping (Schlaug et al., 2009). It should be noted though, that while treatment intensity and duration in ILAT/CIAT and anomia treatment studies were completely identical (3 h/d for 2 weeks), MIT was applied less intensively (1.5 h/d), but with longer duration (~ 16 weeks), resulting in approximately three times higher amounts of overall treatment for MIT than for the other two therapies.
Overall, evidence suggests that intensive aphasia treatment in chronic PSA leads to reorganisation of the functional and structural language network in both hemispheres. The involvement of each hemisphere in neuroplasticity is probably independent from the neuroimaging method used, but may be strongly influenced by the therapy method, its intensity, duration and the language materials and tasks.

More at link.

Optimal transcranial direct current stimulation polarity for enhancing motor recovery from severe post-stroke hemiparesis

If it enhances outcomes write up a fucking stroke protocol.  A great stroke association president would make sure all stroke research with positive outcomes would be written up in a publicly available stroke protocol. Otherwise this research is just wasted.
http://www.brainstimjrnl.com/article/S1935-861X(17)30738-6/abstract
Abstract #76
First page of article
Transcranial direct current stimulation (tDCS) has been shown to enhance outcomes of motor training for subjects with mild to moderate post-stroke motor deficit. To determine which tDCS configuration optimizes motor training in cases of severe post-stroke hemiparesis (≤ 19 out of 60, Fugl-Meyer Assessment (FMA) upper extremity motor score), this study randomized 26 subjects to 1 of 4 conditions: 1) “anodal” (anodal tDCS to the ipsilesional motor cortex); 2) “cathodal” (cathodal tDCS to the contralesional motor cortex); 3) “dual” (anodal tDCS to the ipsilesional motor cortex and cathodal tDCS to the contralesional motor cortex); or 4) “sham” tDCS.

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Stroke research: almost three times as many patients could be disability-free in future

That as a goal is pathetic, 100% recovery for all is the only goal. Quit being lazy.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=176726&CultureCode=en
24 June 2017 B&K Kommunikation
Virtually no other disease has seen such massive strides in treatment in recent years as stroke.(Really? I don't see much in actual results) Recent studies have confirmed that it is still possible to mechanically remove large vessel occlusions in the brain many hours after a stroke occurs. At the European Academy of Neurology Congress in Amsterdam, experts expressed optimism that the proportion of patients with lives free of serious disability after a major stroke could be increased by 270 per cent.
“The past few years have brought about greater advances in the treatment of stroke than the two previous decades,” said Prof Urs Fischer, Secretary General of the European Stroke Organisation (ESO) and stroke expert at the University of Bern’s Department of Neurology, summarising the latest developments. Advances in stroke therapy were one of the key focuses at the 3rd Congress of the European Academy of Neurology in Amsterdam. “The introduction of endovascular therapy means that we can now treat patients with large vessel occlusions, and the latest research findings show that we will be in a position to save far more stroke patients in future and spare them from serious lifetime disability.”
Stroke is the second most common cause of death worldwide
Stroke is already being talked about as the epidemic of the twenty first century. Around one fifth of all women and one sixth of men worldwide have a stroke at some point in their life. More than one in ten deaths are attributable to stroke, making this cerebrovascular condition the second-largest cause of death in the world. Stroke is also the second most frequent cause of lifetime and serious disability.
Large vessel occlusions also removable
A major milestone came 15 years ago when intravenous thrombolysis was first introduced. Under this procedure, stroke-causing blood clots in vessels of the brain are dissolved using medicine. The drawback of this method is that in around 10 to 20 per cent of cases the occlusions are so large that the treatment does not work sufficiently. A mechanical alternative has been available for a number of years now: endovascular thrombectomy involves removing a clot from a blood vessel in the brain using a catheter inserted via the groin. Prof Fischer: “The clinical effects of these acute stroke treatments are often striking. Patients who are admitted to hospital with serious neurological deficits show signs of improvement immediately after recanalisation. A number of them are even well enough to be discharged after just a few days.” The effectiveness of this method is now well documented: “Eight studies unanimously show that endovascular treatment of patients with acute occlusions of large vessels in the brain is superior to treatment with medication only,” Prof Fischer said.
New data: thrombectomy also helps more than six hours after stroke
Although the number of treatments of this kind is increasing all the time, this pioneering approach currently only benefits a few per cent of patients. One reason is that experts previously believed that mechanical clot removal was only possible within six hours of a stroke. The recently unveiled results of the DAWN study disproved this assumption: 48.6 per cent of patients survived without serious disability when they received a thrombectomy and thrombolysis as a combined treatment for a stroke event that had taken place more than six hours earlier. In the control group with medical management alone, just 13.1 per cent had no complications. “This means a relative reduction in disability of 73 per cent,” Prof Fischer summarised. “These new insights may enable us to increase the number of patients able to lead an independent, disability-free life by up to 270 per cent.”
Major variances in care provision in Europe
“We can only harness the full potential of this option if we adapt structures and processes for stroke care to reflect the latest findings,” explained EAN President-elect Prof Franz Fazekas from Austria’s University Hospital Graz. This is why EAN teamed up with five other medical societies last year to publish guidelines on the use of thrombectomy, which define all of the organisational and personnel requirements from selecting suitable instruments to post-operative care. “A pan-European study conducted by ESO, ESMINT and SAFE together with the EAN showed that provision of care is still unsatisfactory in some parts of Europe when it comes to thrombolysis and thrombectomy,” said Prof Fazekas. “Several European countries are not sufficiently equipped for this latest treatment breakthrough.”
In many cases, patients are denied access to the latest neurological innovations because hospitals do not have stroke units or sufficiently trained staff. “But where a person lives should not dictate whether they receive optimal treatment following such a common and serious event as a stroke,” Prof Fazekas added. “EAN will do everything it can to eliminate these differences as quickly as possible. To achieve this we will work very closely with all of the organisations involved in stroke research and stroke care, just as we did when drawing up the survey and the thrombectomy guidelines.”
Need for improvement also in countries where treatment is good
Even countries with highly developed stroke infrastructure still have room for improvement. This question is discussed in a new report by the European Brain Council, “The Value of Treatment for Brain Disorders”. This publication focuses on unmet needs and treatment gaps in neurology.
In many cases, too much time passes between the stroke event and the start of treatment. “Reducing the symptom-to-needle time is a central aspect of improving patient prognoses,” noted Prof Fazekas. “Sadly, many patients wait far too long before calling the emergency services, despite all the campaigns designed to increase awareness. It is particularly regrettable since the time that elapses before treatment starts can determine whether the patient is left disabled or goes on to live an independent life.”
As the expert confirms, there is still room for improvement within the individual treatment centres. According to the guidelines in place in the majority of European countries, no more than an hour should pass between the arrival of the patient and the start of treatment. Prof Fazekas: “Even 15 years after the effectiveness of intravenous thrombolysis was proven, the door-to-needle time for many patients still exceeds 60 minutes.”
Sources: Clinical Mismatch in the Triage of Wake Up and Late Presenting Strokes Undergoing Neurointervention With Trevo (DAWN), ClinicalTrials.gov Identifier: NCT02142283; Aguiar de Sousa et al. ESO ESMINT EAN SAFE Survey On Acute Endovascular Stroke Care In Europe, Abstract ESOC 2017

Parkinson’s disease: early detection crucial, new therapy approaches on the horizon

You need to know about this and your doctor should be up-to-date on how to prevent Parkinsons.

Parkinson’s Disease May Have Link to Stroke


Parkinson’s disease: early detection crucial, new therapy approaches on the horizon

24 June 2017 B&K Kommunikation
Detecting Parkinson’s disease before non-reversible symptoms occur: New approaches to early detection are meant to ensure just that. They are based on detection of alpha-synuclein in the skin or intestines. New therapy approaches such as a potential “vaccination” could improve the prognosis of affected individuals in future. Prof Günther Deuschl, President of the European Academy of Neurology (EAN), summarized the latest findings in research on Parkinson’s’ disease.
New findings on the early detection and treatment of Parkinson’s disease are being discussed at the 3rd Congress of the European Academy of Neurology (EAN) in Amsterdam. “We are getting closer to the big goal of being able to detect Parkinson’s disease at a very early stage,” said EAN President Prof Dr Günther Deuschl from University Hospital Schleswig-Holstein in Kiel. The diagnosis of Parkinson’s disease is difficult particularly in the early phase of the disease (prodromal stage). Although complaints such as sleep disorders, loss of smell, bouts of depression or digestive disorders have been identified as possible early signs of Parkinson’s disease, diagnosis today cannot be carried out with greater certainty until the typical movement disorders manifest themselves, such as tremors and slow, stiff movements. These symptoms are preceded by years of nerve cells dying off.  About 80 per cent of the dopaminergic nerve endings and as many as 50 per cent of the nerve cells in the substantia nigra area of the brain are already destroyed by that stage. A therapy capable of stopping the disease from taking its course is no longer possible at that point in time. The pathological hallmark of Parkinson’s disease is the deposit of pathologic alpha-synuclein in cells of the nervous system.
Early detection with biopsies
Different research groups have reported biopsies of the skin (Donadio et al., 2016), submandibular glands (Adler et al., 2016, Vilas et al., 2016) and colon biopsies (Schneider et al., 2016) showing such alpha synuclein at a very early stage of Parkinson’s disease.  A further major success in early detection was reported recently (Doppler et al., 2017): Pathologic alpha synuclein was demonstrated in REM-sleep behavioural disorder, a condition which leads in about 85 per cent of the sufferers to Parkinson’s disease with the aid of a skin test – and thus, this is many years before the onset of the typical movement disorders. The skin biopsy requires taking only a five millimetre large sample. Detection of pathological deposits of the protein alpha-synuclein in the fine nerve endings of the skin indicates the genesis of the disease.
It has long been known that a high percentage of people suffering from REM sleep behaviour disorders entailing aggressive dreams and violent movements while sleeping will contract Parkinson’s within 15 to 20 years. The study has now been able to identify the biomarker alpha-synuclein in the skin of these patients at risk. Alpha-synuclein is also found in healthy individuals but is present in pathological clumped form in Parkinson’s patients. That results in a malfunction of cell metabolism and ultimately in the degeneration of nerve cells. Prof Deuschl: “The method has great potential for identifying patients for Parkinson’s prevention studies and for winning them over to take part in clinical studies to test disease-modifying medications.” In future, this diagnostic marker should be able to detect Parkinson’s disease at an early stage also in individuals who do not have REM sleep behaviour disorders.
Biomarkers detectable in intestines and salivary glands
However, this is not the only early detection method that is currently the subject of intensive research. Pathologic alpha-synuclein aggregations also form in the enteric nervous system, which consists of the myenteric plexus between the muscle layers of the intestinal wall and the submucous plexus. The protein accumulations in this area cannot be viewed automatically as diagnosis criterion for Parkinson’s disease, however, because they also occur in healthy individuals. Prof Deuschl: “But if aggregations exhibit certain patterns, we can distinguish Parkinson’s patients from healthy individuals with a refined morphometric analysis. Nonetheless, further studies are needed to prove that Parkinson’s can be diagnosed by means of gastrointestinal biopsies.” A Spanish study was also able to prove that alpha-synuclein deposits are detectable by means of a needle biopsy also in the submandibular salivary glands in patients with REM sleep behaviour disorders and thus with early signs of Parkinson’s.
New therapies for mitigation of symptoms
New therapeutic approaches rely on treating the disease already in its early stages and stopping nerve cells in the brain from dying off. In recent years, experts have gained an ever better understanding of how Parkinson’s originates and how it spreads. Prof Deuschl: “Today we know that nerve cells sick from Parkinson’s disease can ‘infect’ other nerve cells in a manner similar to prion diseases. The disease gradually spreads in this way throughout the entire nervous system.” New therapy approaches are being developed based on this finding. Studies pursue the goal developing a “vaccine” against Parkinson’s disease and rely on two different strategies in these efforts: Either stimulate the immune system to generate antibodies against alpha-synuclein or administer synthetic antibodies.
Another new therapy approach relies on binding larger quantities of iron. That is because oxidative stress in the cells also contributes to the development of Parkinson’s disease. This in turn is caused by excessive amounts of iron in certain regions of the brain, which accelerate the demise of the cells.
New definition of diagnostic criteria
One important advance in the early detection of Parkinson’s disease is the new definition of diagnostic criteria for the prodromal stage, during which the classic diagnosis based on motor symptoms is not yet possible. To this end, the Movement Disorder Society drew on clinical studies and statistical studies to create a criteria list that is meant to standardise the clinical research and to facilitate diagnosis in the very early stage (Berg et al., 2015). Prof Deuschl: “The new system for assessing the risk of Parkinson’s disease consists of the age of the patient, environmental triggers such as smoking or caffeine consumption, genetic factors, the results of biomarker tests or prodromal symptoms such as constipation and loss of smell. This system can be expanded at any time if new tests are added for early detection – such as skin biopsies for example.”
Parkinson’s disease is second only to Alzheimer’s as the most frequent neurodegenerative disease of the central nervous system. Parkinson’s affects about two per cent of the population over age 65 and is one of the most common neurodegenerative diseases throughout Europe with 1.2 million people suffering from it. Estimates indicate that the number of cases might at least double by 2030 due to ever longer life expectancy figures.
Sources: Adler CH, Dugger BN, Hentz JG, Hinni ML, Lott DG, Driver-Dunckley E, et al. Peripheral Synucleinopathy in Early Parkinson's Disease: Submandibular Gland Needle Biopsy Findings. Mov Disord. 2016 Feb;31(2):250-6. Berg D, Postuma RB, Adler CH, Bloem BR, Chan P, Dubois B, et al. MDS research criteria for prodromal Parkinson's disease. Mov Disord. 2015 Oct;30(12):1600-11. Donadio V, Incensi A, Piccinini C, Cortelli P, Giannoccaro MP, Baruzzi A, et al. Skin nerve misfolded alpha-synuclein in pure autonomic failure and Parkinson disease. Ann Neurol. 2016 Feb;79(2):306-16. Doppler K, Jentschke HM, Schulmeyer L, Vadasz D, Janzen A, Luster M, et al. Dermal phospho-alpha-synuclein deposits confirm REM sleep behaviour disorder as prodromal Parkinson's disease. Acta Neuropathol. 2017 Apr;133(4):535-45. Schneider SA, Boettner M, Alexoudi A, Zorenkov D, Deuschl G, Wedel T. Can we use peripheral tissue biopsies to diagnose Parkinson's disease? A review of the literature. Eur J Neurol. 2016 Feb;23(2):247-61. Vilas D, Iranzo A, Tolosa E, Aldecoa I, Berenguer J, Vilaseca I, et al. Assessment of alpha-synuclein in submandibular glands of patients with idiopathic rapid-eye-movement sleep behaviour disorder: a case-control study. Lancet Neurol. 2016 Jun;15(7):708-18.

Genetic Variation and Neuroplasticity: Role in Rehabilitation After Stroke

Stop with trying to predict stroke recovery and do something fucking useful for survivors. Research how to get to 100% recovery you blithering lazy idiots. 
https://www.ncbi.nlm.nih.gov/pubmed/28628592

Abstract

BACKGROUND AND PURPOSE:

In many neurologic diagnoses, significant interindividual variability exists in the outcomes of rehabilitation. One factor that may impact response to rehabilitation interventions is genetic variation. Genetic variation refers to the presence of differences in the DNA sequence among individuals in a population. Genetic polymorphisms are variations that occur relatively commonly and, while not disease-causing, can impact the function of biological systems. The purpose of this article is to describe genetic polymorphisms that may impact neuroplasticity, motor learning, and recovery after stroke.

SUMMARY OF KEY POINTS:

Genetic polymorphisms for brain-derived neurotrophic factor (BDNF), dopamine, and apolipoprotein E have been shown to impact neuroplasticity and motor learning. Rehabilitation interventions that rely on the molecular and cellular pathways of these factors may be impacted by the presence of the polymorphism. For example, it has been hypothesized that individuals with the BDNF polymorphism may show a decreased response to neuroplasticity-based interventions, decreased rate of learning, and overall less recovery after stroke. However, research to date has been limited and additional work is needed to fully understand the role of genetic variation in learning and recovery.

RECOMMENDATIONS FOR CLINICAL PRACTICE:

Genetic polymorphisms should be considered as possible predictors or covariates in studies that investigate neuroplasticity, motor learning, or motor recovery after stroke. Future predictive models of stroke recovery will likely include a combination of genetic factors and other traditional factors (eg, age, lesion type, corticospinal tract integrity) to determine an individual's expected response to a specific rehabilitation intervention.
PMID:
28628592
PMCID:
PMC5477674
[Available on 2018-07-01]
DOI:
10.1097/NPT.0000000000000180

Feasibility and efficacy of wearable devices for upper limb rehabilitation in patients with chronic stroke: a randomized controlled pilot study

It is impossible to even attempt to figure out upper limb rehab if you don't even have an objective measurement of what is wrong and can objectively see improvements. This is long overdue. Your therapists and doctors have been flying completely blind about stroke rehab since forever.

Feasibility and efficacy of wearable devices for upper limb rehabilitation in patients with chronic stroke: a randomized controlled pilot study

Saturday, June 24, 2017

North Oaks Medical Center celebrates recertification as Primary Stroke Center - Hammond, LA

Who the hell cares about 'care' We want to know results you lazy fucking idiots.
1. Nothing on 100% recovery statistics.
2. Nothing on 30-day deaths compared to other hospitals.
3. Nothing on the efficacy of their stroke rehab protocols.
4.  Nothing on tPA full efficacy.
5. Nothing on their misdiagnosis percentage of strokes, especially young strokes.
Guidelines prove nothing.
You'll' want to know results so Call that hospital president(




Michele Kidd Sutton, FACHE

general number  (985) 345-2700  and demand to know what the RESULTS are; tPA efficacy, 30 day deaths, 100% recovery, misdiagnosis percentage.
Big fucking whoopee.


The puffery article here:
http://www.theadvocate.com/baton_rouge/news/communities/livingston_tangipahoa/article_bd327c2a-47d9-11e7-ac92-ef1f9ceb390b.html
In conjunction with National Stroke Awareness Month, the North Oaks Medical Center team in Hammond recently celebrated the hospital’s recertification as a Primary Stroke Center by The Joint Commission.
With recertification, the hospital has earned the Joint Commission’s Gold Seal of Approval, as well as the American Heart Association/American Stroke Association’s Heart-Check mark, for using the best practices in providing prompt stroke intervention and care and for improving patient outcomes, according to a news release.
“North Oaks Medical Center has thoroughly demonstrated the greatest level of commitment to the care of stroke patients through its recertification as a Primary Stroke Center,” comments Patrick Phelan, who is executive director of hospital business development for The Joint Commission.
“We congratulate North Oaks Medical Center for achieving this designation,” adds Nancy Brown, chief executive officer of the American Heart Association/American Stroke Association. “By adhering to this very specific set of treatment guidelines, North Oaks has clearly made it a priority to deliver high quality care to all patients affected by stroke.”(Not results!)

Strokes are the No. 4 cause of death in Louisiana, according to the American Heart Association/American Stroke Association. On average in the U.S., someone suffers a stroke every 40 seconds; someone dies of a stroke every 4 minutes; and 795,000 people suffer a new or recurrent stroke each year.
For more information, call North Oaks public relations at (985) 230-6647. For more information about the Stroke Support Group of Hammond, call Dr. Meghan Savage at (985) 230-2346.

So what is so remarkable about neurology anyway?

You'll have to ask your doctor what is in the neurologist stroke checklist.

So what is so remarkable about neurology anyway?

Fluidity of the dietary fatty acid profile and risk of coronary heart disease and ischemic stroke: results from the EPIC-Netherlands cohort study

No clue how to use this, insider and big words were used to confuse the layperson.
http://www.nmcd-journal.com/article/S0939-4753(17)30129-1/fulltext?rss=yes

Highlights

  • This is the first study that investigated whether diets high in fluid fatty acids, either in relative terms (i.e. diets with a low lipophilic index, LI), or in combination with the quantity of fatty acids consumed (lipophilic load, LL), relate to the risk of cardiovascular disease among a European population.
  • In a Dutch population that typically consumes diets high in saturated fatty acids and low in polyunsaturated fatty acids, neither the overall fluidity of the dietary fatty acids consumed (LI), nor the combination of overall fluidity and amount of the dietary fatty acids consumed (LL) related to future risk of CHD or ischemic stroke.
  • Dietary LI and LL calculated in observational studies may have limited added value above original fatty acid classes and food sources in establishing the relation of fatty acid consumption with CVD.

Abstract


Background and aims

The fluidity of dietary fatty acids consumed has been suggested to inversely affect coronary heart disease (CHD) risk. Lipophilic index (LI) represents overall fluidity of the dietary fatty acid profile. Lipophilic load (LL) represents a combination of overall fluidity and absolute intake of dietary fatty acids. We investigated the relations of dietary LI and LL with risk of CHD and ischemic stroke (iStroke).

Methods and results

We used data from the prospective EPIC-NL study, including 36,520 participants aged 20-70 years. LI and LL were calculated using dietary intake data estimated with a validated FFQ. Incident CHD (n=2348) and iStroke (n=479) cases were obtained through linkage to national registers during 15 years follow-up. LI and LL were not associated with CHD risk (HRshighest-versus-lowest-quartiles : 0.93 [95%CI: 0.83, 1.04], and 0.92 [95%CI: 0.79, 1.07], respectively), and neither with iStroke risk (HRs 1.15 (95%CI: 0.89, 1.48), and 0.98 (95%CI: 0.70, 1.38), respectively). Original fatty acid classes (SFA, MUFA and PUFA), and LI and LL stratified by these fatty acid classes, were overall not related to CHD and ischemic stroke either.

Conclusions

In this Dutch population, neither the overall fluidity of the dietary fatty acid profile (LI), nor the combined fluidity and amount of fatty acids consumed (LL) were related to CHD or iStroke risk. Dietary LI and LL may have limited added value above original fatty acid classes and food sources in establishing the relation of fatty acid consumption with CVD.

Physical activity, cognitive decline and risk of dementia: 28-year follow-up of Whitehall II cohort study

So this seems to contradict the research in the NASEM Report that exercise is modestly helpful in preventing dementia. Ask your doctor for clarification. You could try my 19 ideas, because you are completely on your own. You'll be dead before researchers come up with definitive proof on how to prevent dementia.

Dementia prevention 19 ways

NASEM Report Offers Some Hope for Dementia Prevention Evidence for three strategies only modest, but sufficient to talk to patients

Physical activity, cognitive decline and risk of dementia: 28-year follow-up of Whitehall II cohort study

BMJ
Sabia S, et al.
This work examined the hypotheses that physical activity in midlife was not linked to a reduced risk of dementia and that the preclinical phase of dementia was characterised by a decline in physical activity. No evidence was discovered of a neuroprotective effect of physical activity. Previous studies illustrating a lower risk of dementia, among physically active individuals was possibly the result of a reverse causation. This reverse causation was attributed to a decline in physical activity levels, in the preclinical phase of dementia.

Methods

  • This was a prospective cohort study, with a mean follow-up of 27 years.
  • It was carried out at the Civil service departments in London (Whitehall II study).
  • The recruitment consisted of 10308 candidates, aged 35-55 years at study inception (1985-88).
  • Exposures consisted of time spent in mild, moderate to vigorous, and total physical activity assessed seven times between 1985 and 2013 and categorised as “recommended” if duration of moderate to vigorous physical activity was 2.5 hours/week or more.
  • The main measure was a battery of cognitive tests being administered up to four times from 1997 to 2013.
  • The incident dementia cases (n=329) were determined through linkage to hospital, mental health services, and mortality registers until 2015.

Results

  • Mixed effects models did not exhibit any correlation between physical activity and subsequent 15 year cognitive decline.
  • Likewise, the Cox regression did not illustrate any link between physical activity and risk of dementia, over an average 27 year follow-up (hazard ratio in the “recommended” physical activity category 1.00, 95% confidence interval 0.80 to 1.24).
  • For trajectories of hours/week of total, mild, and moderate to vigorous physical activity in people with dementia, compared to those without dementia (all others), no variations were noted between 28 and 10 years prior to the diagnosis of dementia.
  • Nevertheless, the physical activity in people with dementia began to decline up to nine years, before the diagnosis (difference in moderate to vigorous physical activity -0.39 hours/week; P=0.05), and the variation became more prominent (-1.03 hours/week; P=0.005) at diagnosis.

Diagnosis of DWI-negative acute ischemic stroke

Absolutely no clue what this means or how it could be used to get stroke survivors to 100% recovery. More wasted research.
http://www.neurology.org/content/early/2017/06/14/WNL.0000000000004120.short?rss=1

A meta-analysis

  1. Jonathan A. Edlow, MD
  1. Correspondence to Dr. Edlow: bedlow@mgh.harvard.edu
  1. Neurology 10.1212/WNL.0000000000004120
  1. Also available:
  2. Data Supplement

Abstract

Objective: To determine the prevalence of diffusion-weighted imaging (DWI)–negative acute ischemic stroke (AIS) and to identify clinical characteristics of patients with DWI-negative AIS.
Methods: We systematically searched PubMed and Ovid/MEDLINE for relevant studies between 1992, the year that the DWI sequence entered clinical practice, and 2016. Studies were included based upon enrollment of consecutive patients presenting with a clinical diagnosis of AIS prior to imaging. Meta-analysis was performed to synthesize study-level data, estimate DWI-negative stroke prevalence, and estimate the odds ratios (ORs) for clinical characteristics associated with DWI-negative stroke.
Results: Twelve articles including 3,236 AIS patients were included. The meta-analytic synthesis yielded a pooled prevalence of DWI-negative AIS of 6.8%, 95% confidence interval (CI) 4.9–9.3. In the 5 studies that reported proportion data for DWI-negative and DWI-positive AIS based on the ischemic vascular territory (n = 1,023 AIS patients), DWI-negative stroke was strongly associated with posterior circulation ischemia, as determined by clinical diagnosis at hospital discharge or repeat imaging (OR 5.1, 95% CI 2.3–11.6, p <0.001).
Conclusions: A small but significant percentage of patients with AIS have a negative DWI scan. Patients with neurologic deficits consistent with posterior circulation ischemia have 5 times the odds of having a negative DWI scan compared to patients with anterior circulation ischemia. AIS remains a clinical diagnosis and urgent reperfusion therapy should be considered even when an initial DWI scan is negative.
  • Received January 21, 2017.
  • Accepted in final form April 20, 2017.

Effects of morning versus evening statin administration on lipid profile: A systematic review and meta-analysis

I have no clue whether my statins are short or long acting. So this is totally useless for laypersons and I bet your doctor will not be informing you of this.
https://www.mdlinx.com/internal-medicine/medical-news-article/2017/06/16/cholesterol-ldl-hydroxymethylglutaryl-coa-reductase-inhibitors/7213624/?news_id=387&newsdt=062417&subspec_id=4&utm_source=WeeklyNL&utm_medium=newsletter&utm_content=Weeks-Best-Article&utm_campaign=article-section&category=latest-weekly
Journal of Clinical Lipidology
Awad K, et al. – This study explored the impacts of morning versus evening statin administration on lipid profile. As per findings, evening–dose of short–acting statins markedly reduced low density lipoprotein cholesterol (LDL-C) and total cholesterol (TC) levels than morning–dose, whereas, long–acting statins exerted slight but significant impact on LDL-C and displayed equivalent efficacy for both regimens. Overall, it was recommended that long–acting statins should be given at a time that will best aid compliance, whereas, short–acting statins should be given in the evening.

Methods

  • Researchers searched PubMed, SCOPUS, Web of Science and Embase databases (from inception up to July 24th, 2016) to identify the relevant studies.
  • Using a fixed-effect model, they pooled mean differences (MDs) between the change scores in lipid parameters.

Results

  • For this analysis, eleven articles with 1034 participants were found to be eligible.
  • Researchers found that the pooled analysis comparing impacts of morning versus evening administration of statins on plasma total cholesterol (TC) (p=0.10), high density lipoprotein cholesterol (HDL-C) (p=0.90) and triglycerides (TG) (p=0.45) was not statistically significant.
  • They also noted that low density lipoprotein cholesterol (LDL-C) lowering was statistically greater in the evening-dose group (MD: 3.24 mg/dl, 95%CI: 1.23, 5.25, p=0.002).
  • It was demonstrated in subgroup analysis according to statin half-lives that evening-dose of statins was significantly superior to morning-dose for lowering LDL-C in case of both short and long half-life statins (MD: 9.68 mg/dl, 95%CI: 3.32, 16.03, p=0.003, and 2.53 mg/dl, 95%CI: 0.41, 4.64, p=0.02, respectively), and also for TC reduction in case of short half-life statins only (p=0.0005).