Deans' stroke musings

Changing stroke rehab and research worldwide now.Time is Brain!Just think of all the trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 493 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:

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's quite disgusting that this information is not available from every stroke association and doctors group.
My back ground story is here:http://oc1dean.blogspot.com/2010/11/my-background-story_8.html

Wednesday, January 18, 2017

Enhanced Thalamic Functional Connectivity with No fMRI Responses to Affected Forelimb Stimulation in Stroke-Recovered Rats

No idea how anything here could be used to help your recovery.
http://journal.frontiersin.org/article/10.3389/fncir.2016.00113/full?
Woo H. Shim1,2,3,4†, Ji-Yeon Suh1,4†, Jeong K. Kim1, Jaeseung Jeong3* and Young R. Kim4*
  • 1Department of Radiology, ASAN Medical Center, University of Ulsan College of Medicine, Ulsan, South Korea
  • 2ASAN Institute for Life Sciences, ASAN Medical Center, University of Ulsan College of Medicine, Ulsan, South Korea
  • 3Department of Bio and Brain Engineering, Korea Advanced Institute of Science and Technology, Daejeon, South Korea
  • 4Department of Radiology, Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital, Boston, MA, USA
Neurological recovery after stroke has been extensively investigated to provide better understanding of neurobiological mechanism, therapy, and patient management. Recent advances in neuroimaging techniques, particularly functional MRI (fMRI), have widely contributed to unravel the relationship between the altered neural function and stroke-affected brain areas. As results of previous investigations, the plastic reorganization and/or gradual restoration of the hemodynamic fMRI responses to neural stimuli have been suggested as relevant mechanisms underlying the stroke recovery process. However, divergent study results and modality-dependent outcomes have clouded the proper interpretation of variable fMRI signals. Here, we performed both evoked and resting state fMRI (rs-fMRI) to clarify the link between the fMRI phenotypes and post-stroke functional recovery. The experiments were designed to examine the altered neural activity within the contra-lesional hemisphere and other undamaged brain regions using rat models with large unilateral stroke, which despite the severe injury, exhibited nearly full recovery at ∼6 months after stroke. Surprisingly, both blood oxygenation level-dependent and blood volume-weighted (CBVw) fMRI activities elicited by electrical stimulation of the stroke-affected forelimb were completely absent, failing to reveal the neural origin of the behavioral recovery. In contrast, the functional connectivity maps showed highly robust rs-fMRI activity concentrated in the contra-lesional ventromedial nucleus of thalamus (VM). The negative finding in the stimuli-induced fMRI study using the popular rat middle cerebral artery model denotes weak association between the fMRI hemodynamic responses and neurological improvement. The results strongly caution the indiscreet interpretation of stroke-affected fMRI signals and demonstrate rs-fMRI as a complementary tool for efficiently characterizing stroke recovery.

Introduction

Ischemic stroke impairs neurovascular and metabolic functions in the brain and causes neurologic disabilities. Although severely damaged neurons fail to regenerate at the cortical level, interestingly, lost or compromised sensorimotor functions often recover at later stages of stroke. One of the restorative mechanisms underlying such recovery has been linked with the brain plasticity, the brain’s ability to reconstruct neural pathways and synapses in response to the loss of function (Kalénine et al., 2010; Heiss and Kidwell, 2014; Furlan et al., 2015). Despite the high interest and recent efforts, it is as yet unclear whether (or how) the stroke-affected brain areas functionally reposition in unaffected regions and/or reform connections with other brain areas to compensate for the impaired functions.
For identifying brain regions associated with restorative processes, task/stimulus-induced functional MRI (fMRI) has been frequently used to visualize brain activities associated with the neurologic recovery (for review see references Macey et al., 2015; Tang et al., 2015). More recently, resting state fMRI (rs-fMRI) has also provided a platform to explore spatiotemporal changes in neural connection across a wide range of brain regions. In general, by exploiting the temporal correlation of blood oxygenation level-dependent (BOLD) fMRI signals, the rs-fMRI has become an important method to assess the in vivo neuro-network (Carter et al., 2012; Grefkes and Fink, 2014; Thiel and Vahdat, 2015). Previous rs-fMRI investigations have reported that post-stroke loss and recovery of functions were associated with deterioration and subsequent retrieval of functional connectivity in the neural system, especially the interhemispheric connectivity changes (van Meer et al., 2010, 2012; Park et al., 2011). Based on these findings, alterations in the functional fields identified by either evoked fMRI or neural connectivity have been linked with the post-stroke functional recovery.
Past fMRI observations have suggested that remaining brain tissue, particularly the augmented neural activity in the contra-laterally homologous regions likely accounts for the restored sensorimotor function after stroke (Carey et al., 2002; Calautti and Baron, 2003). Typically, the assumption of intact neurovascular coupling underpins the interpretation of altered fMRI signals (Dijkhuizen et al., 2001; Kim et al., 2005). However, this link was challenged by us using multi-faceted fMRI measurements, in which the BOLD/CBV response ratio was significantly smaller in the stroke rats compared to the normal controls (Kim et al., 2005, 2006). Moreover, unclear relationship between fMRI and neurological recovery (i.e., complete absence of fMRI responses corresponding to the behavioral recovery) and questionable baseline physiology (e.g., choice of anesthesia) confounded the clear understanding of previous study results. (Weber et al., 2008; van Meer et al., 2010, 2012) The current study was designed to compare the functional fields and signal amplitudes acquired from both evoked fMRI and rs-fMRI in the stroke rat models exhibiting nearly full neurological recovery. Only using rats with large unilateral lesion encompassing most of the sensory and parts of the motor areas, the study focused on the role of sensorimotor activities in the contra-lesional hemisphere.
We hypothesized that in the chronic phase of stroke recovery, reinforced neural connections among the remaining intact brain regions are utilized more than the simple functional replacement and/or expansion of evoked activation toward the contra-lesional hemisphere. A well-established fMRI protocol with electrical stimulation of the rat forelimb was used to define the active sensorimotor brain regions (Dijkhuizen et al., 2003; Kim et al., 2005) while the BOLD rs-fMRI was used to investigate the functional connectivity networks. Noting that the proper brain function requires not only localized activation but also the integration of neural activities across multiple brain regions, the current study may elucidate the relationship between the different fMRI approaches to improve our understanding of the post-stroke recovery process and offer clues to the underlying neurobiological mechanisms.

More at link.

Hospital Variation in Functional Recovery After Stroke

There should be almost zero variation. If we had objective damage diagnosis, 3d size and location, penumbra included. Then we could measure hospitals against each other since they would be using the exact same stroke rehab protocols. But until we get the fossilized leaders out of stroke progress will not be made. They are all waiting for SOMEONE ELSE TO SOLVE THE PROBLEM. Piss on them. Using the Rankin scale as a measurement device for stroke disability is incredibly stupid. It has nothing objective in it at all except for 6 - death.
http://circoutcomes.ahajournals.org/content/10/1/e002391?etoc=
Janet Prvu Bettger, Laine Thomas, Li Liang, Ying Xian, Cheryl D. Bushnell, Jeffrey L. Saver, Gregg C. Fonarow, Eric D. Peterson

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Abstract

Background—Functional status is a key patient-centric outcome, but there are little data on whether functional recovery post-stroke varies among hospitals. This study examined the distribution of functional status 3 months after stroke, determined whether these outcomes vary among hospitals, and identified hospital characteristics associated with better (or worse) functional outcomes.
Methods and Results—Observational analysis of the AVAIL study (Adherence Evaluation After Ischemic Stroke-Longitudinal) included 2083 ischemic stroke patients enrolled from 82 US hospitals participating in Get With The Guidelines-Stroke and AVAIL. The primary outcome was dependence or death at 3 months (modified Rankin Scale [mRS] score of 3–6). Secondary outcomes included functional dependence (mRS score of 3–5), disabled (mRS score of 2–5), and mRS evaluated as a continuous score. By 3 months post-discharge, 36.5% of patients were functionally dependent or dead. Rates of dependence or death varied widely by discharging hospitals (range: 0%–67%). After risk adjustment, patients had lower rates of 3-month dependence or death when treated at teaching hospitals (odds ratio, 0.72; 95% confidence interval, 0.54–0.96) and certified primary stroke centers (odds ratio, 0.69; 95% confidence interval, 0.53–0.91). In contrast, a composite measure of hospital-level adherence to acute stroke care performance metrics, stroke volume, and bed size was not associated with downstream patient functional status. Findings were robust across mRS end points and sensitivity analyses.
Conclusions—One third of acute ischemic stroke patients were functionally dependent or dead 3 months postacute stroke; functional recovery rates varied considerably among hospitals, supporting the need to better determine which care processes can maximize functional outcomes.

Tuesday, January 17, 2017

Use of Strategies to Improve Door-to-Needle Times With Tissue-Type Plasminogen Activator in Acute Ischemic Stroke in Clinical Practice

This is totally pathetic. The goal should be negative DTN time. With an objective diagnosis in the ambulance with no neurologist needed you should be able to deliver tPA before you get to the hospital. If that is not your goal then get the fuck out of the way and let actual leaders get that done.  No endpoint was measured of total tPA efficacy of reversing the stroke. What a complete fucking waste of otherwise good research. We might have gotten how many minutes do you have to get full recovery. Does no one even know how to run research?
 http://circoutcomes.ahajournals.org/content/10/1/e003227?etoc=

Findings from Target: Stroke

Ying Xian, Haolin Xu, Barbara Lytle, Jason Blevins, Eric D. Peterson, Adrian F. Hernandez, Eric E. Smith, Jeffrey L. Saver, Steven R. Messé, Mary Paulsen, Robert E. Suter, Mathew J. Reeves, Edward C. Jauch, Lee H. Schwamm, Gregg C. Fonarow
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Abstract

Background—The implementation of Target: Stroke Phase I, the first stage of the American Heart Association’s national quality improvement initiative to accelerate door-to-needle (DTN) times, was associated with an average 15-minute reduction in DTN times. Target: Stroke phase II was launched in April 2014 with a goal of promoting further reduction in treatment times for tissue-type plasminogen activator (tPA) administration.
Methods and Results—We conducted a second survey of Get With The Guidelines-Stroke hospitals regarding strategies used to reduce delays after Target: Stroke and quantify their association with DTN times. A total of 16 901 ischemic stroke patients were treated with intravenous tPA within 4.5 hours of symptom onset from 888 surveyed hospitals between June 2014 and April 2015. The patient-level median DTN time was 56 minutes (interquartile range, 42–75), with 59.3% of patients receiving intravenous tPA within 60 minutes and 30.4% within 45 minutes after hospital arrival. Most hospitals reported routinely using a majority of Target: Stroke key practice strategies, although direct transport of patients to computed tomographic/magenetic resonance imaging scanner, premix of tPA ahead of time, initiation of tPA in brain imaging suite, and prompt data feedback to emergency medical services providers were used less frequently. Overall, we identified 16 strategies associated with significant reductions in DTN times. Combined, a total of 20 minutes (95% confidence intervals 15–25 minutes) could be saved if all strategies were implemented.
Conclusions—Get With The Guidelines-Stroke hospitals have initiated a majority of Target: Stroke–recommended strategies to reduce DTN times in acute ischemic stroke. Nevertheless, certain strategies were infrequently practiced and represent a potential immediate target for further improvements.

Pace of Progress in Stroke Thrombolysis Are Hospitals Running To Stand Still?

This is totally pathetic. The goal should be negative DTN time. With an objective diagnosis in the ambulance with no neurologist needed you should be able to deliver tPA before you get to the hospital. If that is not your goal then get the fuck out of the way and let actual leaders get that done. 
http://circoutcomes.ahajournals.org/content/10/1/e003438?etoc=

Scott J. Mendelson, Shyam Prabhakaran
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Stroke is a time-sensitive medical emergency and a leading cause of disability in the United States. Therapies to halt and even reverse ischemic injury to the brain, such as intravenous tissue-type plasminogen activator (tPA), are available, but the systems to deliver them rapidly have not been optimized to ensure timely treatment of as many eligible patients as possible. Although ≈40 000 to 50 000 acute ischemic stroke patients per year receive tPA,1,2 benefits from the drug are not simply related to receiving it or not but rather are closely linked to time from onset to treatment.3,4 Delays to treatment lead to more disability because every additional 5 minutes is tantamount to the permanent loss of nearly 10 million brain cells.5 National guidelines and quality measures have, therefore, emphasized speed of stroke thrombolysis, focusing on the time between patient arrival to the hospital and tPA administration, also known as door-to-needle (DTN) time.6,7 Alarmingly, recommendations that hospitals evaluate acute ischemic stroke patients and administer tPA within 60 minutes(Wrong goal)of a patient’s arrival to the emergency department have existed since the original National Institutes of Neurological Disorders and Stroke tPA trial.8 Despite this, as the first decade of the new millennium closed, US hospitals were not meeting this goal in a majority of patients.

Improving Door-to-Needle Times for Acute Ischemic Stroke

This is totally pathetic. The goal should be negative DTN time. With an objective diagnosis in the ambulance with no neurologist needed you should be able to deliver tPA before you get to the hospital. If that is not your goal then get the fuck out of the way and let actual leaders get that done. 
http://circoutcomes.ahajournals.org/content/10/1/e003242?etoc=

Effect of Rapid Patient Registration, Moving Directly to Computed Tomography, and Giving Alteplase at the Computed Tomography Scanner

Noreen Kamal, Jessalyn K. Holodinsky, Caroline Stephenson, Devika Kashayp, Andrew M. Demchuk, Michael D. Hill, Renee L. Vilneff, Erin Bugbee, Charlotte Zerna, Nancy Newcommon, Eddy Lang, Darren Knox, Eric E. Smith
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Abstract

Background—The effectiveness of specific systems changes to reduce DTN (door-to-needle) time has not been fully evaluated. We analyzed the impact of 4 specific DTN time reduction strategies implemented prospectively in a staggered fashion.
Methods and Results—The HASTE (Hurry Acute Stroke Treatment and Evaluation) project was implemented in 3 phases at a single academic medical center. In HASTE I (June 6, 2012 to June 5, 2013), baseline performance was analyzed. In HASTE II (June 6, 2013 to January 24, 2015), 3 changes were implemented: (1) a STAT stroke protocol to prenotify the stroke team about incoming stroke patients; (2) administering alteplase at the computed tomography (CT) scanner; and (3) registering the patient as unknown to allow immediate order entry. In HASTE III (January 25, 2015 to June 29, 2015), we implemented a process to bring the patient directly to CT on the emergency medical services stretcher. Log-transformed DTN time was modeled. Data from 350 consecutive alteplase-treated patients were analyzed. Multivariable regression showed the following factors to be significant: giving alteplase in the CT (32% decrease in DTN time, 95% confidence interval [CI] 38%–55%), stretcher to CT (30% decrease in DTN time, 95% CI 16%–42%), patient registered as unknown (12% decrease in DTN time, 95% CI 3%–20%), STAT stroke protocol (11% decrease in DTN time, 95% CI 1%–20%), and stroke severity (National Institutes of Health Stroke Scale score 6–8: 19% decrease in DTN time, 95% CI 6%–31%; National Institutes of Health Stroke Scale score >8: 27% decrease in DTN time, 95% CI 17%–37%).
Conclusions—Taking the patient to CT on the emergency medical services stretcher, registering the patient as unknown, STAT stroke protocol, and administering alteplase in CT are associated with lower DTN time.

A Lesion-Proof Brain? Multidimensional Sensorimotor, Cognitive, and Socio-Affective Preservation Despite Extensive Damage in a Stroke Patient

You wouldn't be so baffled by this if you actually had an objective diagnosis done with MRI and PET scans to see the exact areas of damage. She was bilingual which is indicative of better recovery due to better brain reserve.
http://journal.frontiersin.org/article/10.3389/fnagi.2016.00335/full?
  • 1Laboratory of Experimental Psychology and Neuroscience, Institute of Cognitive and Translational Neuroscience, INECO Foundation, Favaloro University, Buenos Aires, Argentina
  • 2National Scientific and Technical Research Council (CONICET), Buenos Aires, Argentina
  • 3Faculty of Elementary and Special Education, National University of Cuyo, Mendoza, Argentina
  • 4Departamento de Estudios Psicológicos, Universidad Icesi, Cali, Colombia
  • 5Universidad Autónoma del Caribe, Barranquilla, Colombia
  • 6Center for Social and Cognitive Neuroscience, School of Psychology, Universidad Adolfo Ibáñez, Santiago de Chile, Chile
  • 7Centre of Excellence in Cognition and its Disorders, Australian Research Council, Sydney, NSW, Australia
In this study, we report an unusual case of mutidimensional sensorimotor, cognitive, and socio-affective preservation in an adult with extensive, acquired bilateral brain damage. At age 43, patient CG sustained a cerebral hemorrhage and a few months later, she suffered a second (ischemic) stroke. As a result, she exhibited extensive damage of the right hemisphere (including frontal, temporal, parietal, and occipital regions), left Sylvian and striatal areas, bilateral portions of the insula and the amygdala, and the splenium. However, against all probability, she was unimpaired across a host of cognitive domains, including executive functions, attention, memory, language, sensory perception (e.g., taste recognition and intensity discrimination), emotional processing (e.g., experiencing of positive and negative emotions), and social cognition skills (prosody recognition, theory of mind, facial emotion recognition, and emotional evaluation). Her functional integrity was further confirmed through neurological examination and contextualized observation of her performance in real-life tasks. In sum, CG's case resists straightforward classifications, as the extent and distribution of her lesions would typically produce pervasive, multidimensional deficits. We discuss the rarity of this patient against the backdrop of other reports of atypical cognitive preservation, expound the limitations of several potential accounts, and highlight the challenges that the case poses for current theories of brain organization and resilience.

Introduction

The mind-brain association, as conceived in clinical neuroscience and neuropsychology, is an abstract generalization. In working with multi-participant samples, behavioral findings stem from data averages while anatomical results are obtained by transforming brain images into a standard coordinate space. In both cases, strict outlier exclusion criteria are applied, so that atypical patterns are removed from ensuing models. These steps are critical and perhaps unavoidable to characterize the organ's functional organization with some degree of external validity. Indeed, thanks to this approach, replicable associations have been established between damage to circumscribed regions and impairments of specific functions, including motor (Zgaljardic et al., 2003), somatosensory (Meyer et al., 2016), socio-cognitive (Gold and Shadlen, 2007; Ibáñez et al., 2010, 2016b; Couto et al., 2013; Baez et al., 2014, 2016b,c; Melloni et al., 2016), interoceptive (Couto et al., 2015; García-Cordero et al., 2016), executive (Rabinovici et al., 2015; Sedeño et al., 2016), linguistic (Ullman, 2008; Cardona et al., 2014; García and Ibáñez, 2014, 2016; Bocanegra et al., 2015; García, 2015; Melloni et al., 2015; García et al., 2016a,b,c; Abrevaya et al., 2017), and pragmatic (Kaplan et al., 1990; Stemmer, 2008) skills.
However, such well established anatomo-clinical links (and the theoretical views construed around them) are sometimes challenged by unusual individual cases which do not easily fit mainstream models in cognitive neuroscience. Such reports include that of a man who efficiently served as a civil servant although he had progressively lost roughly 75% of his brain (Feuillet et al., 2007), that of a housewife with only mild motor symptomatology despite primary cerebellar agenesis (Yu et al., 2015), or multiple patients exhibiting considerable restitution of language skills following early left hemispheromotomy (e.g., Hertz-Pannier et al., 2002). The same is true of studies showing preserved pre- and post-operative temporal functions in patients with large perisylvian arachnoid cysts (Kunz et al., 1988), although such malformations typically impair various cognitive domains (Wester, 2008). Cases such as these are valuable because, in their exceptionality, they invite us to extend our current conceptions of brain organization, plasticity, and functional compensation, beyond the robust patterns that emerge in typical, averaged, normalized data.
Building on these premises, we present the remarkable case of patient CG, who exhibits widespread sparing of sensorimotor, cognitive, and socio-affective functions despite extensive brain damage acquired in adulthood. In particular, as shown below, CG's unusual pattern of preservation was convergently corroborated through neuropsychological assessment, multiple experimental tasks, neurological examination, and even naturalistic observations of her daily functioning. The case could thus prompt new reflections on the functional organization of various neurocognitive systems.

Case Description

More at link.

Saskatchewan Acute Stroke Pathway hastens care for stroke patients

Somehow I missed the time limit for tPA going to 12 hours. Still just talking about care, not results.
http://leaderpost.com/news/local-news/saskatchewan-acute-stroke-pathway-hastens-care-for-stroke-patients
Stroke patients should receive better and quicker care with the launch of the Saskatchewan Acute Stroke Pathway.
Formally launched Monday at the Regina General Hospital, although it has been up and running since summer in most places, the pathway streamlines care for stroke patients.
“This gets people provincewide to the right stroke centre,” said Dr. Michael Kelly, a neurosurgeon from Saskatoon who helped lead the charge on improving stroke care.
“Stroke’s a major disease that sometimes take a backseat to other diseases, but it’s the No. 3 killer of Canadians and it’s the No. 1 cause of long-term disability in Canada, so it’s a major problem.”
With early rehabilitation by a stroke team, there’s “significant reduction” in the length of hospital stay and, so far, about 30 fewer patients requiring permanent institutionalization.
Allison Kesler, CEO of the Saskatchewan Heart & Stroke Foundation, emphasizes the importance of knowing the signs of a stroke: face drooping, inability to raise arms, and slurred or jumbled speech.
If someone is having a stroke, it’s important to call 9-1-1 immediately and say that the patient may be having a stroke. That way, they’ll be transported directly to a stroke care centre in Regina or Saskatoon, or in one of seven smaller cities, including Moose Jaw, Estevan, Yorkton and Swift Current.
Bypassing a smaller rural hospital or care centre, the patient will more quickly obtain proper stroke treatment, which will hasten their recovery. About 1.9 million brain cells die each minute after a stroke.
“It’s time-dependent certainly. That’s one of the problems in a province with such large geography,” said Kelly.
Prior to the pathway, patients who’d shown stroke symptoms for more than 3 ½ hours were considered beyond emergency care, because it was thought a clot-busting drug wouldn’t work on them.
That “always bothered me,” said Kelly.
Now the time limit is 12 hours, which is “one of the big accomplishments” of the pathway.
Stroke patients “need to be cared for by people that have expertise in this, including rehab and therapies and speech language pathology,” said Kelly. “That’s what, by expanding the window, we’ve also been able to implement, is those systems for people that have made a big difference.”
Kelly says about 2,500 people have strokes every year in Saskatchewan.
He said there was minimal cost in creating the pathway; it was more about “implementing best practice to do it better.”
amartin@postmedia.com

Sonothrombolysis in the management of acute ischemic stroke

Only 6 years old, was this enough to add this procedure to tPA administration in your stroke hospital? Or does no one in your hospital read research at all?
https://www.ncbi.nlm.nih.gov/pubmed/20104930

Author information

  • 1Comprehensive Stroke Center, University of Alabama Hospital, Birmingham, Alabama, USA. mrubifu@hotmail.com

Abstract

Multiple in vitro and animal models have demonstrated the efficacy of ultrasound to enhance fibrinolysis. Mechanical pressure waves produced by ultrasound energy improve the delivery and penetration of alteplase (recombinant tissue plasminogen activator [tPA]) inside the clot. In human stroke, the CLOTBUST phase II trial showed that the combination of alteplase plus 2 hours of continuous transcranial Doppler (TCD) increased recanalization rates, producing a trend toward better functional outcomes compared with alteplase alone. Other small clinical trials also showed an improvement in clot lysis when transcranial color-coded sonography was combined with alteplase. In contrast, low-frequency ultrasound increased the symptomatic intracranial hemorrhage rate in a clinical trial. Administration of microbubbles (MBs) may further enhance the effect of ultrasound on thrombolysis by lowering the ultrasound-energy threshold needed to induce acoustic cavitation. Initial clinical trials have been encouraging, and a multicenter international study, TUCSON, determined a dose of newly developed MBs that can be safely administered with alteplase and TCD. Even in the absence of alteplase, the ultrasound energy, with or without MBs, could increase intrinsic fibrinolysis. The intra-arterial administration of ultrasound with the EKOS NeuroWave catheter is another ultrasound application for acute stroke that is currently being studied in the IMS III trial. Operator-independent devices, different MB-related techniques, and other ultrasound parameters for improving and spreading sonothrombolysis are being tested.
PMID:
20104930
DOI:
10.2165/11316850-000000000-00000

NOR-SASS (Norwegian Sonothrombolysis in Acute Stroke Study): Randomized Controlled Contrast-Enhanced Sonothrombolysis in an Unselected Acute Ischemic Stroke Population

No clue what the point of this ultrasound treatment was for. It is safe but why use it? Explained here:

Sonothrombolysis in the management of acute ischemic stroke


http://www.docguide.com/nor-sass-norwegian-sonothrombolysis-acute-stroke-study-randomized-controlled-contrast-enhanced-sonot?

Nacu A, Kvistad C, Naess H, Øygarden H, Logallo N, Assmus J, Waje-Andreassen U, Kurz K, Neckelmann G, Thomassen L; Stroke (Dec 2016)

BACKGROUND AND PURPOSE The NOR-SASS (Norwegian Sonothrombolysis in Acute Stroke Study) aimed to assess effect and safety of contrast-enhanced ultrasound treatment in an unselected acute ischemic stroke population.
METHODS Patients treated with intravenous thrombolysis within 4.5 hours after symptom onset were randomized 1:1 to either contrast-enhanced sonothrombolysis (CEST) or sham CEST. A visible arterial occlusion on baseline computed tomography angiography was not a prerequisite for inclusion. Pulse-wave 2 MHz ultrasound was given for 1 hour and contrast (SonoVue) as an infusion for ≈30 minutes. Magnetic resonance imaging and angiography were performed after 24 to 36 hours. Primary study end points were neurological improvement at 24 hours defined as National Institutes of Health Stroke Scale score 0 or reduction of ≥4 National Institutes of Health Stroke Scale points compared with baseline National Institutes of Health Stroke Scale and favorable functional outcome at 90 days defined as modified Rankin scale score 0 to 1.
RESULTS A total of 183 patients were randomly assigned to either CEST (93 patient) or sham CEST (90 patients). The rates of symptomatic intracerebral hemorrhage, asymptomatic intracerebral hemorrhage, or mortality were not increased in the CEST group. Neurological improvement at 24 hours and functional outcome at 90 days was similar in the 2 groups both in the intention-to-treat analysis and in the per-protocol analysis.
CONCLUSIONS CEST is safe among unselected ischemic stroke patients with or without a visible occlusion on computed tomography angiography and with varying grades of clinical severity. There was, however, statistically no significant clinical effect of sonothrombolysis in this prematurely stopped trial.
CLINICAL TRIAL REGISTRATION URL: http://www.clinicaltrials.gov. Unique identifier: NCT01949961.

Optimal Timing of Anticoagulant Treatment After Intracerebral Hemorrhage in Patients With Atrial Fibrillation

For discussions with your doctor if this applies to you.
http://www.docguide.com/optimal-timing-anticoagulant-treatment-after-intracerebral-hemorrhage-patients-atrial-fibrillation?

Pennlert J, Overholser R, Asplund K, Carlberg B, Van Rompaye B, Wiklund P, Eriksson M; Stroke (Dec 2016)

BACKGROUND AND PURPOSE This study aims to provide observational data on the relationship between the timing of antithrombotic treatment and the competing risks of severe thrombotic and hemorrhagic events in a cohort of Swedish patients with atrial fibrillation and intracerebral hemorrhage (ICH).
METHODS Patients with atrial fibrillation and a first-ever ICH were identified in the Swedish Stroke Register, Riksstroke, 2005 to 2012. Riksstroke was linked with other national registers to find information on treatment, comorbidity, and outcome. The optimal timing of treatment in patients with low and high thromboembolic risk was described through cumulative incidence functions separately for thrombotic and hemorrhagic events and for the combined end point vascular death or nonfatal stroke.
RESULTS The study included 2619 ICH survivors with atrial fibrillation with 5759 person-years of follow-up. Anticoagulant treatment was associated with a reduced risk of vascular death and nonfatal stroke in high-risk patients with no significantly increased risk of severe hemorrhage. The benefit seemed to be greatest when treatment was started 7 to 8 weeks after ICH. For high-risk women, the total risk of vascular death or stroke recurrence within 3 years was 17.0% when anticoagulant treatment was initiated 8 weeks after ICH and 28.6% without any antithrombotic treatment (95% confidence interval for difference, 1.4%-21.8%). For high-risk men, the corresponding risks were 14.3% versus 23.6% (95% confidence interval for difference, 0.4%-18.2%).
CONCLUSIONS This nationwide observational study suggests that anticoagulant treatment may be initiated 7 to 8 weeks after ICH in patients with atrial fibrillation to optimize the benefit from treatment and minimize risk.

Adapted cold shower as a potential treatment for depression

Only 9 years old and I bet your doctor has never considered prescribing this for your post-stroke depression. The bolded line would seem to be an excellent reason for using this as part of your enriched environment as talked about by Dr. Dale Corbett in 2011. This would seem to be similar to the Szechuan pepper that sends the equivalent of 50 light taps to the brain per second.
https://www.ncbi.nlm.nih.gov/pubmed/17993252

Abstract

Depression is a debilitating mood disorder that is among the top causes of disability worldwide. It can be characterized by a set of somatic, emotional, and behavioral symptoms, one of which is a high risk of suicide. This work presents a hypothesis that depression may be caused by the convergence of two factors: (A) A lifestyle that lacks certain physiological stressors that have been experienced by primates through millions of years of evolution, such as brief changes in body temperature (e.g. cold swim), and this lack of "thermal exercise" may cause inadequate functioning of the brain. (B) Genetic makeup that predisposes an individual to be affected by the above condition more seriously than other people. To test the hypothesis, an approach to treating depression is proposed that consists of adapted cold showers (20 degrees C, 2-3 min, preceded by a 5-min gradual adaptation to make the procedure less shocking) performed once or twice daily. The proposed duration of treatment is several weeks to several months. The following evidence appears to support the hypothesis: Exposure to cold is known to activate the sympathetic nervous system and increase the blood level of beta-endorphin and noradrenaline and to increase synaptic release of noradrenaline in the brain as well. Additionally, due to the high density of cold receptors in the skin, a cold shower is expected to send an overwhelming amount of electrical impulses from peripheral nerve endings to the brain, which could result in an anti-depressive effect. Practical testing by a statistically insignificant number of people, who did not have sufficient symptoms to be diagnosed with depression, showed that the cold hydrotherapy can relieve depressive symptoms rather effectively. The therapy was also found to have a significant analgesic effect and it does not appear to have noticeable side effects or cause dependence. In conclusion, wider and more rigorous studies would be needed to test the validity of the hypothesis.
PMID:
17993252
DOI:
10.1016/j.mehy.2007.04.052

Drink for your heart: Caffeine may counter age-related inflammation, cardiovascular disease

From Stanford Medicine. I go for as much coffee as I can get.How long before your doctor has a coffee protocol?
http://scopeblog.stanford.edu/2017/01/16/drink-for-your-heart-caffeine-may-counter-age-related-inflammation-cardiovascular-disease/
There’s a clear connection between chronological age, chronic inflammation, cardiovascular disease and… coffee consumption.
More than 90 percent of all noncommunicable diseases of aging are associated with chronic inflammation. And more than 1,000 papers have provided evidence that chronic inflammation contributes to many cancers, Alzheimer’s disease and other dementias, cardiovascular disease, osteoarthritis and even depression.
It’s also well known — well, at least among the scientists who study this kind of thing — that caffeine intake is associated with longevity. Now, Stanford immunologists David Furman, PhD, and Mark Davis, PhD, and their colleagues have revealed a likely reason why this may be so.
In a study published in Nature Medicine, the researchers conducted extensive analyses of blood samples, survey data and medical and family histories obtained from more than 100 human participants in a multiyear study. Their search revealed a fundamental inflammatory mechanism associated with human aging and the chronic diseases that come with it. In short, this mechanism becomes increasingly likely to kick into high gear as the number of candles on our birthday cake marches relentlessly toward infinity.
The study implicates this same inflammatory process as a driver of cardiovascular disease and increased rates of mortality overall. Metabolites, or breakdown products, of nucleic acids — the molecules that serve as building blocks for our genes — circulating in the blood can trigger this inflammatory process big-time, the study found. Injecting these substances into mice produced massive systemic inflammation, sent their blood pressure soaring and wreaked havoc with their kidneys, among other nasty consequences.
Intriguingly, caffeine and its own metabolites — whose molecular structure, intriguingly, bears a strong family resemblance to the nucleic-acid metabolites — blocked the abysmal action of the latter, possibly explaining why coffee drinkers tend to live longer than abstainers.
Now, the good news: Not all older people, as the study showed, are cursed with the age-related inflammatory hyperdrive discovered by the investigators. And when Furman, Davis et al. looked at the extremes — older people with low levels of this type of inflammation were only one-eighth as likely as the high-level older people to have high blood pressure.  They were also eight times as likely to report having at least one close blood relative who had lived to the age of 90 or older. And of the people in the study who were 85 or more years old in 2008, when the long-term longitudinal study began, those with low levels of the identified type of systemic inflammation were substantially more likely to still be alive in 2016, eight years later.
And sure enough: The study participants with the lowest activation levels of the nasty inflammatory mechanism were the ones who, according to extensive questionnaires, reported the highest caffeine intake.
If that doesn’t enable your coffee addiction, nothing will. Oh, and by the way, black tea and dark chocolate contain compounds similar to caffeine.

Treatment for Stroke That Could Permanently Repair Brain Damage Stroke

I bet nothing will come of this because we have NO stroke leadership and NO stroke strategy. This will join the hundreds and thousands of research pieces I have already talked about that are circling the drain, never to be seen again.
http://www.healthcarepublication.com/treatment-for-stroke-repair-brain/
Researchers from the University of Manchester have developed a new treatment that could limit the damage caused by treatment for stroke and also promote repair in the affected area of the brain. What’s more, the drug they’re using has already been clinically approved.
The researchers’ study is published in Brain, Behavior and Immunity, and it recounts how they developed their treatment using mice bred to develop ischemic treatment for stroke, the most prevalent type of stroke and one that occurs when an artery that supplies oxygen-rich blood to the brain is blocked. Soon after the mice experienced a stroke, the researchers treated them with interleukin-1 receptor antagonist (IL-1Ra), an anti-inflammatory drug that is already licensed for use in treating rheumatoid arthritis.
They noticed a reduction in the amount of brain damage typically observed after a treatment for stroke and also noted that the drug boosted neurogenesis (the birth of new cells) in the areas that did experience brain damage in the days following the treatment. The mice even regained the motor skills they lost due to the stroke.
The researchers’ study is published in Brain, Behavior and Immunity, and it recounts how they developed their treatment using mice bred to develop ischemic treatment for stroke, the most prevalent type of stroke and one that occurs when an artery that supplies oxygen-rich blood to the brain is blocked. Soon after the mice experienced a stroke, the researchers treated them with interleukin-1 receptor antagonist (IL-1Ra), an anti-inflammatory drug that is already licensed for use in treating rheumatoid arthritis.
They noticed a reduction in the amount of brain damage typically observed after a treatment for stroke and also noted that the drug boosted neurogenesis (the birth of new cells) in the areas that did experience brain damage in the days following the treatment. The mice even regained the motor skills they lost due to the stroke.

HOPE FOR A CURE

Treatment for stroke is the fifth leading cause of death in the United States and about 800,000 people suffer from one each year, according to the Centers for Disease Control and Prevention (CDC). They occur when the flow of blood to the brain is interrupted, usually due to a blood clot or a buildup of fat that broke off from the arteries and traveled to the brain. The condition is extremely dangerous because brain cells can die within a few minutes of the treatment for stroke, causing permanent damage or even death.
Must Read:  What is stroke? Treatment for stroke
We still don’t have a treatment to adequately prevent or reverse the damage to the brain caused by treatment for stroke, but the Manchester researchers believe that their development could change that. Though they are still in early stages of clinical trials, they hope to eventually move on to larger trials and eventually human testing. Together with other research, this new study offers hope to the thousands of people whose lives are impacted by strokes worldwide.

Physical activity mediates the relationship between fruit and vegetable consumption and cognitive functioning: A cross-sectional analysis

To improve your cognitive functioning post-stroke your doctor should tell you the exact amount of physical activity needed along with exact fruit and vegetable consumption. In simple words, an exercise protocol and a diet protocol.  Or you could be a bad patient and do this on your own without your doctors knowledge. That would be living life dangerously.
https://www.mdlinx.com/internal-medicine/medical-news-article/2017/01/17/food-and-nutrition-physical-activity-public/7008912/?
Journal of Public Health, 01/17/2017
This study investigated the interrelationships between fruit and vegetable consumption (FVC), body mass index (BMI), physical activity (PA) and cognitive functioning in younger and older adults. Higher PA levels were associated with better cognitive functioning in younger and older adults. Also, higher daily FVC and education levels were associated with better cognitive scores.

Methods

  • Cross–sectional information of 45522 participants (≥30 years) were analyzed from the 2012 annual component of the Canadian Community Health Survey.
  • Cognitive function was evaluated utilizing a single 6–level question of the Health Utilities Index.
  • PA was classified according to the Physical Activity Index kilocalories per kilogram every day as active, moderately active and inactive; BMI was measured in kg/m2 and FVC (servings/day) was classified as low, moderate or high.
  • To evaluate the interrelationship between FVC, BMI, PA, age and cognitive functioning, general linear models and mediation investigations were utilized.

Results

  • Higher BMIs, lower PA and FVC were connected with poorer cognitive functioning.
  • Furthermore, PA statistically mediated the association between FVC and cognitive function (Sobel test: t = –3.15; P < 0.002); and higher education levels and daily FVC were connected with better cognitive function (P < 0.001).
Go to PubMed Go to Abstract Print Article Summary Cat 2 CME Report

Monday, January 16, 2017

Science will be Blockchained by 2025

This would be very useful for stroke but will not occur until we destroy the fucking failures of stroke associations we have now and replace it with a great stroke association.
https://www.linkedin.com/pulse/science-blockchained-2025-sean-manion?
By 2025, all key scientific data will be verifiable by blockchain processes, because science faces a crisis of trust, and blockchain technology is maturing at the right time to fix it.
Coming Crisis. At the foundation of the scientific process is the expectation of reproducible results. This comes from trust in the integrity and verifiability of the data. Unfortunately, the pace of scientific advancement and the current incentive systems have led to numerous problems: falsified data, lack of reproducibility, and limitations of peer-review to name a few.

More at link.

Care suffers when patients berate docs, other medical professionals

Ok, maybe you don't want to follow my suggestion of screaming at your doctor. Then redirect it at the stroke hospital president and the board of directors. You are still getting lousy care if you don't get to 100% recovery and someone needs to step up to the needed leadership skills and solve the problems. How much worse than 10% full recovery rate will you get if you berate your doctor for not knowing anything about stroke recovery?
http://www.fiercehealthcare.com/practices/berating-doctors-other-medical-professionals-can-hurt-medical-care?
Warning to patients, parents and caregivers: Mind your manners.
While much has been written about the need to put an end to some doctors’ rude and bullying behavior, a new study shows the need for patients and families to also control their behavior.
Parents and caregivers who are rude to medical professionals may find it backfires. Indeed, doctors who are subjected to rude behavior may actually provide worse care to their patients even if they don't intend to, according to a study by University of Florida researchers.
Emotions can run high in hospitals, so it's not uncommon for patients or their loved ones to be rude to medical professionals if they think care is inadequate. But that type of bad behavior can lead to worse care for a child, the researchers warn.
Berating a child’s doctors or other medical professionals who provide care has “devastating effects on medical performance,” according to the findings of the study, published in Pediatrics.
A Johns Hopkins study estimated that more than 250,000 deaths are attributed to medical errors in the U.S. each year. The effects of rudeness account for more than 40% of the variance in practitioner performance that can lead to medical errors, according to management professor Amir Erez, Ph.D., one of the study authors.
“People may think that doctors should just 'get over' the insult and continue doing their job. However, the study shows that even if doctors have the best intentions in mind, as they usually do, they cannot get over rudeness because it interferes with their cognitive functioning without an ability to control it," Erez said in an announcement about the study.
In the study, researchers compared teams made up of two doctors and two nurses in 39 neonatal intensive care units in Israel. They simulated five scenarios in which the teams treated infant medical mannequins in emergency situations. An actress playing the baby’s mother scolded some of the teams, while the others were not subjected to rude behavior.
Teams who experienced rudeness performed poorly and were deficient in all of the study’s 11 measures, which included diagnostic accuracy, information sharing, therapy plan and communication. The behavior continued to affect the team members the entire day.
However, teams that participated in a pretest intervention—a computer game intended to raise the threshold of sensitivity to anger and aggression—recognized the mother’s rudeness and were not affected by it. In addition to training healthcare professionals on how to improve their interpersonal skills, the study suggests that hospital administrators should also make it a priority to teach medical professionals how to handle rudeness more effectively.

Millions in Donations Expanding Stroke and Brain Aneurysm Research and Education - Baptist Health, Jacksonville FL

YOU will need to get involved to make sure these donations actually are used to solve some of these problems in stroke. You can't let the researchers decide this on their own they need to be following your strategy, actually doing research that helps survivors. None should go for education, that is just conscience laundering.
http://www.benzinga.com/pressreleases/17/01/p8900380/millions-in-donations-expanding-stroke-and-brain-aneurysm-research-and-

Baptist Health will expand its research and education efforts for stroke and brain aneurysms thanks to recent charitable donations totaling $6 million -- including a $1.1 million gift by a grateful patient. The donation establishes the Ricardo Hanel, MD, and Eric Sauvageau, MD, Chair in Neurovascular Surgery at the Baptist Neurological Institute.
Jacksonville, Fla. (PRWEB) January 12, 2017
Baptist Health will expand its research and education efforts for stroke and brain aneurysms thanks to recent charitable donations totaling $6 million -- including a $1.1 million gift by a grateful patient.
The donation was made by an anonymous patient and spouse to establish the Ricardo Hanel, MD, and Eric Sauvageau, MD, Chair in Neurovascular Surgery at the Baptist Neurological Institute. That donation will be matched by Baptist Health for a total endowment of about $2.5 million, which will provide permanent, ongoing funding for brain treatment and research.
Dr. Hanel, director of the Baptist Neurological Institute, and Dr. Sauvageau, director of the Stroke & Cerebrovascular Center at Baptist Medical Center Jacksonville, are nationally and internationally recognized as leaders in treating brain aneurysms, acute stroke and cerebrovascular conditions using the latest minimally invasive techniques and groundbreaking clinical trials.
"Drs. Hanel and Sauvageau are on a mission to save lives throughout the region," said Hugh Greene, president and CEO of Baptist Health. "Thanks to their tireless efforts, as well the generosity of our donors, Baptist is helping to define the new frontier in stroke and brain aneurysm treatment."
Also funded by the $6 million in donations from corporate and private donors will be endowments focused on clinical program development for treating cerebrovascular conditions in adults and children, as well as expanding community outreach and awareness for stroke and brain aneurysms.
In addition to the anonymous donors, one of the other donations recently came from long-time Beaches residents Cheryl and Tom Rackley who designated $1 million to support neurological needs for Beaches residents and $500,000 to the Baptist Neurological Institute Endowment. Cheryl was treated by Dr. Hanel for a brain aneurysm in 2015.
"The generosity of these gifts are really inspiring," Dr. Hanel said. "The donations allow us to continue doing advanced research and education while providing the best cerebrovascular care in the region for all ages and all socio-economic levels, especially to the under privileged."
"These commitments are truly amazing and will allow us to develop the program further and provide support to educate and reach more people in the community," Dr. Sauvageau added.
Drs. Hanel and Sauvageau, who came to Baptist Health in 2014, helped to establish the Baptist Neurological Institute and Baptist Stroke & Cerebrovascular Center, which leads the region for new minimally invasive treatment of the brain, including clinical trials. Thanks in large part to their leadership, Baptist Jacksonville also now has one of the largest neurointensive care units in the state and the first ER with beds dedicated to neurological needs.


New urine test can quickly detect whether a person has a healthy diet

This won't do you any good since your doctor never setup a stroke diet protocol s/he won't want a test proving that your diet is bad.  And just maybe you want to test for blood clots.

Nanotechnology urine test could detect deadly blood clots

After you pee into the cup ask your doctor for stem cells back.

Turning urine into brain cells could help fight Alzheimer’s, Parkinson’s


https://www.mdlinx.com/internal-medicine/top-medical-news/article/2017/01/16/8

Imperial College London Health News
Scientists have developed a urine test that measures the health of a person's diet.

The five–minute test measures biological markers in urine created by the breakdown of foods such as red meat, chicken, fish and fruit and vegetables.

The analysis, developed by researchers from Imperial College London, Newcastle University and Aberystwyth University, also gives an indication of how much fat, sugar, fibre and protein a person has eaten.

Although the work is at an early stage, the team hope that with future development the test will be able to track patients' diets. It could even be used in weight loss programmes to monitor food intake.

Evidence suggests people inaccurately record their own diets, and under–report unhealthy food while over–reporting fruit and vegetable intake – and that the likelihood of inaccuracies in food diaries increases if a person is overweight or obese.

Professor Gary Frost, senior author of the study from the Department of Medicine at Imperial said: "A major weakness in all nutrition and diet studies is that we have no true measure of what people eat. We rely solely on people keeping logs of their daily diets – but studies suggest around 60 per cent of people misreport what they eat to some extent. This test could be the first independent indicator of the quality of a person's diet – and what they are really eating."

In study, published in the journal Lancet Diabetes and Endocrinology and conducted at the MRC–NIHR National Phenome Centre, the researchers asked 19 volunteers to follow four different diets, ranging from very healthy to very unhealthy. These were formulated using World Health Organisation dietary guidelines, which advise on the best diets to prevent conditions such as obesity, diabetes and heart disease.

The volunteers strictly followed these diets for three days while in a London research facility, throughout which the scientists collected urine samples in the morning, afternoon and evening.

The research team then assessed the urine for hundreds of compounds, called metabolites, produced when certain foods are broken down in the body.

These included compounds that indicate red meat, chicken, fish, fruit and vegetables, as well as giving a picture of the amount of protein, fat, fibre and sugar eaten. They also included compounds that point to specific foods such as citrus fruits, grapes and green leafy vegetables.

From this information the researchers were able to develop a urine metabolite profile that indicated a healthy, balanced diet with a good intake of fruit and vegetables. The idea is this 'healthy diet' profile could be compared to the diet profile from an individual's urine, to provide an instant indicator of whether they are eating healthily.

The scientists then tested the accuracy of the test on data from a previous study. This included 225 UK volunteers as well as 66 people from Denmark. All of the volunteers had provided urine samples, and kept information on their daily diets.

Analysis of these urine samples enabled the researchers in the current study to accurately predict the diet of the 291 volunteers.

Benzodiazepine-like drugs linked to increased stroke risk among Alzheimer's disease patients

You'll have to ask your doctor what the risk for stroke is for you since you have a likely chance of getting dementia. Is this risk just for actual Alzheimer patients?  Or how long prior to Alzheimers/dementia period where the risk lies? Familiar names are Valium and Xanax.

1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.

2. Then this study came out and seems to have a range from 17-66%. December 2013.

3. A 20% chance in this research.   July 2013.

Benzodiazepine-like drugs linked to increased stroke risk among Alzheimer's disease patients

The use of benzodiazepines and benzodiazepine-like drugs was associated with a 20 per cent increased risk of stroke among persons with Alzheimer's disease, shows a recent study from the University of Eastern Finland. Benzodiazepines were associated with a similar risk of stroke as benzodiazepine-like drugs.
The use of benzodiazepines and benzodiazepine-like drugs was associated with an increased risk of any stroke and ischemic stroke, whereas the association with hemorrhagic stroke was not significant. However, due to the small number of hemorrhagic stroke events in the study population, the possibility of such an association cannot be excluded. The findings are important, as benzodiazepines and benzodiazepine-like drugs were not previously known to predispose to strokes or other cerebrovascular events. Cardiovascular risk factors were taken into account in the analysis and they did not explain the association.
The findings encourage a careful consideration of the use of benzodiazepines and benzodiazepine-like drugs among persons with Alzheimer's disease, as stroke is one of the leading causes of death in this population group. Earlier, the researchers have also shown that these drugs are associated with an increased risk of hip fracture.
The study was based on data from a nationwide register-based study (MEDALZ) conducted at the University of Eastern Finland in 2005-2011. The study population included 45,050 persons diagnosed with Alzheimer's disease, and 22 per cent of them started using benzodiazepines or benzodiazepine-like drugs.
Source:
University of Eastern Finland

Sunday, January 15, 2017

Brain-computer interface based motor and cognitive rehabilitation after stroke – state of the art, opportunity, and barriers: summary of the BCI Meeting 2016 in Asilomar

See what state of the art BCI will bring to your stroke rehabilitation. ROFLMAO.
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Non-invasive electroencephalographic (EEG) based brain-computer interfaces (BCIs) are a potential tool to support neuronal plasticity after stroke in the sub-acute and even in the chronic state. A few randomized controlled trials have demonstrated the positive effect on motor rehabilitation. Recent data also indicate that BCI training may improve cognitive rehabilitation. However, important questions remain to be addressed for implementing BCI-based rehabilitation in the clinical routine. This translational effort requires an interdisciplinary approach. The current article provides an overview of a stroke rehabilitation workshop of the 6th International Brain-Computer Interface Meeting in Asilomar, Pacific Grove, USA, held from 30 May to 3 June 2016. This workshop provided an overview of the current state of the art in BCI-based motor and cognitive rehabilitation, presented BCI set-ups shown to be effective, and concluded with a discussion of translational issues and barriers.