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.

Showing posts with label wait on having a stroke. Show all posts
Showing posts with label wait on having a stroke. Show all posts

Thursday, February 3, 2022

Endovascular treatment for acute Basilar Artery Occlusion – a multicenter randomized controlled trial (ATTENTION)

 So don't have an acute basilar artery occlusion until researchers have solved this AND your doctor has created a protocol for this.

Endovascular treatment for acute Basilar Artery Occlusion – a multicenter randomized controlled trial (ATTENTION)

 
First Published February 1, 2022 Research Article 

Background and hypothesis: 

Recently, two multicenter randomized controlled trials (RCT) failed to show a significantly beneficial effect of endovascular treatment (EVT) in patients with acute basilar artery occlusion (BAO). However, both trials suffered from equipoise issues which may have hindered the validity of the trial results. Therefore, additional RCT studies are needed to explore the potential benefit of EVT in patients presenting with BAO. 

Study design: 

ATTENTION is an investigator-initiated, multicenter, prospective, randomized, controlled clinical trial with open-label treatment and blinded outcome assessment (PROBE) of EVT versus best medical management (BMM). The primary effect parameter is a modified Rankin Score of 0-3 at day 90. Discussion: ATTENTION will provide evidence for the efficacy and safety of EVT in stroke patients within 12 hours after BAO.

Tuesday, October 19, 2021

Thrombectomy in Extensive Stroke May Not Be Beneficial and Is Associated With Increased Risk for Hemorrhage

 Good functional outcome was observed in 27.4% is failure by any measure. So you better wait on having this type of stroke until the stroke medical world has created a solution.

Thrombectomy in Extensive Stroke May Not Be Beneficial and Is Associated With Increased Risk for Hemorrhage

 
and for the German Stroke Registry–Endovascular Treatment (GSR-ET)
Originally publishedhttps://doi.org/10.1161/STROKEAHA.120.033101Stroke. 2021;52:3109–3117

Background and Purpose:

This study evaluates the benefit of endovascular treatment (EVT) for patients with extensive baseline stroke compared with best medical treatment.

Methods:

This retrospective, multicenter study compares EVT and best medical treatment for computed tomography (CT)–based selection of patients with extensive baseline infarcts (Alberta Stroke Program Early CT Score ≤5) attributed to anterior circulation stroke. Patients were selected from the German Stroke Registry and 3 tertiary stroke centers. Primary functional end points were rates of good (modified Rankin Scale score of ≤3) and very poor outcome (modified Rankin Scale score of ≥5) at 90 days. Secondary safety end point was the occurrence of symptomatic intracerebral hemorrhage. Angiographic outcome was evaluated with the modified Thrombolysis in Cerebral Infarction Scale.

Results:

After 1:1 pair matching, a total of 248 patients were compared by treatment arm. Good functional outcome was observed in 27.4% in the EVT group, and in 25% in the best medical treatment group (P=0.665). Advanced age (adjusted odds ratio, 1.08 [95% CI, 1.05–1.10], P<0.001) and symptomatic intracerebral hemorrhage (adjusted odds ratio, 6.35 [95% CI, 2.08–19.35], P<0.001) were independently associated with very poor outcome. Mortality (43.5% versus 28.9%, P=0.025) and symptomatic intracerebral hemorrhage (16.1% versus 5.6%, P=0.008) were significantly higher in the EVT group. The lowest rates of good functional outcome (≈15%) were observed in groups of failed and partial recanalization (modified Thrombolysis in Cerebral Infarction Scale score of 0/1–2a), whereas patients with complete recanalization (modified Thrombolysis in Cerebral Infarction Scale score of 3) with recanalization attempts ≤2 benefitted the most (modified Rankin Scale score of ≤3:42.3%, P=0.074) compared with best medical treatment.

Conclusions:

In daily clinical practice, EVT for CT–based selected patients with low Alberta Stroke Program Early CT Score anterior circulation stroke may not be beneficial and is associated with increased risk for hemorrhage and mortality, especially in the elderly. However, first- or second-pass complete recanalization seems to reveal a clinical benefit of EVT highlighting the vulnerability of the low Alberta Stroke Program Early CT Score subgroup.

REGISTRATION:

URL: https://www.clinicaltrials.gov; Unique identifier: NCT03356392.

Brain Mechanisms of Conscious Awareness: Detect, Pulse, Switch, and Wave

 If you present to the hospital with locked-in syndrome you better hope your doctors are sufficiently knowledgeable about it to recognize your consciousness inside. Or you'll have to wait having this type of stroke until your medical staff knows how to treat it.

Brain Mechanisms of Conscious Awareness: Detect, Pulse, Switch, and Wave

First Published October 11, 2021 Research Article 

Consciousness is a fascinating field of neuroscience research where questions often outnumber the answers. We advocate an open and optimistic approach where converging mechanisms in neuroscience may eventually provide a satisfactory understanding of consciousness. We first review several characteristics of conscious neural activity, including the involvement of dedicated systems for content and levels of consciousness, the distinction and overlap of mechanisms contributing to conscious states and conscious awareness of transient events, nonlinear transitions and involvement of large-scale networks, and finally the temporal nexus where conscious awareness of discrete events occurs when mechanisms of attention and memory meet. These considerations and recent new experimental findings lead us to propose an inclusive hypothesis involving four phases initiated shortly after an external sensory stimulus: (1) Detect—primary and higher cortical and subcortical circuits detect the stimulus and select it for conscious perception. (2) Pulse—a transient and massive neuromodulatory surge in subcortical-cortical arousal and salience networks amplifies signals enabling conscious perception to proceed. (3) Switch—networks that may interfere with conscious processing are switched off. (4) Wave—sequential processing through hierarchical lower to higher cortical regions produces a fully formed percept, encoded in frontoparietal working memory and medial temporal episodic memory systems for subsequent report of experience. The framework hypothesized here is intended to be nonexclusive and encourages the addition of other mechanisms with further progress. Ultimately, just as many mechanisms in biology together distinguish living from nonliving things, many mechanisms in neuroscience synergistically may separate conscious from nonconscious neural activity.

 

Friday, October 8, 2021

Timing and Dose of Upper Limb Motor Intervention After Stroke: A Systematic Review

So your doctors and stroke researchers know absolutely nothing on getting your upper limb recovered.  Just lousy guidelines, NOT PROTOCOLS!  You better wait on having your stroke until better interventions exist.

Timing and Dose of Upper Limb Motor Intervention After Stroke: A Systematic Review

 
Originally publishedhttps://doi.org/10.1161/STROKEAHA.121.034348Stroke. ;0:STROKEAHA.121.034348

This systematic review aimed to investigate timing, dose, and efficacy of upper limb intervention during the first 6 months poststroke. Three online databases were searched up to July 2020. Titles/abstracts/full-text were reviewed independently by 2 authors. Randomized and nonrandomized studies that enrolled people within the first 6 months poststroke, aimed to improve(NOT RECOVER! The tyranny pf low expectations in full view.)g 228 (n=9704 participants) unique data sets. The number of studies completed increased from one (n=37 participants) between 1980 and 1984 to 91 (n=4417 participants) between 2015 and 2019. Timing of intervention start has not changed (median 38 days, interquartile range [IQR], 22–66) and study sample size remains small (median n=30, IQR 20–48). Most studies were rated high risk of bias (62%). Study participants were enrolled at different recovery epochs: 1 hyperacute (<24 hours), 13 acute (1–7 days), 176 early subacute (8–90 days), 34 late subacute (91–180 days), and 4 were unable to be classified to an epoch. For both the intervention and control groups, the median dose was 45 (IQR, 600–1430) min/session, 1 (IQR, 1–1) session/d, 5 (IQR, 5–5) d/wk for 4 (IQR, 3–5) weeks. The most common interventions tested were electromechanical (n=55 studies), electrical stimulation (n=38 studies), and constraint-induced movement (n=28 studies) therapies. Despite a large and growing body of research, intervention dose and sample size of included studies were often too small to detect clinically important effects. Furthermore, interventions remain focused on subacute stroke recovery with little change in recent decades. A united research agenda that establishes a clear biological understanding of timing, dose, and intervention type is needed to progress stroke recovery research. Prospective Register of Systematic Reviews ID: CRD42018019367/CRD42018111629.

Footnotes

The Data Supplement is available with this article at https://www.ahajournals.org/doi/suppl/10.1161/STROKEAHA.121.034348.

For Sources of Funding and Disclosures, see page xxx.

Correspondence to: Kathryn S. Hayward, PhD, Departments of Physiotherapy and Medicine, Florey Institute of Neuroscience and Mental Health, University of Melbourne, Level 5 Harold Stokes Bldg, Austin Hospital, Heidelberg, VIC Australia. Email

Risk of Aneurysm Rupture After Thrombolysis in Patients With Acute Ischemic Stroke and Unruptured Intracranial Aneurysms

It is your doctor's responsibility to have protocols in place that will guarantee this won't happen. No protocols, then what research are they initiating to solve this? You'll just have to wait on having your stroke until they get this solved.

Risk of Aneurysm Rupture After Thrombolysis in Patients With Acute Ischemic Stroke and Unruptured Intracranial Aneurysms

 
Jyri Juhani Virta, Daniel Strbian, Jukka Putaala, Miikka Korja

Abstract

Background and Objectives: Unruptured intracranial aneurysms (UIAs) are considered to be a relative contraindication for intravenous thrombolysis (IVT) in acute ischemic stroke (AIS). However, there is currently limited data on the risk of UIA rupture following IVT. Our objective was to assess whether IVT for AIS can lead to a UIA rupture and intracranial hemorrhages (ICHs) in patients with unruptured UIAs.

Methods: Prospective cohort study of consecutive patients treated in a comprehensive stroke center between 2005 and 2019. We assessed radiology reports and records at the Finnish Care Register for Health Care to identify patients with UIAs among all AIS patients treated with IVT at the center. We analyzed patient angiograms for aneurysm characteristics and other brain imaging studies for ICHs after IVT. The main outcome was in-hospital ICHs attributable to an UIA rupture after IVT. Secondary outcomes were in-hospital symptomatic ICHs (ECASS-2 criteria, i.e., NIH Stroke Scale score increase of ≥4 points) and any in-hospital ICHs.

Results: A total of 3 953 patients were treated with IVT during the 15-year study period. One hundred thirty-two (3.3 %) of the 3 953 AIS patients had a total of 155 UIAs (141 saccular and 14 fusiform). The mean diameter of UIAs was 4.7 ± 3.8 mm, with 18.7% being ≥7 mm and 9.7% ≥10 mm in diameter. None of the 141 saccular UIAs ruptured following IVT. Three patients [2.3%, 95% confidence interval (CI) 0.6-5.8%] with large fusiform basilar artery UIAs suffered from a fatal rupture at 27 hours, 43 hours, and 19 days after IVT. All three were administered anticoagulation treatments following IVT and anticoagulation took effect during the UIA rupture. Any ICHs and symptomatic ICHs were detected in 18.9 % (95% CI 12.9-26.2%) and 8.3% (95% CI 4.4-13.8%) of all AIS patients, respectively.

Discussion: IVT appears to be safe in AIS patients with saccular UIAs, including larges UIAs (≥10 mm). Anticoagulation after AIS in patients with large fusiform posterior circulation UIAs may increase the risk of aneurysm rupture.

Sunday, September 26, 2021

Cardiac troponin and recurrent major vascular events after minor stroke or TIA

 Since you don't want any major adverse cardiovascular events after your stroke you'll just have to wait to have your stroke until after your doctors and stroke hospital have initiated the research and come up with EXACT STROKE PROTOCOLS TO PREVENT THAT.  Your responsibility is to wait until then. You can't make any assumption that your stroke hospital can properly treat any type of stroke that comes in until they have defined protocols for all types. NOT GUIDELINES, guidelines are mostly worthless. The 17.2% occurrence rate is too high to not have any protocols addressing that. I wouldn't accept that risk from any medical procedure.

Cardiac troponin and recurrent major vascular events after minor stroke or TIA

First published: 25 September 2021
This article has been accepted for publication and undergone full peer review but has not been through the copyediting, typesetting, pagination and proofreading process, which may lead to differences between this version and the Version of Record. Please cite this article as doi: 10.1002/ana.26225.

Abstract

Objective

To investigate whether high-sensitivity cardiac troponin T (hs-cTnT) is associated with major adverse cardiovascular events (MACE) in patients with minor stroke or transient ischemic attack (TIA), and whether this association differs after risk stratification based on the “Age, Blood pressure, Clinical features, Duration of symptoms, Diabetes” (ABCD2) score.

Methods

INSPiRE-TMS was a randomized controlled trial allocating patients with minor stroke or TIA to an intensified support program or conventional care. In this post-hoc analysis, participants were categorized using hs-cTnT levels (5th Generation, Roche, 99th percentile upper reference limit [URL] 14ng/L). Vascular risk was stratified using the ABCD2 score (lower-risk:0-5 vs. higher-risk:6-7). Cox proportional hazard regression was performed using covariate adjustment and propensity score matching (PSM) for the association between hs-cTnT and MACE (stroke/non-fatal coronary event/vascular death).

Results

Among 889 patients (mean age 70 years, 37% female), MACE occurred in 153 patients (17.2%) during a mean follow-up of 3.2 years. Hs-cTnT was associated with MACE (9.3%/year>URL vs. 4.4%/year≤URL, adjusted HR 1.63 [95%CI 1.13-2.35], adjusted HR (Q4 vs.Q1) 2.57 [95%CI 1.35-4.97], adjusted HR (log-transformed) 2.31 [95%CI 1.37-3.89]). This association remained after PSM (adjusted HR 1.76 [95%CI 1.14-2.72]). There was a significant interaction between hs-cTnT and ABCD2 category for MACE occurrence (pinteraction=0.04). In the lower-risk category, MACE rate was 9.5%/year in patients with hs-cTnT>URL, which was higher than in those ≤URL (3.8%/year) and similar to the overall rate in the higher-risk category.

Interpretation

Hs-cTnT levels are associated with incident MACE within three years after minor stroke or TIA and may help to identify high-risk individuals otherwise deemed at lower-risk based on the ABCD2 score. If confirmed in independent validation studies, this might warrant intensified secondary prevention measures and cardiac diagnostics in stroke patients with elevated hs-cTnT.

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