Longitudinal Trajectories of Global and Domain-Specific Cognition After Stroke Using the Oxford Cognitive Screen

 USELESS! You tell us nothing on how to get cognitive recovery! Ph. D.s and still no brains at all!

You're supposed to solve problems, NOT just describe them you blithering idiots. Hoping comeuppance hits you really hard when you are the 1 in 4 per WHO that has a stroke! 

Longitudinal Trajectories of Global and Domain-Specific Cognition After Stroke Using the Oxford Cognitive Screen

Elise Milosevich, DPhil, Andrea Kusec, PhD https://orcid.org/0000-0003-0128-4677, 

Sarah T. Pendlebury, DPhil https://orcid.org/0000-0003-3603-8388, and Nele Demeyere, PhD https://orcid.org/0000-0003-0416-5147 nele.demeyere@ndcn.ox.ac.uk

Author Info & Affiliations

New online

https://doi.org/10.1161/STROKEAHA.125.054555

Abstract

BACKGROUND:

Cognitive impairment is common after stroke and linked to poor outcomes, yet long-term recovery or decline, particularly across specific cognitive domains, remains unclear. Most studies use brief global screeners with short follow-up, limiting insight into recovery patterns. This study aimed to characterize domain-specific cognitive trajectories over ≥2 years poststroke and identify predictors of persistent impairment.

METHODS:

Participants were recruited at a regional acute stroke unit (John Radcliffe Hospital, Oxford, United Kingdom; 2012–2019) and assessed acutely, at 6 months, and ≥2 years poststroke. The Oxford Cognitive Screen was administered at all timepoints. Global impairment severity was quantified by the proportion of Oxford Cognitive Screen subtasks impaired. Logistic mixed-effects models examined longitudinal change and predictors of domain-specific impairments (language, memory, attention, executive function, and number processing). Latent class growth analysis identified distinct cognitive trajectories. Models were adjusted for acute cognitive impairment severity and time.

RESULTS:

Of 866 patients assessed acutely, 105 were followed up at ≥2 years (98 with complete Oxford Cognitive Screen data; median, 4.1 [interquartile range, 3.3] years; mean age, 69 years, 41% female). Cognitive impairment severity improved substantially by 6 months (β=−0.11; P<0.001) and further long-term (β=−0.15; P<0.001). Acute impairment severity strongly predicted long-term outcomes (β=0.50; P<0.001), while demographic and vascular factors explained minimal variance. Latent class growth analysis identified 4 overall trajectories: no or mild acute impairment with stability (47.6%), moderate-improving (32.3%), large improvement (15.2%), and decline (4.8%). Domain-specific improvements were greatest in memory (odds ratio, 16.40 [95% CI, 5.52–48.7]) and language (odds ratio, 8.17 [95% CI, 3.17–21.1]), more limited in attention (odds ratio, 5.41 [95% CI, 2.52–11.6]) and executive function (odds ratio, 4.14 [95% CI, 1.96–8.75]). Domain models revealed additional classes of persistent or delayed recovery, particularly in executive function and attention.

CONCLUSIONS:

Cognitive recovery is most pronounced within 6 months and continues across domains though executive dysfunction often persists. Acute impairment severity best predicted long-term outcomes, while vascular and demographic factors were less informative. Distinct trajectory classes highlight the need for individualized, long-term cognitive monitoring to guide rehabilitation and prognostication. These findings underscore the importance of long-term cognitive follow-up in stroke care and provide empirical benchmarks for recovery across domains.

Graphical Abstract

Cognitive impairment is common following stroke1,2 and frequently contributes to poor functional outcomes,3,4 increased dependency,5 and reduced quality of life.4 While many individuals experience some degree of cognitive recovery, others may show persistent impairment or delayed decline.3,6 However, the long-term trajectories of change across different cognitive domains remain poorly understood.7 This is partly due to cognitive deficits often being overlooked beyond the immediate postacute period unless dementia develops, which is not an inevitable outcome.6,8,9

Developing the Strategy to Use Silk Spheres for Efficient, Targeted Delivery of Oligonucleotide Therapeutics to Cancer Cells

 If we had ANY FUNCTIONING BRAIN CELLS in our stroke medical 'professionals' this would be looked at as a way to deliver drugs to the brain to increase neurogenesis, dendritic branching and axon pathfinding. But there are NO BRAINS AT ALL IN STROKE!

To prove total incompetence in stroke, nothing was done with this:

Making neurons from stem cells: Molecular mechanisms and spider silk substrates November 2013

Send me hate mail on this: oc1dean@gmail.com. I'll print your complete statement with your name and my response in my blog. Or are you afraid to engage with my stroke-addled mind? Your patients need an explanation of why you aren't trying to get survivors recovered.

Why isn't your 'professional' solving stroke?

Laziness? Incompetence? Or just don't care? NO leadership? NO strategy? Not my job? Not my Problem!

Developing the Strategy to Use Silk Spheres for Efficient, Targeted Delivery of Oligonucleotide Therapeutics to Cancer Cells

Authors Molenda S, Deptuch T , Sikorska A, Lorenc P, Smialek MJ, Florczak-Substyk A , Pawlak P, Dams-Kozlowska H 

Received 28 January 2025

Accepted for publication 16 May 2025

Published 23 June 2025 Volume 2025:20 Pages 8023—8039

DOI https://doi.org/10.2147/IJN.S519906

Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 5

Editor who approved publication: Professor Lijie Grace Zhang

Download Article [PDF] 

Sara Molenda,^{1– 3} Tomasz Deptuch,^1,2 Agata Sikorska,^1,2 Patryk Lorenc,^{1– 3} Maciej Jerzy Smialek,^1,2,* Anna Florczak-Substyk,^1,2 Piotr Pawlak,⁴ Hanna Dams-Kozlowska<sup>1,2

1</sup>Department of Cancer Immunology, Poznan University of Medical Sciences, Poznan, Poland; ²Department of Diagnostics and Cancer Immunology, Greater Poland Cancer Centre, Poznan, Poland; ³Doctoral School, Poznan University of Medical Sciences, Poznan, Poland; ⁴Department of Genetics and Animal Breeding, Poznan University of Life Sciences, Poznan, Poland

*Current address: Biozentrum, University of Basel, Basel, Switzerland, Institute of Human Genetics, Polish Academy of Sciences, Poznan, Poland

Correspondence: Hanna Dams-Kozlowska, Department of Cancer Immunology, Poznan University of Medical Sciences, 15 Garbary St, Poznan, 61-866, Poland, Email hdamskozlowska@ump.edu.pl

Introduction: Oligonucleotide-based drugs, such as siRNA, hold great promise for disease treatment, including cancer. However, their clinical application has challenges related to cell-specific delivery and susceptibility to degradation. The use of drug delivery systems (DDS) may address these problems. Nanoparticles of bioengineered spider silk demonstrate significant potential as DDS due to their biocompatibility and biodegradability. Another advantage of this material is the possibility of functionalization, which allows the control of its property. The main objective of this study was to develop a strategy for targeted delivery of oligonucleotide-based therapeutics into cancer cells using bioengineered silk technology.
Materials and Methods: Two spider silk spheres that bind oligonucleotides and target cancer cells that overexpress HER2 (HER2+) were constructed. One type of sphere was made of a newly designed silk, H2.1MS1KN, which contained two functional peptides: H2.1 for binding HER2 and KN for binding oligonucleotide. The second type of sphere was formed of a blend of two previously described proteins, H2.1MS1 and MS2KN; these proteins differed not only in the functional domain (H2.1 vs KN) but also in the sequence of silk (MS1 vs MS2). The ability of proteins to bind oligonucleotides was analyzed via gel electrophoresis. The biophysicochemical properties of particles were analyzed using an SEM, NanoSight, ZetaSizer, flow cytometry, and scanning confocal microscopy. The silk particle potential was analyzed using siRNA for silencing STAT3 expression in the HER2+ breast cancer model.
Results: Both H2.1MS1KN and H2.1MS1:MS2KN proteins efficiently bound nucleic acid. H2.1MS1:MS2KN formed smaller spheres than H2.1MS1KN. Although both H2.1MS1KN and blended H2.1MS1:MS2KN spheres were effectively loaded with oligonucleotides, only H2.1MS1:MS2KN spheres delivered siRNA to HER2+ cancer cells that successfully silenced STAT3 expression.
Conclusion: Not only the selection of functional peptides but also their quantity and type of silk is crucial when developing an effective silk-based DDS for delivering active siRNA.

Charity 'deeply concerned' about hospital's stroke advice

 And this charity didn't even mention the correct solution! 100% recovery protocols regardless of time admitted! DOESN'T ANYONE IN STROKE THINK AT ALL?

Send me hate mail on this: oc1dean@gmail.com. I'll print your complete statement with your name and my response in my blog. Or are you afraid to engage with my stroke-addled mind? Your patients need an explanation of why you aren't working on 100% recovery protocols.

Why isn't your 'professional' solving stroke?

Laziness? Incompetence? Or just don't care? NO leadership? NO strategy? Not my job? Not my Problem

Charity 'deeply concerned' about hospital's stroke advice

Naj Modak - BBC News

Fri 6 June 2025 at 1:30 pm GMT-4·3-min read

The charity advises anyone who spots any of the signs of a stroke to call 999 straight away [Northern Lincolnshire and Goole NHS Trust]

A charity said it was "deeply concerned" after a hospital advised patients presenting with a suspected stroke not to attend its emergency department.

Northern Lincolnshire and Goole NHS Foundation Trust said its Diana, Princess of Wales Hospital was "not the most appropriate place" for those experiencing symptoms because it did not have a specialist stroke unit. The trust advised patients to call 999 for an ambulance to take them to Scunthorpe General Hospital instead.

However, concerns have been raised by patients on ambulance waiting times.

A spokesperson for the Stroke Association said any lengthy wait for an ambulance was "unacceptable" as every minute could shorten the chance of survival.

'Journey could cost time'

In a social media post on Thursday, the trust said it had seen "a lot of instances recently" of patients arriving at the hospital.

The trust said: "This is not the most appropriate place to be seen, as we don't have a hyper-acute stroke unit at Diana, Princess of Wales Hospital.

"You should instead ring 999 if you've got symptoms and you'll be taken via ambulance to Scunthorpe General Hospital, which has the necessary facilities.

"If you do attend at Grimsby ED, you'll be sent to Scunthorpe via ambulance."

The post received criticism from some social media users with a number of individuals questioning what could happen to them if they were taken ill.

One person wrote: "Why as a member of the public in a state of emergency should we have to ensure we are heading to the right place?"

Others questioned the time taken and distance they would travel to reach the hospital by ambulance.

A user wrote: "The trip to Scunthorpe could add an extra 30-40 [minutes] on the journey."

Another wrote: "If you live closer to Grimsby then maybe that's the natural place you'd automatically think you should go!"

'Systemic challenges'

Samantha Jones, associate director at Stroke Association, said they were "hugely grateful" to medical practitioners who were working tirelessly under extreme pressure.

She said: "Despite their best efforts, systemic challenges are severely compromising ambulance response and hospital treatment times.

"If you spot any of the signs of a stroke in you or someone else, it's vital to call 999 straight away," she said.

A spokesperson for East Midlands Ambulance Service said: "Every 999 call is assessed based on the information provided by the caller and people experiencing a life-threatening emergency are responded to as a priority."

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The NHS Humber Health Partnership said a hyper-acute stroke unit at Scunthorpe General Hospital provides "immediate specialist treatment and high quality care for all stroke patients in our area".

The unit at Scunthorpe was opened in 2013 after an NHS report described stroke services in Grimsby as "inadequate", which led to health bosses consolidating treatment onto one site.

Intracranial Hemorrhage After Reperfusion Therapies in Acute Ischemic Stroke Patients

Well then solve the problem so Intracranial Hemorrhage does not occur. Have you NO BRAINS AT ALL?

Intracranial Hemorrhage After Reperfusion Therapies in Acute Ischemic Stroke Patients

Benjamin Maïer,^1,2,3 Jean Philippe Desilles,^1,2,3 and Mikael Mazighi^1,2,3,*

Author information Article notes Copyright and License information Disclaimer

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Abstract

Reperfusion therapies are the mainstay of acute ischemic stroke (AIS) treatments and overall improve functional outcome. Among the established complications of intravenous (IV) tissue-type plasminogen activator (tPA), intracranial hemorrhage (ICH) is by far the most feared and has been extensively described by seminal works over the last two decades. Indeed, IV tPA is associated with increased odds of any ICH and symptomatic ICH responsible for increased mortality rate during the first week after an AIS. Despite these results, IV tPA has been found beneficial in several pioneering randomized trials and improves functional outcome at 3 months(NOT GOOD ENOUGH; Survivors want  100% recovery, NOT THIS IMPROVES CRAPOLA.). Endovascular therapy (EVT) combined with IV tPA for AIS patients consecutive to an anterior circulation large-vessel occlusion does not increase ICH occurrence. Of note, EVT following IV tPA leads to significantly higher rates of early reperfusion than with IV tPA alone, with no difference in ICH, which challenges the paradigm of reperfusion as a major prognostic factor for ICH complications. However, several blood biomarkers (glycemia, platelet and neutrophil count), clinical factors (age, AIS severity, blood pressure management, diabetes mellitus), and neuroradiological factors (cerebral microbleeds, infarct size) have been identified as risk factors for ICH after reperfusion therapy. In the years to come, the ultimate goal will be to further improve either reperfusion rates and functional outcome, while reducing hemorrhagic complications. To this end, various approaches being investigated are discussed in this review, such as blood-pressure control after reperfusion or the use of new antiplatelet agents as an adjunct to IV tPA and exhibit reduced hemorrhagic potential during the early phase of AIS.

Keywords: acute ischemic stroke, intracranial hemorrhage, thrombolysis, blood pressure, endovascular treatment, thrombectomy, disabilility, mortality

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Introduction

To date, reperfusion therapies represent the mainstay of acute ischemic stroke (AIS) treatments (1, 2). Reperfusion can be performed pharmacologically by the use of intravenous recombinant human tissue-type plasminogen activator (IV tPA; alteplase, Boehringer Ingelheim, Germany) within the first 4.5 h after stroke onset (3), and since 2015, by endovascular therapy (EVT) in case of an anterior circulation large-vessel occlusion (LVO) (4). These different treatments have been found effective in reducing 3 month neurological disability(NOT GOOD ENOUGH; Survivors want  100% recovery, NOT THIS REDUCING CRAPOLA.). Indeed, in a meta-analysis of individual data from randomized controlled trials (RCTs), at 3 months, 32.9% of patients with IV tPA within 3 h after AIS onset had a modified Rankin Scale score 0–1 vs. 23.1% of the placebo group (5). Similarly, EVT following IV tPA vs. IV tPA alone in a setting of LVO of the anterior circulation significantly reduced disability at 3 months (4).

However, these treatments are by no means entirely free of complications, with intracranial hemorrhage (ICH) the most feared. Hemorrhagic complications after reperfusion therapies include a broad spectrum of severity between small petechial hemorrhagic infarcts (HIs) to parenchymal hematomas (PHs) (6–8). ICH, especially with PH, is associated with increased morbidity and mortality (9, 10). This explains in part why ICH and especially symptomatic ICH (sICH) are mandatory safety outcomes of most AIS RCTs. Nevertheless, the ICH description remains challenging, given its several different classifications and timeframe assessment (8). sICH and asymptomatic ICH after AIS have been differentiated, but the prognostic significance of asymptomatic ICH remains largely unknown. In this review, we discuss the implications of ICH after IV tPA and EVT. After examining the different clinical, radiological, and biological baseline characteristics associated with increased ICH occurrence, we review possible modifiable factors and future therapeutic approaches.

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ICH After Intravenous TPA Therapy

Background

The serine protease tPA is mainly synthesized in endothelial cells and scarcely present in blood in the physiological condition. It converts the proenzyme plasminogen into plasmin. The active form of plasmin cleaves fibrin strands into small fibrin degradation products leading to fibrinolysis. This fibrinolysis cascade is tightly regulated under physiological conditions. Especially, at a physiological concentration, tPA can only activate plasminogen into plasmin when associated with fibrin, thus forming the ternary fibrinolysis complex responsible for a highly local fibrinolysis activation (11). However, numerous studies of IV tPA therapy for acute myocardial infarction have found that with tPA in the therapeutic concentration range, plasminogen can also be converted to plasmin in contact with circulating fibrinogen owing to the incomplete fibrin specificity of tPA. Therefore, plasmin can degrade fibrinogen, thus leading to a corresponding fibrinogen consumption and the formation of fibrinogen products (12, 13). The formation of fibrinogen degradation products with anticoagulant properties, called fibrinogen degradation coagulopathy, was linked to a surplus of hemorrhagic complications in acute myocardial infarction studies (14). In a recent study of AIS patients receiving IV tPA, 20% of patients showed fibrinogen degradation coagulopathy defined as a fibrinogen level decrease ≥200 mg/dL at 6 h after IV tPA infusion, which was associated with increased rate of hemorrhagic complications (15).

The natural history of AIS by itself is associated with the occurrence of delayed ICH, usually called hemorrhagic transformation or hemorrhagic infarction. In the European Cooperative Acute Stroke Study (ECASS) 3 trial, the frequency of any ICH in the placebo group reached 17.6%, with 3.5% being sICH according to the National Institute of Neurological Disorders and Stroke (NINDS) definition (3). Notably, the ICH risk in the setting of AIS without IV tPA therapy remains low, with mainly small petechial HIs associated with baseline stroke severity (16) but with limited, if any, impact on 3 month functional outcome in the ECASS 1 and 2 trials (17–19). These HIs were statistically independent of tPA use in the ECASS 1 and 2 trials and had a paradoxical lower proportion in the tPA group as compared with the placebo group (8). Thus, this ICH could be mainly due to the natural history of AIS and not the IV tPA use (19–22). In the late 1980s and early 1990s, when IV tPA was not approved for AIS and primary management was restricted to clinical monitoring, these HIs were frequently described (43%) and usually associated with severe AIS criteria such as brain edema, mass effect, blood–brain barrier disruption, and baseline neurological severity (22). In the setting of LVO AIS, the proportion of these HIs could even reach 50%, and they were associated with early hypodensities on baseline computed tomography (CT) scans (20). The pathophysiological mechanisms underlying HI development are still not elucidated. Reperfusion has long been cited as a main causal factor for the occurrence of HIs or ICH in general, along with blood pressure or hyperglycemia (23). However, this paradigm is now clearly questioned because of the lack of increased ICH risk observed after EVT-induced reperfusion, as discussed below.

ICH and sICH Definitions

As the most severe complication of IV tPA, ICH defined in the setting of AIS is crucial because it involves key safety outcomes in RCTs and may help neurologists in the everyday management of AIS. ICH can be defined clinically (symptomatic vs. asymptomatic), radiologically (HIs vs. PHs) but also within the timeframe of assessment (early vs. late) (8). The notion of sICH in the setting of AIS was first introduced by Levy et al., requiring contemporaneous neurological worsening or a new mass effect on brain CT scan (24, 25). In the NINDS trial (parts 1 and 2), the clinical aspect of ICH was taken into account by the notion of a “temporally related neurologic deterioration,” without further details (6, 8). The Prolyse in Acute Cerebral Thromboembolism (PROACT) II trial, assessing the efficacy of intra-arterial prourokinase for AIS, was the first trial to specifically define the meaning of clinical deterioration after treatment, as an increase from baseline of four points in the National Institutes of Health Stroke Scale (NIHSS) score (8, 26). Because several conditions may increase the NIHSS score in the setting of AIS (e.g., epilepsy, mass effect, ischemic lesion growth), further trials specified ICH as the presumed responsible cause of neurological deterioration (≥4 points in NIHSS score). The rationale for distinguishing sICH and asymptomatic ICH is prognosis. First, and as mentioned above, asymptomatic ICH usually involves HI lesions as opposed to PH lesions, without any impact on 3 month functional outcome (19). However, this last point must be considered with caution in light of recent studies highlighting the association between asymptomatic ICH after EVT and worse clinical outcome (27, 28). Second, such distinction provides a practical and useful tool for RCTs to assess the safety related to IV tPA use (8).

The radiological distinction was introduced in the early 1990s and first distinguished HI and PH on follow-up CT scan (7). These lesions were used in the NINDS study as “acute infarction with punctate or variable hypodensity/hyperdensity, with an indistinct border within the vascular territory” for HIs and “typical homogeneous, hyperdense lesion with a sharp border with or without edema or mass effect” for PHs (29). In the ECASS trials, these definitions were implemented and improved with the distinction between HI1 and HI2 and PH1 and PH2 (Table 1). Therefore, the ECASS definition includes the ICH mass effect that was not considered in the NINDS definition (<30% or ≥30% of the infarct area with or without space-occupying effect) depending on the PH type. PH1 is associated with risk of early neurological deterioration but not disability or death (19). In contrast, PH2 is strongly associated with early neurological deterioration but also with 3 month disability and death (19). In the ECASS 1 trial, PH1 was not associated with neurological deterioration, disability, or death, but PH2 was strongly associated with early neurological deterioration [odds ratio (OR) = 32.3, 95% confidence interval (CI) = 13.4–77.7] and 3 month death (OR = 18, 95% CI = 8.05–40.1) (30). As discussed below, PH2 is strongly associated with tPA use and increases with tPA dose (3-fold for 0.9 mg/kg and 3.6-fold for 1.1 mg/kg) (8). Given its tremendous clinical significance, the Safe Implementation of Thrombolysis in Stroke-Monitoring Study (SITS-MOST) definition used local or remote PH2 on the 22 to 36 h posttreatment CT scan as a surrogate marker for sICH (Table 1) (31). More recently, the ECASS 4, the Extending the Time for Thrombolysis in Emergency Neurological Deficits (EXTEND), and the Echoplanar Imaging Thrombolytic Evaluation trials also used PH2 for defining sICH, when associated with an increase of four points in NIHSS score (32). Finally, the ICH and sICH classifications may differ regarding the timeframe of evaluation. In brief, the NINDS, PROACT II, and ECASS 1 trials assessed early ICH within 36 h after stroke onset (6, 8, 17, 26). In contrast, other trials considered a delayed timeframe for ICH assessment: within 7 days (3, 33). As discussed, delayed assessment could result in poorer correlations with tPA use, notably owing to its known short half-life and also in the context of EVT (8). In this context, the Heidelberg bleeding classification was developed during the XII Thrombolysis Symposium on Thrombolysis, Thrombectomy and Ischemic Stroke treatment with the aim to propose a revised classification that specifies, in a single format, ICH topography (intraparenchymal, subdural, and subarachnoid, to take into account EVT devices complications); localization (within the infarct or remote); symptomatic or asymptomatic aspects; and type of ICH (HI1, 2; PH1, 2) to harmonize everyday practice and RCT designs (Tables 1, ​,2)2) (25). In the Heidelberg Classification, PH2 is considered a distinct entity from other ICHs owing to its pronounced impact on functional outcome and death. Details are also provided in the original publication to help the clinician distinguish the types of PH (25).

 

Language as a Predictor of Motor Recovery: The Case for a More Global Approach to Stroke Rehabilitation

Will you stop trying to predict recovery and just deliver recovery protocols you blithering idiots. There is not a survivor in the world who cares about predictions, they just want the facts about the efficacy of stroke rehab protocols so they know exactly what they have to do to recover. Have you no brains at all? 

Language as a Predictor of Motor Recovery: The Case for a More Global Approach to Stroke Rehabilitation

Deanna Anderlini, MD, Guy Wallis, PhD, Welber Marinovic, PhD

First Published February 13, 2019 Research Article

https://doi.org/10.1177/1545968319829454

Article information

Abstract

Stroke is the third leading cause of death in the developed world and the primary cause of adult disability. The most common site of stroke is the middle cerebral artery (MCA), an artery that supplies a range of areas involved in both language and motor function. As a consequence, many stroke patients experience a combination of language and motor deficits. Indeed, those suffering from Broca’s aphasia have an 80% chance of also suffering hemiplegia. Despite the prevalence of multifaceted disability in patients, the current trend in both clinical trials and clinical practice is toward compartmentalization of dysfunction. In this article, we review evidence that aphasia and hemiplegia do not just coexist, but that they interact. We review a number of clinical reports describing how therapies for one type of deficit can improve recovery in the other and vice versa. We go on to describe how language deficits should be seen as a warning to clinicians that the patient is likely to experience motor impairment and slower motor recovery, aiding clinicians to optimize their choice of therapy. We explore these findings and offer a tentative link between language and arm function through their shared need for sequential action, which we term fluency. We propose that area BA44 (part of Broca’s area) acts as a hub for fluency in both movement and language, both in terms of production and comprehension.

Keywords hemiparesis, aphasia, rehabilitation, Broca, stroke, language

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Vol 33, Issue 3, 2019

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