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.

Friday, July 31, 2020

Post-stroke Cognitive Impairment—Impact of Follow-Up Time and Stroke Subtype on Severity and Cognitive Profile: The Nor-COAST Study

Oh god, more worthless shitworthy research. Describes a problem, offers NO SOLUTION.   Cognitive impairment has been known for centuries, we don't need more research dissecting it another way. SOLUTIONS ONLY PEOPLE!

And you use the crutch of further research needed to explain why you did nothing useful.

Post-stroke Cognitive Impairment—Impact of Follow-Up Time and Stroke Subtype on Severity and Cognitive Profile: The Nor-COAST Study

Stina Aam1,2*, Marte Stine Einstad1, Ragnhild Munthe-Kaas3,4, Stian Lydersen5, Hege Ihle-Hansen3,4,6, Anne-Brita Knapskog6, Hanne Ellekjær1,7, Yngve Seljeseth8 and Ingvild Saltvedt1,2
  • 1Department of Neuromedicine and Movement Science, Faculty of Medicine and Health Science, NTNU-Norwegian University of Science and Technology, Trondheim, Norway
  • 2Department of Geriatric Medicine, Clinic of Medicine, St. Olavs Hospital, Trondheim University Hospital, Trondheim, Norway
  • 3Department of Medicine, Vestre Viken Hospital Trust, Bærum Hospital, Drammen, Norway
  • 4Institute of Clinical Medicine, University of Oslo, Oslo, Norway
  • 5Department of Mental Health, Faculty of Medicine and Health Science, NTNU-Norwegian University of Science and Technology, Trondheim, Norway
  • 6Department of Geriatric Medicine, Oslo University Hospital, Oslo, Norway
  • 7Stroke Unit, Department of Internal Medicine, St. Olavs Hospital, Trondheim University Hospital, Trondheim, Norway
  • 8Medical Department, Ålesund Hospital, Møre and Romsdal Health Trust, Ålesund, Norway
Background: Post-stroke cognitive impairment (PSCI) is common, but evidence of cognitive symptom profiles, course over time, and pathogenesis is scarce. We investigated the significance of time and etiologic stroke subtype for the probability of PSCI, severity, and cognitive profile.
Methods: Stroke survivors (n = 617) underwent cognitive assessments of attention, executive function, memory, language, perceptual-motor function, and the Montreal Cognitive Assessment (MoCA) after 3 and/or 18 months. PSCI was classified according to DSM-5 criteria. Stroke severity was assessed with the National Institutes of Health Stroke Scale (NIHSS). Stroke subtype was categorized as intracerebral hemorrhage (ICH), large artery disease (LAD), cardioembolic stroke (CE), small vessel disease (SVD), or un-/other determined strokes (UD). Mixed-effects logistic or linear regression was applied with PSCI, MoCA, and z-scores of the cognitive domains as dependent variables. Independent variables were time as well as stroke subtype, time, and interaction between these. The analyses were adjusted for age, education, and sex. The effects of time and stroke subtype were analyzed by likelihood ratio tests (LR).
Results: Mean age was 72 years (SD 12), 42% were females, and mean NIHSS score at admittance was 3.8 (SD 4.8). Probability (95% CI) for PSCI after 3 and 18 months was 0.59 (0.51–0.66) and 0.51 (0.52–0.60), respectively and remained constant over time. Global measures and most cognitive domains were assessed as impaired for the entire stroke population and for most stroke subtypes. Executive function and language improved for the entire stroke population (LR) = 9.05, p = 0.003, and LR = 10.38, p = 0.001, respectively). After dividing the sample according to stroke subtypes, language improved for ICH patients (LR = 18.02, p = 0.003). No significant differences were found in the severity of impairment between stroke subtypes except for attention, which was impaired for LAD and CE in contrast to no impairment for SVD (LR = 56.58, p < 0.001).
Conclusions: In this study including mainly minor strokes, PSCI is common for all subtypes, both early and long-term after stroke, while executive function and language improve over time. The findings might contribute to personalizing follow-up and offer new insights into underlying mechanisms. Further research is needed on underlying mechanisms, PSCI prevention and treatment, and relevance for rehabilitation.

Introduction

Stroke is one of two leading causes of disability-adjusted life-years worldwide (1), and post-stroke cognitive impairment (PSCI) has been shown to be common among stroke survivors. Recent reviews and meta-analyses identified a pooled prevalence of PSCI of 53.4% and mild and major PSCI of 36.4–38 and 16% respectively, measured within 1.5 years post-stroke (2, 3).
Previous studies have reported conflicting results regarding the prognosis for patients suffering PSCI; these have indicated deterioration, no progression, and even improvement in cognition over time for subgroups (411). Several cognitive domains are affected in PSCI; of these, impairment in attention and executive function seem to be the most prevalent and severe shortly after and a long time after suffering a stroke (1216). A recent study on PSCI a short time after a stroke showed a high prevalence of impairment in global cognition and in the five most commonly assessed domains: attention, memory, language, perceptual-motor function, and executive function (17).
The underlying pathological mechanisms for suffering a stroke are heterogeneous, and severity and localization of the stroke are important for PSCI (6, 17, 18). About 10–20% of strokes are hemorrhagic; the rest are ischemic and typically related to large artery disease (LAD), cardioembolic stroke (CE), or small vessel disease (SVD), often labeled lacunar infarction, with about 25% in each category (1921). LAD and CE strokes are often cortical strokes of large volume, while SVD strokes are subcortical and of small volume (22). Cognitive impairment has been shown to be less common in the early post-stroke period in SVD compared to other stroke subtypes, but SVD is associated with cognitive decline long after a stroke (16, 17, 23, 24). However, in their review and meta-analyses, Makin et al. found similar proportions to have PSCI in lacunar vs. non-lacunar stroke [OR 0.75 (95% CI 0.47–1.20)] (25, 26). ICH has been reported to be more strongly associated with dementia than ischemic stroke (6), and impairments in processing speed, executive function, episodic memory, language, and visuo-spatial abilities have been found to be most prevalent (19, 21, 27).
There remains a need for additional knowledge about the course of PSCI and the impact of stroke subtypes on PSCI. Therefore, the aim of this study was to investigate whether time and etiological stroke subtype impact the probability for PSCI and its severity and cognitive symptom profile three and 18 months post-stroke.

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