Thursday, October 3, 2024

Understanding Cognitive Decline After Stroke in the Acute Setting

 Survivors don't want to understand cognitive decline post stroke; they want it prevented you BLITHERING IDIOTS! When the hell will you understand survivor requirements and deliver recovery?

Understanding Cognitive Decline After Stroke in the Acute Setting

JAMA Netw Open. 2024;7(10):e2437145. doi:10.1001/jamanetworkopen.2024.37145

The overall effect of a stroke on global cognitive faculties is a matter of debate. While counterintuitive, most deleterious effects of stroke may be felt by patients in daily activities, movement, or emotion control, and not necessarily in overall cognitive capacity. Moreover, whether global cognitive decline on a population level is caused by stroke itself and not by aging or other neurodegenerative diseases is a matter of debate. Most studies investigating this assosciation do not have high-quality cognitive assessments before and after stroke in large populations.

Lo et al1 investigated the association of a first stroke with global cognition compared with prestroke status in an individual patient data study of 20 860 patients. The included participants were derived from 14 cohorts belonging to the Cohort Studies of Memory in an International Consortium (COSMIC). In these populations, patients were followed up for a mean (SD) of 7.5 (4.2) years.1 The occurrence of a first stroke was self-reported, and global cognition was assessed throughout the follow-up period.1 A first stroke event was reported in 1041 patients (5%), which occurred a mean (SD) of 4.55 (3.7) years after inclusion in their respective studies.1 A linear mixed-effects model with regression discontinuity analysis was performed to measure the impact of a first stroke and to estimate the rate of decline in global cognition. The authors1 found that a first stroke was significantly associated with an acute decline in global cognition and in all cognitive domains individually, except for memory.

Poststroke cognitive decline can occur in up to 60% of patients with stroke, with the highest occurrence in the acute poststroke setting; however, the magnitude of the effect size in terms of cognitive decline has not been estimated in this way in previous studies.2,3 Lo et al1 measured the rate and timing of acute cognitive decline and its yearly acceleration while adjusting for baseline demographics, vascular medical history, and baseline (prestroke) cognitive status. The application of regression discontinuity was introduced in 1960 by Thistlethwaite and Campbell,4 and has a quasi-experimental pretest-posttest design that aims to determine the causal effects of interventions, when randomization is unfeasible. It is more powerful in large population studies with high-quality preintervention and postintervention data. From a study design perspective, this individual patient data study is ideal when randomization is unfeasible.5

Data regarding the stroke incident were self-reported by participants in 12 of the 14 COSMIC member studies.1 Regression discontinuity is a powerful tool that mimics a quasi-experimental temporal study design, with each affected patient as their own counterfactual. If the regression model includes time sensitive variables (in this case, time in study and time since stroke), however, it is important to minimize the probability of recall bias, which could cause an overestimation of the found effect. Self-reporting offers no information on the extent of the stroke incident, or of the clinical and radiological confounders which may influence the overall effect. Additionally, follow-up durations of all COSMIC member studies ranged from 3 to 17 years, which constitutes a considerable range, considering participants were a mean age of 75.5 years at study entry. Of these patients, a considerable proportion were at risk to develop neurodegenerative diseases causing additional cognitive decline.1,6,7 Only patients with a history of stroke or dementia at baseline were excluded from the individual patient data analysis.1 The study did not further account for developing neurodegenerative diseases throughout the follow-up period causing additional cognitive decline. A scientific statement from the American Heart Association and American Stroke Association states that up to 33% of patients with stroke are set to develop dementia within the next 5 years after stroke.7 The older median age in the assessed population, the overall risk of dementia after stroke, and the risk of developing other neurodegenerative diseases confound the interpretation of the acceleration of cognitive decline.

Cognitive impairment impacts the quality of life to at least the extent of, or more than, functional disbaility.7 However, in recent decades, research investigating the impact of stroke on cognition has not received the same attention and priority as functional neurological outcomes in the contemporary poststroke literature. Cognitive outcomes are much more granular than the routinely used modified Rankin scale or National Institutes of Health Stroke Scale. Nevertheless, they constitute the next frontier in stroke evaluation. More effort should be dedicated to, on the one hand, improving assessment tools for cognitive outcomes, and on the other hand, to better understanding the impact of cognitive decline after stroke. The absence of a measured effect on memory is also interesting. On the one hand, the explanation might be neuroanatomical, with the archi- and paleo-cortex being less affected by large vessel occlusion of the neocortical structures. On the other hand, the evaluation of memory might be insufficiently granular.

The scientific contribution of Lo et al1 is a major step in the right direction for the future of long-term stroke outcome assessment. As we develop new devices, indications, and time windows for stroke treatment, it may perhaps be wise to ensure trials steer away from simpler outcomes to more complex, granular ones.

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Article Information

Published: October 2, 2024. doi:10.1001/jamanetworkopen.2024.37145

Open Access: This is an open access article distributed under the terms of the CC-BY License. © 2024 Sadigh Y et al. JAMA Network Open.

Corresponding Author: Victor Volovici, MD, PhD, Department of Neurosurgery, Center for Complex Microvascular Surgery, Erasmus MC University Medical Center, Dr Molewaterplein 40, 3015GD, Rotterdam, The Netherlands (v.volovici@erasmusmc.nl).


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