Cognitive Impairment after Mild Stroke: Development and Validation of the SIGNAL2 Risk Score

Kandiah, Nagaendran; Chander, Russell J.; Lin, Xuling; Ng, Aloysius; Poh, Yen Yeong; Cheong, Chin Yee; Cenina, Alvin Rae; Assam, Pryseley Nkouibert

doi:10.3233/jad-150736

Cited by 52 publications

(78 citation statements)

References 31 publications

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“…35 A number of risk scores have been developed recently to predict poststroke dementia (3 months after stroke, area under the curve: 0.74) 36 and cognitive impairment (6 months after stroke, area under the curve: 0.83). 37 Our review, however, shows that cognitive decline seems to become more apparent over a longer followup period, and thus new models could be developed to predict poststroke cognitive impairment and dementia over longer time periods. Currently there are no specific biomarkers that can help discriminate between those at risk and those with better prognosis.…”

Section: Discussionmentioning

confidence: 96%

“…A risk model approach could be used in stroke populations, incorporating some of these variables identified in this review to predict poststroke dementia 35. A number of risk scores have been developed recently to predict poststroke dementia (3 months after stroke, area under the curve: 0.74)36 and cognitive impairment (6 months after stroke, area under the curve: 0.83) 37. Our review, however, shows that cognitive decline seems to become more apparent over a longer follow‐up period, and thus new models could be developed to predict poststroke cognitive impairment and dementia over longer time periods.…”

Section: Discussionmentioning

confidence: 99%

“…There is evidence, however, of a strong relationship between inflammation markers and cognitive performance,39 and this will need further evaluation before being used in potential risk models. Although neuroimaging variables were used in the cognitive impairment model,37 evidence shows that data from magnetic resonance imaging do not significantly improve prediction in all‐cause dementia models 40. Similarly, there may be less focus on incorporating vascular risk factors into these models because results from a recent clinical trial found that intensively managing vascular risk factors in stroke survivors did not alter cognition after 2 years 41…”

Section: Discussionmentioning

confidence: 99%

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Longitudinal Effect of Stroke on Cognition: A Systematic Review

Tang

Amiesimaka

Harrison

et al. 2018

JAHA

144

114

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BackgroundStroke is associated with an increased risk of dementia; however, the impact of stroke on cognition has been found to be variable, such that stroke survivors can show decline, remain stable, or revert to baseline cognitive functioning. Knowing the natural history of cognitive impairment after stroke is important for intervention. The aim of this systematic review is to investigate the longitudinal course of cognitive function in stroke survivors.Methods and ResultsThree electronic databases (Medline, Embase, PsycINFO) were searched using OvidSP from inception to July 15, 2016. Longitudinal studies with ≥2 time points of cognitive assessment after stroke were included. In total, 5952 articles were retrieved and 14 were included. There was a trend toward significant deterioration in cognitive test scores in stroke survivors (8 studies). Cognitive stability (3 studies) and improvement (3 studies) were also demonstrated, although follow‐up time tended to be shorter in these studies. Variables associated with impairment included age, ethnicity, premorbid cognitive performance, depression, stroke location, and history of previous stroke. Associations with APOE*E4 (apolipoprotein E with the E4 allele) allele status and sex were mixed.ConclusionsStroke is associated with an increased risk of cognitive decline, but cognitive decline is not a consequence. Factors associated with decline, such as sociodemographic status, health‐related comorbidity, stroke history, and clinical features could be used in models to predict future risk of dementia after stroke. A risk model approach could identify patients at greatest risk for timely intervention to reduce the frequency or delay the onset of poststroke cognitive impairment and dementia.

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Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Longitudinal Effect of Stroke on Cognition: A Systematic Review

Tang

Amiesimaka

Harrison

et al. 2018

JAHA

144

114

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“…(2003; 2004; 2006) [42], [43], [44]National Neuroscience Institute study (NNI Singapore)Singapore2011–20175063–6m, 1y up to 5y3–6 mo, 1 y up to 5 yInitialYesKandiah et al. (2011; 2014, 2016) [45], [46], [47]Prognosis of Intracerebral Hemorrhage (PITCH)France2004–ongoing5626 mo, 1 y, 2 y, 3 y, 4.5 y, 6 y, 8 y, 10 y1 y, 2 y, 3 y, 4.5 y, 6 y, 8 y, 10 yInitial, 6 mo; 1 y, 2 y, 3 y, 4.5 y, 6 y, 8 y, 10 yYesCordonnier et al. (2010) [48]; Moulin et al.…”

Section: Methodsmentioning

confidence: 99%

STROKOG (stroke and cognition consortium): An international consortium to examine the epidemiology, diagnosis, and treatment of neurocognitive disorders in relation to cerebrovascular disease

Sachdev

Crawford

et al. 2016

Alz & Dem Diag Ass & Dis Mo

Self Cite

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IntroductionThe Stroke and Cognition consortium (STROKOG) aims to facilitate a better understanding of the determinants of vascular contributions to cognitive disorders and help improve the diagnosis and treatment of vascular cognitive disorders (VCD).MethodsLongitudinal studies with ≥75 participants who had suffered or were at risk of stroke or TIA and which evaluated cognitive function were invited to join STROKOG. The consortium will facilitate projects investigating rates and patterns of cognitive decline, risk factors for VCD, and biomarkers of vascular dementia.ResultsCurrently, STROKOG includes 25 (21 published) studies, with 12,092 participants from five continents. The duration of follow-up ranges from 3 months to 21 years.DiscussionAlthough data harmonization will be a key challenge, STROKOG is in a unique position to reuse and combine international cohort data and fully explore patient level characteristics and outcomes. STROKOG could potentially transform our understanding of VCD and have a worldwide impact on promoting better vascular cognitive outcomes.

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“…Due to an aging population and a decline in post-stroke mortality, strategies for timely diagnosis and disease prevention are urgently needed (3)(4)(5)(6). Post-stroke cognitive impairment follows different trajectories, and risk scores based on clinical and neuroimaging variables are promising (7,8), but do not include amyloid biomarkers. Amyloid positivity has been associated with more severe cognitive decline post-stroke in small studies (9,10), and might be included in future prediction models and personalized management.…”

Section: Introductionmentioning

confidence: 99%

No evidence for amyloid pathology as a key mediator of neurodegeneration post-stroke - a seven-year follow-up study

Hagberg

Ihle‐Hansen²,

Fure

et al. 2020

Preprint

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Background: Cognitive impairment (CI) with mixed vascular and neurodegenerative pathologies after stroke is common. The role of amyloid pathology in post-stroke CI is unclear. We hypothesize that amyloid deposition, measured with Flutemetamol (18F-Flut) positron emission tomography (PET), is common in seven-year stroke survivors diagnosed with CI and, further, that quantitatively assessed 18F-Flut-PET uptake after seven years correlates with amyloid-β peptide (Aβ₄₂) levels in cerebrospinal fluid (CSF) at one year, and with measures of neurodegeneration and cognition at seven years post-stroke. Methods: 208 patients with first-ever stroke or transient Ischemic Attack (TIA) without pre-existing CI were included during 2007 and 2008. At one- and seven-years post-stroke, cognitive status was assessed, and categorized into dementia, mild cognitive impairment or normal. Etiologic sub-classification was based on magnetic resonance imaging (MRI) findings, CSF biomarkers and clinical cognitive profile. At seven years, patients were offered 18F-Flut-PET, and amyloid-positivity was assessed visually and semi-quantitatively. The associations between 18F-Flut-PET standardized uptake value ratios (SUVr) and measures of neurodegeneration (medial temporal lobe atrophy (MTLA), global cortical atrophy (GCA)) and cognition (Mini-Mental State Exam (MMSE), Trail-making test A (TMT-A)) and CSF Aβ₄₂ levels were assessed using linear regression. Results: In total, 111 patients completed 7-year follow-up, and 26 patients agreed to PET imaging, of whom 13 had CSF biomarkers from one year. Thirteen out of 26 patients were diagnosed with CI seven years post-stroke, but only one had visually assessed amyloid positivity. CSF Aβ₄₂ levels at one year, MTA grade, GCA scale, MMSE score or TMT-A at seven years did not correlate with 18F-Flut-PET SUVr in this cohort.Conclusions: Amyloid binding was not common in 7-year stroke survivors diagnosed with CI. Quantitatively assessed, cortical amyloid deposition did not correlate with other measures related to neurodegeneration or cognition. Therefore, amyloid pathology may not be a key mediator of neurodegeneration seven years post-stroke.Trial registration: Clinicaltrials.gov (NCT00506818). July 23, 2007. Inclusion from February 2007, randomization and intervention from May 2007 and trial registration in July 2007.

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Cognitive Impairment after Mild Stroke: Development and Validation of the SIGNAL2 Risk Score

Abstract: The seven item risk score adequately identified mild stroke patients who are at an increased risk of developing PSCI.

Cited by 52 publications

References 31 publications

Longitudinal Effect of Stroke on Cognition: A Systematic Review

Longitudinal Effect of Stroke on Cognition: A Systematic Review

STROKOG (stroke and cognition consortium): An international consortium to examine the epidemiology, diagnosis, and treatment of neurocognitive disorders in relation to cerebrovascular disease

No evidence for amyloid pathology as a key mediator of neurodegeneration post-stroke - a seven-year follow-up study

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