Cognitive and Mood Assessment Tools for Use in Stroke

Quinn, Terence J; Elliott, Emma; Langhorne, Peter

doi:10.1161/strokeaha.117.016994

Cited by 88 publications

(100 citation statements)

References 39 publications

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“…Psychological disturbances, including depression, anxiety-impulsivity, aggression-submission, and psychosis are increasingly recognized as a manifestation of the pathological features present in AD and other age-related neurodegenerative diseases [ 12 , 45 , 71 , 95 ]. Adult hAPP-SL mice display significant psychological disturbances such as anxiety- and submissive-like behaviors, and sensorimotor gating deficits compared to their wt littermates (Nguyen TV et al, unpublished data).…”

Section: Resultsmentioning

confidence: 99%

Alzheimer’s associated amyloid and tau deposition co-localizes with a homeostatic myelin repair pathway in two mouse models of post-stroke mixed dementia

Nguyen

Hayes

Zbesko

et al. 2018

acta neuropathol commun

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The goal of this study was to determine the chronic impact of stroke on the manifestation of Alzheimer’s disease (AD) related pathology and behavioral impairments in mice. To accomplish this goal, we used two distinct models. First, we experimentally induced ischemic stroke in aged wildtype (wt) C57BL/6 mice to determine if stroke leads to the manifestation of AD-associated pathological β-amyloid (Aβ) and tau in aged versus young adult wt mice. Second, we utilized a transgenic (Tg) mouse model of AD (hAPP-SL) to determine if stroke leads to the worsening of pre-existing AD pathology, as well as the development of pathology in brain regions not typically expressed in AD Tg mice. In the wt mice, there was delayed motor recovery and an accelerated development of cognitive deficits in aged mice compared to young adult mice following stroke. This corresponded with increased brain atrophy, increased cholinergic degeneration, and a focal increase of Aβ in areas of axonal degeneration in the ipsilateral hemisphere of the aged animals. By contrast, in the hAPP-SL mice, we found that ischemia induced aggravated behavioral deficits in conjunction with a global increase in Aβ, tau, and cholinergic pathology compared to hAPP-SL mice that underwent a sham stroke procedure. With regard to a potential mechanism, in both models, we found that the stroke-induced Aβ and tau deposits co-localized with increased levels of β-secretase 1 (BACE1), along with its substrate, neuregulin 1 (NGR1) type III, both of which are proteins integral for myelin repair. Based on these findings, we propose that the chronic sequelae of stroke may be ratcheting-up a myelin repair pathway, and that the consequent increase in BACE1 could be causing an inadvertent cleavage of its alternative substrate, AβPP, resulting in greater Aβ seeding and pathogenesis.

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Section: Resultsmentioning

confidence: 99%

Alzheimer’s associated amyloid and tau deposition co-localizes with a homeostatic myelin repair pathway in two mouse models of post-stroke mixed dementia

Nguyen

Hayes

Zbesko

et al. 2018

acta neuropathol commun

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“…Although we consider our results as preliminary, they are not without clinical implications. Currently, there is a lack of consensus guidelines on delivering assessments and care focused on cognition following stroke or TIA [68,69]. Most stroke services have insufficient resources to address these issues consistently for all patients, and therefore, it is important to identify who is most likely to experience cognitive impairment.…”

Section: Discussionmentioning

confidence: 99%

Cardiovascular risk factors indirectly affect acute post-stroke cognition through stroke severity and prior cognitive impairment: a moderated mediation analysis

et al. 2020

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Background: Cognitive impairment is an important consequence of stroke and transient ischaemic attack, but its determinants are not fully understood. Simple univariable or multivariable models have not shown clinical utility for predicting cognitive impairment. Cardiovascular risk factors may influence cognition through multiple, direct, and indirect pathways, including effects on prior cognition and stroke severity. Understanding these complex relationships may help clinical teams plan intervention and follow-up strategies. Methods: We analysed clinical and demographic data from consecutive patients admitted to an acute stroke ward. Cognitive assessment comprised Abbreviated Mental Test and mini-Montreal Cognitive Assessment. We constructed bias-corrected confidence intervals to test indirect effects of cardiovascular risk factors (hypertension, vascular disease, atrial fibrillation, diabetes mellitus, previous stroke) on cognitive function, mediated through stroke severity and history of dementia, and we assessed moderation effects due to comorbidity. Results: From 594 eligible patients, we included 587 in the final analysis (age range 26-100; 45% female). Our model explained R 2 = 62.10% of variance in cognitive test scores. We found evidence for an indirect effect of previous stroke that was associated with increased risk of prevalent dementia and in turn predicted poorer cognitive score (estimate = − 0.39; 95% bias-corrected CI, − 0.75 to − 0.13; p = 0.02). Atrial fibrillation was associated with greater stroke severity and in turn with a poorer cognitive score (estimate = − 0.27; 95% bias-corrected CI, − 0.49 to − 0.05; p = 0.02). Conversely, previous TIA predicted decreased stroke severity and, through that, lesser cognitive impairment (estimate = 0.38; 95% bias-corrected CI, 0.08 to 0.75; p = 0.02). Through an association with reduced stroke severity, vascular disease was associated with lesser cognitive impairment, conditional on presence of hypertension and absence of diabetes mellitus (estimate = 0.36; 95% bias-corrected CI, 0.03 to 0.68; p = 0.02), although the modelled interaction effects did not reach statistical significance.

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“…Studies demonstrate greater sensitivity of the OCS scale over the MMSE scale, with a much higher incidence of cognitive impairment detected using the OCS (91% at least one domain impairment) than the MMSE (35%). 23 There is also evidence of better performance of these patients on the evaluation of sub-items of the OCS compared to the MoCA 27 and there is also evidence of greater sensitivity of the MoCA over the MMSE. 14 Overall, it appears that cognitive deficits following stroke are more effectively detected by specially designed tools to capture deficits following stroke than by tools originally designed for dementia.…”

Section: Discussionmentioning

confidence: 99%

Oxford Cognitive Screen – Brazilian Portuguese version (OCS-Br) A pilot study

Ramos

Amado

Borges

et al. 2018

Dement. neuropsychol.

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Cognitive impairment is very common in stroke patients and underdiagnosed. Symptoms such as language, praxis, visuospatial, visuoconstructive and memory impairment are prominent. The screening cognitive tests available do not address some specific characteristics of stroke patients and have major limitations in relation to the most impaired cognitive domains.Objective:To test the applicability of a Brazilian version of the Oxford Cognitive Screen in a convenience sample of individuals with normal cognition.Methods:Thirty neurologically healthy participants underwent the OCS-Br in this pilot study.Results:The mean score on each task was: naming: 3.4 (SD=0.72) (maximum value of 4); semantics: 3 (SD=0) (maximum 3); orientation: 4 (SD=0) (maximum 4); visual field: 4 (SD=0) (maximum 4); sentence reading: 14.53 (SD: 1) (maximum 15); number writing: 2.86 (0.6) (maximum 3); calculation: 3.8 (SD=0.48) (maximum 4); and accuracy on the broken hearts test: 47.3 (3.3) (maximum 50). The scores obtained were similar to those of the English original sample.Conclusion:We observed similar values on each separate OCS task in comparison to the original test, confirming that the Brazilian Portuguese version is comparable to other studies.

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Cognitive and Mood Assessment Tools for Use in Stroke

Abstract: Running title:Cognitive and mood testingWord count:5362

Cited by 88 publications

References 39 publications

Alzheimer’s associated amyloid and tau deposition co-localizes with a homeostatic myelin repair pathway in two mouse models of post-stroke mixed dementia

Alzheimer’s associated amyloid and tau deposition co-localizes with a homeostatic myelin repair pathway in two mouse models of post-stroke mixed dementia

Cardiovascular risk factors indirectly affect acute post-stroke cognition through stroke severity and prior cognitive impairment: a moderated mediation analysis

Oxford Cognitive Screen – Brazilian Portuguese version (OCS-Br) A pilot study

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