Vascular Cognitive Impairment and Post-Stroke Cognitive Deficits

2013 ◽  
Vol 14 (1) ◽  
Author(s):  
HyungSub Shim
Keyword(s):  
Cognitive Impairment ◽  
Cognitive Deficits ◽  
Vascular Cognitive Impairment ◽  
Post Stroke

scholarly journals Post-stroke cognitive impairment on the Mini-Mental State Examination primarily relates to left middle cerebral artery infarcts

2021 ◽  
pp. 174749302098455
Author(s):  
Nick A Weaver ◽  
Angelina K Kancheva ◽  
Jae-Sung Lim ◽  
J Matthijs Biesbroek ◽  
Irene MC Huenges Wajer ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Cognitive Deficits ◽  
Mini Mental State Examination ◽  
Left Middle Cerebral Artery ◽  
Post Stroke ◽  
Lesion Symptom Mapping ◽  
State Examination ◽  
Left Middle

Background Post-stroke cognitive impairment can occur after damage to various brain regions, and cognitive deficits depend on infarct location. The Mini-Mental State Examination (MMSE) is still widely used to assess post-stroke cognition, but it has been criticized for capturing only certain cognitive deficits. Along these lines, it might be hypothesized that cognitive deficits as measured with the MMSE primarily involve certain infarct locations. Aims This comprehensive lesion-symptom mapping study aimed to determine which acute infarct locations are associated with post-stroke cognitive impairment on the MMSE. Methods We examined associations between impairment on the MMSE (<5th percentile; normative data) and infarct location in 1198 patients (age 67 ± 12 years, 43% female) with acute ischemic stroke using voxel-based lesion-symptom mapping. As a frame of reference, infarct patterns associated with impairments in individual cognitive domains were determined, based on a more detailed neuropsychological assessment. Results Impairment on the MMSE was present in 420 patients (35%). Large voxel clusters in the left middle cerebral artery territory and thalamus were significantly (p < 0.01) associated with cognitive impairment on the MMSE, with highest odds ratios (>15) in the thalamus and superior temporal gyrus. In comparison, domain-specific impairments were related to various infarct patterns across both hemispheres including the left medial temporal lobe (verbal memory) and right parietal lobe (visuospatial functioning). Conclusions Our findings indicate that post-stroke cognitive impairment on the MMSE primarily relates to infarct locations in the left middle cerebral artery territory. The MMSE is apparently less sensitive to cognitive deficits that specifically relate to other locations.

scholarly journals Severe carotid artery stenosis evaluated by ultrasound is associated with post stroke vascular cognitive impairment

2016 ◽  
Vol 7 (1) ◽  
pp. e00606 ◽  
Author(s):  
Xuefeng Li ◽  
Xiangling Ma ◽  
Jing Lin ◽  
Xiangqin He ◽  
Feng Tian ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Carotid Artery ◽  
Carotid Artery Stenosis ◽  
Vascular Cognitive Impairment ◽  
Artery Stenosis ◽  
Post Stroke

scholarly journals Towards the concept of disease-modifier in post-stroke or vascular cognitive impairment: a consensus report

BMC Medicine ◽  
2017 ◽  
Vol 15 (1) ◽  
Author(s):  
Régis Bordet ◽  
Ralf Ihl ◽  
Amos D. Korczyn ◽  
Giuseppe Lanza ◽  
Jelka Jansa ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Vascular Cognitive Impairment ◽  
Concept Of Disease ◽  
Post Stroke ◽  
Disease Modifier ◽  
Consensus Report

scholarly journals Vascular Cognitive Impairment: Information from Animal Models on the Pathogenic Mechanisms of Cognitive Deficits

2019 ◽  
Vol 20 (10) ◽  
pp. 2405 ◽  
Author(s):  
Jakub Hort ◽  
Martin Vališ ◽  
Kamil Kuča ◽  
Francesco Angelucci
Keyword(s):  
Cognitive Impairment ◽  
Animal Models ◽  
Cognitive Deficits ◽  
Molecular Mechanisms ◽  
Target Population ◽  
Vascular Cognitive Impairment ◽  
Toxic Waste ◽  
Waste Products ◽  
Cascade Effects ◽  
Vascular Clearance

Vascular cognitive impairment (VCI) is the second most common cause of cognitive deficit after Alzheimer’s disease. Since VCI patients represent an important target population for prevention, an ongoing effort has been made to elucidate the pathogenesis of this disorder. In this review, we summarize the information from animal models on the molecular changes that occur in the brain during a cerebral vascular insult and ultimately lead to cognitive deficits in VCI. Animal models cannot effectively represent the complex clinical picture of VCI in humans. Nonetheless, they allow some understanding of the important molecular mechanisms leading to cognitive deficits. VCI may be caused by various mechanisms and metabolic pathways. The pathological mechanisms, in terms of cognitive deficits, may span from oxidative stress to vascular clearance of toxic waste products (such as amyloid beta) and from neuroinflammation to impaired function of microglia, astrocytes, pericytes, and endothelial cells. Impaired production of elements of the immune response, such as cytokines, and vascular factors, such as insulin-like growth factor 1 (IGF-1), may also affect cognitive functions. No single event could be seen as being the unique cause of cognitive deficits in VCI. These events are interconnected, and may produce cascade effects resulting in cognitive impairment.

Abstract WP155: Delayed Administration of Angiotensin Receptor (AT2-R) Agonist C21 Downregulates Diabetes Induced Pro-Inflammatory Microglia Activation Post-Stroke in Female Rats: Therapeutic Indications for Vascular Cognitive Impairment & Dementia

Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Ladonya Jackson ◽  
Wael Eldahshan ◽  
Guangkuo Dong ◽  
Selin Dumanli ◽  
Sarah Jamil ◽  
...  
Keyword(s):  
Cell Culture ◽  
Cognitive Impairment ◽  
Chronic Inflammation ◽  
Disease Modeling ◽  
Therapeutic Option ◽  
Experimental Studies ◽  
Vascular Cognitive Impairment ◽  
Female Rats ◽  
Post Stroke ◽  
Comorbid Diseases

Post-stroke cognitive impairment (PSCI) occurs in up to 48% of patients, for which there is no therapy. Although 70% of stroke victims present with comorbid diseases such as diabetes and hypertension, the inadequate integration of these comorbidities into experimental studies limited our understanding of the mechanisms involved in the development of PSCI. Based on our recent findings that 1) the increased prevalence of PSCI in male diabetic animals is linked to heightened chronic inflammation and 2) even delayed administration of compound 21 (C21), an angiotensin II Type 2 receptor agonist, effectively reduces PSCI by lowering inflammation in male animals, we hypothesized that a delayed administration of C21 would also lower chronic inflammation post-stroke in female animals. Methods: Diabetes was induced by a high fat diet (HFD) and low dose streptozotocin (STZ) combination. Rats were subjected to 1 h middle cerebral artery occlusion (MCAO) or sham surgery. 3 days post-stroke, rats were administered C21 or vehicle in drinking water at a dose of 0.12 mg/kg/day for 4 weeks. The direct effect of C21 on microglia polarization was determined in mouse cells (C8B4) and the mature:pro BDNF ratio was evaluated through western blot. Samples from freshly harvested brains (B-D slice containing the prefrontal cortex through the hippocampus), and from cell culture were analyzed by flow cytometry. Results: Delayed administration of C21 starting 3 days post-stroke improved inflammation through modulation of the M1/M2 ratio. Cell culture results indicated that along with decreasing the M1/M2 ratio, it also increased the mature/pro-BDNF ratio. Conclusion: Delayed administration of C21 downregulates post-stroke inflammation in both male and female diabetic animals. This study emphasizes the importance of translational disease modeling and suggests that C21 may be a useful therapeutic option to lower inflammation and prevent PSCI in comorbid diseases.

Post-stroke cognitive impairment

2020 ◽  
pp. 381-398
Author(s):  
Sandeep Ankolekar ◽  
Michela Simoni
Keyword(s):  
Cognitive Impairment ◽  
Vascular Dementia ◽  
Vascular Cognitive Impairment ◽  
International Classification Of Diseases ◽  
Great Depth ◽  
Cognitive Disorder ◽  
Post Stroke ◽  
Classification Of Diseases ◽  
Icd 10

‘Post-stroke cognitive impairment’ explores in great depth the burden of post-stroke cognitive impairment, its pathological substrates and clinical characteristics, the causes of these impairments, post-stroke dementia, and the risk factors implicated. The chapter examines common definitions (vascular cognitive impairment, vascular dementia, post-stroke cognitive impairment), the DSM-5 criteria (Diagnostic and Statistical Manual of Mental Disorders-5), ICD-10 criteria (International Classification of Diseases), NINDS-AIREN criteria (National Institute of Neurological Disorders and Stroke and the Association Internationale pour la Recherche et l’Enseignement en Neurosciences) for vascular dementia, and vascular mild cognitive impairment. The VASCOG (vascular cognitive disorder) criteria are also described. A pragmatic approach to investigations and various assessment scales, a description of important clinical trials, and the management of these disorders are also included.

Late-onset-psychosis: cognition

2011 ◽  
Vol 23 (8) ◽  
pp. 1301-1316 ◽  
Author(s):  
Caroline Girard ◽  
Martine Simard ◽  
Robert Noiseux ◽  
Louis Laplante ◽  
Michel Dugas ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Cognitive Deficits ◽  
Clinical Judgment ◽  
Late Onset ◽  
Vascular Cognitive Impairment ◽  
Geriatric Psychiatry ◽  
Psychotic Symptoms ◽  
Significant Difference ◽  
Clinical Diagnoses ◽  
Patient Groups

ABSTRACTBackground: The objectives of the study were to characterize and compare the cognitive profile and natural evolution of patients presenting late-onset psychotic symptoms (LOPS: onset ≥50 years old) to those of elderly patients (≥50 years old) with life-long/early-onset schizophrenia (EOS: onset <40 years old).Methods: Neuropsychological profiles of 15 LOPS patients were compared to those of 17 elderly EOS patients and to those of two control groups (n = 11/group). The evolution of the two patient groups was compared using an independent diagnostic consensual procedure involving a geriatric psychiatry physician/clinician and a neuropsychologist blinded to the initial psychiatric diagnosis.Results: EOS presented significant memory and executive impairments when compared to controls but there was no significant difference between LOPS and their controls when age and education were taken into account. However, a detailed inspection of normative data suggests more executive impairments in LOPS than in EOS. The clinical judgment of experts was in favour of significant cognitive deficits with or without dementia in most LOPS (82.3%–94.1%) and EOS (80.0%–93.3%) patients. Regarding evolution, mild cognitive impairment (MCI) and vascular cognitive impairment (VCI) were the most common clinical diagnoses made by geriatric psychiatry physicians/clinicians for the LOPS (40%). In addition, 20% of LOPS versus 5.9% of EOS patients met the diagnostic criteria for dementia by consensus of the experts. Cerebral abnormalities were confirmed (CT scan; SPECT) in 73.3% of LOPS patients.Conclusion: The present results suggest cognitive deficits (mostly of executive functions) and vascular and neurodegenerative vulnerability in LOPS. Further studies with larger samples are needed to confirm the present findings.

scholarly journals Methods for Improving Screening for Vascular Cognitive Impairment Using the Montreal Cognitive Assessment

2020 ◽  
Vol 47 (6) ◽  
pp. 756-763 ◽  
Author(s):  
Khush-Bakht Zaidi ◽  
Jill B. Rich ◽  
Kelly M. Sunderland ◽  
Malcolm A. Binns ◽  
Linda Truong ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Processing Speed ◽  
Cognitive Assessment ◽  
Roc Curves ◽  
Vascular Cognitive Impairment ◽  
Cognitive Status ◽  
Montreal Cognitive Assessment ◽  
Cut Points ◽  
Post Stroke ◽  
Speed Measure

ABSTRACT:Background:Vascular cognitive impairment (VCI) post-stroke is frequent but may go undetected, which highlights the need to better screen cognitive functioning following a stroke.Aim:We examined the clinical utility of the Montreal Cognitive Assessment (MoCA) in detecting cognitive impairment against a gold-standard neuropsychological battery.Methods:We assessed cognitive status with a comprehensive battery of neuropsychological tests in 161 individuals who were at least 3-months post-stroke. We used receiver operating characteristic (ROC) curves to identify two cut points for the MoCA to maximize sensitivity and specificity at a minimum 90% threshold. We examined the utility of the Symbol Digit Modalities Test, a processing speed measure, to determine whether this additional metric would improve classification relative to the MoCA total score alone.Results:Using two cut points, 27% of participants scored ≤ 23 and were classified as high probability of cognitive impairment (sensitivity 92%), and 24% of participants scored ≥ 28 and were classified as low probability of cognitive impairment (specificity 91%). The remaining 48% of participants scored from 24 to 27 and were classified as indeterminate probability of cognitive impairment. The addition of a processing speed measure improved classification for the indeterminate group by correctly identifying 65% of these individuals, for an overall classification accuracy of 79%.Conclusions:The utility of the MoCA in detecting cognitive impairment post-stroke is improved when using a three-category approach. The addition of a processing speed measure provides a practical and efficient method to increase confidence in the determined outcome while minimally extending the screening routine for VCI.

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