Abstract TMP113: Long-term Cognitive Decline After Intracerebral Hemorrhage

Stroke ◽  
2016 ◽  
Vol 47 (suppl_1) ◽  
Author(s):  
Alessandro Biffi ◽  
Christopher D Anderson ◽  
Alison M Ayres ◽  
Steven M Greenberg ◽  
Jonathan Rosand ◽  
...  

Introduction: Cerebral small vessel disease (CSVD) is the leading cause of Vascular Cognitive Impairment (VCI). Although Intracerebral Hemorrhage (ICH) is the most severe manifestation of CSVD, VCI among ICH survivors has been the subject of limited investigations. Hypothesis: We sought to test these hypotheses: 1) long-term cognitive decline rates are substantial even among initially non-demented ICH survivors; 2) underlying CSVD plays a substantial role in determining post-ICH long-term cognitive decline. Methods: We enrolled survivors of primary ICH, with no evidence of dementia 6 months post-hemorrhage, in a single-center longitudinal observational study. Presence and severity of CSVD was assessed at enrollment using two established markers of CSVD on CT (CT-defined white hatter hypodensity [CT-WMH]) and MRI (cerebral microbleeds [CMBs]). We captured blood pressure measurements during follow-up via review of medical records. Cognitive performance was assessed using the Modified Telephone Interview for Cognitive Status (TICS-m), a standardized validated telephone-based cognitive battery. We constructed multivariate models of cognitive decline rate, defined as slope of TICS-m scores over time. Results: A total of 275 ICH survivors qualified for inclusion in our analyses; of these 83 (30%) developed incident dementia and 33 (12%) developed incident Mild Cognitive Impairment (MCI) at 5 years (Figure). CSVD imaging markers were associated with cognitive decline rate (CT-WMH: p=0.001, CMBs: p=0.003), as were pulse pressure (p=0.003) and systolic blood pressure variation coefficient (p=0.034). Conclusions: Long-term cognitive decline is frequent and substantial among ICH survivors not demented at time of ICH, and strongly associates with severity of underlying CSVD. Our findings suggest that it is the extent of CSVD and not particular ICH characteristics that are most associated with long-term cognitive decline in survivors of ICH.

Author(s):  
Pingping Jia ◽  
Helen W.Y. Lee ◽  
Joyce Y.C. Chan ◽  
Karen K.L. Yiu ◽  
Kelvin K.F. Tsoi

High blood pressure (BP) is considered as an important risk factor for cognitive impairment and dementia. BP variability (BPV) may contribute to cognitive function decline or even dementia regardless of BP level. This study aims to investigate whether BPV is an independent predictor for cognitive impairment or dementia. Literature searches were performed in MEDLINE, Embase, PsycINFO, CINAHL, and Web of Science to May 2021. Longitudinal studies that assessed the risk of dementia or cognitive impairment with BPV as the predictor was included. Meta-analysis and meta-regression were performed to evaluate the effect of BPV on the risk of dementia or cognitive impairment. A total of 5919 papers were identified, and 16 longitudinal studies were included, which had >7 million participants and a median age from 50.9 to 79.9 years and a median follow-up of around 4 years. Thirteen studies reported visit-to-visit BPV and concluded that systolic BPV increases the risk of dementia with a pooled hazard ratio of 1.11 (95% CI, 1.05–1.17), and increases the risk of cognitive impairment with a pooled hazard ratio of 1.10 (95% CI, 1.06–1.15). Visit-to-visit diastolic BPV also increased the risk of dementia and cognitive decline. A meta-regression revealed a linear relationship between higher BPV and risks of dementia and cognitive impairment. Similar findings were observed in the studies with day-to-day BPV. This study suggests that long-term BPV is an independent risk factor for cognitive impairment or dementia, so an intervention plan for reducing BPV can be a target for early prevention of dementia.


Author(s):  
Michael E. Ernst ◽  
Joanne Ryan ◽  
Enayet K. Chowdhury ◽  
Karen L. Margolis ◽  
Lawrence J. Beilin ◽  
...  

Background Blood pressure variability (BPV) in midlife increases risk of late‐life dementia, but the impact of BPV on the cognition of adults who have already reached older ages free of major cognitive deficits is unknown. We examined the risk of incident dementia and cognitive decline associated with long‐term, visit‐to‐visit BPV in a post hoc analysis of the ASPREE (Aspirin in Reducing Events in the Elderly) trial. Methods and Results ASPREE participants (N=19 114) were free of dementia and significant cognitive impairment at enrollment. Measurement of BP and administration of a standardized cognitive battery evaluating global cognition, delayed episodic memory, verbal fluency, and processing speed and attention occurred at baseline and follow‐up visits. Time‐to‐event analysis using Cox proportional hazards regression models were used to calculate hazard ratios (HR) and corresponding 95% CI for incident dementia and cognitive decline, according to tertile of SD of systolic BPV. Individuals in the highest BPV tertile compared with the lowest had an increased risk of incident dementia and cognitive decline, independent of average BP and use of antihypertensive drugs. There was evidence that sex modified the association with incident dementia (interaction P =0.02), with increased risk in men (HR, 1.68; 95% CI, 1.19–2.39) but not women (HR, 1.01; 95% CI, 0.72–1.42). For cognitive decline, similar increased risks were observed for men and women (interaction P =0.15; men: HR, 1.36; 95% CI, 1.16–1.59; women: HR, 1.14; 95% CI, 0.98–1.32). Conclusions High BPV in older adults without major cognitive impairment, particularly men, is associated with increased risks of dementia and cognitive decline. Registration URL: https://www.clinicaltrials.gov ; Unique identifier: NCT01038583; isrctn.com . Identifier: ISRCTN83772183.


Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Wenjun Deng ◽  
David McMullin ◽  
Lindsay Fisher ◽  
Richard Chou ◽  
Jared Jacobson ◽  
...  

Background: Hypertension (HTN) is a well-recognized risk factor for vascular cognitive decline. Poorly controlled HTN is common in the outpatient setting, with multi-factorial components including a lack of consistent, continuous and accurate reporting of blood pressure (BP) to help clinicians to tailor therapy. In the current prospective study, we explore the association of stroke patients’ at-home BP self-monitoring compliance with clinical and imaging risk markers of developing cognitive impairment. Method: 146 consecutive stroke outpatients with diagnosed HTN were recruited per IRB protocol. All patients received BP education at their first clinical visit and were encouraged to monitor BP at home on a daily basis for two weeks three times during the course of the 5-year study. Compliance with BP monitoring was evaluated by completed BP log and questionnaire in follow-up visits at fixed intervals. At the end of the study, white matter disease (WMD) severity was estimated by Fazekas and Sheltens scores. Cognitive impairment was assessed using Montreal Cognitive Assessment (MoCA) scales. Result: Only 16.4% (n=24) patients had “good compliance,” monitoring their home BP regularly and consistently as instructed. The compliant group had better controlled systolic and diastolic BP (Figure A, p<0.05). As measured by Fazekas and Sheltens scales, patients compliant with BP monitoring had lower WMD burden (Figure B, p<0.05), and higher MoCA scores (Figure C, p=0.012) compared to noncompliant patients. Conclusion: Compliance with at-home BP monitoring is essential for better BP control in vascular cognitive impairment (VCI) patients post stroke. Consistent home BP monitoring resulted in decreased imaging-apparent small vessel disease and better long-term cognitive performance. Expanded study with a larger patient cohort is ongoing to account for other behavioral and psycho-social factors and to create improved home monitoring technology and treatment strategies.


2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Yu-Hui Liu ◽  
Ye-Ran Wang ◽  
Qing-Hua Wang ◽  
Yang Chen ◽  
Xian Chen ◽  
...  

Abstract Background Understanding the long-term effects of coronavirus disease 2019 (COVID-19) on cognitive function is essential for monitoring the cognitive decline in the elderly population. This study aims to assess the current cognitive status and the longitudinal cognitive decline in elderly patients recovered from COVID-19. Methods This cross-sectional study recruited 1539 COVID-19 inpatients aged over 60 years who were discharged from three COVID-19-designated hospitals in Wuhan, China, from February 10 to April 10, 2020. In total, 466 uninfected spouses of COVID-19 patients were selected as controls. The current cognitive status was assessed using a Chinese version of the Telephone Interview of Cognitive Status-40 (TICS-40) and the longitudinal cognitive decline was assessed using an Informant Questionnaire on Cognitive Decline in the Elderly (IQCODE). Cognitive assessments were performed 6 months after patient discharge. Results Compared with controls, COVID-19 patients had lower TICS-40 scores and higher IQCODE scores [TICS-40 median (IQR): 29 (25 to 32) vs. 30 (26 to 33), p < 0.001; IQCODE median (IQR): 3.19 (3.00 to 3.63) vs. 3.06 (3.00 to 3.38), p < 0.001]. Severe COVID-19 patients had lower TICS-40 scores and higher IQCODE scores than non-severe COVID-19 patients [TICS-40 median (IQR): 24 (18 to 28) vs. 30 (26 to 33), p < 0.001; IQCODE median (IQR): 3.63 (3.13 to 4.31) vs. 3.13 (3.00 to 3.56), p < 0.001] and controls [TICS-40 median (IQR): 24 (18 to 28) vs. 30 (26 to 33), p < 0.001; IQCODE median (IQR) 3.63 (3.13 to 4.31) vs. 3.06 (3.00 to 3.38), p < 0.001]. Severe COVID-19 patients had a higher proportion of cases with current cognitive impairment and longitudinal cognitive decline than non-severe COVID-19 patients [dementia: 25 (10.50 %) vs. 9 (0.69 %), p < 0.001; Mild cognitive impairment (MCI): 60 (25.21 %) vs. 63 (4.84 %), p < 0.001] and controls [dementia: 25 (10.50 %) vs. 0 (0 %), p < 0.001; MCI: 60 (25.21 %) vs. 20 (4.29 %), p < 0.001)]. COVID-19 severity, delirium and COPD were risk factors of current cognitive impairment. Low education level, severe COVID-19, delirium, hypertension and COPD were risk factors of longitudinal cognitive decline. Conclusions Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is associated with an increased risk of long-term cognitive decline in elderly population. COVID-19 patients, especially severe patients, should be intensively monitored for post-infection cognitive decline.


Stroke ◽  
2017 ◽  
Vol 48 (suppl_1) ◽  
Author(s):  
Alessandro Biffi ◽  
Christina Kourkoulis ◽  
Kristin Schwab ◽  
Alison M Ayres ◽  
M. Edip Gurol ◽  
...  

Introduction: Survivors of Intracerebral Hemorrhage (ICH) are at high risk for developing long-term incident cognitive decline and depression. However, owing largely to limited data on long-term post-ICH depression risk, the degree to which these two forms of post-hemorrhage clinical deterioration overlap is unknown. Hypothesis: post-ICH depression is highly incident, and associated with long-term cognitive decline risk. Methods: We followed longitudinally 695 ICH survivors with no prior history of depression. Exposures of interest included clinical information, known genetic risk factors for ICH / post-ICH dementia (APOE ε2/ε4), and imaging manifestations of cerebral small vessel disease on CT (CT-defined white matter disease [CT-WMD]). We captured outcomes (incident depression and dementia) during follow-up using validated scales administered via telephone every 6 months. Results: A total of 271/695 ICH survivors (40%) developed new-onset mood disorder during a median follow-up time of 49.6 months (Figure). We estimated an incidence rate of 6.9% yearly (95% CI 5.5-8.8%) for post-ICH depression. Independent risk factors for post-ICH depression included lower educational achievements, APOE ε4, and moderate/severe CT-WMD (all p<0.05). Depression and dementia were co-diagnosed in 135/214 individuals (63%). Depression preceded post-ICH dementia in 108/135 cases (80%, 95% CI 71-88%, p = 0.002), with median anticipation of 17.5 months (IQR = 12.8-23.9). Conclusions: we conducted the first-ever systematic evaluation of long-term post-ICH depression, which affects a large proportion of ICH survivors and shares risk factors (education, APOE genotype, CT-WMD severity) with risk for ICH recurrence and post-ICH dementia. Newly diagnosed depression often signals impending onset of dementia after ICH.


2020 ◽  
Vol 30 (Supplement_5) ◽  
Author(s):  
P S Kostadinova ◽  
G N Atanasova ◽  
S D Kostadinov ◽  
S S Kostadinov

Abstract Background Metabolic syndrome (MetS), a risk factor for many vascular conditions, may be a prodromal manifestation of vascular cognitive impairment. Diagnosing early stages of cerebrovascular pathology can lead to prevention and delay of the progression of pathological conditions such as vascular cognitive impairment. Methods The objective of the study was to investigate new biomarkers for early diagnosis of MetS and cognitive decline as a follow-up. A cardiological, neuropsychological and neurological study was conducted among 75 Bulgarian participants. Beta amyloid in the blood, procalcitonin (PCT), NT-proBNP as predictors of cognitive impairment in patients with metabolic syndrome were identified. Clinical, anthropometric, biochemical, neuropsychological, cognitive and statistical data processing. Plasma amyloid beta (Aβ) levels, procalcitonin, NT-proBNP in MetS were investigated in participants with MetS and in group of healthy people. Results In the present study, plasma levels of Aβ42 and Aβ40 were found to be reduced in MetS participants. Procalcitonin concentration was significantly higher in males than in females. NT-proBNP was significantly higher in females than in males (p &lt; 0.001). Regression analysis showed a positive relationship between NT-proBNP and systolic blood pressure (p &lt; 0.001) and fasting blood glucose (p &lt; 0.05). An inverse relation between NT-proBNP and diastolic blood pressure, waist circumference, triglycerides, HDL- and LDL cholesterol was found. Conclusions There was a positive association between PCT levels, decreased levels of Aβ42 and Aβ40, as well as elevated NT-proBNP and cognitive impairment in people with MetC. A concentration of NT-proBNP of 60 pg / ml or greater could be an indicator of metabolic abnormalities and early cognitive decline. Key messages Metabolic syndrome may be a prodromal manifestation of vascular cognitive impairment. The use of new biomarkers for diagnosis can lead to preventing and slowing the progression of complications associated with MetS.


2003 ◽  
Vol 15 (S1) ◽  
pp. 71-75 ◽  
Author(s):  
Paul G. Ince ◽  
Malee S. Fernando

Understanding of vascular substrates of cognitive decline in the elderly is evoloving to include a major emphasis on the impact of small vessel disease (SVD). While existing concepts of multi-infarct dementia and strategic infarct dementia remain valid, they present difficulty in generalizing clinicopathological correlations from patient to patient. The range and significance of lesions that should be included as manifestations of SVD are unresolved, as is their impact on, and association with, neurodegenerative changes. This mini-review summarizes the authors' views on SVD substrates leading to cognitive decline and proposes priorities for pathological investigations of human cerebrovascular mechanisms leading to cognitive decline.


2021 ◽  
pp. 1-15
Author(s):  
Manu J. Sharma ◽  
Brandy L. Callahan

Background: Mild cognitive impairment (MCI) is considered by some to be a prodromal phase of a progressive disease (i.e., neurodegeneration) resulting in dementia; however, a substantial portion of individuals (ranging from 5–30%) remain cognitively stable over the long term (sMCI). The etiology of sMCI is unclear but may be linked to cerebrovascular disease (CVD), as evidence from longitudinal studies suggest a significant proportion of individuals with vasculopathy remain stable over time. Objective: To quantify the presence of neurodegenerative and vascular pathologies in individuals with long-term (>5-year) sMCI, in a preliminary test of the hypothesis that CVD may be a contributor to non-degenerative cognitive impairment. We expect frequent vasculopathy at autopsy in sMCI relative to neurodegenerative disease, and relative to individuals who convert to dementia. Methods: In this retrospective study, using data from the National Alzheimer’s Coordinating Center, individuals with sMCI (n = 28) were compared to those with MCI who declined over a 5 to 9-year period (dMCI; n = 139) on measures of neurodegenerative pathology (i.e., Aβ plaques, neurofibrillary tangles, TDP-43, and cerebral amyloid angiopathy) and CVD (infarcts, lacunes, microinfarcts, hemorrhages, and microbleeds). Results: Alzheimer’s disease pathology (Aβ plaques, neurofibrillary tangles, and cerebral amyloid angiopathy) was significantly higher in the dMCI group than the sMCI group. Microinfarcts were the only vasculopathy associated with group membership; these were more frequent in sMCI. Conclusion: The most frequent neuropathology in this sample of long-term sMCI was microinfarcts, tentatively suggesting that silent small vessel disease may characterize non-worsening cognitive impairment.


Diagnostics ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 1051
Author(s):  
Valentina Bessi ◽  
Salvatore Mazzeo ◽  
Silvia Bagnoli ◽  
Giulia Giacomucci ◽  
Assunta Ingannato ◽  
...  

The Huntingtin gene (HTT) is within a class of genes containing a key region of CAG repeats. When expanded beyond 39 repeats, Huntington disease (HD) develops. Individuals with less than 35 repeats are not associated with HD. Increasing evidence has suggested that CAG repeats play a role in modulating brain development and brain function. However, very few studies have investigated the effect of CAG repeats in the non-pathological range on cognitive performances in non-demented individuals. In this study, we aimed to test how CAG repeats’ length influences neuropsychological scores in patients with subjective cognitive decline (SCD) and mild cognitive impairment (MCI). We included 75 patients (46 SCD and 29 MCI). All patients underwent an extensive neuropsychological battery and analysis of HTT alleles to quantify the number of CAG repeats. Results: CAG repeat number was positively correlated with scores of tests assessing for executive function, visual–spatial ability, and memory in SCD patients, while in MCI patients, it was inversely correlated with scores of visual–spatial ability and premorbid intelligence. When we performed a multiple regression analysis, we found that these relationships still remained, also when adjusting for possible confounding factors. Interestingly, logarithmic models better described the associations between CAG repeats and neuropsychological scores. CAG repeats in the HTT gene within the non-pathological range influenced neuropsychological performances depending on global cognitive status. The logarithmic model suggested that the positive effect of CAG repeats in SCD patients decreases as the number of repeats grows.


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