scholarly journals Cognitive Trajectories Following Acute Infection in Older Patients With and Without Cognitive Impairment: An 1-Year Follow-Up Study

2021 ◽  
Vol 12 ◽  
Author(s):  
Ana Rita Silva ◽  
Patrícia Regueira ◽  
Ana Luísa Cardoso ◽  
Inês Baldeiras ◽  
Isabel Santana ◽  
...  

Introduction: Dementia is a known risk factor for both delirium and acute systemic infections which may also play a significant role in promoting or accelerating neurodegenerative disease. Infections are both the main causes of hospitalization of dementia patients and can be a major precipitant of delirium but currently it is not possible to predict the risk of cognitive decline in older patients exposed to acute infection.Objectives: We aimed to determine the level of cognitive change at 1-year follow up in individuals with different patterns of cognitive function (dementia, delirium, delirium superimposed on dementia) at the time of their hospitalization due to a systemic infection and to correlate these cognitive patterns with clinical status variables.Methods: We recruited 53 hospitalized geriatric patients with a systemic infection, and we collected 12-months follow up data for 34 patients. These patients were classified in four groups: no cognitive impairment (controls—C), delirium only (D), dementia only (Dem), and delirium superimposed to dementia (DD). Cognitive performance was measured by change in score on the Montreal Cognitive Assessment (MoCA) and delirium was identified using Confusion Assessment Measure (CAM). We examined performance on the MoCA in the first year after hospitalization, controlling for demographic characteristics, coexisting medical conditions, and type of infection.Results: For the 34 patients to whom follow-up data was available, delirium presence in individuals with prior dementia (DD group) was associated with a negative mean change score of 3-point (p < 0.02) at 1 year follow up, whereas dementia patients without delirium had a mean change score of 1.5-point lower at 12-months (p = 0.04), when comparing follow-up and baseline MoCA scores. Cognitively healthy patients did not significantly decrease their MoCA score at follow-up (p = 0.15). MoCA and NPI scores during hospitalization were significantly correlated with the level of cognitive decline in the four groups (r = 0.658, p < 0.01 and r = 0.439, p = 0.02, respectively).Conclusions: Premorbid dementia and delirium superimposed on dementia during hospitalization in older patients with acute infections predict cognitive decline at 1 year following admission. Taken together, our findings suggest a pathophysiological interaction between neurodegenerative changes, acute infection, and delirium.

Author(s):  
Iván Galtier ◽  
Antonieta Nieto ◽  
María Mata ◽  
Jesús N. Lorenzo ◽  
José Barroso

ABSTRACT Objective: Subjective cognitive decline (SCD) and mild cognitive impairment (MCI) in Parkinson’s disease (PD) are considered as the risk factors for dementia (PDD). Posterior cortically based functions, such as visuospatial and visuoperceptual (VS-VP) processing, have been described as predictors of PDD. However, no investigations have focused on the qualitative analysis of the Judgment of Line Orientation Test (JLOT) and the Facial Recognition Test (FRT) in PD-SCD and PD-MCI. The aim of this work was to study the VS-VP errors in JLOT and FRT. Moreover, these variables are considered as predictors of PDD. Method: Forty-two PD patients and 19 controls were evaluated with a neuropsychological protocol. Patients were classified as PD-SCD and PD-MCI. Analyses of errors were conducted following the procedure described by Ska, Poissant, and Joanette (1990). Follow-up assessment was conducted to a mean of 7.5 years after the baseline. Results: PD-MCI patients showed a poor performance in JLOT and FRT total score and made a greater proportion of severe intraquadrant (QO2) and interquadrant errors (IQO). PD-SCD showed a poor performance in FRT and made mild errors in JLOT. PD-MCI and QO2/IQO errors were independent risk factors for PDD during the follow-up. Moreover, the combination of both PD-MCI diagnosis and QO2/IQO errors was associated with a greater risk. Conclusions: PD-MCI patients presented a greater alteration in VS-VP processing observable by the presence of severe misjudgments. PD-SCD patients also showed mild difficulties in VS-SP functions. Finally, QO2/IQO errors in PD-MCI are a useful predictor of PDD, more than PD-MCI diagnosis alone.


2020 ◽  
Vol 32 (S1) ◽  
pp. 91-91

AUTHORS:Kerstin Johansson, Karolina Thömkvist, Ingmar Skoog and Sacuiu SF* (*presenter)OBJECTIVE:To determine the effects of electroconvulsive therapy (ECT) in major depression in relation to the development of dementia during long-term follow-up.METHOD:In an observational clinical prospective study of consecutive patients 70 years and older diagnosed with major depression at baseline 2000-2004 (n=1090), who were free of dementia and received antidepressant treatment, with or without ECT, we sought to determine if cognitive decline (mild cognitive impairment and dementia) during 15 -year follow-up was associated with receiving ECT at baseline. The control group was selected among the participants in the Gothenburg H70 Birth Cohort Studies matched by age group and sex 1:1.RESULTS:Among patients with affective syndromes 7% received ECT. During follow-up, 157 patients were diagnosed with dementia, equal proportions among those who received ECT (14.5%) and those who did not receive ECT (14.5%). The relation between ECT and cognitive decline remained non-significant irrespective antidepressive medication or presence of mild cognitive impairment at baseline.CONCLUSION:Preliminary results indicate that ECT was not associated with the development of cognitive decline in the long-term in a hospital-based cohort of 70+ year-olds. The results remain to verify against controls from a representative community sample.


2020 ◽  
Vol 11 ◽  
Author(s):  
Jing Zhang ◽  
Zixiao Li ◽  
Xingxing Cao ◽  
Lijun Zuo ◽  
Wei Wen ◽  
...  

We investigated the association between poststroke cognitive impairment and a specific effective network connectivity in the prefrontal–basal ganglia circuit. The resting-state effective connectivity of this circuit was modeled by employing spectral dynamic causal modeling in 11 poststroke patients with cognitive impairment (PSCI), 8 poststroke patients without cognitive impairment (non-PSCI) at baseline and 3-month follow-up, and 28 healthy controls. Our results showed that different neuronal models of effective connectivity in the prefrontal–basal ganglia circuit were observed among healthy controls, non-PSCI, and PSCI patients. Additional connected paths (extra paths) appeared in the neuronal models of stroke patients compared with healthy controls. Moreover, changes were detected in the extra paths of non-PSCI between baseline and 3-month follow-up poststroke, indicating reorganization in the ipsilesional hemisphere and suggesting potential compensatory changes in the contralesional hemisphere. Furthermore, the connectivity strengths of the extra paths from the contralesional ventral anterior nucleus of thalamus to caudate correlated significantly with cognitive scores in non-PSCI and PSCI patients. These suggest that the neuronal model of effective connectivity of the prefrontal–basal ganglia circuit may be sensitive to stroke-induced cognitive decline, and it could be a biomarker for poststroke cognitive impairment 3 months poststroke. Importantly, contralesional brain regions may play an important role in functional compensation of cognitive decline.


2016 ◽  
Vol 19 (2) ◽  
pp. 104-111 ◽  
Author(s):  
Inge Petersen ◽  
Matt McGue ◽  
Qihua Tan ◽  
Kaare Christensen ◽  
Lene Christiansen

A complex interrelation exists between change in depression symptomatology and cognitive decline. Studies indicate either that depression is a direct risk factor for cognitive change over time, or vice versa. Longitudinal twin studies provide the possibility to unravel cause and effect of correlated traits. Here, we have applied twin modeling approaches to shed light on the genetic correlation between both level and change of depression symptomatology and cognitive functioning, and to further explore the bidirectionality of any such correlation using assessments of both phenotypes at two occasions 10 years apart. The study included 2,866 Danish twins with a mean age of 56.8 years at intake (range: 45–68 years). Of these, 1,267 were intact pairs. A total number of 1,582 twins (55%), of whom 557 were intact pairs, participated in the follow-up survey. We found stable cross-sectional heritability estimates of approximately 60% for general cognitive abilities and 30% for affective depressive symptoms. There was a considerable decline in the mean cognitive performance over 10 years, whereas the mean affective depression symptoms score was stable and with no genetic contribution to any individual change. Additionally, we saw a small but significant cross-trait correlation at both occasions (-0.11 and -0.09, respectively), but cross-trait cross-occasion analysis revealed no evidence that either of the two traits predicts the other over a 10-year interval. Thus, our study was not able to detect any causal association between change in depressive symptomatology and cognitive decline in middle-aged and elderly people over a 10-year interval.


2018 ◽  
Vol 45 (3-4) ◽  
pp. 232-242 ◽  
Author(s):  
Adam P. Mecca ◽  
Hannah R. Michalak ◽  
Julia W. McDonald ◽  
Emily C. Kemp ◽  
Erika A. Pugh ◽  
...  

Background: We investigated the relationship between sleep disturbance and cognitive decline or clinical conversion in individuals with normal cognition (CN), as well as those with mild cognitive impairment (MCI) and dementia due to Alzheimer disease (AD-dementia). Methods: Secondary analysis of 1,629 adults between 48 and 91 years of age with up to 24 months of follow-up from the ADNI (Alzheimer’s Disease Neuroimaging Initiative), a longitudinal cohort study. Results: Sleep disturbance was not associated with decline in memory, executive function, or global cognition. The presence of sleep disturbance did not significantly increase the risk of diagnostic conversion in CN, early MCI, or late MCI participants. Conclusion: This study investigated the effect of sleep disturbance on cognitive decline using several outcomes and does not support the hypothesis that sleep disturbance predicts subsequent cognitive decline.


2020 ◽  
Vol 78 (2) ◽  
pp. 573-585
Author(s):  
Hyemin Jang ◽  
Hee Jin Kim ◽  
Yeong Sim Choe ◽  
Soo-Jong Kim ◽  
Seongbeom Park ◽  
...  

Background: As Alzheimer’s disease (AD) and cerebral small vessel disease (CSVD) commonly coexist, the interaction between two has been of the considerable interest. Objective: We determined whether the association of Aβ and tau with cognitive decline differs by the presence of significant CSVD. Methods: We included 60 subcortical vascular cognitive impairment (SVCI) from Samsung Medical Center and 82 Alzheimer’s disease-related cognitive impairment (ADCI) from ADNI, who underwent Aβ (florbetaben or florbetapir) and tau (flortaucipir, FTP) PET imaging. They were retrospectively assessed for 5.0±3.9 and 5.6±1.9 years with Clinical Dementia Rating-sum of boxes (CDR-SB)/Mini-Mental State Examination (MMSE). Mixed effects models were used to investigate the interaction between Aβ/tau and group on CDR-SB/MMSE changes. Results: The frequency of Aβ positivity (45% versus 54.9%, p = 0.556) and mean global FTP SUVR (1.17±0.21 versus 1.16±0.17, p = 0.702) were not different between the two groups. We found a significant interaction effect of Aβ positivity and SVCI group on CDR-SB increase/MMSE decrease (p = 0.013/p < 0.001), and a significant interaction effect of global FTP uptake and SVCI group on CDR-SB increase/MMSE decrease (p < 0.001 and p = 0.030). Finally, the interaction effects of regional tau and group were prominent in the Braak III/IV (p = 0.001) and V/VI (p = 0.003) not in Braak I/II region (p = 0.398). Conclusion: The association between Aβ/tau and cognitive decline is stronger in SVCI than in ADCI. Therefore, our findings suggested that Aβ positivity or tau burden (particularly in the Braak III/IV or V/VI regions) and CSVD might synergistically affect cognitive decline.


2009 ◽  
Vol 22 (2) ◽  
pp. 291-299 ◽  
Author(s):  
Graciela Muniz Terrera ◽  
Carol Brayne ◽  
Fiona Matthews ◽  

ABSTRACTBackground: Cognitive decline in old age varies among individuals. The identification of groups of individuals with similar patterns of cognitive change over time may improve our ability to see whether the effect of risk factors is consistent across groups.Methods: Whilst accounting for the missing data, growth mixture models (GMM) were fitted to data from four interview waves of a population-based longitudinal study of aging, the Cambridge City over 75 Cohort Study (CC75C). At all interviews global cognition was assessed using the Mini-mental State Examination (MMSE).Results: Three patterns were identified: a slow decline with age from a baseline of cognitive ability (41% of sample), an accelerating decline from a baseline of cognitive impairment (54% of sample) and a steep constant decline also from a baseline of cognitive impairment (5% of sample). Lower cognitive scores in those with less education were seen at baseline for the first two groups. Only in those with good performance and steady decline was the effect of education strong, with an increased rate of decline associated with poor education. Good mobility was associated with higher initial score in the group with accelerating change but not with rate of decline.Conclusion: Using these analytical methods it is possible to detect different patterns of cognitive change with age. In this investigation the effect of education differs with group. To understand the relationship of potential risk factors for cognitive decline, careful attention to dropout and appropriate analytical methods, in addition to long-term detailed studies of the population points, are required.


2011 ◽  
Vol 24 (1) ◽  
pp. 1-5 ◽  
Author(s):  
Karen Ritchie ◽  
Craig W Ritchie

Cognitive decline has commonly been considered an inevitable result of brain aging and has been of clinical interest principally because of related difficulties with everyday functioning. Since the 1990s the “normality” of age-related cognitive decline has been called into question, being commonly attributed to a number of underlying disorders. Numerous concepts have been proposed which link subclinical cognitive change to pathological states (mild cognitive disorder, mild neurocognitive disorder, mild cognitive impairment). Of these, mild cognitive impairment (MCI) has become the most popular, driven on the one hand by industrial interests seeking to extend new dementia treatments for a more prevalent subclinical syndrome, and on the other by researchers attempting to identify at-risk populations. MCI has been both criticized for “medicalizing” behavior still within normal limits (Stephan et al., 2008; Moreira et al., 2008) and welcomed in that it suggests cognitive decline with aging may not be inevitable, but rather due to abnormalities which could ultimately be treated. Recently, in both Europe (DuBois et al., 2007) and the USA (Albert et al., 2011), panels of experts have scrutinized the concept of MCI and more broadly the pre-dementia stages of neurodegenerative diseases and offered new research diagnostic criteria. These proposed criteria have highlighted the (potential) value of biomarkers in assisting diagnosis, although some have considered the elevation of biomarkers to this level of importance in diagnosing disease before dementia develops to be premature given both the extent and quality of diagnostic biomarker data currently available (McShane et al., 2011a; 2011b).


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