Imaging Mild Cognitive Impairment and Dementia in Parkinson's Disease.
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ABSTRACT:
SUBMITTER: Sasikumar S
PROVIDER: S-EPMC7005138 | biostudies-literature | 2020
REPOSITORIES: biostudies-literature
Publications
Imaging Mild Cognitive Impairment and Dementia in Parkinson's Disease.
Sasikumar Sanskriti S Strafella Antonio P AP
Frontiers in neurology 20200131
Cognitive dysfunction is a significant non-motor feature of Parkinson's disease, with the risk of dementia increasing with prolonged disease duration. Multiple cognitive domains are affected, and the pathophysiology cannot be explained by dopaminergic loss alone. Sophisticated neuroimaging techniques can detect the nature and extent of extra-nigral involvement by targeting neurotransmitters, abnormal protein aggregates and tissue metabolism. This review identifies the functional and anatomical i ...[more]
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Project description:Background: Cognitive impairment in Parkinson's disease (PD) includes a spectrum varying from Mild Cognitive Impairment (PD-MCI) to PD Dementia (PDD). The main aim of the present study is to evaluate the incidence of PD-MCI, its rate of progression to dementia, and to identify demographic and clinical characteristics which predict cognitive impairment in PD patients. Methods: PD patients from a large hospital-based cohort who underwent at least two comprehensive neuropsychological evaluations were retrospectively enrolled in the study. PD-MCI and PDD were diagnosed according to the Movement Disorder Society criteria. Incidence rates of PD-MCI and PDD were estimated. Clinical and demographic factors predicting PD-MCI and dementia were evaluated using Cox proportional hazard model. Results: Out of 139 enrolled PD patients, 84 were classified with normal cognition (PD-NC), while 55 (39.6%) fulfilled the diagnosis of PD-MCI at baseline. At follow-up (mean follow-up 23.5 ± 10.3 months) 28 (33.3%) of the 84 PD-NC at baseline developed MCI and 4 (4.8%) converted to PDD. The incidence rate of PD-MCI was 184.0/1000 pyar (95% CI 124.7-262.3). At multivariate analysis a negative association between education and MCI development at follow-up was observed (HR 0.37, 95% CI 0.15-0.89; p = 0.03). The incidence rate of dementia was 24.3/1000 pyar (95% CI 7.7-58.5). Out of 55 PD-MCI patients at baseline, 14 (25.4%) converted to PDD, giving an incidence rate of 123.5/1000 pyar (95% CI 70.3-202.2). A five time increased risk of PDD was found in PD patients with MCI at baseline (RR 5.09, 95% CI 1.60-21.4). Conclusion: Our study supports the relevant role of PD-MCI in predicting PDD and underlines the importance of education in reducing the risk of cognitive impairment.
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Project description: Not available
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Project description:INTRODUCTION:Identification of factors associated with progression of cognitive symptoms in Parkinson's disease (PD) is important for treatment planning, clinical care, and design of future clinical trials. The current study sought to identify whether prediction of cognitive progression is aided by examining baseline cognitive features, and whether this differs according to stage of cognitive disease. METHODS:Participants with PD in the Pacific Udall Center Clinical Consortium who had longitudinal data available and were nondemented at baseline were included in the study (n = 418). Logistic and Cox regression models were utilized to examine the relationship between cognitive, demographic, and clinical variables with risk and time to progression from no cognitive impairment to mild cognitive impairment (PD-MCI) or dementia (PDD), and from PD-MCI to PDD. RESULTS:Processing speed (OR = 1.05, p = 0.009) and working memory (OR = 1.01, p = 0.03) were associated with conversion to PDD among those with PD-MCI at baseline, over and above demographic variables. Conversely, the primary predictive factor in the transition from no cognitive impairment to PD-MCI or PDD was male sex (OR = 4.47, p = 0.004), and males progressed more rapidly than females (p = 0.01). Further, among females with shorter disease duration, progression was slower than for their male counterparts, and poor baseline performance on semantic verbal fluency was associated with shorter time to cognitive impairment in females but not in males. CONCLUSIONS:This study provides evidence for sex differences in the progression to cognitive impairment in PD, while specific cognitive features become more important indicators of progression with impending conversion to PDD.
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Project description:BackgroundCognitive deficit in Parkinson disease (PD) is an important cause of functional disability in these patients and early detection, with sensitive instruments, can contribute to longitudinal monitoring.ObjectiveTo investigate the diagnostic accuracy, sensitivity, and specificity of the Addenbrooke's Cognitive Examination-III in patients with PD, using the comprehensive neuropsychological battery as reference method.MethodsCross-sectional, observational, case-control study.Settingrehabilitation service. A total of 150 patients and 60 healthy controls matched for age, sex, and education. For level I assessment, Addenbrooke Cognitive Examination (ACE-III) was used. Level II assessment used a comprehensive neuropsychological battery of standardized tests for this population. All patients remained in on-state during the study. The diagnostic accuracy of the battery was investigated through the receiver operating characteristic (ROC) analysis.ResultsThe clinical group was divided into 3 subgroups: normal cognition in Parkinson's disease (NC-PD-16%), mild cognitive impairment due to Parkinson's disease (MCI-PD-69.33%), and dementia due to Parkinson's disease (D-PD-14.66%). ACE-III optimal cutoff scores for detecting MCI-PD and D-PD were 85/100 (sensitivity 58.65%, specificity 60%) and 81/100 points (sensitivity 77.27%, specificity 78.33%), respectively. Age was inversely associated with the performance of the scores (totals and domains of the ACE-III), while the level of education had a significantly positive correlation in the performance of these scores.ConclusionsACE-III is a useful battery for assessing the cognitive domains and to differentiate individuals with MCI-PD and D-PD from healthy controls. Future research, in a community setting, is necessary to provide discriminatory capacity of ACE-III in the different severities of dementia.
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Project description:BackgroundDementia is common in Parkinson's disease, but the underlying brain pathology is not yet fully understood.AimTo examine the changes in the brain of patients with Parkinson's disease with mild cognitive impairment (MCI) and dementia, using structural magnetic resonance imaging.MethodsUsing voxel-based morphometry, the grey matter atrophy on brain images of patients with Parkinson's disease and dementia (PDD; n = 16) and Parkinson's disease without dementia (PDND; n = 20), and healthy elderly subjects (n = 20) was studied. In the PDND group, 12 subjects had normal cognitive status and 8 had MCI. Standardised rating scales for motor, cognitive and psychiatric symptoms were used.ResultsWidespread areas of cortical atrophy were found in patients with PDD compared with normal controls (in both temporal and frontal lobes and in the left parietal lobe). Grey matter reductions were found in frontal, parietal, limbic and temporal lobes in patients with PDD compared with those with PDND. In patients with PDND with MCI, areas of reduced grey matter in the left frontal and both temporal lobes were found.ConclusionThese findings show that dementia in Parkinson's disease is associated with structural neocortical changes in the brain, and that cognitive impairment in patients with PDND may be associated with structural changes in the brain. Further studies with larger groups of patients are needed to confirm these findings.
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Project description:IntroductionNo known studies have compared longitudinal characteristics between individuals with incident mild cognitive impairment due to Parkinson's disease (PD-MCI) versus Alzheimer's Disease (AD-MCI).MethodsWe used longitudinal data from the National Alzheimer's Coordinating Center's Uniform Data Set to compare 41 PD-MCI and 191 AD-MCI participants according to their demographics, presence of ≥1 APOE e4 allele, and baseline and change over time in clinical characteristics, neuropsychological test scores, and Clinical Dementia Rating sum of boxes (CDR-SB). Multivariable linear regression models with generalized estimating equations were used to account for clustered data and to test for baseline and longitudinal differences in neuropsychological test scores.ResultsPD-MCI and AD-MCI participants differed by many demographic and clinical characteristics. Significantly fewer PD-MCI participants developed dementia over one year. Compared to AD-MCI participants, PD-MCI participants performed better at baseline and over time on a global measure of cognition (Mini Mental State Exam), memory measures (immediate and delayed Logical Memory), and a language measure (Boston Naming Test), and additionally performed better over time on an attention measure (Digit Span Forward), a language measure (Vegetable List), a processing speed measure (Digit Symbol), and an overall measure of memory and functional impairment (CDR-SB).ConclusionOur study provides further evidence that PD-MCI is clinically distinct from AD-MCI and requires different tools for diagnosis and monitoring clinical progression. More importantly, this study suggests that PD-MCI takes longer to convert into dementia than AD-MCI, findings that require replication by other studies.
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Project description:This study aimed to investigate the cortical neural correlates of dementia conversion in Parkinson's disease with mild cognitive impairment (PD-MCI). We classified 112 patients with drug-naïve early stage PD meeting criteria for PD-MCI into either PD with dementia (PDD) converters (n = 34) or nonconverters (n = 78), depending on whether they developed dementia within 4 years of PD diagnosis. Cortical thickness analyses were performed in 34 PDD converters and 34 matched nonconverters. Additionally, a linear discriminant analysis was performed to distinguish PDD converters from nonconverters using cortical thickness of the regions that differed between the two groups. The PDD converters had higher frequencies of multiple domain MCI and amnestic MCI with storage failure, and poorer cognitive performances on frontal/executive, memory, and language function domains than did the nonconverters. Cortical thinning extending from the posterior cortical area into the frontal region was observed in PDD converters relative to nonconverters. The discriminant analysis showed that the prediction model with two cortical thickness variables in the right medial superior frontal and left olfactory cortices optimally distinguished PDD converters from nonconverters. Our data suggest that cortical thinning in the frontal areas including the olfactory cortex is a marker for early dementia conversion in PD-MCI.
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