scholarly journals Comparison of Test Your Memory and Montreal Cognitive Assessment Measures in Parkinson’s Disease

2016 ◽  
Vol 2016 ◽  
pp. 1-6 ◽  
Author(s):  
Emily J. Henderson ◽  
Howard Chu ◽  
Daisy M. Gaunt ◽  
Alan L. Whone ◽  
Yoav Ben-Shlomo ◽  
...  

Background.MoCA is widely used in Parkinson’s disease (PD) to assess cognition. The Test Your Memory (TYM) test is a cognitive screening tool that is self-administered.Objectives.We sought to determine (a) the optimal value of TYM to discriminate between PD patients with and without cognitive deficits on MoCA testing, (b) equivalent MoCA and TYM scores, and (c) interrater reliability in TYM testing.Methods.We assessed the discriminant ability of TYM and the equivalence between TYM and MoCA scores and measured the interrater reliability between three raters.Results.Of the 135 subjects that completed both tests, 55% had cognitive impairment according to MoCA. A MoCA score of 25 was equivalent to a TYM score of 43-44. The area under the receiver operator characteristic (ROC) curve for TYM to differentiate between PD-normal and PD-cognitive impairment was 0.82 (95% CI 0.75 to 0.89). The optimal cutoff to distinguish PD-cognitive impairment from PD-normal was ≤45 (sensitivity 90.5%, specificity 59%) thereby correctly classifying 76.3% of patients with PD-cognitive impairment. Interrater agreement was high (0.97) and TYM was completed in under 7 minutes (interquartile range 5.33 to 8.52 minutes).Conclusions.The TYM test is a useful and less resource intensive screening test for cognitive deficits in PD.

2021 ◽  
Vol 13 ◽  
Author(s):  
Song’an Shang ◽  
Hongying Zhang ◽  
Yuan Feng ◽  
Jingtao Wu ◽  
Weiqiang Dou ◽  
...  

Background: Cognitive deficits are prominent non-motor symptoms in Parkinson’s disease (PD) and have been shown to involve the neurovascular unit (NVU). However, there is a lack of sufficient neuroimaging research on the associated modulating mechanisms. The objective of this study was to identify the contribution of neurovascular decoupling to the pathogenesis of cognitive decline in PD.Methods: Regional homogeneity (ReHo), a measure of neuronal activity, and cerebral blood flow (CBF), a measure of vascular responses, were obtained from patients with PD with mild cognitive impairment (MCI) and normal cognition (NC) as well as matched healthy controls (HCs). Imaging metrics of neurovascular coupling (global and regional CBF-ReHo correlation coefficients and CBF-ReHo ratios) were compared among the groups.Results: Neurovascular coupling was impaired in patients with PD-MCI with a decreased global CBF-ReHo correlation coefficient relative to HC subjects (P < 0.05). Regional dysregulation was specific to the PD-MCI group and localized to the right middle frontal gyrus, right middle cingulate cortex, right middle occipital gyrus, right inferior parietal gyrus, right supramarginal gyrus, and right angular gyrus (P < 0.05). Compared with HC subjects, patients with PD-MCI showed higher CBF-ReHo ratios in the bilateral lingual gyri (LG), bilateral putamen, and left postcentral gyrus and lower CBF-ReHo ratios in the right superior temporal gyrus, bilateral middle temporal gyri, bilateral parahippocampal gyri, and right inferior frontal gyrus. Relative to the HC and PD-NC groups, the PD-MCI group showed an increased CBF-ReHo ratio in the left LG, which was correlated with poor visual–spatial performance (r = −0.36 and P = 0.014).Conclusion: The involvement of neurovascular decoupling in cognitive impairment in PD is regionally specific and most prominent in the visual–spatial cortices, which could potentially provide a complementary understanding of the pathophysiological mechanisms underlying cognitive deficits in PD.


CNS Spectrums ◽  
2018 ◽  
Vol 23 (1) ◽  
pp. 77-77 ◽  
Author(s):  
Daniel Weintraub ◽  
James Norton ◽  
Bruce Coate ◽  
Candace Andersson ◽  
Doral Fredericks ◽  
...  

AbstractObjectiveA planned subgroup analysis of a phase 3 study was performed to evaluate the efficacy and safety of pimavanserin (PIM) in Parkinson’s disease psychosis (PDP) patients withglobal cognitive impairment.BackgroundPDP is frequent, distressing, a leading cause of institutionalization, complicates PD management and is linked to increased morbidity, incident dementia and mortality. PIM, a selective serotonin receptor (5-HT2A) inverse agonist/antagonist, is newly FDA-approved for the treatment of hallucinations and delusions associated with PDP.MethodsIn Study 020, a 6-week FDA registration study, 199 patients with baseline Mini-Mental State Examination (MMSE) score ≥21, moderate-severe psychosis, and on stable PD meds, were randomized to PIM (34 mg/day) or placebo (PBO) for 6 weeks. This subgroup analysis evaluates efficacy and safety between two groups: those with MMSE total score ≥21 but <25 (cognitively impaired; equivalent to Montreal Cognitive Assessment [MoCA] score 15-19) and those with score ≥25 (cognitively normal; equivalent to MoCA score 20-30). Safety assessments were performed on the full safety dataset (i.e., three 6-week placebo-controlled studies) including 614 subjects (PIM=382, PBO=231).ResultsOverall, patients in the PIM group experienced a statistically significant improvement in SAPS-PD scores from baseline to Day 43 compared with PBO (-5.79 vs. -2.73; p=0.001). In the subgroup analysis stratifying by baseline MMSE score, the change from baseline to Day 43 compared with PBO in the cognitively-impaired group (N=50) was numerically larger (-7.11 vs. -0.47; p=0.002). In the full safety dataset examining cognitively impaired patients, there were no between-group (PIM vs. PBO) differences in any treatment-emergent adverse event (TEAE) (57.6% vs. 56.1%) or serious TEAE (6.8% vs. 5.3%). The most common TEAEs occurring at ≥5% in either group were fall (7.4% vs.10.5%), confusional state (6.5% vs.1.8%), and orthostatic hypotension (0.0% vs. 8.8%).ConclusionsIn this subgroup analysis of PDP patients, the treatment effect of PIM on SAPS-PD was larger in the cognitively-impaired group, with similar TEAE and serious TEAE rates. These results hold promise for cognitively-impaired patients that will be further elucidated in future studies.Funding AcknowledgementsClinical study was funded by ACADIA Pharmaceuticals Inc.


2020 ◽  
Author(s):  
Arturo Moreno ◽  
Nijee Luthra ◽  
Luke Bonham ◽  
Jonathan Lin ◽  
Lauren Broestl ◽  
...  

Abstract Aging is the primary risk factor for Parkinson’s disease (PD) and cognitive impairment from PD is a major and unmet biomedical challenge. Klotho, a pleiotropic protein, extends lifespan and enhances cognition. Whether longevity factors such as klotho can counteract PD-related mortality and deficits in mice or associate with resistance to PD in humans is unknown. Here we show that transgenic elevation of klotho increased lifespan, improved synaptic and cognitive, but not motor, functions in mice, and decreased steady state α-synuclein levels in the brains of mice that express wildtype human α-synuclein. In humans, a genetic variant of KLOTHO that increases circulating klotho levels associated with better executive cognition and less CSF abnormalities of α-synuclein in individuals with PD. Thus, klotho can counteract cognitive deficits related to PD, possibly modulating α-synuclein levels – and these findings may be relevant to new therapeutic pathways for human PD.


2021 ◽  
Vol 11 ◽  
Author(s):  
Kye Won Park ◽  
Sungyang Jo ◽  
Mi Sun Kim ◽  
Sang Ryong Jeon ◽  
Ho-Sung Ryu ◽  
...  

Background: Cognitive impairment is very common in Parkinson's disease (PD) and constitutes the most debilitating complication of this disease. However, to date, few studies have investigated a genome-wide association in the development of cognitive impairment of PD. We aimed to identify the genetic loci associated with cognitive impairment in patients with sporadic PD by ethnicity-specific genotyping.Materials and methods: We recruited 1,070 patients with PD and performed a genome-wide association study using the Korean Chip, a microarray chip containing 827,400 single-nucleotide polymorphisms (SNPs) optimized for the Korean population. Multiple logistic regression models adjusting for age, sex, years of education, and disease duration were used to compare between patients with and without cognitive impairment, which was defined using the Mini-Mental Status Examination (MMSE) score (MMSE score ≥ 26 vs. &lt; 26) or the Montreal Cognitive Assessment (MoCA) score (MoCA score ≥24 vs. &lt; 24).Results:RYR2 SNP rs10495397 was most significantly associated with cognitive impairment based on the MMSE scores (OR = 3.21; 95% CI = 1.96–5.25, P = 3.36 × 10−6) and CASC17 showed the strongest association with cognitive impairment based on the MoCA scores. However, none of the SNPs were statistically significant after Bonferroni correction.Conclusion:RYR2 may play a role in cognitive impairment in PD by the pathogenic mechanism of neuroinflammation. However, more studies are needed to replicate and validate the results of our functional study.


2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
Alexandru Hanganu ◽  
Oury Monchi

Cognitive impairment in patients with Parkinson’s disease is a major challenge since it has been established that 25 to 40% of patients will develop cognitive impairment early in the disease. Furthermore, it has been reported that up to 80% of Parkinsonian patients will eventually develop dementia. Thus, it is important to improve the diagnosing procedures in order to detect cognitive impairment at early stages of development and to delay as much as possible the developing of dementia. One major challenge is that patients with mild cognitive impairment exhibit measurable cognitive deficits according to recently established criteria, yet those deficits are not severe enough to interfere with daily living, hence being avoided by patients, and might be overseen by clinicians. Recent advances in neuroimaging brain analysis allowed the establishment of several anatomical markers that have the potential to be considered for early detection of cognitive impairment in Parkinsonian patients. This review aims to outline the neuroimaging possibilities in diagnosing cognitive impairment in patients with Parkinson’s disease and to take into consideration the near-future possibilities of their implementation into clinical practice.


2019 ◽  
Vol 13 (4) ◽  
pp. 394-402
Author(s):  
Yunier Broche-Pérez ◽  
Danay Bartuste-Marrer ◽  
Miriam Batule-Domínguez ◽  
Filiberto Toledano-Toledano

ABSTRACT Cognitive deficits in Parkinson’s disease typically affect executive functions. Recently, the concept of Mild Cognitive Impairment (MCI) has been related to PD (PD-MCI). PD-MCI is considered a transition phase to Parkinson’s disease Dementia. Therefore, it is important to identify PD-MCI in a reliable way. Objective: To evaluate the sensitivity and specificity of the INECO Frontal Screening (IFS) in detecting cognitive deficits in PD-MCI. Additionally, we compare the IFS and the Addenbrook Cognitive Examination Revised (ACE-R) between three groups; PD-MCI, MCI, and controls. Methods: The IFS and ACE-R were administered to 36 patients with PD-MCI, 31 with MCI (amnestic-multidomain subtype) and 92 healthy controls. Sensitivity and specificity were determined using ROC analysis. The groups were compared using one-way analysis of variance. Results: The IFS had adequate accuracy in differentiating patients with PD-MCI from healthy controls (AUC=0.77, sensitivity=0.82, specificity=0.77), and good accuracy in differentiating PD-MCI from MCI patients (AUC=0.80, sensitivity=0.82, specificity=0.61). However the IFS had low accuracy in differentiating MCI patients from healthy controls (AUC=0.47, sensitivity=0.52, specificity=0.41). On the ACE-R, the PD-MCI group had low performance in Fluency and Language. Only patients with PD-MCI had difficulties on the IFS, specifically in inhibitory control and visual working memory. This dysexecutive profile explains the sensitivity and specificity values found in the IFS. Conclusion: The present study results suggest that the IFS is a suitable screening tool for exploring cognitive dysfunction in PD-MCI, especially in those patients with a dysexecutive profile.


2021 ◽  
Vol 12 ◽  
Author(s):  
Xiaojuan Dan ◽  
Yang Hu ◽  
Junyan Sun ◽  
Linlin Gao ◽  
Yongtao Zhou ◽  
...  

Background: Cognitive impairment is one of the most prominent non-motor symptoms in Parkinson's disease (PD), due in part to known cerebellar dysfunctions. Furthermore, previous studies have reported altered cerebellar functional connectivity (FC) in PD patients. Yet whether these changes are also due to the cognitive deficits in PD remain unclear.Methods: A total of 122 non-dementia participants, including 64 patients with early PD and 58 age- and gender-matched elderly controls were stratified into four groups based on their cognitive status (normal cognition vs. cognitive impairment). Cerebellar volumetry and FC were investigated by analyzing, respectively, structural and resting-state functional MRI data among groups using quality control and quantitative measures. Correlation analysis between MRI metrics and clinical features (motor and cognitive scores) were performed.Results: Compared to healthy control subjects with no cognitive deficits, altered cerebellar FC were observed in early PD participants with both motor and cognitive deficits, but not in PD patients with normal cognition, nor elderly subjects showing signs of a cognitive impairment. Moreover, connectivity between the “motor” cerebellum and SMA was positively correlated with motor scores, while intracerebellar connectivity was positively correlated with cognitive scores in PD patients with cognitive impairment. No cerebellar volumetric difference was observed between groups.Conclusions: These findings show that altered cerebellar FC during resting state in early PD patients may be driven not solely by the motor deficits, but by cognitive deficits as well, hence highlighting the interplay between motor and cognitive functioning, and possibly reflecting compensatory mechanisms, in the early PD.


2018 ◽  
Vol 76 (3) ◽  
pp. 145-149
Author(s):  
Carlos Henrique Ferreira Camargo ◽  
Augusto Bronzini ◽  
Eduardo de Souza Tolentino ◽  
Camila Medyk ◽  
Gustavo Leopold Schultz-Pereira

ABSTRACT The Consortium to Establish a Registry for Alzheimer's Disease (CERAD) neuropsychological battery was created to assess cognitive impairment in Alzheimer's disease (AD) but it is widely-used for various dementias. The aim of this study was to analyze the efficacy of using the CERAD battery in the assessment of patients with Parkinson's disease. Forty-nine patients with Parkinson's disease were divided into two groups (one with dementia and one without) using the Movement Disorder Society criteria for Parkinson's disease dementia. Cognitive deficits were assessed with the Clinical Dementia Rating Scale as the gold standard, and the CERAD. The ROC curve for the CERAD battery had an area under the curve = 0.989 (95% CI = 0.967 – 1, p<0.0001). Among the CERAD subtests, verbal fluency had the worst accuracy, and word list learning had the best accuracy. Despite the limits of this study, the CERAD battery can be efficient for assessment of cognitive deficits in Parkinson's disease patients.


1991 ◽  
Vol 4 (2) ◽  
pp. 89-102 ◽  
Author(s):  
H. J. Sagar

Multiple cognitive deficits have been recognized in many neurological disorders but the specificity of the findings and the relationship to the underlying neuropathology remain obscure. Definitions of dementia have been proposed based on symptom profiles of the cognitive disorder and qualitative differences have been claimed between dementias of different aetiology. Some conditions have been claimed to show patterns of cognitive deficit that are distinguished from dementia and related to specific neuropathology or psychological processes, e.g. frontal lobe deficits in Parkinson's disease. Sometimes, a relationship has been established between certain cognitive deficits and particular neurochemical deficits which has led to the notion of specific drug treatment, e.g. cholinergic deficits and memory failure in Alzheimer's disease. However, these conclusions are often potentially flawed by methodological inadequacies. This critique presents some methodological issues relevant to the study of brain-behaviour and drug-behaviour relationships in syndromes of multiple cognitive deficit, using Parkinson's disease as the model. The following recommendations are made: rigid diagnostic criteria; representative patient groups; avoidance of arbitrary quantitative criteria to limit definitions of dementia; matching of groups for overall level of cognitive impairment in the search for qualitative cognitive differences related to neuropathology or effects of particular drugs; the use of suitable controls in patient groups, neuropsychological tests and treatment regimes; the use of specific quantitative tests of cognition, affect and motor disability; and longitudinal, compared with cross-sectional, study design.


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