Specific pattern of linguistic impairment in Parkinson's disease patients with subjective cognitive decline and mild cognitive impairment predicts dementia.

OBJECTIVE: Parkinson's disease patients with subjective cognitive decline (PD-SCD) and mild cognitive impairment (PD-MCI) have an increased risk of dementia (PDD). Thus, the identification of early cognitive changes that can be useful predictors of PDD is a highly relevant challenge. Posterior cortically based functions, including linguistic processes, have been associated with PDD. However, investigations that have focused on linguistic functions in PD-MCI are scarce and none of them include PD-SCD patients. Our aim was to study language performance in PD-SCD and PD-MCI. Moreover, language subcomponents were considered as predictors of PDD. METHOD: Forty-six PD patients and twenty controls were evaluated with a neuropsychological protocol. Patients were classified as PD-SCD and PD-MCI. Language production and comprehension was assessed. Follow-up assessment was conducted to a mean of 7.5 years after the baseline. RESULTS: PD-MCI patients showed a poor performance in naming (actions and nouns), action generation, anaphora resolution and sentence comprehension (with and without center-embedded relative clause). PD-SCD showed a poor performance in action naming and action generation. Deficit in action naming was an independent risk factor for PDD during the follow-up. Moreover, the combination of deficit in action words and sentence comprehension without a center-embedded relative clause was associated with a greater risk. CONCLUSIONS: The results are of relevance because they suggest that a specific pattern of linguistic dysfunctions, that can be present even in the early stages of the disease, can predict future dementia, reinforcing the importance of advancing in the knowledge of linguistic dysfunctions in predementia stages of PD.

Analyses of Visuospatial and Visuoperceptual Errors as Predictors of Dementia in Parkinson's Disease Patients with Subjective Cognitive Decline and Mild Cognitive Impairment.

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.

The organization of the basal ganglia functional connectivity network is non-linear in Parkinson's disease.

The motor symptoms in Parkinson's disease (PD) have been linked to changes in the excitatory/inhibitory interactions of centers involved in the cortical-subcortical closed-loop circuits which connect basal ganglia (BG) and the brain cortex. This approach may explain some motor symptoms of PD but not others, which has driven the study of BG from new perspectives. Besides their cortical-subcortical linear circuits, BG have a number of subcortical circuits which directly or indirectly connect each BG with all the others. This suggests that BG may work as a complex network whose output is the result of massive functional interactions between all of their nuclei (decentralized network; DCN), more than the result of the linear excitatory/inhibitory interactions of the cortical-subcortical closed-loops. The aim of this work was to study BG as a DCN, and to test whether the DCN behavior of BG changes in PD. BG activity was recorded with MRI methods and their complex interactions were studied with a procedure based on multiple correspondence analysis, a data-driven multifactorial method which can work with non-linear multiple interactions. The functional connectivity of twenty parkinsonian patients and eighteen age-matched controls were studied during resting and when they were performing sequential hand movements. Seven functional configurations were identified in the control subjects during resting, and some of these interactions changed with motor activity. Five of the seven interactions found in control subjects changed in Parkinson's disease. The BG response to the motor task was also different in PD patients and controls. These data show the basal ganglia as a decentralized network where each region can perform multiple functions and each function is performed by multiple regions. This framework of BG interactions may provide new explanations concerning motor symptoms of PD which are not explained by current BG models.

Subjective cognitive decline and progression to dementia in Parkinson's disease: a long-term follow-up study.

INTRODUCTION: Increasing evidence suggests that subjective cognitive decline is associated with Alzheimer's disease pathology and with an increased risk for future dementia development. However, the clinical value of subjective cognitive decline in Parkinson's disease (PD-SCD) is unclear. The aim of the present work was to characterize PD-SCD and its progression to dementia. METHODS: Forty-three PD patients and twenty normal controls were evaluated with a neuropsychological protocol. Patients were classified as PD-SCD and PD with mild cognitive impairment (PD-MCI). Follow-up assessment was conducted to a mean of 7.5 years after the baseline. RESULTS: Thirteen patients were diagnosed with PD-SCD (30.2%) and 22 patients were classified as PD-MCI (51.2%) at the baseline. Difficulties in language (60.5%) and memory (51.5%) were the most frequent cognitive complaints. PD-MCI showed alterations in processing speed, executive functions, visuospatial skills, memory and language. No significant differences were found between normal controls and PD-SCD in any of the neuropsychological measures. Conversion to clinically diagnosed dementia during the follow-up was 50% in PD-MCI, 33.3% in PD-SCD and 14.3% in patients without subjective cognitive complaints. Discriminant function analyses and logistic regression analyses revealed that language domain and, especially memory domain are good predictors of dementia. CONCLUSIONS: The present investigation is the first to conduct a long-term follow-up study of PD-SCD and its relationship with the development of dementia. The results provide relevant data about the characterization of SCD in PD patients and show that PD-SCD is a risk factor for progression to dementia.

Mild Cognitive Impairment in Parkinson's Disease: Clustering and Switching Analyses in Verbal Fluency Test.

OBJECTIVES: Mild cognitive impairment is common in non-demented Parkinson disease patients (PD-MCI) and is considered as a risk factor for dementia. Executive dysfunction has been widely described in PD and the Verbal Fluency Tests (VFT) are often used for executive function assessment in this pathology. The Movement Disorder Society (MDS) published guidelines for PD-MCI diagnosis in 2012. However, no investigation has focused on the qualitative analysis of VFT in PD-MCI. The aim of this work was to study the clustering and switching strategies in VFT in PD-MCI patients. Moreover, these variables are considered as predictors for PD-MCI diagnosis. METHODS: Forty-three PD patients and twenty normal controls were evaluated with a neuropsychological protocol and the MDS criteria for PD-MCI were applied. Clustering and switching analysis were conducted for VFT. RESULTS: The percentage of patients diagnosed with PD-MCI was 37.2%. The Mann-Whitney U test analysis showed that PD-MCI performed poorly in different cognitive measures (digit span, Wisconsin Card Sorting Test, judgment of line orientation, and comprehension test), compared to PD patients without mild cognitive impairment (PD-nMCI). Phonemic fluency analyses showed that PD-MCI patients produced fewer words and switched significantly less, compared to controls and PD-nMCI. Concerning semantic fluency, the PD-MCI group differed significantly, compared to controls and PD-nMCI, in switches. Discriminant function analyses and logistic regression analyses revealed that switches predicted PD-MCI. CONCLUSIONS: PD-MCI patients showed poor performance in VFT related to the deficient use of production strategies. The number of switches is a useful predictor for incident PD-MCI. (JINS, 2017, 23, 511-520).

Mild cognitive impairment in Parkinson's disease: Diagnosis and progression to dementia.

INTRODUCTION: Mild cognitive impairment is common in nondemented Parkinson disease patients (PD-MCI) and is considered as a risk factor for dementia (PDD). Recently, the Movement Disorder Society (MDS) published guidelines for PD-MCI, although the studies available are still limited. The aim of this work was to characterize PD-MCI and its progression to dementia. Moreover, the study variables could be considered as predictors for the progression of cognitive impairment. METHOD: The study included 43 patients with idiopathic PD (mean age = 59.19 years, SD = 9.64) and 20 healthy and neurologically normal controls (mean age = 60.85 years, SD = 12.26). The criteria proposed by the MDS Task Force were applied for the PD-MCI diagnosis. Follow-up assessments were conducted within six to eight years after the diagnosis of PD-MCI. RESULTS: The results showed that 60.5% of the patients were diagnosed with PD-MCI when a comprehensive assessment was performed (MDS criteria Level 2), while 23.3% of the patients met MCI criteria when a brief assessment was used (MDS criteria Level 1). Multiple domain impairment was the most frequent impairment (96.2%). A total of 42.3% of PD-MCI patients had dementia in the follow-up study. Logistic regression showed that the Hoehn and Yahr stage and education significantly contributed to the prediction of PD-MCI. Moreover, the Hoehn and Yahr stage and memory domain significantly contributed to the prediction of dementia. CONCLUSIONS: The results of the study: (a) provide relevant data about the process of validation of the MDS PD-MCI criteria, (b) reinforce the hypothesis that PD-MCI is more frequent than previous studies showed without applying MDS criteria, and (c) confirm that PD-MCI is a risk factor for the onset of dementia. Finally, the study shows that neurological impairment, educational level and memory impairment were predictors for the progression of cognitive impairment.

Cognitive impairment in Parkinson’s disease: more than a frontostriatal dysfunction

Cognitive deficit in Parkinson’s disease has been traditionally considered as being mainly related to executive dysfunction secondary to frontostriatal affectation. However, this traditional consideration has recently been challenged. Forty-three nondemented PD patients (mean age = 59.19; SD = 9.64) and twenty control group subjects (mean age = 60.85; SD = 12.26) were studied. They were assessed on a wide range of cognitive functions. Patients showed motor slowing (p = .012), along with alterations in visuoperceptive (p = .001), visuospatial (p = .007) and visuoconstructive functions (p = .017), as well as in visual span (direct: p = .008; inverse: p = .037). Regarding executive functions, differences were not observed in classical measures for verbal fluency (phonetic: p = .28; semantic: p = .27) or in response inhibition (Stroop test: p = .30), while execution was altered in other prefrontal tasks (Wisconsin Test: p = .003; action fluency: p = .039). Patients showed altered performance in verbal learning processes (p = .005) and delayed memory (free: p = .032; cued: p = .006), visuospatial learning (p = .016) and linguistic functions (naming: p < .001; comprehension: p = .007). Poor performance in visuospatial memory is predicted by deficits in working memory and visuospatial perception. Taken together, the observed alterations not only suggest prefrontal affectation, but also temporal and parietal systems impairment. Thus, cognitive dysfunction in nondemented PD patients cannot be exclusively explained by frontostriatal circuit affectation and the resulting executive dysfunction (AU)

No disponible

Cognitive impairment in Parkinson's disease: more than a frontostriatal dysfunction.

Cognitive deficit in Parkinson's disease has been traditionally considered as being mainly related to executive dysfunction secondary to frontostriatal affectation. However, this traditional consideration has recently been challenged. Forty-three nondemented PD patients (mean age = 59.19; SD = 9.64) and twenty control group subjects (mean age = 60.85; SD = 12.26) were studied. They were assessed on a wide range of cognitive functions. Patients showed motor slowing (p = .012), along with alterations in visuoperceptive (p = .001), visuospatial (p = .007) and visuoconstructive functions (p = .017), as well as in visual span (direct: p = .008; inverse: p = .037). Regarding executive functions, differences were not observed in classical measures for verbal fluency (phonetic: p = .28; semantic: p = .27) or in response inhibition (Stroop test: p = .30), while execution was altered in other prefrontal tasks (Wisconsin Test: p = .003; action fluency: p = .039). Patients showed altered performance in verbal learning processes (p = .005) and delayed memory (free: p = .032; cued: p = .006), visuospatial learning (p = .016) and linguistic functions (naming: p < .001; comprehension: p = .007). Poor performance in visuospatial memory is predicted by deficits in working memory and visuospatial perception. Taken together, the observed alterations not only suggest prefrontal affectation, but also temporal and parietal systems impairment. Thus, cognitive dysfunction in nondemented PD patients cannot be exclusively explained by frontostriatal circuit affectation and the resulting executive dysfunction.