Cognitive speed in nondemented Parkinson's disease

Smith, Mikel D.; Goldman, William P.; Janer, Kevin W.; Baty, Jack; Morris, John C.

doi:10.1017/s1355617798466074

Cited by 13 publications

(9 citation statements)

References 37 publications

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“…For this later group, only those times-of-assessment where PD was diagnosed were included. Thus PD patients reported here are a subset of a larger clinical cohort reported previously 1,2,4,5,12 with the important distinction of having been assessed at least 3 times so changepoint models have sufficient repeated measures data to be estimated. Thus all PD participants enrolled without cognitive impairment (i.e., CDR 0); and there were sufficient number of repeated measures to estimate MRC change points.…”

Section: Methodsmentioning

confidence: 99%

Onset of Mild Cognitive Impairment in Parkinson Disease

Johnson

Langford²,

Garnier‐Villarreal³

et al. 2016

Alzheimer Disease &Amp; Associated Disorders

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Objective Characterize the onset and timing of cognitive decline in PD from the first recognizable stage of cognitively symptomatic PD - mild cognitive impairment (PD-MCI) - to PD dementia (PDD). Thirty-nine participants progressed from PD to PDD and 25 remained cognitively normal. Method Bayesian estimated disease-state models described the onset of an individual’s cognitive decline across 12 subtests with a changepoint. Results Subtests measuring working memory, visual imagery, and crystalized memory changed significantly 3–5 years before their first non-zero CDR and progressively worsened from PD to PD-MCI to PDD. Crystalized memory deficits were the hallmark feature of imminent conversion of cognitive status. Episodic memory tasks were not sensitive to onset of PD-MCI. For cognitively intact PD, all 12 subtests showed modest linear decline without evidence of a changepoint. Conclusions Longitudinal disease-state models support a prodromal dementia stage (PD-MCI) marked by early declines in working memory and visuospatial processing beginning 5 years prior to clinical diagnosis of PDD. Cognitive declines in PD affect motor ability (bradykinesia), working memory and processing speed (bradyphrenia) resulting in PD-MCI where visuospatial imagery and memory retrieval deficits manifest before eventual development of overt dementia. Tests of episodic memory may not be sufficient to detect and quantify cognitive decline in PD.

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Section: Methodsmentioning

confidence: 99%

Onset of Mild Cognitive Impairment in Parkinson Disease

Johnson

Langford²,

Garnier‐Villarreal³

et al. 2016

Alzheimer Disease &Amp; Associated Disorders

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“…It has been suggested that the finding of reduced cognitive speed may very well have been caused by the inclusion of patients with mild dementia or depression (Smith, 1998). For an excellent and comprehensive review of the literature on cognitive deficits in PD, one is advised to read the chapter by Pillon and co-workers in the recent Handbook of Neuropsychology (Pillon, 2001).…”

Section: Cognitive Deficits In Non-demented Pd Patientsmentioning

confidence: 99%

Cognitive dysfunction and dementia in Parkinson?s disease

2004

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Summary. Parkinson's disease (PD) is a slowly progressive neurodegenerative disorder mainly characterized by degeneration of dopaminergic neurons in the substantia nigra and the ventral tegmental area, in combination with a varying loss of central noradrenergic (locus coeruleus), cholinergic (nucleus basalis of Meynert) and serotonergic (dorsal raphe nuclei) integrity, leading to a multitude of motor and non-motor behavioral disturbances.Apart from the clinical motor hallmarks, in the early stages of disease, subtle cognitive dysfunction might be seen comprising mainly executive dysfunction, with secondary visuospatial and mnemonic disturbances. In about 20-40% of patients, these problems may eventually proceed to dementia, which constitutes an important risk factor for caregiver distress, decreased quality of life and nursing home placement. Dementia in PD is typically characterized by a progressive dysexecutive syndrome with attentional deficits and fluctuating cognition, often accompanied by psychotic symptoms. It is thought to be the result of a combination of both subcortical and cortical changes. PD-related dopaminergic deficiency in the nucleus caudatus and mesocortical areas (due to degeneration of projections from the substantia nigra and ventral tegmental area) and cholinergic deficiency in the cortex (due to degeneration of ascending projections from the nucleus basalis of Meynert), combined with additional Alzheimer-pathology and cortical Lewy bodies, may greatly contribute to dementia.Current treatment of dementia in PD is based on compensation of the profound cholinergic deficiency. Recent studies with the cholinesterase inhibitors galantamine, donepezil and rivastigmine show promising results in improving cognition and ameliorating psychotic symptoms, which must further be confirmed in randomized controlled trials.

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“…Using the SIRP, Smith and colleagues did not find slowing of the motor component of the response time in a group of dopaminergically depleted patients with Parkinson's disease. 24 Specific task characteristics, including the type of motor response required (for example button press, as in the current study, versus a response that requires a larger movement) may provide a partial explanation of these contrasting findings. 38 In addition, although the motor component of the SIRP is conceptually similar to simple response time, it differs in that it is a derived measure (the y intercept of the regression line) that isolates the motor component of response time.…”

Section: Discussionmentioning

confidence: 71%

“…[22][23][24] The SIRP is a choice-reaction time test that dissociates the motor and cognitive components of response time. Accurate responses are predicated upon a temporarily stored representation of the targets that must be maintained in working memory for the duration of the trial.…”

mentioning

confidence: 99%

Cognitive slowing in Parkinson's disease resolves after practice

Press

Mechanic²,

Tarsy³

et al. 2002

Journal of Neurology, Neurosurgery &Amp; Psychiatry

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Objective: To assess the effect of dopaminergic repletion on working memory in Parkinson's disease. Methods: The role of dopaminergic state on working memory in patients with Parkinson's disease was determined using the Sternberg item recognition paradigm, a continuous performance task that dissociates the motor and cognitive components of response time. Ten patients with Parkinson's disease were tested in an "on" state (on dopaminergic drug treatment) and a practical "off" state in two sessions held one week apart in counterbalanced order; 10 controls matched for age and education were studied at the same time points. Results: Patients with Parkinson's disease showed impaired working memory, independent of motor slowing. During session 1, the performance of the patients was worse than the controls, regardless of dopaminergic state. The patients showed a significant improvement in the cognitive component of task performance during the second session, such that they no longer differed from the controls. The performance of the control subjects remained stable over the two sessions. Conclusions: Working memory performance of patients with Parkinson's disease did not change in association with dopaminergic state; rather, the performance improved over time. The pattern of improvement over time suggests a delay in proceduralising the task, similar to the deficits shown by such patients in procedural learning of other tasks.

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Cognitive speed in nondemented Parkinson's disease

Cited by 13 publications

References 37 publications

Onset of Mild Cognitive Impairment in Parkinson Disease

Onset of Mild Cognitive Impairment in Parkinson Disease

Cognitive dysfunction and dementia in Parkinson?s disease

Cognitive slowing in Parkinson's disease resolves after practice

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