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Original Articles

Computerized testing in Parkinson’s disease: Performance deficits in relation to standard clinical measures

, ORCID Icon, , & ORCID Icon
Pages 1062-1073 | Received 04 Nov 2017, Accepted 31 May 2018, Published online: 06 Jul 2018
 

ABSTRACT

Objective: This study assessed deficits associated with Parkinson’s disease (PD) at two time points separated by 1 year using a computerized neuropsychological battery, and determined interrelationships with conventional clinical measures of cognitive functioning (Montreal Cognitive Assessment; MoCA) and motor impairment (Part III of the Unified PD Rating Scale; UPDRS), as well as other factors known to influence cognitive dysfunction in PD. Method: Participants included 37 with PD and 47 controls. Linear mixed-effects models were developed for each computerized task. Results: Results showed that the PD group performed worse than controls on all of the computerized tasks at both time points. In contrast, MoCA scores differed between PD and controls only at follow-up. However, the MoCA detected decline over the year in the PD group, whereas only one of the computerized tasks did. In both groups, higher MoCA scores predicted better performance on some but not all of the computerized tasks. Surprisingly, UPDRS-rated motor impairment did not predict performance on any of the computerized tasks, and aside from older age, which predicted poorer performance on all but one task, the other factors—education, affective and impulsivecompulsive symptoms, sleep quality, dopaminergic medication—generally had no relationship with performance on the computerized tasks. Conclusions: The presence of performance deficits for all of the computerized tasks in the PD group compared to controls, but not for the MoCA at initial testing, indicates that the computerized battery was better able to detect deficits. However, in contrast to the MoCA, the current results call into question the suitability of the computerized battery as measured here for tracking decline.

Acknowledgment

The authors thank Michael Yung for his contribution.

Disclosure statement

No potential conflict of interest was reported by the authors.

Additional information

Funding

This work was supported by the Neurological Foundation of New Zealand [grant number 1517-SPG] and the University of Otago.

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