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. 2010 Sep;133(9):2677-89.
doi: 10.1093/brain/awq197. Epub 2010 Aug 5.

Visual working memory deficits in patients with Parkinson's disease are due to both reduced storage capacity and impaired ability to filter out irrelevant information

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Visual working memory deficits in patients with Parkinson's disease are due to both reduced storage capacity and impaired ability to filter out irrelevant information

Eun-Young Lee et al. Brain. 2010 Sep.

Abstract

Given that Parkinson's disease broadly affects frontostriatal circuitry, it is not surprising that the disorder is associated with a reduction of working memory. We tested whether this reduction is due to diminished storage capacity or impaired ability to exclude task-irrelevant items. Twenty-one medication-withdrawn patients and 28 age-matched control subjects performed a visuospatial memory task while their electroencephalograms were recorded. The task required them to remember the orientations of red rectangles within the half of the screen that was cued while ignoring all green rectangles. Behavioural and electroencephalogram measures indicated that patients with Parkinson's disease were impaired at filtering out distracters, and that they were able to hold fewer items in memory than control subjects. The results support recent suggestions that the basal ganglia help control access to working memory.

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Figures

Figure 1
Figure 1
Example of a 2-red–2-green condition in which the left hemifield was task relevant. SOA = stimulus onset asynchrony; ITI = inter-trial interval.
Figure 2
Figure 2
(A) Mean K scores of control subjects and patients with Parkinson's disease (n = 28 and 21, respectively) as a function of trial type: K = N*(H−FA), where N is the relevant set size, H is the hit rate and FA is the false alarm rate. (B) Mean amplitudes of CDA at 600–1200 ms after memory array onset as a function of trial type for controls and patients. Error bars represent standard errors of the mean.
Figure 3
Figure 3
K scores (number of relevant items held in and retrieved from working memory) in the 4-red condition for control subjects and patients with Parkinson's disease, respectively.
Figure 4
Figure 4
(A) Mean K scores of high- and low-capacity controls and patients as a function of trial type: K = N*(H − FA), where N is the relevant set size, H is the hit rate and FA is the false alarm rate. (B) Mean amplitudes of CDA at 600–1200 ms after memory array onset as a function of trial type, for participants with estimated high and low overall storage capacity. Error bars represent standard errors of the mean.
Figure 5
Figure 5
Correlation between estimated capacity of visual working memory (K score in the 4-red condition) and unnecessary storage (K score difference: 2-red minus 2-red-2-green) for control subjects (A) and patients with Parkinson's disease (B).
Figure 6
Figure 6
Grand averaged CDA waveforms time-locked to the onset of the memory array averaged across the posterior parietal, posterior temporal and occipital electrode sites for controls (A) and patients with Parkinson's disease (B) as a function of trial type. Negative voltage is plotted upwards.
Figure 7
Figure 7
Grand averaged CDA waveforms as a function of trial type for high-capacity controls and patients (A, upper panel) and low-capacity controls and patients (B, lower panel).

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