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Long reaction times are associated with delayed brain activity in Lewy body dementia

Published version
Peer-reviewed

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Authors

Firbank, MJ 
O'Brien, JT 
Taylor, JP 

Abstract

A significant symptom of Lewy body dementia (LBD) is slow cognitive processing or bradyphrenia. In a previous fMRI task-based study, we found slower responses in LBD, accompanied by greater deactivation in the default mode network. In this study, we investigated the timing and magnitude of the activations and deactivations with respect to reaction time to determine whether the slower responses in LBD were associated with delayed neuronal activity. Using fMRI, we examined the magnitude and latency of activations and deactivations during an event-related attention task in 32 patients with LBD and 23 healthy controls using predefined regions of interest. Default mode network deactivations did not significantly differ in their timing between groups or task conditions, while the task-related activations in the parietal, occipital, frontal, and motor cortex were all significantly later in the LBD group. Repeating the analysis with reaction time as a parametric modulator of activation magnitude produced similar findings, with the reaction time modulator being significant in a number of regions including the default mode network, suggesting that the increased deactivation in LBD is partly explained by slower task completion. Our data suggest that the default mode network deactivation is initiated at the start of the task, and remains deactivated until its end, with the increased magnitude of deactivation in LBD reflecting the more prolonged cognitive processing in these patients. These data add substantially to our understanding of the neural origins of bradyphrenia, which will be essential for determining optimum therapeutic strategies for cognitive impairment in LBD.

Description

Keywords

bradyphrenia, Lewy body dementia, default mode network, reaction time

Journal Title

Human Brain Mapping

Conference Name

Journal ISSN

1065-9471
1097-0193

Volume Title

Publisher

Wiley
Sponsorship
Funded by: National Institute for Health Research, Newcastle Biomedical Research Unit based at Newcastle Hospitals NHS Foundation Trust, Newcastle University, Wellcome Trust. Grant Number: WT088441MA