Poststroke action slowing increases with task complexity and is linked to broader brain recruitment
- PMID: 39933229
- DOI: 10.1016/j.cortex.2024.12.024
Poststroke action slowing increases with task complexity and is linked to broader brain recruitment
Abstract
Despite its high prevalence, the mechanisms of slowing in stroke remain surprisingly poorly understood. Our objectives were (1) to determine the profile of slowing as a function of test complexity and (2) to examine the relationship between this complexity effect, test sensitivity and the recruitment of brain areas. The study focused on the 371 stroke patients and 581 controls of the GRECogVASC study assessed with eight time-limited tests: finger tapping, simple reaction time, line cancellation, Trail Making Test parts A and B, coding, and semantic and phonemic fluency tests. Action speed of patients was slower than that of controls (p = .0001); slowing worsened with test complexity (p = .0001) by 7.7% at each step of increasing complexity. The highest test sensitivity was observed (p = .0001) for more complex tests. The number of lesioned voxels associated with action speed increased with test complexity. The sensitivity of the tests roughly paralleled (p = .007) the volume of recruited brain areas. The individual slopes of action duration with test complexity correlated with the volume of lesion (p = .002), white matter hyperintensities (p = .0001) and parenchymal brain fraction (p = .0001). The effect of stroke on slowing is due both to small slowing on simple tests and to a general slowing of processing speed. The test sensitivity reflects the size of recruited brain network and its proportional vulnerability to lesion. In addition to their clinical implications, these results shed light on the organization of the systems that optimize action speed in humans.
Keywords: Attention; Dementia; Executive functions; Lesion-symptom mapping; Psychomotor speed; Stroke.
Copyright © 2025 Elsevier Ltd. All rights reserved.
Conflict of interest statement
Declaration of competing interest Olivier Godefroy reports funding for travel and meetings from Biogen, Roche, and Bristol-Myers Squibb outside the submitted work. Sandrine Canaple has nothing to disclose. Pierre-Andrea Cervellera has nothing to disclose. Jeremy Neel has nothing to disclose. Sophie Tasseel-Ponche reports travel and meeting support from LFB Biomedicaments, Icomed, Ipsen, Merz, Jean-Manuel Toussaint IHTM, Allergan, B3TSI, EISAI SAS and DJO France SAS outside the submitted work. Ardalan Aarabi has nothing to disclose. Mickael Aubignat reports funding for travel and meetings from Abbvie, Orkyn, Elivie, Biogen, Medtronic and Boston scientific. Martine Roussel has nothing to disclose.
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