Executive control deficits and lesion correlates in acute left hemisphere stroke survivors with and without aphasia

In contrast to the traditional definition of the disorder, many individuals with aphasia exhibit non-linguistic cognitive impairments, including executive control deficits. Classic lesion studies cite frontal lobe damage in executive dysfunction, but more recent lesion symptom-mapping studies in chronic aphasia present mixed results. In this study, we compared executive control abilities of acute stroke survivors with and without aphasia and investigated lesion correlates of linguistic and non-linguistic cognitive tasks. Twenty-nine participants with acute left hemisphere stroke resulting in aphasia (n = 14) or no aphasia (n = 15) completed clinical MRI and testing, including three NIH Toolbox Cognition Batteries (Pattern Comparison Processing Speed, Flanker Inhibitory Control and Attention, and Dimensional Change Card Sort Tests) and the Boston Naming Test. We compared performance between groups using Wilcoxon rank sum tests. We used Least Absolute Shrinkage and Selection Operator Regression to identify neural markers (percent regional damage, hypoperfusion within vascular territories, and total lesion volume) of executive control deficits and anomia. Group performance was comparable on the Pattern Comparison Processing Speed Test, but people with aphasia had poorer standard scores, lower accuracy, and slower response times on the Dimensional Change Card Sort Test than people without aphasia. Damage to extrasylvian regions (dorsolateral prefrontal cortex, intraparietal sulcus) was related to executive control deficits, whereas language network damage (to inferior frontal and superior and posterior middle temporal gyri) was linked to naming impairments. These results suggest people with aphasia can exhibit comorbid executive control impairments linked to damage outside classic language network areas.