Mechanisms of lexical selection: The relative contributions of linguistic and executive control deficits

Dynamic aphasia (DA) remains a relatively understudied form of aphasia. Patients with DA demonstrate a reduced spontaneous speech output despite that lower linguistic levels (that is, production and comprehension of single words and short sentences) are relatively well-preserved. Previous studies have suggested that DA is driven either by a deficit in executive functions (more specifically, planning or sequencing), or impaired lexical selection. We aim to study the relative contributions of these two mechanisms to spontaneous speech impairment in DA.

We are performing detailed assessments of linguistic and executive control abilities in two groups of patients: those who are diagnosed with DA following the left frontal lobe lesions, and a control group – patients with left frontal lobe lesions who do not have DA. The assessment includes a variety of tests measuring deficits at the specific stages of language processing that are frequently impaired in DA, and the concurrent executive control deficits. To obtain a detailed neuroanatomical profile of the patients’ lesions, they undergo structural and diffusion-weighted magnetic resonance imaging. We plan to test the hypothesis that DA is driven by a disruption of connectivity between the frontal lobe areas subserving executive control, and the language network. We expect that two different mechanisms may cause DA depending on the specific pattern of connectivity disruption. Namely, we expect that a disruption of connectivity between posterior frontal areas and the prefrontal cortex impairs the abilities to plan extended spontaneous speech. At the same time, a disruption of connectivity between the supplementary motor and inferior frontal cortices may impair lexical selection. We hypothesize that both mechanisms contribute to the overall spontaneous speech reduction despite well-preserved lower linguistic levels, that is, dynamic aphasia.

The study was supported by the RF Government Grant, ag. No. 14.641.31.0004.