The Cortical Organization of Syntax: Insights into Grammatical Deficits in Aphasia

About This Grant

PROJECT SUMMARY Syntax, the ability to combine words into phrase and sentence structures, is a central component of language that is commonly impaired in aphasia. Deficits in sentence production are common in post-stroke aphasia, and sentence comprehension deficits are typically more persistent and severe than word comprehension deficits. Sentence comprehension often show little to no recovery by one year post-stroke, whereas word comprehension deficits typically recover well. Finally, people with chronic aphasia express a strong desire for greater fluidity of connected speech in fully structured sentences. Altogether, syntactic deficits are a major barrier to communication and participation in society for people with post-stroke aphasia. However, dominant neurocognitive models of syntax are supported by indirect measures of syntactic processing which do not segregate out effects of semantic processing and working memory. These models also do not account for the distinct patterns of syntactic deficits and patterns of recovery that emerge from different patterns of brain damage. Finally, these models do not account for the syndrome of paragrammatism, or syntactic deficits in in fluent aphasia, which has overall received highly limited attention in the research literature. We recently established a theoretical model of the cortical organization of syntax that addresses these issues and makes predictions that we will assess in the following research Aims. Specific Aim 1 will identify lesion correlates of receptive syntax in chronic post-stroke aphasia using grammaticality judgments and lesion mapping, Specific Aim 2 will identify lesion correlates and behavioral profile of agrammatic and paragrammatic speech in chronic post-stroke aphasia using a novel elicitation task, objective coding scheme and lesion mapping. We predict that that results will support models which make fundamental distinctions between syntactic and semantic processing and ascribe distinct syntactic functions to frontal and posterior temporal cortex and provide evidence against models which do not make the same distinctions. This work will clarify how distinct syntactic production and comprehension deficits result from damage to different specific brain networks and how these syndromes relate to each other, thereby providing a foundation for future treatment approaches. This proposal is innovative because of the novel theoretic approach informed by neuroscience in aphasia and healthy individuals, and will advance state-of-the-art neuroimaging techniques using arterial spin labeling and graph-theoretic connectivity analyses that account for lesion effects. This proposal is significant because it address poorly understood yet prevalent and persistent syntactic deficits in aphasia which are a priority for treatment as expressed by people who suffer from this condition.