Neurocognitive Mechanisms of Syntactic Recovery in Agrammatism

Results of neuroimaging studies (using functional magnetic resonance imaging; fMRI) show a left lateralized neural network for syntactic processing in healthy individuals. When this network is damaged by stroke or other neurological disease syntactic abilities (i.e., sentence processing and production) are disrupted, resulting in agrammatic aphasia (agrammatism). This presentation will discuss (a) research examining the nature of syntactic processing deficits in agrammatism, for example, the results of eye tracking studies showing a failure to integrate lexical and syntactic information (see Thompson & Choy, 2009, for review) as well as (b) the results of research detailing patterns of syntactic recovery induced by treatment (see, for example, Thompson et al., 2010). Central to the talk will be discussion of research focused on the neural mechanisms of recovery and factors that affect it. Neural structures both within and outside the normal network for syntactic processing have potential to be recruited to support recovery, however, lesion characteristics (e.g., volume and location), vascular neuropathology (e.g., hypoperfusion) and other variables influence neural recruitment patterns (Bonakdarpour, Parrish, & Thompson, 2007; den Ouden et al., 2012; Thompson et al., 2010). Results of studies aimed at identifying these factors to determine the brain’s neuroplastic potential, i.e., biomarkers of recovery from brain damage, will be discussed.