摘要：Caplan et al. (2007) have proposed that the sentence processing deficit in agrammatic aphasia is aconsequence of intermittent deficiency (ID) in the capacity to carry out syntactic, semantic, and taskrelated computations. We operationalize ID as a specific impairment in a cognitive architecture forsentence processing. We also implement a complementary hypothesis of slowed processing (SP),which ascribes the deficit to a pathological slowdown (Hanne et al., 2011). We contrast theseprocessing deficit accounts with a representational deficit account, the Trace Deletion Hypothesis(TDH) (Grodzinsky, 2000), which claims that patients suffer from impairment in their syntacticrepresentation.
