title: No right to speak? The relationship between object naming and semantic impairment: neuropsychological evidence and a computational model.
abstract: The processes required for object naming were addressed in a study of patients with semantic dementia (a selective decline of semantic memory resulting from progressive temporal lobe atrophy) and in a computational model of single-word production. Although all patients with semantic dementia are impaired in both single-word production and comprehension, previous reports had indicated two different patterns: (a) a parallel decline in accuracy of naming and comprehension, with frequent semantic naming errors, suggesting a purely semantic basis for the anomia and (b) a dramatic progressive anomia without commensurate decline in comprehension, which might suggest a mainly postsemantic source of the anomia. Longitudinal data for 16 patients with semantic dementia reflected these two profiles, but with the following additional important specifications: (1) despite a few relatively extreme versions of one or other profile, the full set of cases formed a continuum in the extent of anomia for a given degree of degraded comprehension; (2) the degree of disparity between these two abilities was associated with relative asymmetry in laterality of atrophy: a parallel decline in the two measures characterized patients with greater right- than left-temporal atrophy, while disproportionate anomia occurred with a predominance of atrophy in the left-temporal lobe. In an implemented computational model of naming, semantic representations were distributed across simulated left- and right-temporal regions, but the semantic units on the left were more strongly connected to left-lateralized phonological representations. Asymmetric damage to semantic units reproduced the longitudinal patient profiles of naming relative to comprehension, plus additional characteristics of the patients' naming performance. On the basis of both the neuropsychological and computational evidence, we propose that semantic impairment alone can account for the full range of word production deficits described here.
authors.affiliation: University of Bristol, Bristol, UK. matt.lambon-ralf@bristol.ac.uk
authors.forename: M A
authors.initials: MA
authors.lastname: Lambon Ralph
authors.forename: J L
authors.initials: JL
authors.lastname: McClelland
authors.forename: K
authors.initials: K
authors.lastname: Patterson
authors.forename: C J
authors.initials: CJ
authors.lastname: Galton
authors.forename: J R
authors.initials: JR
authors.lastname: Hodges
mesh_terms: D000849:Anomia / Q000503:physiopathology*; D001041:Aphasia, Wernicke / Q000503:physiopathology*; D015331:Cohort Studies; D003704:Dementia / Q000503:physiopathology*; D007839:Functional Laterality / Q000502:physiology; D006801:Humans; D008959:Models, Neurological; D009483:Neuropsychological Tests; D010700:Phonetics; D010775:Photic Stimulation; D013702:Temporal Lobe / Q000503:physiopathology