BACKGROUND: Verbal working memory is an essential component of many language functions, including sentence comprehension and word learning. As such, working memory has emerged as a domain of intense research interest both in aphasiology and in the broader field of cognitive neuroscience. The integrity of verbal working memory encoding relies on a fluid interaction between semantic and phonological processes. That is, we encode verbal detail using many cues related to both the sound and meaning of words. Lesion models can provide an effective means of parsing the contributions of phonological or semantic impairment to recall performance. METHODS AND PROCEDURES: We employed the lesion model approach here by contrasting the nature of lexicality errors incurred during recall of word and nonword sequences by 3individuals with progressive nonfluent aphasia (a phonological dominant impairment) compared to that of 2 individuals with semantic dementia (a semantic dominant impairment). We focused on psycholinguistic attributes of correctly recalled stimuli relative to those that elicited a lexicality error (i.e., nonword → word OR word → nonword). OUTCOMES AND RESULTS: Patients with semantic dementia showed greater sensitivity to phonological attributes (e.g., phoneme length, wordlikeness) of the target items relative to semantic attributes (e.g., familiarity). Patients with PNFA showed the opposite pattern, marked by sensitivity to word frequency, age of acquisition, familiarity, and imageability. CONCLUSIONS: We interpret these results in favor of a processing strategy such that in the context of a focal phonological impairment patients revert to an over-reliance on preserved semantic processing abilities. In contrast, a focal semantic impairment forces both reliance upon and hypersensitivity to phonological attributes of target words. We relate this interpretation to previous hypotheses about the nature of verbal short-term memory in progressive aphasia.
BACKGROUND: Verbal working memory is an essential component of many language functions, including sentence comprehension and word learning. As such, working memory has emerged as a domain of intense research interest both in aphasiology and in the broader field of cognitive neuroscience. The integrity of verbal working memory encoding relies on a fluid interaction between semantic and phonological processes. That is, we encode verbal detail using many cues related to both the sound and meaning of words. Lesion models can provide an effective means of parsing the contributions of phonological or semantic impairment to recall performance. METHODS AND PROCEDURES: We employed the lesion model approach here by contrasting the nature of lexicality errors incurred during recall of word and nonword sequences by 3individuals with progressive nonfluent aphasia (a phonological dominant impairment) compared to that of 2 individuals with semantic dementia (a semantic dominant impairment). We focused on psycholinguistic attributes of correctly recalled stimuli relative to those that elicited a lexicality error (i.e., nonword → word OR word → nonword). OUTCOMES AND RESULTS:Patients with semantic dementia showed greater sensitivity to phonological attributes (e.g., phoneme length, wordlikeness) of the target items relative to semantic attributes (e.g., familiarity). Patients with PNFA showed the opposite pattern, marked by sensitivity to word frequency, age of acquisition, familiarity, and imageability. CONCLUSIONS: We interpret these results in favor of a processing strategy such that in the context of a focal phonological impairment patients revert to an over-reliance on preserved semantic processing abilities. In contrast, a focal semantic impairment forces both reliance upon and hypersensitivity to phonological attributes of target words. We relate this interpretation to previous hypotheses about the nature of verbal short-term memory in progressive aphasia.
Entities:
Keywords:
Aphasia; Progressive Nonfluent Aphasia; Recall; Semantic Dementia; Working Memory
Authors: J M S Pereira; G B Williams; J Acosta-Cabronero; G Pengas; M G Spillantini; J H Xuereb; J R Hodges; P J Nestor Journal: Neurology Date: 2009-05-12 Impact factor: 9.910
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Authors: M Grossman; J Mickanin; K Onishi; E Hughes; M D'Esposito; X S Ding; A Alavi; M Reivich Journal: J Cogn Neurosci Date: 1996 Impact factor: 3.225
Authors: J D Rohrer; E McNaught; J Foster; S L Clegg; J Barnes; R Omar; E K Warrington; M N Rossor; J D Warren; N C Fox Journal: Neurology Date: 2008-10-28 Impact factor: 9.910