The problem of naming in SDAT: A relative deficit

Abstract

Research relating to language disorder in senile dementia of the Alzheimer type (SDAT) has focused primarily on naming impairment, formally termed anomia or nominal aphasia/dysphasia. Data resulting from this research have been insufficiently informed by a comparative linguistic framework in which performance on naming tasks is contrasted with performance on other forms of language tasks. The present study involves the comparison of 21 adults with SDAT and 18 demographically controlled normal elderly adults on the Test for Syntactic Complexity and fifteen subtests of the Western Aphasia Battery. Performance on naming is compared with performance on oral language variables of repetition, yes/no response, auditory word recognition, sequential commands, syntactic processing, as well as with performance on reading tasks and non-verbal tasks. Findings relating to oral language tasks show that structured syntactic processing requiring explicit interpretation and sequential commands are significantly more difficult for the SDAT sample than are three of four naming tasks. Further, significant SDAT performance variability is found across naming tasks. The generative categorical naming task is found to be significantly more difficult for the SDAT patient than are the other three naming tasks. It is concluded that the generative categorical naming task should be regarded as a meta-naming task. In sum, it is found that although language dysfunction in SDAT has anomic components, the essential character of the language disorder is not best conceptualized as a problem of naming.

Noninfarct vascular dementia and Alzheimer dementia spectrum

“…Analysis of the seven subtests of the Western Aphasia Battery revealed that both vascular samples had deficits at the 0.0001 level when compared with normal elderly persons on the word fluency task, which is a metanaming [37] task assessing capability for generative naming (e.g., bname as many foods as you canQ). The infarct sample was also impaired at the 0.0001 level when compared to normal elderly on reading comprehension and sequential commands tasks, whereas the noninfarct sample was impaired in relation to normals on these tasks at the 0.004 and 0.0004 levels ( Table 4).…”

“…Comparisons between both vascular samples and normal elderly on repetition and auditory comprehension were also statistically significant (Table 4). There were no significant differences between either the infarct or noninfarct patients in relation to normal elderly persons on oral language tasks of responsive speech and sentence completion, which are the least complex of language tasks involving overlearned language sequences (e.g., broses are red, violets are what?Q) [33][34][35]37].…”

Reclassification of the Vascular Dementias: Comparisons of Infarct and Noninfarct Vascular Dementias

“…Oral language processing was measured by six subtests from the Western Aphasia Battery (WAB; Kertesz, 1982) and by the Boston Naming Test (BNT; Kaplan et al, 1983). Oral language variables assessed were repetition, naming, auditory verbal comprehension, and grammatical-syntactic processing (Emery, 1985(Emery, ,1986(Emery, ,1993(Emery, ,1996Emery & Breslau, 1988Kertesz, 1979Kertesz, , 1982Yngve, 1986). The WAB Repetition test requires the participant to repeat 14 items.…”

Phonological and Articulatory Impairment in Alzheimer's Disease: A Case Series

“…Despite the negative findings summarized above, therefore, it is perhaps not surprising that other evidence suggests a degree of vulnerability of articulatory and phonological processing (Hart, 1988). An abnormal rate of phonological errors has been either occasionally noted, or even specifically investigated and reported, both in spontaneous speech (Gavazzi, Luzzatti, & Spinnler, 1986;Loebel, Dager, Berg, & Hyde, 1990;Shuren, Geldmacher, & Heilman, 1993) and in more formal word and sentence production tasks (Biassou et al, 1995;Emery & Breslau, 1988;Glosser, Friedman, Kohn, Sands, & Grugan, 1998;Glosser, Kohn, Friedman, Sands, & Grugan, 1997;Obler & Albert, 1984;Price et al, 1993). Because phonological and/or articulatory disruption is characteristic of several other neurodegenerative diseases which may be contenders in the differential diag- (Cummings, Darkins, Mendez, Hill, & Benson, 1988;Gordon & Illes, 1987;Hier, Hagenlocker, & Shindler, 1985;Holland, McBurney, Moossy, & Reinmuth, 1985)], if reported speech output deficits in probable AD were infrequent, and only referred to cases lacking pathological confirmation, one might question whether such deficits were actually associated with non-Alzheimer pathology in cases which had accidentally been included in a probable AD group.…”