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  • Title: [Neuro-cognitive models of spelling and Alzheimer disease: mutual clarification].
    Author: Eustache F, Lambert J.
    Journal: Rev Neurol (Paris); 1996 Nov; 152(11):658-68. PubMed ID: 9033940.
    Abstract:
    The neuro-cognitive models developed over the last twenty years have considerably added to the understanding of disorders of spelling and writing resulting from brain lesions. These models differentiate between central processes, damage to which explains linguistic disorders, and peripheral processes, damage to which results in praxia and related disorders. This article analyses studies which have applied these distinctions to disorders observed in Alzheimer's disease. This disease causes unusual pathological situations which show certain types of agraphia rarely seen in the relevant literature, particularly certain peripheral forms. Several studies considered demonstrate the frequency of lexical agraphia in Alzheimer's disease. These lexical disorders of written expression seem to be independent of the lexico-semantic disorders found in other areas of the intellectual processes, Central writing disorders-lexical but also phonological-would appear to be the result of relatively focussed dysfunctionings, the left gyrus angularis and left gyrus supramarginalis respectively, as is suggested in brain metabolism studies. Moreover, certain patients develop peripheral writing disorders which are at present less well known, on a cognitive and neurobiological point of view. Inferences from other pathological contexts reveals that these disorders are often associated with diffuse cerebral lesions. Therefore disorders of written expression in Alzheimer's disease may be the result of two different pathological mechanisms: central disorders arising from localized areas of dysfunctioning at the left temporo-parietal intersection; peripheral disorders linked to the dysfunctioning of a much wider network involving the parietal and frontal regions of both cerebral hemispheres. To account for the diversity of clinical pictures, we suggest a physiopathological hypothesis which could also be used as a therapeutic model in Alzheimer's disease.
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