ABSTRACT
There is a scientific paradigm (Kuhn, 1962) within which research in aphasia is conducted. This paradigm encompasses the tacit assumptions about the underlying nature of the disorder (aphasia in this case) and in general dictates the kind of the research questions and methods used for answering them that is acceptably conducted by its practitioners. The paradigm is determined by the majority of the scientists working in the discipline. Although there is the possibility of coexisting paradigms for the clinical practice in aphasia on the one hand and theory-driven investigation of aphasia on the other, the practice of science in most Western cultures dictates coherence between them and the theoretical perspective typically holds more capital than the clinical one. That is, because it is generally believed that theory is the guiding principle for practice, the theoretical paradigm typically has a strong and perhaps dominating influence on the clinical paradigm. Such is the case with clinical aphasiology. This theoretical paradigm may be best characterized as the centers and pathways paradigm and is a direct descendent of the Wernicke/Lichtheim model of aphasia (Eggert, 1977). It is based on the notion that there are language centers in the brain that house specific linguistic rules and representations and that these centers are connected to one another by direct pathways. To illustrate, within this centers and pathways conceptualization of aphasia, the arcuate fasciculus pathway connects the posterior temporal lobe (putative) language comprehension center (Wernicke’s area) to the inferior and posterior two-thirds of the third frontal convolution (putative) speech production center (Broca’s Area). These centers and this specific pathway allow the association of representations and the performance of specific linguistic computations and language tasks (e.g., speech repetition in this instance). The aphasia classification system adhered to by the majority of aphasiologists best represents this scientific paradigm and is firmly grounded in this “anatomical connectionist” (not to be confused with “computational connectionist”) models of aphasia. Within this model of aphasia, damage to a specific center (e.g., Wernicke’s area) or a specific pathway (e.g., the arcuate fasciculus) will yield a specific pattern of language (Wernicke’s Aphasia) or modality (repetition deficit in “Conduction Aphasia”) deficit respectively, which corresponds to a “classical” type or category of aphasia (Geschwind, 1965a, 1965b; Goodglass, Kaplan, & Barresi, 2001; Kertesz, 1979). In general, this model of aphasic deficits, and the adherents of its derived classification system have tended to view aphasia as a loss of representations subserving specific language functions due to the damaged language center or the damaged or disconnected pathway. In its strongest formulations, it is assumed that the rules and the representations have either been deleted from the patient’s repertoire or become permanently inaccessible because of a structural lesion in the relevant neural substrates responsible for the language computation or association. This assumption is reflected in definitions of aphasia as a “loss” of language (Benson, 1979), and in some formal theories and hypotheses proposed to account for specific signs and symptoms of aphasia such as the “trace deletion hypothesis” of Grodzinsky (2000), which was proposed to account for the failure of specific syntactic operations. Proponents of the centers and pathways model have tended to emphasize the differences among persons with aphasia by dividing them into the model-derived behavioral categories arranged along modality and psycholinguistic dimensions.
