We claim that the animate and inanimate conceptual categories represent evolutionarily adapted domain-specific knowledge systems that are subserved by distinct neural mechanisms, thereby allowing for their selective impairment in conditions of brain damage. On this view, (some of) the category-specific deficits that have recently been reported in the cognitive neuropsychological literature - for example, the selective damage or sparing of knowledge about animals - are truly categorical effects. Here, we articulate and defend this thesis against the dominant, reductionist theory of category-specific deficits, which holds that the categorical nature of the deficits is the result of selective damage to noncategorically organized visual or functional semantic subsystems. On the latter view, the sensory/functional dimension provides the fundamental organizing principle of the semantic system. Since, according to the latter theory, sensory and functional properties are differentially important in determining the meaning of the members of different semantic categories, selective damage to the visual or the functional semantic subsystem will result in a category-like deficit. A review of the literature and the results of a new case of category-specific deficit will show that the domain-specific knowledge framework provides a better account of category-specific deficits than the sensory/functional dichotomy theory.

Priming for semantically related concepts was investigated using a lexical decision task designed to reveal automatic semantic priming. Two experiments provided further evidence that priming in a single presentation lexical decision task (McNamara & Altarriba, 1988) derives from automatic processes. Mediated priming, but no inhibition or backward priming was found in this type of lexical decision task. Experiments 3 and 4 demonstrated that automatic priming was found only for associated word pairs, as determined by word association norms, and not for word pairs that are semantically related but not associated. It is argued that automatic priming in the lexical decision task occurs at a lexical level not at a semantic level.

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We report on two brain-damaged subjects who exhibit the uncommon pattern of loss of object color knowledge, but spared color perception and naming. The subject P.C.O., as in previously reported patients, is also impaired in processing other perceptual and functional properties of objects. I.O.C., in contrast, is the first subject on record to have impaired object color knowledge, but spared knowledge of object form, size and function. This pattern of performance is consistent with the view that semantic information about color and other perceptual properties of objects is grounded in modality-specific systems. Lesion analysis suggests that such grounding requires the integrity of the mesial temporal regions of the left hemisphere.

We present the case of a fluent aphasic patient who is impaired at producing nouns relative to verbs in picture naming, sentence completion, and sentence generation tasks, but is better at both producing and comprehending concrete nouns than abstract nouns. Moreover, he displays a selective difficulty in producing the plural forms of some nouns and pseudowords presented as nouns, but was able to produce the phonologically identical third-person singular forms of corresponding verb homonyms and of the same pseudowords presented as verbs. This pattern of performance casts doubt on the hypothesis that grammatical class effects are always epiphenomena of more general semantic impairments that affect the naming of actions or of concrete objects, and suggests that these effects may arise instead from damage to syntactic processes pertaining specifically to the grammatical properties of words. We also discuss the implications of such damage for models of morphological processing.

The investigation of language processing following brain damage may be used to constrain models of normal language processing, We review the literature on semantic and lexical processing deficits, focusing on issues of representation of semantic knowledge and the mechanisms of lexical access, The results broadly support a componential organization of lexical knowledge-the semantic component is independent of phonological and orthographic form knowledge, and the latter are independent of each other. Furthermore, the results do not support the hypothesis that word meaning is organized into modality-specific subcomponents. Wealso discuss converging evidence from functional imaging studies in relation to neuropsychological results.The investigation of cognitive deficits in brain-damaged individuals can provide powerful constraints for theories of normal cognition. Brain damage does not lead to an undifferentiated loss of cognitive abilities but to richly structured patterns of impaired and spared performance. Thus, for example, a patient might show severe difficulties in orally producing the names ofpictures but show no comparable difficulties in writing them. Or a patient might show great difficulty in producing nouns but not verbs and adjectives. Furthermore, in most cases impaired performance deviates from normal performance in instructive ways. For example, in a picture naming task a patient might produce phonological distortions of the target response (e.g., chair~"share, chail"), suggesting the possibility that the correct lexical node has been accessed but that subsequent processes are damaged. Or the patient might produce well-formed, semantically related responses (e.g., chair~"table, not that but close, something you sit on"), suggesting that motor programming and articulatory processes are intact but that lexical selection mechanisms are malfunctioning. The analysis of the dissociation and association of symptoms and their related error patterns severely constrains possible interpretations of the locus of functional impairment in the normal language production system. The logic of inferences from impaired performance to normal cognition is straightforward: We prefer a theory of normal cognition over alternative theories if that theory can explain both normal performance and the various ways in which a system breaks down in conditions ofbrain damage. One area 5 that has benefited greatly from neuropsychological investigations is lexical processing.A basic assumption shared by almost all current theories of the lexicon is that it is composed of several distinct components. This assumption supports the expectation that brain damage could result in the selective disruption of each of the components that constitutes the lexical system. The ways in which a cognitive system can be damaged depends on how it is organized in the brain. Functionally independent lexical components can be damaged selectively only if they are neuroanatomically separable.' But, within the constraints imposed by the neuroanatomical organ...

This study reports data from two dysgraphic patients, TH and PB, whose errors in spelling most often occurred in the final part of words. The probability of making an error increased monotonically towards the end of words. Long words were affected more than short words, and performance was similar across different output modalities (writing, typing and oral spelling). This error performance was found despite the fact that both patients showed normal ability to repeat the same words orally and to access their full spelling in tasks that minimized the involvement of working memory. This pattern of performance locates their deficit to the mechanism that keeps graphemic representations active for further processing, and shows that the functioning of this mechanism is not controlled or "refreshed" by phonological (or articulatory) processes. Although the overall performance pattern is most consistent with a deficit to the graphemic buffer, the strong tendency for errors to occur at the ends of words is unlike many classic "graphemic buffer patients" whose errors predominantly occur at word-medial positions. The contrasting patterns are discussed in terms of different types of impairment to the graphemic buffer.

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