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At least 235 records · Page 13Linked to original sources
PubMed1993

Single-character processing in a case of pure alexia.

The processing of single characters in a pure alexic patient was studied in an attempt to identify the impairment responsible for his reading disorder. Observations from Experiments 1 to 4 suggested a deficit of identification of alphanumeric stimuli without any impairment affecting the elaboration of a structural description of visual stimulation. Experiment 5 indicated that the identification disorder results from a defect in the selective processes--activation and/or inhibition--that must come into play for achieving an appropriate match between a structural description of the stimulation and representations of the identities of known stimuli. The possible implications of this deficit in single-character identification for word reading are discussed.

Adult↗
PubMed1996

Reading speed in pure alexia.

This study investigated possible causes of differences in reading speed between two alexic patients who read words letter by letter. As both patients appeared to rely on serial left-to-right processing of letters within words, the difference in reading speed did not seem to be related to any differences in the extent to which the patients could recognize letters in words in parallel or 'ends-in'. Differences in reading speed also seemed to be unrelated to the patients ability to identify individual letters since their letter recognition accuracy was very similar. Furthermore, although patient PD was significantly slower at reading words aloud than patient DC, PD was in fact significantly quicker than DC on a test that has previously been used to assess letter recognition skills in letter-by-letter readers. It is therefore concluded that PD reads words more slowly because of an additional impairment at the level of the word form system. The results therefore reinforce the distinction between Type 1 and Type 2 letter-by-letter readers that was first drawn by Patterson and Kay.

Adult↗
PubMed1988

Internal representations and the conceptual operation of color in pure alexia with color naming defects.

This research examined the structure of internal representation and the conceptual operation of color in two pure alexic cases (Case I and Case II) with color naming defects. Experiment I investigated the structure of the internal representation of different kinds of colors using a similarity judgment task. Experiment II examined categorical judgments of perceived colors using a two-alternative-forced choice task. Experiment III tested the classification of perceived colors using a color sorting task. The performance of Case I essentially fell within the normal range while the results of Case II showed some impairment in the conceptual operation of color. Analysis of the responses obtained from these experiments indicated that the color naming defects in Case I can be explained in terms of visual-verbal disconnection. However, the naming defects in Case II reflect disfunction in some other higher cortical processes coupled with visual-verbal disconnection.

Color Perception↗
PubMed1994

Associative visual agnosia and alexia without prosopagnosia.

Disagreement over the neuroanatomical substrate of associative visual agnosia encompasses such basic issues as: (1) the necessity for bilateral lesions; (2) the intrahemispheric locus of damage; and (3) the roles of disconnection versus cortical damage. We examined three patients whose associative visual agnosia encompassed objects and printed words but spared faces. CAT scans revealed unilateral dominant occipitotemporal strokes. CAT scans of four previously reported cases with this same profile of associative agnosia were obtained. Dominant parahippocampal, fusiform and lingual gyri were the most extensively damaged cortical regions surveyed and were involved in all cases. Of white matter tracts surveyed, only temporal white matter including inferior longitudinal fasciculus was severely and universally involved. Splenium of the corpus callosum was frequently but not always involved. We conclude there is a form of associative visual agnosia with agnosia for objects and printed words but sparing face recognition which has a characteristic unilateral neuropathology. Damage or disconnection of dominant parahippocampal, fusiform and lingual gyri is the necessary and sufficient lesion.

Aged↗
PubMed2003

Alexia and related reading disorders.

Peripheral dyslexias are the result of impairment to processes that convert letters on the page into an abstract orthographic representation. Many aspects of these disorders are difficult to understand in depth. Invariably, there is evidence that some type of word-level perception occurs rapidly in many patients with LBL reading or neglect dyslexia, yet apparently contradictory evidence indicates that part of the word has been misperceived or that the letters must be analyzed laboriously for conscious identification to occur. Current theories attempt to synthesize these different aspects of the patients' performance, but their development is at an early stage. Questions remain also about the domain specificity of the perceptual impairment in LBL reading and about the nature of spatial attention and spatial frames in neglect dyslexia and other forms of attentional disorder. Current understanding of central dyslexias has perhaps advanced further. Well-developed computational models exist of these dyslexias, as do plausible experimental techniques for revealing the activity of semantic and non-semantic routes in normal readers. Nevertheless, the difficult issue of domain specificity arises again with respect to some of the mechanisms invoked, and in this regard, central and peripheral dyslexias continue to pose the same challenge.

Attention↗