1992
DOI: 10.1016/0093-934x(92)90022-7
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Lesion localization of phonological agraphia

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Cited by 65 publications
(48 citation statements)
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“…As mentioned previously, these effects are occurring in the ventral left visual processing pathway-precisely where they would be expected to occur on the basis of anatomical and human lesion data. Attributing these effects to phonological access is less consistent with available lesion data, which link phonological impairments -including phoneme recognition deficits, phonological dyslexias, phonemic paraphasia and phonological dysgraphia -to lesions in the superior temporal lobe and temporoparietal junction (Alexander et al, 1992;Beauvois and Derouesne, 1979;Caplan et al, 1995;Damasio and Damasio, 1980;Marin, 1980) rather than to lesions in the ventral visual pathway.…”
Section: Discussionmentioning
confidence: 94%
“…As mentioned previously, these effects are occurring in the ventral left visual processing pathway-precisely where they would be expected to occur on the basis of anatomical and human lesion data. Attributing these effects to phonological access is less consistent with available lesion data, which link phonological impairments -including phoneme recognition deficits, phonological dyslexias, phonemic paraphasia and phonological dysgraphia -to lesions in the superior temporal lobe and temporoparietal junction (Alexander et al, 1992;Beauvois and Derouesne, 1979;Caplan et al, 1995;Damasio and Damasio, 1980;Marin, 1980) rather than to lesions in the ventral visual pathway.…”
Section: Discussionmentioning
confidence: 94%
“…Similarly, it has been proposed that damage to the frontal operculum played a central role in the pathogenesis of phonological dyslexia (Fiez and Petersen, 1998;Fiez et al, 2006), but there are also reports of patients with lesions confined to posterior perisylvian cortex (for a review, see Lambon Ralph and Graham, 2000). Thus, lesion-deficit correlations to date have failed to identify a single cortical area essential for sublexical reading and spelling, leading some investigators to propose that phonological dyslexia and dysgraphia may be caused by damage to a number of perisylvian cortical regions that are components of a distributed neural network dedicated to phonological processing (Alexander et al, 1992;Rapcsak and Beeson, 2002;Henry et al, 2007). The distributed nature of phonological processing is supported by functional imaging studies in normal individuals that typically reveal activation in multiple functionally linked perisylvian cortical regions during speech production/perception and phonological awareness tasks (for reviews, see Binder and Price, 2001;Vigneau et al, 2006).…”
Section: Introductionmentioning
confidence: 99%
“…In brief, semantic processing is thought to engage anterior and inferolateral temporal regions (BA 38,20,21) as well as inferior prefrontal cortex (BA 47), and the angular gyrus (BA 39;Binder & Price, 2001;Mummery et al, 2000;Vandenberghe et al, 1996). The phonological codes involved in spelling rely on a network of perisylvian cortical regions, including Broca's area, Wernicke's area, the supramarginal gyrus, and insula (Alexander et al, 1992;Fiez, 1997;Omura et al, 2004;Roeltgen et al, 1983). Orthographic knowledge of lexical representations for reading and spelling is thought to engage a critical region within temporo-occipital cortex (BA 37), sometimes referred to as the visual word form area (Beeson et al, 2003b;Cohen & Dehaene, 2004;Nakamura et al, 2002;Rapcsak & Beeson, 2004).…”
Section: Introductionmentioning
confidence: 99%