Article

The double-deficit hypothesis: a comprehensive analysis of the evidence.

Department of Educational Psychology, University of British Columbia, Vancouver.
Journal of learning disabilities (Impact Factor: 1.77). 01/2006; 39(1):25-47. DOI: 10.1177/00222194060390010401
Source: PubMed

ABSTRACT The double-deficit hypothesis of developmental dyslexia proposes that deficits in phonological processing and naming speed represent independent sources of dysfunction in dyslexia. The present article is a review of the evidence for the double-deficit hypothesis, including a discussion of recent findings related to the hypothesis. Studies in this area have been characterized by variability in methodology--how dyslexia is defined and identified, and how dyslexia subtypes are classified. Such variability sets limitations on the extent to which conclusions may be drawn with respect to the double-deficit hypothesis. Furthermore, the literature is complicated by the persistent finding that measures of phonological processing and naming speed are significantly correlated, resulting in a statistical artifact that makes it difficult to disentangle the influence of naming speed from that of phonological processing. Longitudinal and intervention studies of the double-deficit hypothesis are needed to accumulate evidence that investigates a naming speed deficit that is independent of a phonological deficit for readers with dyslexia. The existing evidence does not support a persistent core deficit in naming speed for readers with dyslexia.

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    ABSTRACT: The double-deficit hypothesis of dyslexia posits that both rapid naming and phonological impairments can cause reading difficulties, and that individuals who have both of these deficits show greater reading impairments compared to those with a single deficit. Despite extensive behavioral research, the brain basis of poor reading with a double-deficit has never been investigated. The goal of the study was to evaluate the double-deficit hypothesis using functional MRI. Activation patterns during a printed word rhyme judgment task in 90 children with a wide range of reading abilities showed dissociation between brain regions that were sensitive to phonological awareness (left inferior frontal and inferior parietal regions) and rapid naming (right cerebellar lobule VI). More specifically, the double-deficit group showed less activation in the fronto-parietal reading network compared to children with only a deficit in phonological awareness, who in turn showed less activation than the typically-reading group. On the other hand, the double-deficit group showed less cerebellar activation compared to children with only a rapid naming deficit, who in turn showed less activation than the typically-reading children. Functional connectivity analyses revealed that bilateral prefrontal regions were key for linking brain regions associated with phonological awareness and rapid naming, with the double-deficit group being the most aberrant in their connectivity. Our study provides the first functional neuroanatomical evidence for the double-deficit hypothesis of developmental dyslexia.
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