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In this discussion paper, I review a number of common misconceptions about the phonological deficit theory (PDH) of dyslexia. These include the common but mistaken idea that the PDH is simply about phonemic awareness (PA), and, consequently, is a circular “pseudo”-explanation or epiphenomenon of reading difficulties. I argue that PA is only the “tip of the phonological iceberg” and that “deeper” spoken-language phonological impairments among dyslexics appear well before the onset of reading and even at birth. Furthermore, not even reading-specific expressions of phonological deficits—PA or pseudoword naming, can be considered circular if we clearly distinguish between reading proper—real meaning-bearing words, or real text, and the mechanisms (subskills) of reading development (such as phonological recoding). I also explain why an understanding of what constitutes an efficient writing system explains why phonology is necessarily a major source of variability in reading ability and hence a core deficit (or at least one core deficit) among struggling readers whether dyslexic or non-dyslexic. I also address the misguided notion that the PDH has now fallen out of favor because most dyslexia researchers have (largely) ceased studying phonological processing. I emphasize that acceptance of the PDH does not imply repudiation of other non-phonological hypotheses because the PDH does not claim to account for all the variance in reading ability/disability. Finally, I ask where neurobiology enters the picture and suggest that researchers need to exercise more caution in drawing their conclusions.

In this discussion paper, I review a number of common misconceptions about the phonological deficit theory (PDH) of dyslexia. These include the common but mistaken idea that the PDH is simply about phonemic awareness (PA), and, consequently, is a circular "pseudo"-explanation or epiphenomenon of reading difficulties. I argue that PA is only the "tip of the phonological iceberg" and that "deeper" spoken-language phonological impairments among dyslexics appear well before the onset of reading and even at birth. Furthermore, not even reading-specific expressions of phonological deficits-PA or pseudoword naming, can be considered circular if we clearly distinguish between reading proper -real meaning-bearing words, or real text, and the mechanisms (subskills) of reading development (such as phonological recoding). I also explain why an understanding of what constitutes an efficient writing system explains why phonology is necessarily a major source of variability in reading ability and hence a core deficit (or at least one core deficit) among struggling readers whether dyslexic or non-dyslexic. I also address the misguided notion that the PDH has now fallen out of favor because most dyslexia researchers have (largely) ceased studying phonological processing. I emphasize that acceptance of the PDH does not imply repudiation of other non-phonological hypotheses because the PDH does not claim to account for all the variance in reading ability/disability. Finally, I ask where neurobiology enters the picture and suggest that researchers need to exercise more caution in drawing their conclusions.

Impaired verbal 'phonological' short-term memory is considered a cardinal feature of the logopenic variant of primary progressive aphasia (lv-PPA) and is assumed to underpin most of the language deficits in this syndrome. Clinically, examination of verbal short-term memory in individuals presenting with PPA is common practice and serves two objectives: (i) to help understand the possible mechanisms underlying the patient's language profile and (ii) to help differentiate lv-PPA from other PPA variants or from other dementia syndromes. Distinction between lv-PPA and the non-fluent variant of PPA (nfv-PPA), however, can be especially challenging due to overlapping language profiles and comparable psychometric performances on verbal short-term memory tests. Here, we present case vignettes of the three PPA variants (lv-PPA, nfv-PPA, and the semantic variant (sv-PPA)) and typical Alzheimer's disease (AD). These vignettes provide a detailed description of the short-term and working memory profiles typically found in these patients and highlight how speech output and language comprehension deficits across the PPA variants differentially interfere with verbal memory performance. We demonstrate that a combination of verbal short-term and working memory measures provides crucial information regarding the cognitive mechanisms underlying language disturbances in PPA. In addition, we propose that analogous visuospatial span tasks are essential for the assessment of PPA as they measure memory capacity without language contamination.