Authors: John Stein.

Article: Theories about Developmental Dyslexia.

Publication: Brain Sciences (MDPI). 13, no. 2: 208 2023 | DOI: 10.3390/brainsci13020208

[Full Text]


Despite proving its usefulness for over a century, the concept of developmental dyslexia (DD) is currently in severe disarray because of the recent introduction of the phonological theory of its causation. Since mastering the phonological principle is essential for all reading, failure to do so cannot be used to distinguish DD from the many other causes of such failure. To overcome this problem, many new psychological, signal detection, and neurological theories have been introduced recently. All these new theories converge on the idea that DD is fundamentally caused by impaired signaling of the timing of the visual and auditory cues that are essential for reading. These are provided by large ‘magnocellular’ neurons which respond rapidly to sensory transients. The evidence for this conclusion is overwhelming. Especially convincing are intervention studies that have shown that improving magnocellular function improves dyslexic children’s reading, together with cohort studies that have demonstrated that the magnocellular timing deficit is present in infants who later become dyslexic, long before they begin learning to read. The converse of the magnocellular deficit in dyslexics may be that they gain parvocellular abundance. This may often impart the exceptional ‘holistic’ talents that have been ascribed to them and that society needs to nurture.

Tagged as: dyslexic talents, magnocellular, parvocellular, phonologi, and temporal processing


Stein, John. 2023. “Theories about Developmental Dyslexia” Brain Sciences 13, no. 2: 208.

Excerpts from Full Text / Notes:

For over a century, developmental dyslexia was recognised by neurologists and other
doctors as a useful diagnosis for which the key criteria were a significant discrepancy between a child’s backward reading, yet normal or high speech and oral comprehension and reasoning skills, together with a strong family history. However, since the turn of the millennium, this consensus has been thoroughly undermined.

To simplify, the essence of reading is
to learn to translate letters into the sounds they stand for, which are ‘phonemes’. However, phonemes do not actually exist as a consistent, standard acoustic signal. Their acoustic form varies according to the preceding and succeeding sounds in the spoken word; thus, children have to learn a semi-abstract concept, the ‘phonological principle’

This new emphasis on phonology meant that DD became attributed entirely to failure to learn the phonological principle properly, and the ‘phonological theory’ of dyslexia became dominant.

More than 90% of the new neurones born in the foetal brain in the last few months of pregnancy fail to thrive and are eliminated jn early infancy because they fail to make successful and useful connections [60]. This means that the most numerous neurones, parvocells (parvus, Latin for small), may be able to flourish more than usual. Since parvocells are normally more extensively connected than magnocells, and their superabundance in dyslexia implies that their connectivity might be even greater. Thus, the magnocellular timing deficit could be matched by a superabundance of parvocells in DD.

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