[5][6][7] Dyslexia was seen as an issue with reading achievement specifically, caused by deficits in discrimination of written word sounds as opposed to a broader disorder of brain function.
[8] Specifically, it's been shown that "Relatively high heritabilities were observed for both reading ability and dyslexia indicating substantial genetic influences.
Theories should not be viewed as competing, but as attempting to explain the underlying causes of a similar set of symptoms from a variety of research perspectives and background.
[15][16]: 84 In attempting to explain all the many known reading and non-reading dyslexic symptoms, therapies and theories as well as the presence of only cerebellar and related vestibular neurophysiological signs in dyslexics, the cerebellum was postulated to coordinate in time and space all signals (visual, auditory, tactile, proprioceptive, motion) entering and leaving the brain as well as signal interconnections.
The quality and severity of the many symptoms characterizing each dyslexic was reasoned to depend on the diverse cerebral cortical and other brain processors receiving scrambled signals due to a cerebellar dysfunction.
Helpful therapies were reasoned to enhance cerebellar fine tuning (e.g., the use of cerebellar-vestibular stabilizing antimotion sickness medications) and/or improve descrambling and other compensatory cognitive capabilities (e.g., tutoring, biofeedback).
In many societies around the world the majority of the population do not use the visual notation of speech as a form of communication and do not use reading skills, and therefore have no dyslexia.
It was thus hypothesized that genetic dyslexia may represent an ontogenetic recapitulation of a pre-reading state in phylogeny and that ontogeny extended beyond the embryo into childhood and occasionally beyond, thus perhaps explaining late and even late-late blooming.
[27] The speed with which an individual can engage in the rapid automatized naming of familiar objects or letters is a strong predictor of dyslexia.
[29] The concept of a perceptual noise exclusion deficit (impaired filtering of behaviorally irrelevant visual information in dyslexia or visual-noise) is an emerging hypothesis, supported by research showing that subjects with dyslexia experience difficulty in performing visual tasks (such as motion detection in the presence of perceptual distractions) but do not show the same impairment when the distracting factors are removed in an experimental setting.
They assert that dyslexic symptoms arise because of an impaired ability to filter out both visual and auditory distractions, and to categorize information so as to distinguish the important sensory data from the irrelevant.
The phonological theory explains a reading impairment when using an alphabetic writing system which requires learning the grapheme/phoneme correspondence, the relationship between the graphic letter symbols and speech sounds which they represent.
Support for this theory arises from evidence that people with dyslexia show poor performance on a number of auditory tasks, including frequency discrimination and temporal order judgment.
A 2007 review reported that no specific cognitive processes are known to be influenced by the proposed genes and that scientists had begun to include neurophysiological (e.g., event-related potential) and imaging (e.g., functional MRI) procedures in their phenotype characterisation of people with dyslexia.
[47] Also suspected are convergence insufficiency and poor accommodation, both of which are uncommon in children, can interfere with the physical act of reading but not with decoding.
[50][needs update] People with dyslexia have been commonly associated with working memory deficits, along with reduced activity in the pre-frontal and parietal cortex.
In particular, Elliot and Gibbs argue that "attempts to distinguish between categories of 'dyslexia' and 'poor reader' or 'reading disabled' are scientifically unsupportable, arbitrary and thus potentially discriminatory".
[55] While acknowledging that reading disability is a valid scientific curiosity, and that "seeking greater understanding of the relationship between visual symbols and spoken language is crucial" and that while there was "potential of genetics and neuroscience for guiding assessment and educational practice at some stage in the future", they conclude that "there is a mistaken belief that current knowledge in these fields is sufficient to justify a category of dyslexia as a subset of those who encounter reading difficulties".
It argues that the common understanding of dyslexia is not only false but makes it more difficult to provide the reading help that hundreds of thousands of children desperately need.
Drawing on years of intensive academic research on both sides of the Atlantic, it challenged the existence of dyslexia as a separate condition, and highlighted the many different forms of reading styles.
Julian Elliot, an educational psychologist at Durham University in the United Kingdom, disputes the characterization of dyslexia as a medical condition, and believes it should be treated simply as a reading difficulty.
"[57] Elliot believes that children of all levels of intelligence may struggle with learning to read, and that all can be helped by educational strategies appropriate to their needs.