How dyslexics might see a text
In this post I will touch upon an exciting field of genetic neuropsychology in relation to dyslexia. I will talk about the dual route cascaded model of reading and two types of dyslexia which could occur be either of the routes impaired: Surface and Phonological dyslexia.
I will then discuss methods used in determining the causes of dyslexia; particularly studies of normally developing twins and use of genetic modelling.
I will then discuss methods used in determining the causes of dyslexia; particularly studies of normally developing twins and use of genetic modelling.
Dual Route Cascaded Model of Reading
Below you can find a dual route cascaded model of reading (Coltheart et al., 2003), which suggests that there are two routes which process written language simultaneously. One of them is a lexical route, which develops and accesses a lexical store. It involves semantic comprehension of the words. The second route is phonological; it does not have any support from the semantic system, and is responsible for converting graphemes into phonemes, or, letters into sounds.
Surface and Phonological Dyslexia
Dyslexia literally means 'difficulty with words'. It affects up to 17.5% of children despite their level of intelligence, education level, family environment and other factors. Depending on which route is impaired, two types of dyslexia may occur. Surface dyslexia affects the lexical route, and makes it impossible for a person to store and access sounds of familiar words, in other words, use a lexical store. Patients with surface dyslexia are able to read words with regular spelling, as their phonological route is still at work. However, they will have difficulty reading irregular words such as 'yacht' and 'Edinburgh', as these words can not be pronounced right based on regular grapheme-phoneme correspondence.
Phonological dyslexia affects phonological route, causing difficulties in translating written words with no meaning cues into spoken words. Patients with phonological dyslexia will have difficulty reading non-words such as 'slomb' out-loud. Non-words are not stored, and thus cannot be found in the lexical store, thus we would need the phonological route to be intact to translate meaningless graphemes into phonemes.
Phonological dyslexia affects phonological route, causing difficulties in translating written words with no meaning cues into spoken words. Patients with phonological dyslexia will have difficulty reading non-words such as 'slomb' out-loud. Non-words are not stored, and thus cannot be found in the lexical store, thus we would need the phonological route to be intact to translate meaningless graphemes into phonemes.
Heritability
Numerous studies found that dyslexia is familial. It tends to affect more than one member of the family, and there is normally a family history of reading disorder. It shows that either shared genes or shared environment could be a cause. To learn more about the possible effects of these factors, many studies have been conducted of both monozygotic (MZ) and dyzygotic (DZ) twins. MZ twins share 100% of genes and 100% of environment, while DZ twins - 50% of genes and 100% of environment. Thus, the role of genes and shared environment can be studied by comparing the variance between families to within-family differences between MZ and DZ twins - increased MZ over DZ similarity being evidence for genetic influences.
There have been many studies of normal twins reared together which aimed to find how much of familial similarity in reading depended on shared genes, how much - on shared environment and how much - on unique (random) environment.
1. Unique/random Environment effect:
E = 1 - rMZ
2. Heritable effect/Additive genetic effect:
A = 2 * (rMZ - rDZ)
3. Shared/Common environment:
C = rMZ - A
Using the concept of genetic modelling, we could imagine reading as a sum of these three factors. Some large studies showed, that Additive genetic effect for reading disorders is over 7%; similar results has been found around the world. Common environment has its effects prior to the age of 4 years old, but by 8-9 years old these effects are reduced to zero, and are replaced with increased genetic effects.
There have been many studies of normal twins reared together which aimed to find how much of familial similarity in reading depended on shared genes, how much - on shared environment and how much - on unique (random) environment.
1. Unique/random Environment effect:
E = 1 - rMZ
2. Heritable effect/Additive genetic effect:
A = 2 * (rMZ - rDZ)
3. Shared/Common environment:
C = rMZ - A
Using the concept of genetic modelling, we could imagine reading as a sum of these three factors. Some large studies showed, that Additive genetic effect for reading disorders is over 7%; similar results has been found around the world. Common environment has its effects prior to the age of 4 years old, but by 8-9 years old these effects are reduced to zero, and are replaced with increased genetic effects.
Genetic Model of Reading
A Genetic Model of Reading was devised by Bates et al. (2007) in order to see how the arrow-box model of reading (dual cascaded model) works in relation to the genetic research:
There are different genes that are responsible solely for the lexical route (Airr), some - for the phonological route (Anon), and some - for both (Ag, g standing for general). Similarly, unique environment can either have an effect on both or one of the routes. We can also see here, that Common environment (C) does not affect reading.