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Dyslexia Causes: What the Latest Research Reveals

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Most problems can only be solved if one knows what causes that particular problem. A disease such as pellagra took the lives of thousands in the Southern States of America during the early part of the twentieth century. Data is sketchy, but by 1912, the State of California alone reported 30,000 cases and a mortality rate of 40%. Today, pellagra is virtually unknown because we know that it is caused by a vitamin B3 deficiency.  A viable point of departure would thus be to ask: what causes dyslexia?

Dyslexia causes: Genetic influences

Clinicians have known for a long time that dyslexia runs in families. Soon after developmental dyslexia was first described by Pringle-Morgan (1896) and Kerr (1897), several reports of familial aggregation appeared (Hinshelwood, 1907, 1917; Stephenson, 1907; Thomas, 1905).

A large-scale study of twins with dyslexia yielded a concordance rate of 68% in identical twins, as compared with 38% in non-identical twins.

DeFries and colleagues (1978) initiated a large family study of dyslexia. They recruited a sample of 133 children who were identified by teachers as having significant reading difficulty. The researchers tested them in the laboratory with an extensive battery to confirm their reading problems and related cognitive disabilities. A matched group of 125 children with no reading problems was also identified and tested, as well as the parents and siblings of both groups. The main result of the DeFries family study was clear: There was strong evidence for the familial transmission of dyslexia. The relatives of the children ascertained with dyslexia were significantly more likely to also have reading problems, compared to the relatives of children with normal-range reading abilities.

The relative contributions of genetic influences and shared family environment can be dissected in twin studies. It has been shown robustly that concordance for a qualitative diagnosis of dyslexia is significantly higher in identical twins, who have a virtually identical genetic makeup, than it is in non-identical twins who (like ordinary siblings) share about half of their segregating alleles. A large-scale study of twins with dyslexia yielded a concordance rate of 68% in identical twins, as compared with 38% in non-identical twins, indicating a substantial genetic component (DeFries & Alarcón, 1996).

Dyslexia causes: Cognitive deficits

Although some causes of dyslexia have a genetic origin, and environmental factors play an important role, cognition mediates brain-behavior relationships and therefore offers a sufficient level of explanation for the development of principled interventions. We thus need to understand the cognitive difficulties that underpin reading failure, regardless of whether their origin is constitutional or environmental (Elliott & Grigorenko, 2014).

Dyslexia research has been dominated by the quest for a single cognitive deficit that is necessary and sufficient to cause all behavioral characteristics of the disorder. Until the 1950s, the belief was that dyslexia is attributable to visual processing problems, perhaps also including motor skill problems. But in 1957 Noam Chomsky published his seminal book, Syntactic Structures, which suggested that humans are genetically endowed with an “encapsulated linguistic processor” which mediates a “Universal Grammar” that underlies all languages. These ideas quickly transformed the study of language and with it, reading. Dyslexia became attributed to a fault in Chomsky’s linguistic processor, and any role for visual processing was abandoned. Dyslexia became a linguistic, phonological problem, not a visual one. In an influential book, Dyslexia: Theory and Research, Vellutino (1979) argued that many of the apparent visual problems could actually be attributed to language difficulties — especially to deficient phonological awareness.

Phonological deficit theory

The phonological deficit theory became the most well-developed and supported of the theories of dyslexia. The U.S. researchers have united in adopting the phonological deficit hypothesis since the early 1980s, and this united front has led to the investment of more than $15 million annually by the US government, via the National Institute for Child Health and Human Development (NICHD) (Fawcett, 2001). This research program into the causes and remediation of reading disabilities continues until the present day.

Phonological awareness (PA) refers to an individual’s awareness of the phonological structure, or sound structure, of language. It is a listening skill that includes the ability to distinguish units of speech, such as rhymes, syllables in words, and individual phonemes in syllables. PA is often confused with phonics, but it is different. Phonics requires students to know and match letters or letter patterns with sounds, learn the rules of spelling, and use this information to decode (read) and encode (write) words. PA relates only to speech sounds, not to alphabet letters or sound-spellings, so alphabet knowledge is not necessary to develop a basic phonological awareness of language. Phonemic awareness is a subset of PA that focuses on recognizing and manipulating phonemes, the smallest units of sound. The two most important phonemic awareness skills are segmenting and blending.

The ability to segment and blend phonemes is said to be critical for the development of reading skills, including decoding and fluency, and even that it predicts reading ability (Edwards & Taub, 2016). It is also claimed that PA training can prevent and correct reading difficulties (Kilpatrick, 2016, p. 13). Moustafa, however, points out that correlation does not establish causation. “In statistics, the word predicts means nothing more than that there is a high correlation between two phenomena” (Moustafa, 2001, p. 248).

Not all studies support phonological and phonemic awareness training (Pape-Neumann et al., 2015; Krashen, 1999a; Krashen 1999b). Blomert and Willems (2010) investigated children at familial risk for dyslexia in kindergarten and first grade. The familial risk was genuine; 40% developed reading deficits in first grade. However, they did not find any relationship between a PA or other phonological processing deficits in kindergarten and reading deficits in first grade. In a study by Daigle et al. (2016), the inefficiency of phonological processing could not explain the spelling delay in a group of French children with dyslexia. Taylor (1998) points out that while children’s early cognition develops from concrete experiences to abstract understandings, phonemic awareness training begins with abstract exercises. Stein (2018) concludes that the phonological theory does not provide a helpful explanation for dyslexic reading problems because it is set at too high a cognitive level.

Some findings indicate that phoneme awareness may develop as a consequence of exposure to reading and writing, while other support an intermediate view, “that phonological awareness and alphabetic literacy learning influence each other reciprocally” (Manolitsis & Tafa, 2011, p. 31). Some researchers claim that phonological factors may be less important than is commonly accepted (Byrne, 2011). Not all children with reading disabilities demonstrate a phonological deficit, and Catts and Adlof (2011) point out that children with poor phonological abilities can nevertheless develop good reading skills. Also, a single cognitive deficit model cannot account for comorbidity. Dyslexia co-occurs more often than would be expected by chance with other developmental disorders, such as ADHD and specific language impairment.

Multiple deficits

Given that a single phonological deficit is not necessary or sufficient to cause a reading disability, current thinking sees this as one of multiple deficits that are likely to interact to cause reading disability (Pennington, 2006; Peterson & Pennington, 2012). Van Bergen et al. (2014) summarize Pennington’s multiple deficit model as follows:

In his model, multiple genetic and environmental risk factors operate probabilistically by increasing the liability to a disorder; conversely, protective factors decrease the liability. These etiological factors produce the behavioral symptoms of developmental disorders by influencing the development of relevant neural systems and cognitive processes. Importantly, there is no single etiological or cognitive factor that is sufficient to cause a disorder. Instead, multiple cognitive deficits (each due to multiple etiological factors) need to be present to produce a disorder at the behavioral level. Some of the etiological and cognitive risk factors are shared with other disorders. As a result, comorbidity among developmental disorders is to be expected, rather than something that requires additional explanations. Finally, from Pennington’s multi-deficit model (MBM) it follows that “the liability distribution for a given disease is often continuous and quantitative, rather than being discrete and categorical” (Pennington, 2006, p 404).

In addition to phonological awareness, cognitive psychology has now linked many brain-based skills to dyslexia:

  • verbal fluency (Moura et al., 2015);
  • attention and executive functions (Menghini et al., 2010);
  • visual attention, i.e. our ability to rapidly select the most relevant visual information ranges when we are engaged in various reading tasks (Elliott, 2015; Valdois et al., 2004);
  • visuospatial abilities (Giovagnoli et al., 2016; Menghini et al., 2010; Helland & AsbjØrnsen, 2003);
  • processing speed (Moura et al., 2015; Stoodley & Stein, 2006);
  • short-term memory (Cowan et al., 2017; Majerus & Cowan, 2016);
  • auditory working memory (Vender, 2017; Weiss et al., 2014);
  • visual and visual sequential memory (Talepasand et al. 2018; Guthrie & Goldberg, 1972);
  • visual long-term memory (Binamé et al., 2015), especially for details (Huestegge et al., 2014);
  • verbal long-term memory (Helland & Morken, 2015); and
  • rapid naming (Brizzolara, 2006; Denckla & Rudel, 1976).

Video: Dyslexia intervention based on the multiple deficit model


Why do these cognitive skills matter?

Weak cognitive skills prevent a process called orthographic mapping. Every word has three forms: its sounds, spelling, and meaning. The process of orthographic mapping involves the brain linking the three forms of the word and storing them together in long-term memory. Orthographic mapping allows for instant word recognition, fluent reading, and accurate spelling.

Dyslexia causes: Brain differences

There is old but famous evidence consistent with the idea that there is something wrong in the brain of some persons who have persistent unexpected difficulty in learning to read. Specifically, Galaburda and colleagues (1985) reported several anatomical anomalies in the brains of a few persons with reading difficulties. Although those findings are intriguing, they are far from decisive. The samples were extremely small (a total of 4 men and 3 women) and included participants with evidence for neurological or psychiatric conditions and participants with impairments not limited to written language, who should have been excluded from a study purporting to examine brain correlates of dyslexia. The control group was also very small, effectively precluding reliable estimation of the specificity of any findings.

As technology advanced, neuroscience contributed more and more to dyslexia research. Unfortunately, most studies have too small samples to permit reliable conclusions to be drawn, and many results are inconsistent (Protopapas & Parrila, 2018). In a meta-analysis of functional neuroimaging studies of dyslexia, Martin et al. (2016) list studies in which differences between groups with and without dyslexia were found in specific brain regions. The most consistent findings concerned the left occipitotemporal cortex, which includes the so-called visual word form area (VWFA), though to be critical for reading.

Neuroscientists at Georgetown University Medical Center discovered that skilled readers can recognize words at a lightning-fast speed when they read because the word has been placed in a sort of visual dictionary. This part of the brain, the VWFA (shown in yellow), functions separately from an area that processes the sounds of written words (Glezer et al., 2016).

Data using fMRI indicate three neural systems for reading (shown in the image above). These are all located in the left side of the brain: one in the front of the brain (shown in green, in the region of the inferior frontal gyrus [Broca’s area]) and two in the back of the brain (one in the parietotemporal region, shown in red, and a second in the occipito-temporal region, shown in yellow). The latter system is of particular importance for skilled, fluent reading and is termed the visual word-form area (Shaywitz, 2005).

Glezer and her coauthors tested word recognition in 27 volunteers in two different experiments using fMRI. They were able to see that words that were different, but sound the same — like ‘hare’ and ‘hair’ — activate different neurons, akin to accessing different entries in a dictionary’s catalog. If the sounds of the word had any influence in this part of the brain, we would expect to see that they activate the same or similar neurons. This, however, was not the case — ‘hair’ and ‘hare’ looked just as different as ‘hair’ and ‘soup’. In addition, the researchers found a different distinct region that was sensitive to the sounds, where ‘hair’ and ‘hare’ did look the same. The researchers thus showed that the brain has regions that specialize in doing each of the components of reading: one region is doing the visual piece and the other is doing the sound piece.

These findings negate the dual-access theory which suggests that visual word recognition in skilled readers is not based on visual processing alone, but that we access both the phonology and the visual perception of a word (Frost, 1998).

The left inferior parietal lobule came in a close second in the meta-analysis study by Martin and colleagues (shown in red). This part of the brain is said to be involved in word analysis, grapheme-to-phoneme conversion, and general phonological and semantic processing.

Imaging also reveals compensatory overactivation in other parts of the reading system (shown in green). The compensatory neural systems allow a dyslexic person to read more accurately. However, the critical visual word-form area remains disrupted and difficulties with rapid, fluent, automatic reading persist. The dyslexic continues to read slowly (Shaywitz, 2005).

It should be noted that brain differences do not equal brain disorders. After reviewing the scientific evidence of the last few decades, Protopapas and Parrila (2018) conclude:

Differences in brains are certain to exist whenever differences in behavior exist, including differences in ability and performance. Therefore, findings of brain differences do not constitute evidence for abnormality; rather, they simply document the neural substrate of the behavioral differences. We suggest that dyslexia is best viewed as one of many expressions of ordinary ubiquitous individual differences in normal developmental outcomes. Thus, terms such as “dysfunctional” or “abnormal” are not justified when referring to the brains of persons with dyslexia…

[A] statement such as ‘My child can’t read because he’s dyslexic’ is not an explanation, rather it is a circular redescription of the problem.” This is because the term “dyslexia” is merely a label for poor word reading that persists in spite of appropriate educational experiences, rather than referring to an underlying cause for it..

It should also be noted that brain differences may be the cause of reading difficulties, and not the result. In one study, published online in the Journal of Neuroscience, researchers analyzed the brains of children with dyslexia and compared them with two other groups of children: an age-matched group without dyslexia and a group of younger children who had the same reading level as the children with dyslexia. Although the children with dyslexia had less gray matter than age-matched children without dyslexia, they had the same amount of gray matter as the younger children at the same reading level. Krafnick et al. (2014) say this suggests that the anatomical differences reported in left-hemisphere language-processing regions of the brain appear to be a consequence of reading experience as opposed to a cause of dyslexia.

Video: Overcoming dyslexia

Meet Susan, Vivienne’s mom. Vivienne was adopted from China at age 5. This video is about Susan helping her 11-year-old daughter catch up on development delays, including dyslexia. They started with the Edublox program 13 weeks ago. Click here to follow their journey to learning success.


Key takeaways


NEXT: Page 5: Dyslexia types

Authored by Susan du Plessis (B.A. Hons Psychology; B.D.) who has 30+ years’ experience in the LD field.
Page last reviewed: May 21, 2021.
Next review due: May 21, 2023.

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