In 1896 a paper entitled ‘A case of congenital word blindness’ in the British Medical Journal (Morgan, 1896) reported the case of a 14-year-old whose inability to learn to read was in striking contrast to their overall intellectual abilities. This was the first recorded report of developmental dyslexia.
Dyslexia simply means “difficulty with reading”, a catch-all term that has perhaps added more confusion to the world of reading disorders than clarity and has led to misunderstanding, misinterpretation and even dispute as to the condition’s existence. Difficulty with reading can be caused by myriad issues from misdiagnosed auditory deficits, poor teaching, low IQ and socio-economic disadvantage. However, these sensory, neurological and environmental influences cannot all be the same condition. Furthermore, it is estimated between 5 and 17% of children in the United States suffer with dyslexia (Shaywitz, 2003); but why is the upper figure so high and why is the range so large? Again, confusion obfuscates as the number is reliant on the threshold used to define impairment. The prevalence of dyslexia and the actual percentage depends upon an arbitrary criterion for reading normality. This arbitrariness has led to accusations that dyslexia is merely a social construct – a conflation between behaviour and health problems in our overmedicalised western world (Dehaene, 2010) - and that it doesn’t actually exist.
DOES DYSLEXIA EXIST?
There are two main indicators that suggest that dyslexia is not a social construct and point to the conclusion that its origins are cerebral. Firstly, largescale genetic studies confirm the genetic heritability of reading disorders (DeFries et al., 1987). It is not, however, linked to the mutation of a single gene but appears to be linked to several genes, impairment to any one of which may be the cause of disruption to the acquisition of a cultural ability such as reading. As Stanislas Dehaene (2010) posits, ‘Expert reading depends on a fortuitous combination of cerebral connections that luckily pre-exist in our primate brains and take years of training to convert to a new use. One mishap in the circuitry is enough to bring the fragile process of neuronal recycling to a grinding halt.’ (2010:238).
Secondly, the erratic nature of international dyslexia reporting initially seemed to suggest that it was indeed a social construction invented in Britain and America as a cultural label. When an Italian research team (Paulesu, 2001) investigated the paradox that dyslexia was hardly ever reported in Italy compared to France, Britain and the United States they also found that it was reported with far less frequency in France than in the English-speaking nations. This led the researchers to ask the radical question whether the same proportions of children suffered from dyslexia in all countries, but the symptoms only appeared in cultures whose writing systems were so opaque that they placed impossible stresses on the brain circuits that linked vision to language (Italian has a relatively transparent orthography, French is opaquer with English being the most opaque). Visualising brain imaging data from the study revealed a clear anomaly between the dyslexic group and the control group. A whole portion of their left temporal lobe showed reduced brain activity compared to the control group. This was observed in the same area and in the same degree for all three nationalities and has been the case for all brain imaging studies of dyslexia (Shaywitz et al.,1999; Shaywitz et al. 2002; McCrory et al., 2004). Paulelesu et al’s. (2001) study was conducted on older dyslexics but the same was found by Shaywitz et al. (2002) for younger readers with the crucial addition that greater brain disfunction correlated with more severe reading deficit. Thus, for alphabetic writing systems there appeared to be a universal cerebral origin for dyslexia with the left temporal lobe seeming to be systematically disorganised. (For readers of Chinese who struggle, Siok et al. (2004) found a different area of the brain that appeared to have reduced activity. The area is that associated with motor memory which may be more important for assisting the remembering of the 3000 Chinese characters required for reading.)
A PHONOLOGICAL DEFICIT?
Although there are a number of models that propose etiologies for dyslexia, converging evidence seems to identify the core phonological deficit model (Stanovich, 1988) as the most accommodating of the current research indicating that most poor readers have difficulty segmenting, blending and manipulating the phonemes that they hear in spoken words (Rayner et al., 2012). In reading, deficient phonological representations impede grapheme-phoneme translation and efficient word recognition (more here on word recognition) (Griffiths and Snowling, 2002) with phonological deficits also impacting negatively on verbal short-term memory and naming (Berninger et al., 2006). Weak or indistinct representations appears to be the central processing problem for dyslexic readers who seem to suffer from a faulty representation of speech sounds which prevent the precise processing of spoken words and the pairing of these spoken words with visual symbols. Though dyslexic children may be able to apply phonic rules when decoding, they have not developed fast, automatic retrieval of these codes, nor the connections that allow them to use the codes for the quick recognition of words. Thus, dyslexia appears to be a problem with single-word decoding due to an impairment in grapheme-phoneme conversion and is ‘characterised by difficulties with accurate and/or fluent word recognition and poor spelling and decoding abilities….’ (National Institute for Health – Lyon et al., 2003).
And what does the left temporal lobe that was found to lack activation in dyslexics actually do when we’re reading? One of its functions is the processing of phonological information in speech; another is the visual identification of written words.
It would, therefore, appear that deficits in the brain’s speech processing networks create phonological problems in dyslexics with the resultant difficulties in phonemic awareness undermining the acquisition of the alphabetic principle. This in turn impacts the brain letterbox area with the ensuing difficulty in word recognition. However, some studies (McCrory et al., 2004) suggest that in dyslexics the letterbox area is of itself impaired indicating a double deficit; both a phonological and visual deficit. As Berninger and Richards (2002) advance, it is the point at which orthographic (word) and phonological information become linked that is impaired leading to difficulties with fluent word recognition so critical for skilled reading. Strikingly, brain imaging indicates that compared to normal readers, dyslexics exhibit (Georgiewa et al., 2002) hyperactivity in the Broca’s area (critical for syntax and articulation) suggesting a strategy of explicit speech production to compensate for lack of automatic decoding – ‘a brave but fruitless endeavour’ (Dehaene, 2010:247).
A DOUBLE DEFICIT?
When Denckla and Rudel (1974, 1976) found that when they tested children’s serial naming speed of 50 objects, colours, digits or letters, naming rates correlated with reading achievement it led to the suggestion that slower rapid automatised naming (RAN) may predict variances in reading. Further research (Landerl and Wimmer, 2008; Lervåg and Hulme, 2009) seemed to support this with the suggestion that dyslexic readers can be grouped into those with poor phonemic awareness, those with slow naming speeds and those with both - the double-deficit (Wolf and Bowers, 1999). This double-deficit hypothesis was able to account for the vast majority of poor readers (Katzir et al., 2008). Furthermore, genetic studies (Compton et al., 2001) appeared to support the existence of two distinct genetic contributors to dyslexia indicating two separate heritability patterns for phonemic awareness and RAN speed. The majority of dyslexic readers Katzir et al. (2008) suggest are affected by a phonological deficit alone or in conjunction with slow naming. Slow naming alone is far rarer.
IS DYSLEXIA A DISCREPENCY BETWEEN IQ AND READING LEVEL?
Historically, dyslexia has been diagnosed on the observation of a discrepancy between a child’s aptitude and their reading level. Thus, a reading score a few standard deviations below a child’s IQ indicated dyslexia. This had some unfortunate consequences. Firstly, very bright children with average reading levels were being diagnosed as dyslexic. Secondly, children with an average IQ who had memorised significant words by shape and gave the appearance of average reading ability were not identified as poor readers until much later in their schooling thereby missing out on essential early intervention. Perhaps more worrying is the growing evidence that the fundamental assumption behind the discrepancy-based formula may be incorrect. Stuebing et al. (2002) found in their meta-analysis symptoms of poor word reading and spelling across the range of normal and above normal IQs and were uncorrelated with the discrepancy between their IQ and reading achievement. A discrepancy between IQ and reading achievement may have an obvious cause (poor teaching, low socioeconomic status, poor educational environment) not indicated by the formula. Fletcher et al. (2007) noted that despite the recommended abandonment of this discrepancy-based diagnosis in schools it continued to maintain traction.
IS DYSLEXIA A PROBLEM WITH EYE MOVEMENTS?
‘A case of congenital word blindness’ (Morgan, 1896) certainly suggested some element of visual impairment in dyslexic readers. Faulty eye movements may indeed impair reading; however, evidence suggests that dyslexia is not caused by this defect. Nevertheless, dyslexic readers make more fixations, longer fixations and shorter saccades (Rayner, 1998) (see here for more on eye movements). This may seem obvious; if you were to read text in a foreign language you would register similar occurrences and erratic eye movements. Thus, Tinker (1958) was emphatic that eye movements were not a cause of reading problems, but a reflection of the underlying difficulties experienced by the reader. Stanley et al. (1983) found that dyslexic readers and normal readers exhibited the same eye movements when engaged in non-reading tasks but that eye movements differed significantly between the two groups when reading text. These movements differed further when longer and less-familiar words were introduced (Hyönä and Olsen, 1995). Thus, Stanovich (1986) and Rayner (1983, 1985) concluded that eye movements in and of themselves are not the cause of the reading problem but that the erratic eye movements are a symptom of the problem. The American Academy of Pediatrics and The American Academy of Opthamologists have issued repeated warnings about the unproven benefits of vision therapy concluding that ‘vision problems do not cause dyslexia’ (AAP, 2009).
BUT WHAT ABOUT COLOURED OVERLAYS?
Coloured overlays (Irlen,1991) have been ubiquitous for dyslexic relief for many years and are even approved for use in standardised testing (Denton and Meindl, 2016). A Google search will reveal numerous sites selling these overlays as support resources for dyslexia. There is growing evidence that beyond a placebo effect they are of little value (Ritchie et al., 2011) and rather worryingly may have a deleterious effect (Denton and Meindl, 2016).
BUT WHAT ABOUT LETTERS ‘MOVING’ ON THE PAGE AND REVERSING LETTERS?
Left-right confusion seems to have entered the public consciousness as a primary symptom of dyslexia (remember the singularly unfunny graffiti from the 1970s, ‘dyslexia rules k.o’?). Mirror errors occur naturally in humans (as a result of the part of the brain that recognises symmetry in faces being utilised for reading – the brain never evolved for reading despite the whole language theorists believing/hoping it did) and peak at between 7 and 10 years old after which they disappear…for almost all of us. For a very few, however, left-right confusion persists and results in reversal of letters, confusion of letters within strings and even inverted word order (McCloskey et al., 1995). Spatial relations are never stable and seem in perpetual fluctuation hence the reports of letter and word instability. This is sometimes referred to as mirror dyslexia. It is so exceptional that it probably ‘raises more questions than it answers’ (Dehaene, 2010:298).
BUT ISN’T DYSLEXIA A PROCESSING PROBLEM?
Although the bulk of evidence from research supports the model that dyslexia is a phonological-core deficit some theorists suggest that the condition is one of deficiencies of processing speed. The root of word-level reading problems, the theory posits, lies in the auditory, visual and motor system processing problems that are manifest when rapid sequences of information (speech sounds, dots in motion) are presented (Lovegrove et al., 1980; Nicolson et al., 2001). The appeal of the theory is that it accounts for differences among dyslexic readers. However, although these sensorimotor deficits are relatively common among dyslexic readers these deficits are not tightly correlated with reading problems (White et al., 2006). So, although some dyslexic readers have sensorimotor deficits, not all of those with sensorimotor deficits are dyslexic (Robertson et al., 2009; Milne et al., 2002). Ziegler et al.’s (2009) research suggested that what many regard as a sensorimotor deficit may actually be a noise exclusion deficit. Poor readers performed equally as well as normal readers in no noise conditions; it was only in high-noise conditions that their detection thresholds compared less favourably.
IS THERE A CURE?
Dyslexia is not a pathology. It does not condemn a child to never being able to read, write or spell. There is therefore no need for the hopeless prognosis often accompanying its diagnosis. A child does not ‘have’ dyslexia in the same way that it may ‘have’ chickenpox. It is not a virus. A child is dyslexic in the same way that a child is diabetic (Rayner et al., 2012) indicating an ongoing neurological state that manifests itself in certain symptoms. In the same way that a diabetic can control their insulin, a dyslexic reader is able to become asymptomatic. However, early diagnosis and effective intervention seem to be the key to achieving this asymptomatic status. When children fall behind in their reading this is rarely due to a temporary lag in cognitive development (Shaywitz et al., 1999; Snowling et al., 1997). Without intervention they are unlikely to catch up!
BUT WHAT INTERVENTION?
As Vellutino et al.’s (1996) longitudinal study showed, most children with early reading problems (acquired for whatever reason – often poor teaching) benefit from supplementary decoding instruction whether they are diagnosed with dyslexia or not. As most dyslexic children exhibit a phonological deficit, early assessments of phonological awareness are essential and interventions that concentrate on building phonological and phonemic awareness have proven to be most effective especially those that encourage children to manipulate letters and sounds (Torgesen, 2005). Interventions must be intense and prolonged (Dehaene, 2010). Reassuringly, brain imaging technology has shown that with intensive intervention the brain activation profiles of dyslexic readers can be normalised with a net gain in activation of the left temporal region (Shaywitz, et al., 2004, Simos et al., 2002). There also appear to be some compensatory results with observed increases in activity in symmetrical areas of the right hemisphere.
SO, IT’S ALL ROSY THEN?
Unsurprisingly, difficulties acquiring fluency for dyslexic readers allied to the time and effort commitment required to normalise word recognition results in legacy issues. Reduced exposure to print as a result of dyslexia and the necessary concentration on the phonological deficit means that reading automaticity takes longer. This often manifests itself in slower reading rates whilst readers enrich their visual vocabulary of graphemes, morphemes and words (Dehaene, 2012). It is therefore essential that dyslexic readers continue to build this print exposure. This is not always easy to motivate when reading has been a struggle throughout one’s life. It may also be unhelpful to market a ‘love of reading’ as a nirvana for these children. It may have to be enough that they have not acquired a pathological hatred of a necessary activity that has brought them so much anxiety, struggle, pain and exhaustion. Furthermore, in the small percentage of children where slow serial naming speed is an issue, this factor appears to be the most difficult to remediate with little evidence of effective intervention (Levråg and Hulme, 2009; Powell et al., 2014). More research is required in this complex area.
Perhaps the most pertinent issue with dyslexia is not so much its early diagnosis as the perception that dyslexic readers need to learn to read in a different way to other readers and are categorically different from other children who struggle to read. Velluntino et al.’s (1996) longitudinal study showed that almost all children with early reading problems (whether dyslexic or not) benefit from supplemental decoding instruction and early diagnosis of this phonological deficit was crucial in remediation. It would seem that code-based reading instruction is therefore the most likely to, firstly, identify phonological deficits and, secondly, offer a route to remedy the deficit. The instruction may require supplemental input, reduced pace and intensive intervention but it is, however, founded on the same principle. The idea that if phonics hasn’t worked then a child requires a different approach (Glazzard, 2017; Adoniou, 2017 – see here) would thus appear to be not only fallacious but detrimental and possibly even irresponsible. It is clear (see above) that many dyslexics can decode but struggle to develop effective recognition of orthographic representations. This, however, is not an argument that phonics instruction is ineffective or spurious for dyslexic readers. On the contrary, instant word recognition is ultimately dependent on efficient grapheme-phoneme mapping for all readers and is the core problem for the vast majority of struggling readers (Roberts et al.,2011). For dyslexic readers, this takes longer, requires much harder work and a lot more patience.
The study of dyslexia has a long and complex history. Much of our knowledge has come though the study of acquired dyslexia.
Acquired Dyslexia (alexia) – this occurs as a product of brain damage to the left hemisphere of the brain which often results in reading difficulties as a result of the injuries. Its study has led to other sub-definitions:
Surface dyslexia – people with surface dyslexia typically exhibit better reading of pseudowords and regular words rather than irregular words (Marshall and Newcombe, 1973).
Phonological dyslexia – people with phonological dyslexia, unlike surface dyslexia, struggle to read unfamiliar words and pseudowords which they sound out but can read familiar irregular words (Patterson, 1982).
Deep dyslexia - similar to phonological dyslexia, people with deep dyslexia (Coltheart et al., 1980) make errors reading new words and pseudowords but their ability to read familiar words is more stable. However, in addition, they also make characteristic semantic errors (paralexias) eg. Reading ‘kitten’ as ‘cat’.
The study, diagnosis, treatment and remediation of dyslexia is, understandably, a contentious, emotive and febrile area of reading development. This short post cannot possibly cover all of the aspects pertaining to this particular condition, and I do not in any way claim to be an expert on the subject. It does, I hope, demystify some of the polemic, address some of the misconceptions and offer some hope and encouragement particularly to teachers of reading and particularly early reading. As Stanislas Dehaene (2012) points out, although teaching reading is complex enough, we (teachers) are not defenceless against a genetic brain impairment that started before birth. Genes do not dictate ironclad, inalterable laws that govern us for the rest of our lives. The brain is a plastic organ which is able to rebuild itself and for which experience is as important as genes. If we learn how to teach reading with expertise according to the scientific and empirical evidence at our disposal, and we apply that knowledge to those children who struggle to learn to read with a greater intensity, resolve and patience, avoiding the lure of what ‘feels’ right as opposed to what research and evidence suggest ‘is’ right, we do our pupils, and ourselves, the best service we can.