DEVELOPMENTAL DYSLEXIA: A CONDENSED REVIEW OF LITERATURE

In this article we provide a condensed review of literature on developmental dyslexia. Starting with the historical background to this language-based reading disorder, we discuss four key components for a valid and operational deinition of developmental dyslexia. We then present the major theoretical explanations of developmental dyslexia in order to gain a better understanding of the causes of this reading disorder. hese causal explanations are addressed in the context of Morton and Frith’s (1995) model. Four major theories of developmental dyslexia are discussed: the phonological deicit theory, the double-deicit theory, the magnocellular theory, and the cerebellar theory. he last section of this review addresses the model of reading development proposed by Frith (1986). Understanding the developmental progression of children’s abilities in reading is crucial in order to detect in which phase of this progression a breakdown attributed to dyslexia occurs.


Developmental dyslexia: a bit of history
he word dyslexia is of Greek origin: the preix dys means diicult and the root, lexia, means words.herefore, the literal translation of dyslexia is diiculty with words (Payne & Turner, 1999). he German professor Rudolf Berlin, an ophthalmologist working in Stuttgart, coined this term in 1887 to refer to a group of six adult patients who had lost their ability to read (Shaywitz, 2003). 1 hese adult patients attracted the attention of Berlin, who monitored them for twenty years.Based on a postmortem analysis, Berlin detected brain lesions in the let hemisphere and associated these lesions to diiculties in reading.
Earlier clinical evidence for similar behavior in reading was described by the term word-blindness (Wortblindheit in German),[which was] coined by another German physician, Adolf Kussmaul, in 1877.Interested in neurologically impaired adults with reading diiculties, he observed patients who demonstrated poor ability to recognize written words ater having sufered cerebral vascular injury.Of interest was the fact that the patients' intelligence, luency in speaking, and eyesight were not afected by the injury they had sufered.he physician was puzzled by the fact that these abilities remained intact and, seeking to understand the problem, he continued further investigations of lesions around the let angular gyrus, a region of the brain in the parietal lobe.Based on his indings, Kussmaul concluded that a lesion in the let angular gyrus was responsible for reading diiculties.herefore, Kussmaul was the irst scientist to associate reading disability with a lesion in this brain region.
Other clinicians such as the German physician Johann Schmidt, the British neurologist William Broadbent, and the French neurologist Joseph Dejerine also reported cases of dyslexia (Elliott & Grigorenko, 2014;Ott, 1997;Shaywitz, 2003). 2 However, it is important to bear in mind that these clinicians described atypical reading patterns in adults who had achieved normal levels of reading skills; i.e., prior to brain lesions these adults were literate.Today, this condition is termed acquired dyslexia.Acquired dyslexia, which is also termed alexia, is a reading disorder which emerges in premorbidly literate individuals who lose previously developed reading skills ater brain injury (Leong & Joshi, 2013).Similar atypical reading patterns are also observed in people who have never achieved the expected reading level.he term developmental dyslexia applies to this condition.In light of this, the nature of reading disability in acquired dyslexia and developmental dyslexia is diferent (Jackson & Coltheart, 2001).
Noteworthy, there are reasons to be wary of claims that acquired dyslexia is always related to adults and brain damage as its cause, while developmental dyslexia is only encountered in school-aged children (Jackson & Coltheart, 2001).Cumulative evidence from case studies on dyslexia has revealed that age and brain damage are not necessarily associated with the type of dyslexia.For example, there are cases of children who, despite being typical readers and demonstrating progress in the development of reading skills, suddenly lose their reading ability and competence.his is a case of acquired dyslexia.On the other hand, an elderly woman at the age of 80 who has always had great diiculties with reading is an example of developmental dyslexia, not acquired dyslexia, because she has never been a competent reader.
Additionally, brain damage is not always indicative of acquired dyslexia because there are cases of acquired dyslexia in which brain damage is not necessarily the source of reading diiculties.Jackson and Coltheart (2001) give an example of a man who used to be a skilled reader, but one day he woke up and perceived his diiculties in reading.Neither alterations in brain function, nor brain damage were detected in this patient.Nevertheless, his case received the diagnosis of acquired dyslexia.As regards developmental dyslexia, alterations in brain function associated with defective brain maturation are central to the explanation of this reading disorder (Habib, 2000;Shaywitz et al., 2002).
he irst report of developmental dyslexia, entitled A case of Congenital Word Blindness, was published by the British physician Dr. William Pringle Morgan in 1896 (Shaywitz, 2003;Snowling, 2000).In his report, Morgan described a 14-year-old boy named Percy F. as a case of developmental dyslexia (Cook & Ryan, 2016).Despite being bright and intelligent, quick at games, the boy had severe diiculties in learning to read.Percy struggled with reading simple sentences, making mistakes in every single word, except for articles, prepositions and conjunctions.Moreover, he made many spelling errors, including in his own name, which he used to spell as Precy.Morgan also tested his ability to read numbers and do mathematical operations like multiplication and was puzzled by the fact that the boy performed these tasks easily.In light of accumulated evidence, Morgan concluded that Percy's inability to learn to read was due to a congenital alteration in the let angular gyrus, since similar diiculties were observed in adults with injury in this region. 3 With the passage of years, more cases of developmental dyslexia were reported in Europe and the United States (Elliott & Grigorenko, 2014;Shaywitz, 2003).During the 1920s one of the most prominent was the American neurologist Dr. Samuel Torrey Orton.His inluential work Reading, Writing and Speech Diiculties in Children was published in 1937.Orton proposed a theory of cerebral dominance suggesting that, in dyslexics, neither hemisphere was dominant and that would explain basic symptoms of developmental dyslexia, such as reversals of letters, syllables, and words.Even though his hypothesis was refuted, many of his observations had a profound impact on understanding dyslexia and sparkled a great deal of debate in the literature (Høien & Lundberg, 2000).One year ater Orton's death in 1948, the Orton Dyslexia Society was founded with the mission to continue his work on the prevention, treatment, and study of this disorder.he Orton Dyslexia Society is the former name of the International Dyslexia Association (IDA), a non-proit education and advocacy organization dedicated to this reading disorder in the USA.
As can be seen from this brief historical account, research on dyslexia began more than a century ago and since then important contributions have been made to dyslexia research (Jackson & Coltheart, 2001).Today, there is a general consensus that developmental dyslexia is a disorder of neurobiological origin characterized by diiculties in reading and writing skills (Cook & Ryan, 2016).With advanced neuroimaging techniques (fMRI, EEG, MEG), it is possible to detect neuronal abnormalities associated with this disorder.However, despite a plethora of reports with detailed descriptions of the behavioral symptoms observed in developmental dyslexia, the deinition of dyslexia has been subject of debate over the last 50 years.Researchers agree that developmental dyslexia may have several underlying causes and is generally accompanied by other developmental disorders, such as attention deicit hyperactivity disorder (ADHD) (Joshi & Aaron, 2016).Various deinitions of developmental dyslexia have been proposed.he next section aims at presenting important characteristics of developmental dyslexia, which should be accounted for its deinition.

Deinitions of dyslexia
Despite years of research, there is still considerable debate on the appropriate deinition for developmental dyslexia (Castles & Coltheart, 1993;Fisher & DeFries, 2002;Fletcher, 2009;Lyon et al., 2003).Much disagreement concerns the underlying causes of developmental dyslexia (hereater, dyslexia), which in turn also implicates appropriate forms of assessment.Rice and Brooks (2004) reviewed over 1200 book chapters and papers and analyzed many deinitions of dyslexia.he researchers distinguish two types of deinitions: descriptive and explanatory (Rice & Brooks, 2004).Descriptive deinitions of dyslexia are those that purely describe developmental diiculties, such as poor word decoding (reading) and encoding (spelling).his type of deinition aims at facilitating the early diagnosis of dyslexia, which in turn leads to early intervention.However, descriptive deinitions lack explanatory elements with respect to possible underlying causes of dyslexia.Explanatory deinitions rely on explanatory theories.What type of deinition is the most applicable remains a contentious issue among researchers and clinicians.Tunmer and Greaney (2010) sought to contribute to this debate by providing answers to three interrelated questions: What is dyslexia?What causes it?What can be done about it?(p.229).According to the researchers, the conceptualization of how dyslexia is deined, what causes diiculties in learning to read, and which intervention is the most efective is strongly inluenced by a broader conceptualization of what reading is and how it is acquired.On the basis of answers to the above question, Tunmer and Greaney (2010) strongly advocate that the plausible deinition of dyslexia should encompass the following four components: (1) persistent literacy learning diiculties, (2) exclusionary factors, (3) exposure to evidence-based instruction and intervention, and (4) inclusionary factors.
A deinition that encompasses these four components is the one developed by a working group of the International Dyslexia Association (Lyon et al., 2003). he deinition of Lyon and colleagues (2003) is commonly accepted and cited in the literature of dyslexia (Elliott & Grigorenko, 2014;Fletcher, 2009). he following deinition is an updated version of their working deinition of 1994: Dyslexia is a speciic learning disability that is neurobiological in origin.It is characterized by diiculties with accurate and/or luent word recognitionand by poor spelling and decoding abilities.hese diiculties typically result from a deicit in the phonological component of language that is oten unexpected in relation to other cognitive abilities and the provision of efective classroom instruction.Secondary consequences may include diiculties in reading comprehension and reduced reading experience that can impede growth of vocabulary and background knowledge (Lyon et al., 2003, p.2).
his deinition provides essential characteristics of dyslexia.In the opening sentence of the deinition, Lyon and colleagues (2003) refer to the speciicity of dyslexia towards learning skills as well as to its neurobiological origin.It is noteworthy that this deinition also goes beyond the established view of dyslexia as single word decoding diiculties.Decoding abilities of pseudowords, 4 for instance, and poor spelling are also considered as a manifestation of reading comprehension diiculties and reduced reading experience.hese consequences, in turn, may lead to limited growth in vocabulary and background knowledge.he deinition of Lyon and colleagues (2003) also includes the core causal explanation of dyslexia, the phonological processing deicit, which is not related to intelligence and classroom instruction.
It is important to state that traditionally, clinicians have identiied dyslexic individuals with the help of standardized tests that measure intelligence and cognitive abilities in order to attest that literacy learning diiculties of dyslexics are not directly caused by low intelligence. 5As a consequence, many deinitions of dyslexia hold with the idea of the discrepancy-based criterion, i.e., the discrepancy between mental age, measured by an intelligence quotient (IQ), and reading age, measured by standardized tests of reading accuracy and comprehension, in comparison to chronological age (Bishop & Snowling, 2004;Fletcher, 2009;Lyon et al., 2003;Ramus, 2003).An example of a discrepancy-based deinition is that proposed by an inluential diagnostic system, the ICD-10 Classiication of Mental and Behavioural Disorders (Health Organization-WHO, 1993).

heories of developmental dyslexia
he deinition and explanation of dyslexia have become a matter of debate, in which the nature and features of this disorder are central (Elliott & Grigorenko, 2014).In order to achieve a better understanding of this disorder, the irst step is to distinguish between the diferent levels of existing explanation for dyslexia.Morton and Frith (1995) have proposed a causal model, which clearly distinguishes the three major levels of explanation: biological, cognitive, and behavioral.By providing full causal explanation for this disorder, this causal model has become widely acknowledged and commonly referenced (Frederickson, 2009;Nicolson & Fawcett, 2008;Pavey, 2007;Snowling, 2000).Here we describe this causal model and discuss current explanatory theories of dyslexia in the context of the model.he choice to address theories of dyslexia by means of Morton and Frith's (1995) model is attributed to the fact that it brings together diferent levels of explanation, thus contributing to a thorough understanding of dyslexia.
he lack of an agreed deinition as well as the debate over the underlying causes of dyslexia motivated two developmental psychologists, John Morton and Uta Frith, to think about a neutral framework, which would compare diferent theories of development disorders and ind the common ground between them (Morton & Frith, 1995). he framework proposed by Morton and Frith (1995) incorporates three levels of explanation: the biological level, the cognitive level, and the behavioral level.According to Morton and Frith (1995), all three levels are equally important and complement each other.Additionally, the researchers included environmental factors in the framework, as these may have an impact on one or all of these levels.
It is well assumed that clinicians diagnose dyslexia based on speciic behavioral manifestations.Morton and Frith (1995) suggest that all behavioral manifestations of dyslexia should be associated with the behavioral level of the framework.Given that dyslexia is a disorder of neurobiological origin, Morton and Frith (1995) pay special attention to the diferences, in the neurobiological substrates, between dyslexic and typically developing individuals.he biological level, which is the deepest level of explanation of dyslexia, includes contributions from genetic and brain imaging research.here is evidence from molecular genetics that a number of inherited genes (for example, DYX1C1, KIAA0319, DCDC2 and ROBO1) may contribute to the development of dyslexia (Fisher & DeFries, 2002;Fisher &Francks, 2006).Additionally, dyslexia is a congenital neurobiological disorder caused by abnormal brain structure, in particular abnormal magnocellular pathways and abnormal cerebellum (Shastry, 2007).hese brain abnormalities are associated with explanation at the biological level of the framework.
According to Morton and Frith (1995), valuable contributions to the understanding of dyslexia come from the cognitive level, where causes of dyslexia are associated with deicient information-processing mechanisms.Current theoretical explanations of dyslexia at the cognitive level include deicits in shortterm or working memory, phonological awareness, incomplete automatization, and slow processing (Reid, Soler, & Wearmouth, 2003).For instance, there is a general consensus about the phonological deicit theory, which suggests that the core deicit in dyslexia is related to phonological processing (Ramus et al., 2003).
Overall, Morton and Frith (1995) highlight the importance of each level as well as of environmental factors when analyzing diferent explanatory perspectives on dyslexia.he researchers claim that investigating causes of dyslexia at the proposed levels as well as causal links between these levels will be helpful in understanding and explaining this disorder.In addition, this framework integrates the potentially disparate theoretical accounts of dyslexia, which may seem to be in conlict with each other at irst sight.An example of this is an integration of two commonly referenced theories that explain dyslexia as resulting from a phonological deicit and from a magnocellular deicit, respectively.As previously stated, the phonological deicit theory is associated with the cognitive level of explanation, where a deicit in phonological processing is the source of reading diiculties among dyslexics.he magnocellular deicit theory, in turn, assumes that there is alteration in the magnocellular system of dyslexics, which causes reading diiculties.his theory is attributed to the biological level of explanation.From the perspective of Morton and Frith's (1995) model, both theories are compatible with each other, and not mutually exclusive.he researchers claim that theoretical explanations should not be conined to a particular level of the framework: they may originate at one level and extend to others.
Taking into account a range of causal explanations at the biological and cognitive levels, Morton and Frith's (1995) emphasize the importance of considering not only behavioral manifestations for a diagnosis of dyslexia, such as poor reading accuracy and speed, but also evidence of alterations in brain function and cognitive deicits.According to Morton and Frith (1995), contemporary theories of dyslexia may be modelled in the three-level framework.Next we address some of these theories, which explain neurocognitive causes of dyslexia.

he phonological deicit theory
Over the 40 last years, research in dyslexia has accumulated robust empirical evidence in support of both the phonological deicit in dyslexia and efective intervention programs based on phonological training (Lyon et al., 2003;Fawcett & Nicolson, 1995;Joanisse et al., 2000;Ramus, 2003;Snowling, 1995). he description of the phonological processing deicit comprises three main components: poor phonological awareness, poor verbal short-term memory and slow lexical retrieval (Ramus, 2004).
Phonological processing diiculties in dyslexics are well-documented (Ramus, 2003;Snowling, 2000;Vellutino et al., 2004).hese diiculties are especially detectable in task requiring phonological awareness, i.e., the ability to manipulate speech sounds (phonemes) and their combinations (syllables) consciously (Ramus, 2004).Having poor phonological awareness, dyslexic individuals have diiculties in performing tasks such as syllable counting, phoneme deletion or substitution.A deicit in phonological processing manifests in tasks that require memory for phonological sequences (Ramus, 2004).Dyslexics demonstrate severe diiculties in tasks aimed at remembering sequences of sounds or letters or repeating non-words.he phonological processing deicit also afects lexical retrieval, which is an undeniable skill for reading (Ramus, 2004).Dyslexics are seriously challenged by tasks that require the ability to name aloud letters or objects rapidly.According to Ramus (2004), phonological awareness, verbal short-term memory, and lexical retrieval are responsible for the representation, storage, and retrieval of linguistic material, i.e., information processing at the cognitive level.Failures in one or all of these abilities may explain a variety of behavioral manifestations in dyslexia.
In terms of the causal model proposed by Morton and Frith (1995), the behavioral signs of a phonological deicit are associated with alterations in the lethemisphere language system (Démonet, Taylor, & Chaix, 2004).In particular, there are abnormal responses in the let inferior frontal region with increased activation, the let parietal-temporal regions and the let inferior temporal-occipital regions with reduced activation during both phonological and reading tasks (Démonet et al., 2004;Hoet et al., 2006;Shaywitz & Shaywitz, 2005).Importantly, diiculties in phonological processing are neither related to auditory impairments, where an individual cannot reproduce a sound due to inadequate hearing, nor to visual impairments caused by physical diiculties with the eyes.
he model also predicts that various environmental factors, such as orthography, teaching methods, and literacy values, have a strong impact on the acquisition of grapheme-phoneme knowledge.For instance, the type of orthography may inluence the developmental progress of children learning to read (Vellutino et al., 2004).Languages with opaque orthographies, i.e., languages with no consistent relationship between graphemes and phonemes, such as English, present a signiicantly greater challenge to many beginning learners than languages with transparent orthographies, i.e., languages with consistent relationship between graphemes and phonemes, such as German or Italian.Moreover, teaching methods play an important role in building phonological skills, and societal values strongly inluence the acquisition of literacy acquisition.
he phonological deicit theory has become the most commonly referenced theoretical explanation of dyslexia.Although this theory provides a reasonable and coherent explanation of dyslexia, controversy still exists because not all dyslexics demonstrate diiculties in phonological processing. he main criticism of the phonological deicit theory is that it typiies the idea of a phonological deicit as exclusive in nature.In the next subsection, the role of two distinct cognitive deicits responsible for information processing, i.e., a phonological deicit and a rapid-naming deicit, is addressed in terms of the double-deicit theory.

he double-deicit theory
A number of scholars defend the notion that dyslexics' diiculties are not exclusively or mainly associated with a deicit in phonological processing (Lovett, Steinbach, & Frijters, 2000;Wimmer, Mayringer, & Landerl, 2000;Wolf & Bowers, 2000).herefore, the double-deicit theory, which is an extension of the dominant phonological deicit theory, has been proposed (Wolf & Bowers, 2000). he double-deicit theory recognizes the role of phonological processing skills for reading development.However, according to this theory, dyslexics have a deicit in rapid serial/automatized naming (RAN), which is an equally important skill for reading development.he double-deicit theory proposes that dyslexic individuals have a single deicit in one of these skills or the double deicit in both skills.
Based on extensive investigations, Wolf and Bowers (2000) claim the existence of three subtypes of dyslexic readers: the irst subtype exhibiting a single deicit in phonological skills, but intact naming speed, the second subtype exhibiting a single naming-speed deicit, but intact phonological skills, and the third subtype exhibiting a double deicit, when both phonological and rapid-naming skills are impaired.A phonological deicit has a strong relationship with decoding accuracy, whereas a naming-speed deicit is strongly associated with reading luency.
An important implication of this theory is that individuals with a single naming-speed deicit require adequate intervention, not solely based on the training of phonological skills.In line with this, training phonological skills may not be so efective for languages with transparent orthographies.For instance, in languages like Italian and German, in which skills in phonological processing play a less important role, naming speed becomes a powerful predictor of reading performance (Nijakowska, 2010).Noteworthy is the evidence that individuals with a double deicit, i.e., with diiculties in both reading accuracy and speed, are the most severely impaired subtype, thus suggesting a more intensive intervention based on training both phonological and rapid-naming skills.
he double-deicit theory has been intensely investigated by providing a substantial body of evidence for its main assumptions (Lovett et al., 2000;Wolf, Bowers, & Biddle, 2000).For instance, Lovett and colleagues (2000) conducted a study with 166 children with severe reading disabilities with age ranging from 7 to 13 years old. he researchers aimed at categorizing children's diiculties according to the presence or absence of a phonological and naming-speed deicit (Lovett et al., 2000). he data of 84% of the sample (140 children) were submitted to further analysis, revealing that 54% of the sample demonstrated a double deicit, 24% had a single naming-speed deicit and 22% had a phonological deicit.It should be noted that children with the double deicit were more severely impaired in comparison to children with single deicits.Based on evidence in support to a double deicit in dyslexic individuals, Wolf and colleagues (2000) argue that a phonological deicit is not the only core deicit in dyslexia.here is a second core naming speed deicit, which inluences reading performance in terms of luency.According to the researchers, intervention programs for dyslexics should include practices on both skills (Wolf et al., 2000).
In hindsight, the two theories of dyslexia presented above have a causal explanation at the cognitive level.According to Morton and Frith (1995), the cognitive level constitutes a crucial link between the biological and behavioral levels, with underlying causes of cognitive deicits arising from structural abnormalities of the brain.Owing to the assumption of a causal model of Morton and Frith (1995), behavioral manifestations of language processing diiculties in dyslexia are caused by brain abnormalities.herefore, the dyslexic brain has attracted researchers' attention as the likely source of language processing diiculties (Galaburda, 2005;Habib, 2000;Shaywitz et al., 2002;Shaywitz & Shaywitz, 2005).
Before discussing the theoretical explanations of dyslexia in relation to alterations in the brain, it is important to give credit to the earliest investigations of the dyslexic brain.Norman Geschwind, an American neurologist, had the idea to undertake neuroanatomical analysis of dyslexic brains and compare them to those of non-dyslexics (Galaburda, 2005).As stated by Galaburda (2005) in his review article, Geschwind conirmed a let-right hemisphere asymmetry in volume of the planum temporale in dyslexics and explained this inding as insuicient amount of brain tissues in the let hemisphere, which is heavily involved in language processing.Geschwind hypothesized that an insuiciency of brain tissues in the let hemisphere could be triggered by an improper development of language regions in fetus, particularly during the migration of young neurons to their inal destination in the brain.
Geschwind's ideas were further investigated by Galaburda and colleagues (Galaburda, Sherman, Rosen, Aboitiz, & Geschwind, 1985), who were among the irst interested in the brain organization of dyslexic individuals.Galaburda's group observed neural abnormalities (ectopias), i.e., dismigration and disorganization of the neurons, in many areas of dyslexic cerebral cortex, especially in language areas in the let hemisphere.A plausible account of ectopias in combination with a phonological deicit is that anomalous neural development is more pronounced in the language areas of the let hemisphere, particularly the perisylvian region.
Interesting indings were revealed comparing four male and three female dyslexic brains (Galaburda et al., 1985;Humphreys, Kaufmann, & Galaburda, 1990).he number of participants was limited as these were two postmortem investigations.he researchers concluded that the location of neural abnormalities was diferent in males and females.In dyslexic males, the brain showed symmetry of the planumtemporale and predominantly let-sided microscopic abnormalities in the cerebral cortex.Regarding the female dyslexic brain, the researchers also concluded that the brain had a symmetrical planumtemporale, but there were fewer abnormalities, which varied in location, when compared to the brain of male dyslexics (Humphreys et al., 1990).It is important to state that the planumtemporale in typically developing individuals has a letward asymmetry with greater size (Bloom, Garcia-Barrera, Miller, Miller, & Hynd, 2013).

he magnocellular deicit theory
Reading involves fast and accurate visual identiication of letters and words.According to Stein (2001), the visual system is crucial to reading, and dyslexia is the result of abnormalities in the neural pathways of this system.he visual system is divided into two distinct pathways: the magnocellular and the parvocellular (Greatrex & Drasdo, 1995) pathways.Each pathway has diferent functions and properties. he magnocellular pathway is responsible for the fast input transmission from the retina to the occipital and parietal brain regions, and the parvocellular pathway processes the details of this input.
In the magnocellular deicit theory, poor reading performance of dyslexics is due to abnormally reduced sensitivity in the magnocellular system (Livingstone, Rosen, Drislane, &Galaburda, 1991;Lovegrove, Bowling, Badcock, & Blackwood, 1980;Skottun, 2000;Stein et al., 2000).In particular, the visual sensory abnormalities are the result of magnocells shrinkage (magnocells are about 27% smaller in dyslexics) and disorganization in lateral geniculate nucleus, whereas the parvocells are intact (Greatrex & Drasdo, 1995;Livingstone et al., 1991).A reduced ability to detect visual stimuli rapidly can result in visual stress.hus, dyslexics manifest a variety of symptoms of visual stress, such as headaches, eye strain, poor concentration, diiculty to remember what has been read, omission of words and lines when reading (Kelly & Phillips, 2016).
In terms of the causal model proposed by Morten and Frith (1995), there are causal connections between abnormalities in the magnocellular system and behavioral signs of dyslexia.Fluency and accuracy in reading are dependent on fast and accurate processing of both visual and auditory information.As Stein (2001) proposes, dyslexics have lower sensitivity to both visual and auditory stimuli in comparison to typically developing individuals.At the cognitive level, diiculties of dyslexics are attributed to a general temporal processing dysfunction.As a consequence, this dysfunction leads to a visual magnocellular deicit and an auditory deicit.he temporal auditory deicit is thought to cause a deicit in phonological processing.At the behavioral level, the visual magnocellular deicit explains dyslexics' diiculties with tasks that require the perception of motion.Diiculties associated with the temporal auditory deicit are poor tone discrimination, poor speech development, and poor reading.
In addition to the visual and auditory deicits, the magnocellular deicit theory also explains the cerebellar deicit in dyslexics (Stein, 2001).Taking into account that the cerebellum receives information from the magnocellular system, the cerebellum is also afected by a more general magnocellular dysfunction.hus, the cerebellar deicit theory has been proposed, which is reviewed next.

he cerebellar deicit theory
he cerebellum has been traditionally viewed as the area involved in learning and the automatization of motor skills (Nicolson & Fawcett, 2008;Stein & Glickstein, 1992).However, during the last two decades the assumption that the cerebellum might be involved in cognitive skills, particularly in language processing, has gained support (Fabbro, Moretti, & Bava, 2000;Justus & Ivry, 2001;Marien, Engelborghs, Fabbro, & De Deyn, 2001).Recent brain imaging studies have provided evidence to this assumption by detecting activation in the cerebellum during reading tasks (e.g., Carreiras, Mechelli, Estévez, & Price, 2007;Joubert et al., 2004;Mechelli, Gorno-Tempini, & Price, 2003).Based on the converging evidence for cerebellar dysfunction in dyslexics, Nicolson and Fawcett (2008) proposed the cerebellar deicit theory.According to Nicolson and Fawcett (2008), dyslexic individuals fail to develop automaticity in reading skills due to a dysfunction in the cerebellum.In particular, this dysfunction was reported in brain imaging studies as a reduced activation in the right cerebellum conirming that the magnocellular deicit also afects the cerebellum (Nicolson et al., 1999;Rae et al., 1998).Frith (1999) proposes a causal connection between cerebellar alterations and behavioral signs of dyslexia.An impaired cerebellum implies a temporal processing deicit at the cognitive level.Slower-than-normal temporal processing is associated with deicits in phonological and motor skills.At the behavioral level, the motor control deicit explains poor naming speed, poor time estimation, poor motor development, and poor balance.Diiculties associated with the phonological deicit are poor naming speed and poor reading.
Altogether, the cerebellar deicit theory treats dyslexia as a general learning disability (Nicolson, Fawcett, & Dean, 1995;Nicolson, Fawcett, & Dean, 2001).Diiculties in reading and writing are caused by a deicit in the cerebellum, which is responsible for skill automatization.herefore, the supporters of the cerebellar theory claim that diiculties in phonological processing and motor skills experienced by dyslexics should be attributed to a dysfunction in the cerebellum (Fawcett & Nicolson, 1994;Nicolson, Fawcett, & Dean, 1995;Nicolson, 1994).he cerebellar deicit theory as well as the magnocellular deicit theory explain the phonological deicit as caused by a more general temporal processing deicit, thus suggesting that intervention at the sensory level can also be helpful (Tallal et al., 1996).
We will now move on to a review of the model proposed by Frith (1986), which describes the developmental progression of children's abilities in reading and accounts for the breakdown in this progression that is associated with dyslexia

Typical reading development
here has been considerable interest in the reading literature about children`s progress in reading development (Elbro, 1996;Kirby, Desrochers, Roth, & Lai, 2008;Nation & Snowling, 1998), and a developmental model of reading can serve many purposes.First, a developmental model can inform about crucial abilities for reading, such as decoding, as well as explain the developmental progression of these abilities.Moreover, a developmental model can establish the relation between reading and cognitive abilities involved in this process.
An example of such model is the one proposed by Uta Frith (1986), which is currently one of the most prominent and inluential models of literacy development (Gathercole & Baddeley, 2014).Frith's model of reading development takes into account her research and practice about children`s learning to read (Nunes & Bryant, 2013).Although it was proposed more than three decades ago, this model is widely accepted and commonly referenced by many scholars and still is considered applicable today (Adelman, 2012;Beaton, 2004;Hulme & Snowling, 2013). he model describes how typically developing reading abilities change and progress while children learn to read an alphabetic orthography such as English.According to the model, in order to reach success in reading, children should go through three phases: the logographic phase, the alphabetic phase, and the orthographic phase (Frith, 1986).
During the logographic phase, children`s earliest attempts to read take place.However, these attempts do not involve a phonological strategy, since letter sequence is neglected, and are based on a purely visual strategy.Children recognize familiar words relying on highly distinctive visual cues such as size, shape, and length.In other words, children memorize words as visual entities, called logographs.Using this visual strategy, children are able to read or perceive words that are signiicant to them and are stored in their limited vocabulary.For instance, children recognize their own names, names of shops, and common signs.However, the strategy is not always reliable and, because it is not generative, it will not help them read unfamiliar words later.At this early phase of literacy development, children are not aware of the alphabetic principle, i.e., understanding that individual graphemes and their combinations correspond to certain sounds.he chronological age of children associated with this phase may vary from 3 to 5 years old (Bielby, 1999).
Having quite good experience with the visual forms of words, children`s visual discrimination abilities become more reined.It is in the second phase-the alphabetic phase--that children develop the notion of alphabetic principle.Unlike the irst phase, the alphabetic strategy does not usually develop spontaneously.Children need to be exposed to some kind of formal instruction from more competent readers, such as parents, relatives, and teachers, who can explain to them the grapheme-to-phoneme conversion rules.his input motivates children to analyze the relationship between graphemes and sounds in spoken and written words.he chronological age of children attributed to this phase may vary from 5 to 7 years old (Bielby, 1999).
he alphabetic phase plays a crucial role in the development of the subsequent orthographic strategy.In the orthographic phase, children develop the orthographic strategy, which enables them to recognize words automatically and access their meaning immediately from the lexical memory.Word recognition and word retrieval occur without much efort because children are able to break down words into orthographic segments automatically without graphemeto-phoneme conversion, i.e., without sounding out each grapheme as in the alphabetic phase. he orthographic segments correspond to morphemes that are stored in memory.he analysis of words into orthographic segments takes place much faster than the phonological analysis.Frequent words are decoded and read much faster than infrequent ones. he chronological age of children attributed to this phase may vary from 7 to 9 years old (Bielby, 1999).
According to Frith (1986), typical literacy acquisition is characterized by the progression in each phase and the development of each strategy in the above mentioned sequence.he progress and change from one phase to the next one are not random.hey are the consequence of biological (maturation) and cultural (teaching) inluence.he expected outcome of this sequential development is a competent reader who demonstrates luency and accuracy in reading.Importantly, this ixed sequential development is not restricted to the use of one strategy independently and once at a time.Sometimes children may employ two diferent strategies at the same time, in particular when they still do not have full control of a new strategy and use aprevious strategy on their way to adapt to a new condition.
Another relevant issue that Frith (1986) raises in her model of reading development is that, over the course of learning, children do not always demonstrate gradual improvement in reading.At any moment of their reading development, children may have a decline in performance because the transition from one phase to another implies the acquisition of a new strategy and its integration with the already acquired strategy.he transition through phases is very sensitive and delicate and may be associated with either breakthrough or breakdown.According to Whitebread (2002), the advantage of this model is that the deined phases are quite useful and practical for instructors because they can monitor the progress made by children at a particular phase and identify whether there is some nonconformity or decline in progression, whether the decline is temporal or long-lasting, and whether early intervention is mandatory.
Although the model proposed by Frith (1986) has particular authority in the literature on reading development, it has also received criticism (Beech, 2005;Graham & Kelly, 2012). he main criticism comes from Ehri (1995) and has to do with inadequacies in Friths' deinition of each phase.For instance, Ehri (1995, p. 118) states that the term logographic is misleading "because beginners in the irst phase do not read words like mature readers of logographic orthographies such as Chinese".According to Ehri (1995), the concept of alphabetic processing is crucial to the deinition of developmental phases in reading.herefore, she proposes a new model of reading development consisting of four phases that are distinguished by the involvement of the alphabetic system. he phases are labelled pre-alphabetic, partial alphabetic, full alphabetic, and consolidated alphabetic. he pre-alphabetic phase is equivalent to Frith`s logographic phase.Frith`s (1986) alphabetic phase is divided by Ehri (1995) into two: partial and full.According to Ehri (1995), the diference between these two phases lies in the ability to map graphemes to phonemes: whereas in the partial alphabetic phase this ability is initial, in the full alphabetic phase it is fully developed.Despite the criticism of Ehri (1995), the model proposed by Frith (1986) is currently one of the most inluential developmental models of reading (Gathercole & Baddeley, 2014) and has also been adopted to explain developmental disorders of reading like dyslexia (Høien & Sundberg, 2000;Mortimore & Dupree, 2008;̛odej, 2016).
he idea that reading strategies are acquired at diferent time courses and in a ixed and continuous sequence enables the identiication of a developmental failure within one of these strategies.According to Frith (1986), the failure may be observed at diferent phases, and the type of developmental disorder will depend on where exactly the failure occurs.It is reasonable to suggest that in the presence of a failure, the child tries to develop some compensatory strategies.If the child faces diiculties at one particular phase, the child may over-develop a previously acquired strategy in order to compensate for these diiculties, or s/he may simulate the use of a necessary strategy for a certain performance.Under the last presupposition, a simulated behavior like guessing words from context is easily detectable because it requires more time and, hence, reduces luency, accuracy, prosody, and also comprehension (Mather &Wendling, 2011).A failure in developing a new strategy should receive a parsimonious explanation because not all children may advance from one phase to the following one at the same or similar pace.Noteworthy, this temporal developmental delay should not be considered a developmental disorder.
When comparing developmental delay and developmental disorder, Frith (1986) argues that the crucial diference is about the time course of children's diiculties.In developmental delay, the strategy is acquired slowly and diiculties are overcome by the end of each phase, whereas in developmental disorder, despite the use of compensatory strategies, diiculties still persist.An example of the second condition is the case of successful dyslexics who manage to develop good reading abilities ater having been exposed to efective intervention and training, but who still need to make great efort while reading, in comparison to typical readers (Frith, 1999).For this reason, dyslexia must be deined in terms of a developmental disorder and not in terms of a developmental delay, because in developmental delay the diiculty is no longer detectable in the following phase (Frith, 1999).
Additionally, Frith (1986) also claims that the gravity of a reading disorder depends on where (which developmental phase) a failure occurs, i.e., the later the failure, the less severe the disorder.Moreover, Frith (1986) states that it is not possible to fail at one phase and succeed in the next phase.For instance, the child cannot learn the orthographic strategy if s/he has failed the previous strategy, i.e., the alphabetic strategy, which serves as the basis for the next one.According to Frith (1986), a failure in acquiring the alphabetic strategy results in dyslexia.he researcher also explains that dyslexic individuals are able to master the logographic strategy, but there is a failure to develop the alphabetic strategy, in which the grapheme-to-phoneme correspondence rules are at stake.In other words, dyslexics cannot make progress beyond the logographic phase because they cannot grasp the alphabetic grapheme-to-phoneme associations.In a similar vein, they also face great diiculty to move on to the orthographic phase, in which luency in reading is mastered, because they have not succeeded in the previous phase.

Conclusion
Developmental dyslexia is the most common developmental language disorder of neurological origin in school-aged children with normal intelligence and sensory abilities (Baillieux et al., 2009;Fisher & Defries, 2002;Fletcher, 2009;Petterson & Pennington, 2015;Vellutino et al., 2004). he estimates of the afected school age population around the world vary from 5 to 17and it is estimated that 80% of all individuals diagnosed with some type of learning disability are dyslexic (D'Mello & Gabrieli, 2018).Consequently, dyslexia may be considered an epidemiology in our society, where literacy skills are crucial.his explains why dyslexia has attracted much attention and why it is important to understand the nature of this language disorder.Dyslexia manifests itself in reading and writing diiculties in diferent languages, be they alphabetic, like English, or non-alphabetic, like Chinese.Although dyslexia has been studied for more than 100 years, it is still a challenge for professionals to identify this speciic reading disability, explain its underlying causes and, as a result, provide efective intervention (e.g., Démonet et al., 2004;Fisher & DeFries, 2002;Fletcher, 2009;Nicolson & Fawcett, 2008;Tunmer & Greaney, 2010;Vellutinoet al., 2004).With this condensed review, we hope to have highlighted the basics about dyslexia by presenting the historical background to the research on this disorder, summarizing important theories of dyslexia, and addressing an inluential model of reading development.