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In recent years, the field of knowledge about dyslexia has undergone

significant changes as a result of considerable scientific and educational research (Reid, 2001). Different potential explanations have been

offered to account for the observed symptoms of dyslexia (Doyle, 2002). According to Reid (2001) there are a number of hypotheses

(explanations) which can be associated with dyslexia, as: Phonological Deficit hypotheses, Temporal Processing hypothesis, Working Memory hypothesis, Intelligence and Cognitive Profiles hypothesis.

These hypotheses each refer to different theoretical approaches supported by researchers (Snowling, 2000; Reid, 2001; Frith, 1999;

Regan and Wood, 2000) to explain dyslexia from causal perspective. Dyslexia can be caused by a combination of phonological, visual and

auditory processing deficits (Reid, 2002). The deficit model focuses on language processing tasks and the cluster model focuses on an individual displaying a range of characteristics (Dale, 2002). All these

models are trying to show and explain dyslexia by separating the environment in biological, cognitive and behavioural levels. However,

there is no consensus among experts on a definition of dyslexia, nor is there any agreement on its exact causes (DfES, 2004a).

Uta Frith (1999) has provided a useful framework for thinking about the nature of developmental difficulties (see table 1). According to Frith

(1999) there are three main perspectives on any given developmental condition: a biological, a cognitive and a behavioural one. In addition to

this there are environmental factors that can have a role in the accounts offered from these perspectives.

Biological explanation:

In the last twenty years, efforts have been made to identify the genetic

basis for dyslexia. For example, Gilger, Pennington and Defries (1991) estimated that the risk of a son being dyslexic if he has a dyslexic father

is about 40 per cent. If genetic factors are associated with dyslexia and this, of course, can lead to the early identification of the condition or, at

least, of some very early warning signs in a child being at risk of being dyslexic. The structure of the brain of a dyslexic individual is different

particularly in the language areas. New technologies such as positron emission tomography (PET) and magnetic resonance imaging (MRI) have enabled researchers to identify the differences in the structure of

the brain of a dyslexic and non+dyslexic (DfES, 2004a). Differences in form and function of brain, particularly interaction between right and left

hemispheres affect speech processing, as well as more general motor control processes including time estimation and balance (Too, 2000). In

particular, brains of people with dyslexia often show an unusual symmetry across hemispheres of a region called the ,

which is larger in the left hemisphere and is involved in auditory and language processing (Kalat, 2001). There is evidence that this planum

symmetry may relate to poor phonological skills (Larsen et al., 1990). Brunswick et al. (1999) reported that PET scans of young dyslexic adults

while reading aloud and word and non+ word recognition tasks showed less activation than controls in the left hemisphere.

There is also evidence of visual factors relating to dyslexia (Reid, 2001).

Stein (1994) provides evidence of some perceptual difficulties in dyslexia for tasks involving the processing of rapidly changing information, such as the perception of flicker or motion. Such difficulties

implicate the magnocellular visual system (Eden et al., 1996; Stein and Walsh, 1997). According to DfES (2004, p.37)

Literacy difficulties may be a result of the impaired development of a system of large neurones in the brain (magnocells) that is responsible for timing sensory and motor events.

That means that the visual magnocellular is connected with the visual

demands of reading, so any weakness can lead to visual confusion of letter order and poor visual memory for the written word.

Cognitive explanation:

Riddick (1996) argues that the actual manifest problems are more readily observed in the cognitive area. The cognitive model focuses on

phonological processing difficulties caused by difficulties such as short term and working memory, organising, sequencing and synthesising

information within the brain, writing and learning new information (Too, 2000). However, these difficulties have an additional feature in

common; they contain a phonological component (Reid, 2001). They involve the processing of speech sounds in short+ term memory. It is

therefore possible to suggest that a deficit in phonological processing may provide an explanation of dyslexia (Muter, Hulme and Snowling,

that dyslexics can have difficulties with phonological processing and naming speed.

According to Fawcett and Nicolson (1994); Peer and Reid (2003a)

difficulties in automaticity implies that dyslexic student may not establish new learning and because of that they find it difficult to change inappropriate learning habits. The concept of automatisation refers to

the gradual reduction in the need for conscious control as a new skill is learned.

This leads to greater speed and efficiency and a decreased likelihood of breakdown of performance under stress, as well as the ability to perform a second task at the same time with minimal disruption to either behaviour. (Peer and Reid., 2003a, p. 46)

Fawcett and Nicolson (1994) highlight that the dyslexic children could have Dyslexic Automatisation Deficit and Conscious Compensation

Hypothesis. This means that the dyslexic children could have difficulty in acquiring automaticity, but in many cases they can hide this deficit by working harder. However, a general automatisation deficit would be

most evident during complex, highly demanding, multi+sensory tasks such as learning to read and write (Fawcett and Nicolson, 1994).

Behavioural explanation:

Biological and cognitive perspectives offer theoretical explanations that

require experimental validation, although behavioural perspectives tend to be less debated because the behaviours can be directly observed

(Too, 2000). The behavioural model includes difficulties in areas such as reading, remembering and generating sequences (letters, sounds, and

days of the week), copying and generating oral or written language, characterised by slow speed, spelling errors, syllabification, blending

segmentation and rhyme, confusing between right/left, letter reversals (Frith 1999; Too, 2000; Regan and Woods, 2000; Snowling, 2005). A

dyslexic person may exhibit specific difficulties with number work or difficulty in learning to read; a gap between listening comprehension

and reading comprehension (Too, 2000). That means that dyslexia is a genetic term covering various learning disabilities, which cut across the whole curriculum.

Research in dyslexia can be viewed from different perspectives.

According to Rice and Brooks (2004) there might be either one cause, or more than one cause of dyslexia.

If there is only one cause, it has to be either biological or experiential. However, if there is more than one cause, the causes might be either biological, or experiential, or part biological and part experiential. If there is more than one cause, the causes might take effect separately or in combination.

(Rice and Brooks, 2004, p.19)

Any single level of description, taken in isolation, will provide an incomplete explanation of what might cause the behavioural symptoms

(Frith, 1999). Frith (1999) suggests that the case of dyslexia illustrates a general finding that few condition are caused by a single biological

problem, which affects a single cognitive process and which ends in a set of behavioural symptoms.

According to Frith (1999, p. 211):

Defining dyslexia at a single level of explanation+ biological, cognitive or behavioural+ will always lead to paradoxes. For a full understanding of dyslexia we need to link together the three levels and consider the impact of cultural factors which can aggravate or ameliorate the condition.

The environment (physical, psychological and biological) can impact on all these levels and either exacerbate or temper the severity of condition

as a result (Snowling, 2005).