Biological theories of dyslexia

Dyslexia was first identified by Oswald Berkhan in 1881, the term 'dyslexia' was later coined in 1887 by Rudolf Berlin , an ophthalmologist practicing in Stuttgart, Germany. Since then generations of researchers have been investigating what Dyslexia is, and tring to identify the biological causes.(See History section of the Dyslexia Article. The Theories of Dyslexia have and are evolving with each new generation of Dyslexia Researchers, and the more recent theories of Dyslexia tend to enhance one or more of the older theories as our understanding of the nature Dyslexia evolves.

Theories of Developmental Dyslexia

The following theories should not be viewed as competing, but viewed as theories trying to explain the underlying causes of a similar set of symptoms from a variety of research perspectives and background.

• Evolutionary hypothesis

This theory posits that reading is an unnatural act, and carried out by humans for an exceedingly brief period in our evolutionary history (Dalby, 1986). It has been less than a hundred years that most western societies promoted reading by the mass population and therefore the forces that shape our behavior have been weak. Many areas of the world still do not have access to reading for the majority of the population. There is no evidence that "pathology" underlies dyslexia but much evidence for cerebral variation or differences. It is these essential differences that are taxed with the artificial task of reading.

• Phonological Deficit Theory

The phonological deficit theory postulates that people with dyslexia have a specific impairment in the representation, storage and/or retrieval of speech sounds. It explains the reading impairment of people with dyslexia on the basis that learning to read an alphabetic system requires learning the grapheme/phoneme correspondence, i.e. the correspondence between letters and constituent sounds of speech. If these sounds are poorly represented, stored or retrieved, the learning of grapheme/phoneme correspondences, the foundation of reading by phonic methods for alphabetic systems, will be affected accordingly.

Children with phonological dyslexia seem to have a general deficiency in representing and processing speech stimuli.

• Rapid auditory processing theory

The rapid auditory processing theory is an alternative to the phonological deficit theory, which specifies that the primary deficit lies in the perception of short or rapidly varying sounds. Support for this theory arises from evidence that people with dyslexia show poor performance on a number of auditory tasks, including frequency discrimination and temporal order judgment. Backward masking tasks, in particular, demonstrate a 100-fold (40 dB) difference in sensitivity between people with and without dyslexia. Abnormal neurophysiological responses to various auditory stimuli have also been demonstrated. The failure to correctly represent short sounds and fast transitions would cause further difficulties in particular when such acoustic events are the cues to phonemic contrasts, as in /ba/ versus /da/. There is also evidence that people with dyslexia may have poorer categorical perception of certain contrasts.

• Visual Theory

The visual theory (Lovegrove et al., 1980 ; Livingstone et al., 1991; John Stein and Walsh, 1997 ) reflects another long standing tradition in the study of dyslexia, that of considering it as a visual impairment giving rise to difficulties with the processing of letters and words on a page of text. This may take the form of unstable binocular fixations, poor vergence, or increased visual crowding. The visual theory does not exclude a phonological deficit, but emphasizes a visual contribution to reading problems, at least in some dyslexic individuals. At the biological level, the proposed etiology of the visual dysfunction is based on the division of the visual system into two distinct pathways that have different roles and properties: the magnocellular and parvocellular pathways. The theory postulates that the magnocellular pathway is selectively disrupted in certain dyslexic individuals, leading to deficiencies in visual processing, and, via the posterior parietal cortex, to abnormal binocular control and visuospatial attention. Evidence for magnocellular dysfunction comes from anatomical studies showing abnormalities of the magnocellular layers of the lateral geniculate nucleus (Livingstone et al., 1991 ), psychophysical studies showing decreased sensitivity in the magnocellular range, i.e. low spatial frequencies and high temporal frequencies in people with dyslexia, and brain imaging studies.

• Cerebellar Theory

Yet another view is represented by the automaticity/cerebellar theory of dyslexia. Here the biological claim is that the cerebellum of people with dyslexia is mildly dysfunctional and that a number of cognitive difficulties ensue. First, the cerebellum plays a role in motor control and therefore in speech articulation. It is postulated that retarded or dysfunctional articulation would lead to deficient phonological representations. Secondly, the cerebellum plays a role in the automatization of overlearned tasks, such as driving, typing and reading. A weak capacity to automatize would affect, among other things, the learning of grapheme-to-phoneme correspondences. Support for the cerebellar theory comes from evidence of poor performance of people with dyslexia in a large number of motor tasks, in dual tasks demonstrating impaired automatization of balance, and in time estimation, a non-motor cerebellar task. Brain imaging studies have also shown anatomical, metabolic and activation differences in the cerebellum of people with dyslexia.

• Magnocellular Theory

There is a unifying theory that attempts to integrate all the findings mentioned above. A generalization of the visual theory, the magnocellular theory postulates that the magnocellular dysfunction is not restricted to the visual pathways but is generalized to all modalities (visual and auditory as well as tactile). Furthermore, as the cerebellum receives massive input from various magnocellular systems in the brain, it is also predicted to be affected by the general magnocellular defect (John Stein et al., 2001). Through a single biological cause, this theory therefore manages to account for all known manifestations of dyslexia: visual, auditory, tactile, motor and, consequently, phonological. Beyond the evidence pertaining to each of the theories described previously, evidence specifically relevant to the magnocellular theory includes magnocellular abnormalities in the medial as well as the lateral geniculate nucleus of the brains of people with dyslexia, poor performance of people with dyslexia in the tactile domain, and the co-occurrence of visual and auditory problems in certain people with dyslexia.

• Perceptual visual-noise exclusion hypothesis

The concept of a perceptual noise exclusion (Visual-Noise) deficit is an emerging hypothesis, supported by research showing that subjects with dyslexia experience difficulty in performing visual tasks such as motion detection in the presence of perceptual distractions, but do not show the same impairment when the distracting factors are removed in an experimental setting. The researchers have analogized their findings concerning visual discrimination tasks to findings in other research related to auditory discrimination tasks. They assert that dyslexic symptoms arise because of an impaired ability to filter out both visual and auditory distractions, and to categorize information so as to distinguish the important sensory data from the irrelevant.

Theories of Alexia (Acquired Dyslexia)

There are three key types of acquired dyslexia with different patterns of deficits: surface dyslexia, phonological dyslexia, and deep dyslexia.