What Causes Dyslexia
A significant percentage of school-age children fail to learn to read in spite of normal intelligence, adequate environment and educational opportunities.

The deficit thus defined, is usually considered of constitutional origin, but its actual mechanisms are still being gradually understood and currently remain the subject of researchers endeavors’ in various neuroscientific areas and along several theoretical frameworks.

Accumulated evidence favours the theory of a dysfunction of neural systems known to participate in the normal acquisition and achievement of reading and other related cognitive functions.

Neuropathological studies of brains from dyslexic individuals have drawn attention towards a possible abnormality in specific stages of prenatal maturation of the cerebral cortex and suggested a role of atypical development of brain asymmetries.

These studies have confirmed some subtle differences in brain anatomy - and neuropsychological studies have provided considerable evidence that one of the primary mechanisms leading to these children's learning difficulties is phonological in nature, namely a basic defect in segmenting and manipulating the phoneme constituents of speech.

Impairment in brain visual mechanisms of reading as a possible contributing factor are also postulated and this approach has led to an important conceptual advance with the suggestion of a specific involvement of one subsystem of vision pathways.

Both the phonological and the visual hypotheses have received valuable contribution from modern functional imaging techniques with a sensible interpretation of available evidence pointing to dyslexia as a multi-system deficit possibly based on a fundamental incapacity of the brain in performing tasks requiring processing of brief stimuli in rapid temporal succession.

Temporal processing impairment as a theory of dyslexia could also account for at least some of the perceptual, motor and cognitive symptoms very often associated with the learning disorder.

Over time dyslexia has become a fertile ground for transdisciplinary studies and a model for elucidating biological, educational and socio-cultural factors of brain and cognition interactions and development.

The first near accurate description of the issue related to dyslexia was researched from the brain of a dyslexic boy who had demonstrated evidence of difficulties learning to read in his schooling years. This child also had a family history of migraine and learning disorders and this was especially the case in his only brother. Pathological examination of his brain showed a series of brain malformations principally in the cortical gyri of the left inferior parietal region, including ectopias in the outer (molecular) cortical layer. This pattern of cortical abnormalities, which was suggestive of defective brain maturation, is now central to the description given in more recent studies and to pathophysiological hypotheses which have been proposed since then.

To summarize - two main observations should be understood when we consider the details of the brain studies. First, at the microscopic level, a meticulous analysis of serial coronal slices compared with a similar analysis of non-dyslexic brains discloses specific cortical malformations including ectopias (small neuronal congregations in an abnormal superficial layer location), mainly distributed across both frontal regions and in the left language areas; loss of characteristic architectural organization of the cortical neurons, mainly subjacent to the site of ectopias; and more rarely, vascular micro-malformations. The main lesson drawn from these microscopic observations is that all the brains studied differed from control brains in a way that suggested abnormal cortical development. Since neuronal migration is thought to take place during the sixth gestational month, the mechanism leading to these cortical lesions was presumed to occur before or during this period of the foetal brain development. Finally, in addition to these neuronal abnormalities, the female brains showed glial scars in the border zones between the arterial territories, suggesting a vascular mechanism, supposedly of immune origin.

Additionally it has been noticed in studies that most of the dyslexic brains display a macroscopic peculiarity, namely an absence of the usual left > right asymmetry of the planum temporale. Since this asymmetry is believed to parallel the functional linguistic preponderance of the left hemisphere, and by reference to the above-mentioned evidence of incomplete lateralization in dyslexics, this region deserves greater understanding in time to come. Although the developmental mechanisms leading to such atypical symmetry still remain a subject of debate, these findings, combined with the above-mentioned microscopic features, have been generally considered good evidence of maturational deviance being at the origin of the learning difficulties of dyslexics.

(This poor or inadequate brain lateralization, especially for language may suggest that the lateralization of language functions to the left hemisphere may be delayed in dyslexics, so that the language prerequisites for learning to read could not develop normally -- For instance, the high incidence of left-handers and the mirror-writing phenomenon can be considered as evidence for abnormal lateralization in these children.)

Dyslexia may be expressed as a specific and significant impairment in the reading ability of a child which is unexplainable by any kind of deficit in general intelligence, learning opportunity, general motivation or sensory acuity.

Children with this condition often have associated deficits in related domains such as oral language acquisition writing abilities, mathematical abilities, motor coordination, postural stability and dexterity, temporal orientation, visuospatial abilities, and attentional abilities. In fact if parents have been noticing any of these issues even at a level they would categorize as minor, the fact is that the condition is serious enough for them to sit up and take notice. Deficits noticed do not vanish over time, and neither do children outgrow their problems.

Besides their multiple possible interrelations and associations, all these developmental syndromes listed above share in common their relative `specificity', i.e. the fact that general intelligence is intact, as reflected in a normal or above normal non-verbal IQ.

Such comorbidity may also suggest a common origin involving either genetic factors or prenatal environmental influences, or both with children who fail to achieve normal reading performances making the same type of errors: visual confusions between morphologically similar letters, especially those having a symmetrical counterpart (such as b and d), difficulty in acquiring global logographic strategies which would allow them to recognize common words presented briefly, and difficulty in generalizing previously learned grapheme to phoneme rules (especially for complex letter clusters). This latter aspect appears as the core dysfunction in dyslexia.

Due to the multitude of possible combinations of the basic dysfunctions, a rational remedial approach usually involves specific and specialized intervention, which may take months or (more often) years of remedial effort. Eventually reading becomes possible, although often clumsy and effortful, sometimes with persisting errors, especially with irregular or exceptional words, as well as in the area of comprehension. Even with intensive intervention we notice that spelling impairment normally persists as the permanent hallmark of the developmental disorder - and stands as a valuable indicator for retrospective diagnosis of dyslexia in adults.

Current research in the field of dyslexia and related disorders is indicating that there is a fundamental linkage to a constitutional characteristic of the brain. Evidence for a genetic origin of dyslexia has been increasingly accumulating during the last few years. For present purposes we can say that dyslexia is very probably of genetic origin, since it occurs most often in families. However, genetic transmission is probably complex and non-exclusive. In particular, it is conceivable that different forms of dyslexia may occur within the same family, whereas different genes have been implicated in different aspects of the reading disorders.

From a neurological point of view, the large prevalence of oral or written language deficits among learning disordered children suggests a special vulnerability of the left hemisphere cortical systems subserving various aspects of language-related abilities to aetiological factors.

In spite of contradictory evidence - there is currently a consensus towards the conception of a complex link between several traits including non-right-handedness’, immune diseases, sex hormones and verbal learning disorders, but the nature of this link, although probably genetic, remains totally speculative.

One intriguing finding in current research is the suggestion that in addition to interhemispheric asymmetry, it would be interesting to consider intrahemispheric asymmetries, i.e. the relative importance, within each hemisphere, of the temporal and parietal banks of the posterior sylvian fissure.

In fact it has been demonstrated that intensive training in the modality that neuroplasticity intervention (See T.R.A.I.N™) uses can modify the degree of asymmetry in the posterior auditory region. This finding is in line with neuroplasticity studies in animals, showing that direct training notably alters the sensory neural maps at the neuronal level.

Besides theories pointing to defective brain lateralization, another frequently proposed potential mechanism is abnormal collaboration and/or communication between the hemispheres. This hypothesis relies on well-documented evidence of impaired interhemispheric transfer of sensory or motor information in dyslexics.

Besides the neuroanatomical aspect given above research is currently in progress from different perspectives in order to elucidate how the dyslexic brain functions or malfunctions.

Neuroscientific research has explored three main pathways during the past decade: the phonological, the visual and the temporal. These are represented in the inability to manipulate in an abstract form the sound constituents of oral language, making errors that follow visual rather than strictly phonetic laws, e.g. confusions between symmetrical (b/d) or visually close (m/n) letters and problems with the phonetic distance and not the pure temporal order difficulty which is reflected in a dyslexic child's poor performance in temporal order judgment tasks.

(Neurological accounts of dyslexia usually ascribe at least some of the symptoms observed to a left-hemisphere dysfunction. That the left hemisphere is a good candidate for subserving the role of rapid processing of brief stimuli is also widely admitted. In addition, older adults who often report difficulty-understanding speech despite normal hearing, exhibit a temporal sequencing decrement. There is, thus, converging evidence to suspect that the left hemisphere is specifically pre-wired to support the function of processing transient sensory events, especially when these events become meaningful through their temporo-spectral characteristics.)

There are numerous circumstances where dyslexic children seem to have trouble with various aspects of temporal processing, well beyond the sole sensory motor level. It is very common to find severe delays in time duration awareness, sequential naming problems for concepts pertaining to time (such as the days of a week), errors in time relocation of memories, and vagueness of temporal distance or remoteness appreciation. It is not rare to see a parent of a dyslexic child, who was formerly dyslexic, admitting his or her own persisting problems occasionally emerging when confronted by situations where time constraints have to be handled.

From a neurobiological point of view, one may speculate that the dyslexic brain, perhaps due to abnormal maturational neuronal migration and assembly and/or connectivity, especially in the left-hemisphere language areas, is normally unable to hold any kind of functions requiring temporal simultaneity and/or coordination between even remote neuronal zones. Synchrony of activity between groups of neurons is viewed as one of the fundamental features of electrical activity of the brain. Furthermore, it is possible that the same general brain property is also responsible for processing all kinds of brain signals whose significance relies on their temporal characteristics. Moreover, such temporal coordination of activity in different, even remote, cortical regions probably requires control from one or more `pacemaker' structures, able to homogenize spontaneous or evoked activity in groups of neurons normally functioning in concert. Anatomically, the cerebellum appears as one of the best candidates to carry out this task, since spontaneous rhythmic activity and remote propagation of this activity has been clearly demonstrated there. Recent evidence of reduced cerebellar activity in dyslexics performing a motor learning task provides an interesting basis for further testing of this hypothesis in normal readers and dyslexics.

Dyslexic individuals also have been known to show subtle impairments in naming pictures of objects in addition to their difficulties with reading – which is leading us to question that can word reading and picture naming deficits in children with dyslexia be reduced to a common neurological impairment that may explain what is happening in the brains of such children.

Children with dyslexia who have been studied in detail have been known to demonstrate a reduced activation in a left occipitotemporal area during both word reading and picture naming tasks. Abnormal activation in this region may reflect a more general impairment in integrating phonology and visual information. These may point to a common neurological basis for deficits in word reading and picture naming in developmental dyslexia.

As an example it has been proposed that the cognitive processes engaged when reading a word overlap considerably with those engaged when a dyslexic child tries to name a known object. In both instances children perceive and identify a visual stimulus and retrieve its associated lexical form, which is then output during articulation. It is also well established that picture naming provides a means to index literacy skill. Naming performance in kindergarten, for example, represents a powerful predictor of later reading ability. It is therefore not surprising that dyslexic children show early impairments on tasks of picture naming in addition to their difficulties with reading. For example, if a child is dyslexic she will present with impairments on tasks of rapid automatic naming, in which a series of pictures are named sequentially. The cognitive complexity of this task precludes a straightforward explanation of this impairment – but in contrast, the same child’s impairments in confrontation naming, in which individual pictures are named discretely, can generally be thought to be attributable to a phonological impairment

During both reading and naming, children from their brains retrieve a stored code and this code is likely to consist of certain segments that are activated and assembled into a sequence that controls production of output. When a child is non-impaired, these tasks of letter, colour and picture naming have been shown to implicate a common neural system incorporating the left posterior inferior temporal lobe and the left frontal operculum. Typically, frontal regions are associated with later stages of retrieval, including articulation while posterior areas are activated during earlier stages of phonological retrieval. When a child is wired perfectly or near perfectly, all systems are a go and glide smoothly, however when a child is impaired, activity levels in all three regions of the brain that are responsible for processing are much lower. The resulting output on both platforms can help a parent understand and a professional make predictions that are relevant to the diagnosis and treatment of the problem of dyslexia.