The Neurobiology of Dyslexia

Alan A. Beaton

It is now almost universally accepted (but see Ehri, 1992) that dyslexia is a constitutional condition, almost certainly genetic, rooted in the biology of the central nervous system. The question is, how do the relevant genes have the effect that they do? To show that a particular gene locus is implicated in, for example, phonological awareness does not explain how the gene (or more probably genes) code for biological mechanisms which underlie this ability. One step towards solving this problem might be to relate relevant gene loci to particular brain structures and mechanisms. Presumably, genetic factors determine in part the relative size or efficiency of regions of the brain involved in language and other processes relevant to reading and its component skills.

Figure 1 shows a diagram of the eyes and brain. Defects at every stage from the retina (Grosser & Spafford, 1989, 1992; Stordy, 2000) through the midbrain to the cerebral cortex and the cerebellum have been said to be involved in dyslexia. Figure 2 shows the main features of the human brain which are referred to in this chapter.

The brain consists of two apparently symmetrical halves or hemispheres. It has an uneven surface made up of ridges, known as convolutions, or gyri, and troughs, known as sulci. There is some individual variability in the pattern of convolutions, but there is also sufficient similarity between different brains for individual gyri and sulci to be identified and named. To the naked eye, there is no

Alan A. Beaton, Senior Lecturer, Department of Psychology, University of Wales, Swansea SA2 8PP, UK.

The Study of Dyslexia, edited by Turner and Rack. Kluwer Academic Publishers. New York, 2004.

Dyslexia People Wales
Primay visual cortex
Visual Receptor Brain
Figure 1. Pathway from the visual receptors in the retina to the brain.

conspicuous difference between the brains of dyslexic and other people although it has been claimed that one kind of gyral pattern is relatively more frequent in dyslexics than controls (Hynd & Hiemenz, 1997). This pattern is also found in non-dyslexics, but the functional significance of small variations in gyral patterning is unknown.

The first published report of a postmortem examination of the brain of a purportedly dyslexic individual concerned a boy named Billy who died suddenly of a brain haemorrhage at approximately 12 years of age. The author of the report

Examination Health Boys

Figure 2. (a) Lateral view of the left hemisphere and (b) dorsal view of the cerebral cortex in humans. The major features of the cortex include the four cortical lobes and various key gyri. Gyri (singular is gyrus) are separated by sulci (singular is sulcus) and result from the folding of the cerebral cortex that occurs during development of the nervous system, to achieve an economy of size.

Figure 2. (a) Lateral view of the left hemisphere and (b) dorsal view of the cerebral cortex in humans. The major features of the cortex include the four cortical lobes and various key gyri. Gyri (singular is gyrus) are separated by sulci (singular is sulcus) and result from the folding of the cerebral cortex that occurs during development of the nervous system, to achieve an economy of size.

(Drake, 1968) wrote: "in the cerebral hemispheres, anomalies were noted in the convolution pattern of the parietal lobes bilaterally. The cortical pattern was disrupted by penetrating deep gyri that appeared disconnected. Related areas of the corpus callosum appeared thin" (p. 496). Billy was said to have marked difficulty with reading and writing, and some difficulty with arithmetic, although by age 12 years 2 months his performance on standard tests suggests that he performed at a more or less satisfactory level in reading and spelling. Other aspects of the report suggest that he would today be classified as showing attention-deficit hyperactivity disorder (ADHD). Billy's medical history included "dizzy spells" and "blackouts" occurring from age 6 as well as recurring left frontal headaches during the 2 years prior to his death. In short, the extent to which Billy could be regarded as a "representative" dyslexic person is unclear.

It has been known for over 100 years that the majority of people speak with only one side of their brain. A stroke affecting the left hand side of the brain (left cerebral hemisphere) may produce devastating effects on language, whereas damage affecting the right hand side (right cerebral hemisphere) may leave language functions relatively intact. The qualification "relatively" is important. It seems that some aspects of language, such as prosody or the appreciation of metaphor or humour, for example, can be impaired by right-sided brain damage.

Damage due to injury, stroke, or other disease (referred to simply as lesions) to two so-called "classical" brain areas produce different effects. Lesions involving the inferior frontal gyrus, or Broca's area, tend to make speech effortful and dysfluent; the patient has difficulty in finding the right word and omits "little" words (prepositions, conjunctions) so that speech takes on the character of a telegram in which only the main words are retained. This is known as Broca's aphasia after the 19th century French neuroanatomist and physician who first linked speech difficulties to damage in the inferior, or third, frontal gyrus of the left hemisphere.

In contrast to Broca's aphasia, damage to the posterior region of the superior temporal gyrus on the left side, Wernicke's area, tends to produce fluent language which may be devoid of meaning, or even gibberish. Patients with this form of aphasia, named after a German neurologist of the late 19th century, have difficulty in understanding what is said to them. Neither of these descriptions should be regarded as providing hard and fast rules—Broca's aphasics may have difficulty in understanding certain kinds of grammatical constructions and Wernicke's aphasics may have word-finding difficulties. Nonetheless, the two classifications are useful approximations and are widely used among neurologists and speech professionals. Nor should it be thought that Broca's and Wernicke's areas are the only two regions of the brain involved in language. Deficits in spoken (or written) language can be produced by lesions in other cortical and sub-cortical areas. Damage to the thalamus, for example, has been linked to particular aphasic symptoms (Crosson, 1985) while damage to the cerebellum is associated with impairments of articulation.

If the fundamental problem of dyslexia is, as has been claimed, in the phonological domain (rather than visual as on the face of it might naively be imagined), then it makes sense to look for differences between dyslexics and controls in language-related areas of the brain.

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