01 NRDC Dyslexia 1-88 update - Texthelp
01 NRDC Dyslexia 1-88 update - Texthelp 01 NRDC Dyslexia 1-88 update - Texthelp
26 Research Report The causes of these outgrowths and infoldings have yet to be determined. Their origin does not appear to be directly genetic (Galaburda et al., 2001). Possible environmental causes include the adverse effects of testosterone upon fetal neuronal development (Geschwind & Galaburda, 1985), viral inflammation from influenza (Livingston et al., 1993) and toxic substances such as lead or alcohol (Hynd & Semrud-Clikeman, 1989). Although it is possible that individual differences in susceptibility to environmental hazards could be heritable and although some developmental abnormalities are heritable in the form of genetic mutations or chromosomal defects (Baraitser, 1997; McKusick, 1994; Weatherall, 1991), there is no need to assume that every developmental abnormality is heritable. Ectopias and microgyria develop before birth, at a late stage of neuronal migration (Galaburda et al., 2001). They are associated with higher degrees of connectivity, both within their own cerebral hemisphere and between the two hemispheres (Galaburda et al., 1989). The effect that these microscopic abnormalities have upon human cognitive functioning must be inferred from laboratory experiments with rats and mice, where there is evidence that they impair both auditory processing (Galaburda et al., 2001; Peiffer et al., 2002) and the normal balance of arousal and inhibition (Gabel & Turco, 2002; Redecker et al., 1998). Cerebral asymmetries have an ancient ancestry in primate evolution (Steele, 1998). Perhaps for this reason, they may be related more closely to handedness than to language lateralisation (Annett, 1985; Corballis, in press; McManus, 1999). In the course of individual human development, planar asymmetries (differences between the brain hemispheres in the planum temporale) are established before birth (Wada et al., 1975). While the extent to which asymmetries are influenced by heredity and environment is unclear (Eckert et al., 2002), it is plausible that genes are the major cause of asymmetric neural tissue development (McManus, 1999). However, there is no uniform pattern of asymmetry. In the general population, about three in four people have left-greater-than-right asymmetry, whereas about one in 12 have no detectable asymmetry and about one in eight have right-greater-than-left asymmetry (Shapleske et al., 1999). Language functions may not always be lateralised in the cerebral hemisphere with the larger planum temporale (Moffatt et al., 1998). The degree of planar asymmetry appears to be reflected in individual differences between verbal and nonverbal ability (Riccio & Hynd, 2000), in which case it could represent normal variation rather than a pathological state. However, a reduction in planar asymmetry has been found in schizophrenics (Saugstad, 1999), where it is associated with disordered language but not with difficulty in learning to read. The significance of abnormalities in the magnocellular system is particularly difficult to determine in relation to dyslexia. For a more detailed consideration of the evidence, readers are referred to the later section on dyslexia and processing speed. However, some words of caution are appropriate. Although evidence from the post-mortem studies could be interpreted to support distinctions both between dyslexics and ‘normal’ readers and also between dyslexics and ordinary poor readers, there are three reasons why this interpretation is tenuous. First, the post-mortem research involves few brains. The numbers vary from one study to another, but studies typically involve between three and seven brains. From small samples like these, the findings are at best suggestive rather than definitive.
Developmental dyslexia in adults: a research review 27 Second, it is unclear whether the brains in the post-mortem studies are representative of dyslexic brains in general (Beaton, 2002). Even if that were the case, it would be unsafe to assume that the abnormalities in those brains are specific to dyslexia, because the full nature and extent of the cognitive and behavioural problems experienced by their donors was not identified before they died (Bishop, 2002). The specificity of the post-mortem brain abnormalities is questionable with respect to planum temporale symmetry, since it is possible that dyslexia (defined as a phonologically-based reading disability) might be associated with asymmetrical brain structures, whereas symmetrical brain structures might be associated with the linguistic deficit known as Specific Language Impairment (Leonard et al., 1998). Third, the evidence from brain imaging studies offers no support for the notion that there is a causal relationship between dyslexia and an absence of left-greater-than-right asymmetry of the planum temporale: one non-dyslexic brain in three shows similar symmetry or reversed asymmetry; some researchers find abnormally large right plana, while others find abnormally small left plana; patterns of symmetry or asymmetry vary from study to study; and it has not been established that deviations from normal asymmetry are exclusive to dyslexia (Beaton, 2002; Cossu, 1999; Habib, 2000; Heiervang et al., 2000; Robichon et al., 2000b; Rumsey et al., 1997a; Shapleske et al., 1999). Whether ‘dyslexic’ brains differ in structure from ‘normal’ brains is not a question that can be determined on the evidence of the post-mortem research. While there are undoubted abnormalities in the autopsied brains, their relationship to dyslexia is open to question. Although the post-mortem findings have suggested interesting new lines of investigation, lack of convergence with findings from more recent in vivo studies is an obstacle to their acceptance. Evidence from in vivo studies: structural differences Although no consistent morphological correlates have been associated with developmental dyslexia in children or in adults (Cossu, 1999), there is broad agreement about the main regions of interest. Thus, in vivo studies of ‘dyslexic’ and ‘normal’ brains examine two kinds of structural anomaly. They consider both the patterns of symmetry in the temporal lobes and the cerebellum and also the connectivity between left and right cerebral hemispheres. At the time of writing, magnetic resonance imaging (MRI), the technique employed for this purpose, cannot be used to resolve details as fine as the microscopic abnormalities reported in the post-mortem studies. The question of symmetry in the temporal lobes has typically focused on the planum temporale, which is considered above. Additionally, dyslexia appears to be associated with lack of normal asymmetry in the cerebellum, which may also be associated with mixed handedness in ways that have yet to be explained (Rae et al., 2002). Connectivity between the two sides of the brain is a function of the corpus callosum, the mass of white-matter fibres that connects the brain’s two hemispheres. The issue of the link between anatomical observations and clinical abnormalities in the corpus callosum remains fundamentally unresolved (Habib & Robichon, 2002). Atypical development of the corpus callosum may be characteristic of dyslexics (Hynd et al., 1995; Rumsey et al., 1996; von Plessen et al., 2002), although the evidence is conflicting (Habib et al., 2000a). While it is possible for qualitative differences in corpus callosum morphology to have biological origins (Robichon et al., 2000a), it is also possible that they could be caused by atypical experience
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Developmental dyslexia in adults: a research review 27<br />
Second, it is unclear whether the brains in the post-mortem studies are representative of<br />
dyslexic brains in general (Beaton, 2002). Even if that were the case, it would be unsafe to<br />
assume that the abnormalities in those brains are specific to dyslexia, because the full nature<br />
and extent of the cognitive and behavioural problems experienced by their donors was not<br />
identified before they died (Bishop, 2002). The specificity of the post-mortem brain<br />
abnormalities is questionable with respect to planum temporale symmetry, since it is<br />
possible that dyslexia (defined as a phonologically-based reading disability) might be<br />
associated with asymmetrical brain structures, whereas symmetrical brain structures might<br />
be associated with the linguistic deficit known as Specific Language Impairment (Leonard et<br />
al., 1998).<br />
Third, the evidence from brain imaging studies offers no support for the notion that there is a<br />
causal relationship between dyslexia and an absence of left-greater-than-right asymmetry of<br />
the planum temporale: one non-dyslexic brain in three shows similar symmetry or reversed<br />
asymmetry; some researchers find abnormally large right plana, while others find abnormally<br />
small left plana; patterns of symmetry or asymmetry vary from study to study; and it has not<br />
been established that deviations from normal asymmetry are exclusive to dyslexia (Beaton,<br />
2002; Cossu, 1999; Habib, 2000; Heiervang et al., 2000; Robichon et al., 2000b; Rumsey et al.,<br />
1997a; Shapleske et al., 1999).<br />
Whether ‘dyslexic’ brains differ in structure from ‘normal’ brains is not a question that can be<br />
determined on the evidence of the post-mortem research. While there are undoubted<br />
abnormalities in the autopsied brains, their relationship to dyslexia is open to question.<br />
Although the post-mortem findings have suggested interesting new lines of investigation, lack<br />
of convergence with findings from more recent in vivo studies is an obstacle to their<br />
acceptance.<br />
Evidence from in vivo studies: structural differences<br />
Although no consistent morphological correlates have been associated with developmental<br />
dyslexia in children or in adults (Cossu, 1999), there is broad agreement about the main<br />
regions of interest. Thus, in vivo studies of ‘dyslexic’ and ‘normal’ brains examine two kinds of<br />
structural anomaly. They consider both the patterns of symmetry in the temporal lobes and<br />
the cerebellum and also the connectivity between left and right cerebral hemispheres. At the<br />
time of writing, magnetic resonance imaging (MRI), the technique employed for this purpose,<br />
cannot be used to resolve details as fine as the microscopic abnormalities reported in the<br />
post-mortem studies.<br />
The question of symmetry in the temporal lobes has typically focused on the planum<br />
temporale, which is considered above. Additionally, dyslexia appears to be associated with<br />
lack of normal asymmetry in the cerebellum, which may also be associated with mixed<br />
handedness in ways that have yet to be explained (Rae et al., 2002).<br />
Connectivity between the two sides of the brain is a function of the corpus callosum, the mass<br />
of white-matter fibres that connects the brain’s two hemispheres. The issue of the link<br />
between anatomical observations and clinical abnormalities in the corpus callosum remains<br />
fundamentally unresolved (Habib & Robichon, 2002). Atypical development of the corpus<br />
callosum may be characteristic of dyslexics (Hynd et al., 1995; Rumsey et al., 1996; von<br />
Plessen et al., 2002), although the evidence is conflicting (Habib et al., 2000a). While it is<br />
possible for qualitative differences in corpus callosum morphology to have biological origins<br />
(Robichon et al., 2000a), it is also possible that they could be caused by atypical experience