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.