Reading Difficulties 255individual’s overall advantage (irrespective of whether or not additional
neurodevelopmental symptoms are present).
Causation of SRD
SRD is not a uniform condition, though it is not clear if the heterogeneity
is best conceptualised in dimensional or categorical terms. It seems likely
that the aetiology and pathogenesis of SRD are also heterogeneous.
In most cases, phonological problems seem central. These make it much
harder for affected individuals to increase their reading vocabulary by
sounding out new words and thereby familiarising themselves with them.
In a minority of cases, visual perceptual problems may be more important
than language-related problems. Little is known about children who do
well on tests of reading accuracy but poorly on tests of reading compre-
hension, except that they tend to have poor vocabulary and syntactic skills,
and fail to use context clues.
SRD was initially investigated in English-speaking populations. Does
the link between phonological problems and SRD primarily reflect the
notorious unpredictability of English spelling? Surprisingly, phonological
problems are also linked to SRD in phonologically predictable languages
such as Italian and German. For children with SRD who speak these
languages, sounding words out is not so difficult, but automatising this
process is problematic.
Twin and family studies have demonstrated a substantial heritability,
particularly among those with higher IQ. Linkage studies have implicated
the short arm of chromosome 6 – a replicated finding that has led to
the identification of two candidate genes (DCDC2, KIAA0319) whose
mutations may disturb cortical neuronal migration. The psychosocial en-
vironment is also of great importance, as shown, for example, by the fact
that SRD was more than twice as common in inner London than on the
Isle of Wight.
Children and adolescents with neurological conditions such as cerebral
palsy or epilepsy are at much greater risk of SRD than other children
and adolescents with comparable IQs. In children with dyslexia in the
absence of overt neurological disorders, it has been suggested that SRD
arises from developmental anomalies in language-related areas of the left
hemisphere. Neuroanatomical and neuroradiological studies have focused
interest on the planum temporale, a region of the temporal lobe involved
in phonological processing. In individuals who read normally, the planum
temporale is typically larger on the left side of the brain than on the right
side; this asymmetry often seems to be lost in individuals with SRD. The
finding of an excess of strong left-handers and strong right-handers among
children with SRD is intriguing. Annett’s genetic model of handedness sug-
gests that strong left- and right- handers are mainly homozygotes, whereas
mild and moderate right-handers are mainly heterozygotes. Perhaps there
is a heterozygote advantage for reading (analogous to the heterozygote
advantage of the sickle cell trait).