Neural Correlates of Processing Syntax in Music and ... - PubMan

Specific Language Impairment 83
Biological, genetic and psychosocial risk factors
Biological and genetic influences on SLI are mainly discussed, since more boys than
girls suffer from language impairment and some evidence that SLI is highly heritable
and tends to run in families (Stromswold, 1998, 2001).
Genetic influences on language development and the occurrence of SLI are an issue of
intensive discussion (see, e.g., Bishop, Adams, & Norbury, 2006; S. E. Fisher, Vargha-
Khadem, Watkins, Monaco, & Pembrey, 1998; Gopnik, 1997; Kovas et al., 2005; Meaburn,
Dale, Craig, & Plomin, 2002; Palmour, 1997; SLI Consortium, 2004; Viding et
al., 2004). It was shown, that SLI tends to run in families (Stromswold, 1998) and has a
much higher concordance in monozygotic compared to dizygotic twins (Tomblin &
Buckwalter, 1998).
The search for genetic factors is hampered by the heterogeneity of the deficiencies, i.e.
the absence of a phenotype of this impairment: This is reflected by the lack of replication
(see, e.g., Meaburn et al., 2002; SLI Consortium, 2004) for the finding of the gene
FOXP2 on chromosome 7 responsible for SLI (Lai, Fisher, Hurst, Vargha-Khadem, &
Monaco, 2001) – in this region a point mutation was observed in the affected members
of the KE family and one unrelated person (the pattern of disorders in the KE family has
been extensively studied, as half of them are affected by SLI). In contrast, the SLI consortium
(2002, 2004) localized possible risk factors for SLI on regions on chromosome
16 (SLI1, correlated especially with the non-word-repetition-performance), on chromosome
19 (SLI2, correlated with performance in expressive language). Other studies
found such regions on chromosome 13 (SLI3, see Bartlett et al., 2002), and on chromosome
3 (SSD, related to speech sound disorder, see also Stein et al., 2004). Newbury et
al. (2005) differentiated, relying on this evidence, genetic risk factors for phonological
working memory, and for deficiencies in the development of morphosyntax. They further
describe risk factors in the child’s environment. However, none of these factors is
regarded as an exclusive explanation for SLI (see also Bishop et al., 2006).
Biological risk factors might be the lack of specialization of the two brain hemispheres,
delays in the brain development, and differences in brain anatomy. SLI seems to have
some relation to hemispheric dominance and there is an above-average proportion of
non-right-handed children that suffer from SLI, whose handedness is less pronounced
(Bishop, 2005; Grimm, 2003; Leonard, 1998; Neils & Aram, 1986). Ors et al. (2005)
proposed differences in brain development and lateralization as a risk factor for SLI.
They found a symmetrical instead of the (usual) asymmetrical pattern of cerebral blood
flow. Locke (1997) assumed delayed brain development (resulting from genetic predisposition)
which may cause language impairment – especially, if critical periods are