584 Dorothy V.M. Bishop et al. they found signiﬁcant differences at electrode Fz, whereas we saw only a nonsigniﬁcant trend at this site. Despite this group difference, a substantial propor- tion of children with SLI had age-appropriate wave- forms in this time interval. These ﬁndings are similar to those of Tonnquist-Uhlén et al. (1996), who noted that many children with SLI had a normal N1, but neverthe- less the proportion with atypical ﬁndings was higher than in controls. Which children have atypical waveforms? This study conﬁrms suggestions that children with SLI are heterogeneous, with some showing normal auditory ERPs and others differing from controls (Neville et al., 1993; Tonnquist-Uhlén et al., 1996). If atypical wave- forms characterize only a subset of those with SLI, then we will need large samples in order to have sufﬁcient power to detect group differences, yet many studies in this area include 12 or fewer. One way forward is to identify the characteristics of those children with atypi- cal waveforms, in order to reduce heterogeneity in future studies. The only difference that we found between children with typical and atypical waveforms was in terms of subtype of SLI: those with receptive SLI were more likely than controls to have atypical waveforms, whereas this was not the case for children with purely expressive problems. One might expect that the link between atypical auditory ERPs and receptive SLI might be an indicator of abnormal function of auditory cortex leading to poor speech discrimination; however, like McArthur and Bishop (2005), but in contrast to Neville et al. (1993), we did not ﬁnd that abnormal performance on auditory tasks characterized those children who had atypical waveforms. However, it must be noted that the auditory assessments used with this sample were fairly limited. More studies are needed to clarify the functional signiﬁc- ance for auditory and language processing of having an atypical auditory ERP. As argued below, it is possible that the atypical ERPs reﬂect unusual patterns of under- lying brain morphology. If so, these may be correlated with SLI without having any signiﬁcance for auditory discrimination skills. What does an atypical waveform signify? The ICC analysis, coupled with overall scrutiny of the brain maps, suggests that there is atypical lateralization of brain responses to sounds in some children with SLI. The laterality effect (lower ICCs in SLI on the right but not the left fronto-central regions) is consistent with © 2007 The Authors. Journal compilation © 2007 Blackwell Publishing Ltd. several other studies that have reported anomalous cerebral lateralization in some cases of SLI using mea- sures of brain structure (Gauger, Lombardino & Leon- ard, 1997; De Fossé, Hodge, Makris, Kennedy, Caviness, McGrath, Steele, Ziegler, Herbert, Frazier, Tager- Flusberg & Harris, 2004; Herbert, Ziegler, Deutsch, O’Brien, Kennedy, Filipek, Bakardjiev, Hodgson, Takeoka, Makris & Caviness, 2005) or function (Mason & Mellor, 1984; Dawson, Finley, Phillips & Lewy, 1989; Chiron, Pinton, Masure, Duvelleroy-Hommet, Leon & Billard, 1999; Shafer, Schwartz, Morr, Kessler & Kurtz- berg, 2000). Atypical lateralization of ERPs has also been reported in infants who have a family risk for SLI (Benasich, Choudhury, Friedman, Realpe-Bonilla, Chojnowska & Gou, 2006). Also, unusually large, posi- tive, right-hemisphere responses to /ga/ were found in infants who subsequently turned out to have poor recep- tive language (Guttorm, Leppänen, Poikkeus, Eklund, Lyytinen & Lyytinen, 2005). There are three broad classes of explanation for such an effect. The ﬁrst, which we may term the ‘atypical brain’ hypothesis, maintains that the brain is not optim- ally wired up for language learning. According to this view, brain organization in some children with SLI is qualitatively different from that in typical development, presumably because of genetic inﬂuences on prenatal brain development. An alternative ‘epigenetic’ hypo- thesis maintains that brain differences between children with SLI and controls are not a cause but a consequence of the language disorder: if verbal signals are not meaning- ful to the child, then these may be tuned out, and brain networks for processing language may show aberrant development. Circumstantial evidence against this expla- nation comes from our ﬁndings that (a) only a subset of cases with receptive SLI have atypical ERPs and (b) abnormal auditory ERPs are seen in response to nonverbal as well as verbal sounds. A ﬁnal ‘maturational lag’ hypothesis maintains that electrophysiological dif- ferences in auditory responses of children with SLI vs. controls are indicators of neurodevelopmental imma- turity, rather than any stable differences in underlying brain structure. For instance, we know that the cerebral commissures continue to myelinate throughout child- hood (Giedd, Rumsey, Castellanos, Rajapakse, Kaysen, Vaituzis, Vauss, Hamburger & Rapoport, 1996). It is possible that the differences in lateralization between receptive SLI and typically developing children reﬂect some delay in maturation of interhemispheric trans- mission: this kind of explanation has been proposed for learning disabilities, though it is highly speculative (Njiokiktjien, de Sonneville & Vaal, 1994; Von Plessen, Lundervold, Duta, Heiervang, Klauschen, Smievoll, Ersland & Hugdahl, 2002). Bishop and McArthur