neuroimaging studies. For instance, in studies using structural MRI, Jernigan, Hesselink, Sowell and Tallal (1991) and Leonard, Lombardino, Walsh, Eckert, Mockler, Rowe, Williams and DeBose (2002) reported that SLI was associated with small cerebral volume, but Herbert et al. (Herbert, Ziegler, Makris, Bakardjiev, Hodgson, Adrien, Kennedy, Filipek & Caviness, 2003) found just the opposite. Abnormalities of gyral development in frontal and temporal cortical regions are rather more common in people with SLI than in unaffected individuals, but the relationship is weak and probabilistic (Plante & Jackson, 1997; Clark & Plante, 1998). Such ﬁndings suggest that we need to use methods that allow us to identify neurobiological abnormalities at the level of the individual, rather than averaging results across a group. One line of evidence comes from electrophysiological studies of auditory event-related potentials (ERPs). With ERPs we can obtain an index of the brain’s responses to auditory stimuli in real time while minim- izing performance demands on the child. To date, there have been a handful of studies looking at passively elicited auditory ERPs in children with SLI vs. controls, but analysis has largely focused on com- paring mean amplitudes and latencies of ERP peaks at the group level. The P1, N1 and P2 peaks have been a particular focus of interest, because they provide a window on the earliest stages of processing in auditory cortex: if it were possible to demonstrate abnormal brain responses at this level, this would provide evidence against the view that perceptual abnormalities in SLI are conﬁned to linguistically relevant stimuli (e.g. Nittrouer, 2002). Results, however, have been inconsistent. Mason and Mellor (1984), using a slow presentation rate (2000 ms stimulus onset asynchrony; SOA) found no abnormalities of N1 and P2 latency or amplitude at cen- tral or temporal sites in eight children with SLI, when compared with 12 controls, although there was some suggestion of atypical lateralization of responses in tem- poral regions in the children with SLI. The sample was not very well speciﬁed, with few details of language and cognitive test results. Other studies that found no differ- ences in amplitude or latency of N1 and P2 when com- paring children with SLI and controls include Lincoln, Courchesne, Harms and Allen (1995) (electrode Cz with SOA of 2000 ms) and Marler, Champlin and Gillam (2002) (electrodes C3, Cz and C4, with SOA of 500 or 1000 ms). These studies contrast with results from Korpilahti and Lang (1994) and Tonnquist-Uhlén and colleagues (Tonnquist-Uhlén, 1996a, 1996b; Tonnquist- Uhlén, Borg, Persson & Spens, 1996). Korpilahti and Lang (1994) were not able to compare N1 and P2 in their sample of 14 children with SLI and 12 controls because they used a rapid presentation rate (SOA 450 ms) © 2007 The Authors. Journal compilation © 2007 Blackwell Publishing Ltd. Atypical auditory ERPs in SLI 577 and these peaks were often not present, but they did report a signiﬁcant delay in the latency of N2 in those with SLI. However, the control group was apparently not given any psychological tests, and thus was not matched to the SLI group on nonverbal ability. Tonnquist-Uhlén and colleagues (Tonnquist-Uhlén, 1996a, 1996b; Tonnquist-Uhlén et al., 1996) examined N1, P2, N2 and the T-complex, for a 500 Hz tone pre- sented with SOA of 900 ms. They used topographic analyses as well as measures of peak amplitude and latency. Unfortunately, the psychological description of their sample is sketchy, and so it is not possible to estab- lish whether the control group was matched, or indeed assessed for language and cognitive function. Nor can one tell how severe the language disorders were, nor whether all children scored within normal limits on performance IQ; it is more appropriate therefore to refer to these as children with language impairment (LI) rather than SLI. Nine of the 20 participants with LI were judged to have pathological EEGs (Bø, Marklund, Hamsten, Persson & Tonnquist-Uhlén, 1992). Tonnquist- Uhlén et al. (1996; Tonnquist-Uhlén, 1996a) noted that the overall topography of N1 and P2 was generally similar in LI and control groups, but both peaks were signiﬁcantly later in those with LI compared to 20 con- trols, this effect being seen for N1 only after right-ear stimulation. In addition, topographic maps were com- pared to a control grand average for the time window corresponding to N1, and a higher rate of deviant topo- graphy was seen in the LI group. Overall, it was con- cluded that when information on N1 latency, amplitude and topography were combined, the majority of those with abnormal results were in the LI group. Neverthe- less, many of the LI children had waveforms comparable to those seen in controls. An intriguing feature of these data was that the latency of N1 decreased with age (from 9 to 15 years) in the control group, but not in the LI group, and inspection of the scatterplots indicates that this is because the N1 latencies of the older LI children (aged 13 to 16 years) were more similar to those of younger control children than to their own age group. The authors suggested that this could indicate a persistent abnor- mality or a delay in maturation. Delayed maturation was also suggested as an explanation of ﬁndings by Jirsa and Clontz (1990), who studied a group of children who had language impairments accompanied by poor scores on a central auditory processing test battery. Unlike the other studies reviewed here, they adopted an active paradigm, with ERPs recorded as children pressed a button when detecting a deviant tone. They found that 12/18 children in the clinical group had N1 latencies more than 2 SE from a control mean, and 8/18 had equivalent delays in P2. No controls had abnormal N1