The Neurobiology of Sensory and Language Processing in Language-Impaired Children

Abstract

Clinical, behavioral, and neurophysiological studies of developmental language impairment (LI), including reading disability (RD), have variously emphasized different factors that may contribute to this disorder. These include abnormal sensory processing within both the auditory and visual modalities and deficits in linguistic skills and in general cognitive abilities. In this study we employed the event-related brain potential (ERP) technique in a series of studies to probe and compare Merent aspects of functioning within the same sample of LI/RD children. Within the group multiple aspects of processing were affected, but heterogeneously across the sample. ERP components linked to processing within the superior temporal gyrus were abnormal in a subset of children that displayed abnormal performance on an auditory temporal discrimination task. An early component of the visual ERP was reduced in amplitude in the group as a whole. The relevance of this effect to current conceptions of substreams within the visual system is discussed. During a sentence processing task abnormal hemispheric specialization was observed in a subset of children who scored poorly on tests of grammar. By contrast the group as a whole displayed abnormally large responses to words requiring contextual integration. The results imply that multiple factors can contribute to the profile of language impairment and that different and specific deficits occur heterogeneously across populations of LI/RD children.

Neural plasticity following auditory training in children with learning problems

“…Second, increased neural synchrony, which has been linked to perceptual learning (Merzenich et al, 1999), can be demonstrated through changes in evoked potentials. Third, auditory evoked potentials have been shown to reflect perception in normal and impaired children (Neville et al, 1993;Ponton et al, 1996;Tonnquist-Uhlen, 1996;Jordan et al, 1997;Cunningham et al, 2000Cunningham et al, , 2001. Fourth, deficits in the encoding of speech signals in quiet have been demonstrated at the auditory brainstem level and in both quiet and noise at cortical levels in learning-impaired children (Kraus et al, 1996;Schulte-Koerne et al, 1998;Cunningham et al, 2001).…”

Development of structure and function in the infant brain: Implications for cognition, language and social behaviour

“…Neville et al, (1993) reported an atypical early negative ERP component in a subgroup of SLI children who demonstrated poor auditory temporal performance behaviourally. This component, time-locked to tones, was found to be reduced over the right hemisphere and delayed in latency, especially over temporal and parietal sites in the left hemisphere.…”

“…One should always remember that brain and behaviour relationships are extremely complex and that behaviour is likely to rely on circuitry dispersed across the brain, rather than a distinct circumscribed area. As noted by Neville et al (1993), ''the developing organism displays a high degree of change both in different neural systems and in cognition, and thus provides an important opportunity to link variability in one trajectory to variability in the other.'' However, the careful use of increasingly fine-grained behavioural assessments in conjunction with stateof-the art brain imaging methods provides an unparalleled and increasing opportunity to obtain a clearer, more detailed picture of how neural development interacts with environmental influences across time to produce complex behaviours and individual variability in brain function.…”

Neurophysiological indices of attention to speech in children with specific language impairment

“…However, results from several studies are consistent with the suggestion that attention to speech and/or auditory information may differ between SLI and TLD groups. Specifically, several studies have found later latency of N1 in, at least, a subset of Language Impaired (LI) children (Jirsa & Clontz, 1990;Neville, et al, 1993;Tonnquist-Uhlen, Borg, Persson & Spens, 1996), although this was not seen in other studies (e.g., Lincoln, et al, 1995;Marler, Champlin & Gillam, 2002). These differences in N1 latency could be due to reduced N1 negativity leading to the appearance of later N1 peak latency.…”