Biomedical subjects

Paula Tallal

Publications and source records attributed to Paula Tallal.

4 recordsLinked to original sources

PubMed2003

Neural deficits in children with dyslexia ameliorated by behavioral remediation: evidence from functional MRI.

Developmental dyslexia, characterized by unexplained difficulty in reading, is associated with behavioral deficits in phonological processing. Functional neuroimaging studies have shown a deficit in the neural mechanisms underlying phonological processing in children and adults with dyslexia. The present study examined whether behavioral remediation ameliorates these dysfunctional neural mechanisms in children with dyslexia. Functional MRI was performed on 20 children with dyslexia (8-12 years old) during phonological processing before and after a remediation program focused on auditory processing and oral language training. Behaviorally, training improved oral language and reading performance. Physiologically, children with dyslexia showed increased activity in multiple brain areas. Increases occurred in left temporo-parietal cortex and left inferior frontal gyrus, bringing brain activation in these regions closer to that seen in normal-reading children. Increased activity was observed also in right-hemisphere frontal and temporal regions and in the anterior cingulate gyrus. Children with dyslexia showed a correlation between the magnitude of increased activation in left temporo-parietal cortex and improvement in oral language ability. These results suggest that a partial remediation of language-processing deficits, resulting in improved reading, ameliorates disrupted function in brain regions associated with phonological processing and produces additional compensatory activation in other brain regions.

Brain↗

PubMed2002

Infant discrimination of rapid auditory cues predicts later language impairment.

The etiology and mechanisms of specific language impairment (SLI) in children are unknown. Differences in basic auditory processing abilities have been suggested to underlie their language deficits. Studies suggest that the neuropathology, such as atypical patterns of cerebral lateralization and cortical cellular anomalies, implicated in such impairments likely occur early in life. Such anomalies may play a part in the rapid processing deficits seen in this disorder. However, prospective, longitudinal studies in infant populations that are critical to examining these hypotheses have not been done. In the study described, performance on brief, rapidly-presented, successive auditory processing and perceptual-cognitive tasks were assessed in two groups of infants: normal control infants with no family history of language disorders and infants from families with a positive family history for language impairment. Initial assessments were obtained when infants were 6-9 months of age (M=7.5 months) and the sample was then followed through age 36 months. At the first visit, infants' processing of rapid auditory cues as well as global processing speed and memory were assessed. Significant differences in mean thresholds were seen in infants born into families with a history of SLI as compared with controls. Examination of relations between infant processing abilities and emerging language through 24 months-of-age revealed that threshold for rapid auditory processing at 7.5 months was the single best predictor of language outcome. At age 3, rapid auditory processing threshold and being male, together predicted 39-41% of the variance in language outcome. Thus, early deficits in rapid auditory processing abilities both precede and predict subsequent language delays. These findings support an essential role for basic nonlinguistic, central auditory processes, particularly rapid spectrotemporal processing, in early language development. Further, these findings provide a temporal diagnostic window during which future language impairments may be addressed.

Apgar Score↗

PubMed2002

A major susceptibility locus for specific language impairment is located on 13q21.

Children who fail to develop language normally-in the absence of explanatory factors such as neurological disorders, hearing impairment, or lack of adequate opportunity-are clinically described as having specific language impairment (SLI). SLI has a prevalence of approximately 7% in children entering school and is associated with later difficulties in learning to read. Research indicates that genetic factors are important in the etiology of SLI. Studies have consistently demonstrated that SLI aggregates in families. Increased monozygotic versus dizygotic twin concordance rates indicate that heredity, not just shared environment, is the cause of the familial clustering. We have collected five pedigrees of Celtic ancestry that segregate SLI, and we have conducted genomewide categorical linkage analysis, using model-based LOD score techniques. Analysis was conducted under both dominant and recessive models by use of three phenotypic classifications: clinical diagnosis, language impairment (spoken language quotient <85) and reading discrepancy (nonverbal IQ minus non-word reading >15). Chromosome 13 yielded a maximum multipoint LOD score of 3.92 under the recessive reading discrepancy model. Simulation to correct for multiple models and multiple phenotypes indicated that the genomewide empirical P value is <.01. As an alternative measure, we also computed the posterior probability of linkage (PPL), obtaining a PPL of 53% in the same region. One other genomic region yielded suggestive results on chromosome 2 (multipoint LOD score 2.86, genomic P value <.06 under the recessive language impairment model). Our findings underscore the utility of traditional LOD-score-based methods in finding genes for complex diseases, specifically, SLI.

Autistic Disorder↗

PubMed2002

Developmental language learning impairments.

Developmental language learning impairments (LLI) are one of the most prevalent of all developmental disabilities, can occur in children for a wide variety of reasons, and have been shown to co-occur frequently with other developmental social, emotional and behavioral disorders, as well as with academic achievement problems. Research pertaining to developmental LLI of unknown origin, with an emphasis on the continuum between oral and written language impairment, is the focus of this review. Given the complexity of language learning, research has focused on multiple levels of analysis, including linguistic, neuropsychological, genetic, neurobiological, and remediation studies. To date, the vast majority of data on LLI derive from studies focused on a single level of analysis. Although attempts have been made to integrate data across studies and multiple levels of analysis, this has proven to be problematic, given the heterogeneity of the subject populations used to study LLI, as well as the differences in ages, degree of impairment, and types of impairment included in each study. Given that LLI is a complex developmental disability, it is suggested that future research would benefit from taking a multiple levels of analysis approach with the same individuals, incorporating mathematical models designed to analyze dynamically changing complex systems, and studying individual differences in language learning, prospectively and longitudinally, throughout the most dynamic stages of the process.

Brain↗