PubMed Health⌕ Search

PubMed · 14657303

Speech delay in children: a functional MR imaging study.

Abstract

PURPOSE: To determine if children with speech delay who have been sedated have patterns of activation to passive language paradigms that are different than those of children with normal speech. MATERIALS AND METHODS: Seventeen children with speech delay (age range, 2-7 years; mean, 4.0 years) and 35 age-matched children with normal speech (age range, 2-8 years; mean, 4.2 years) were evaluated. The subjects in the control group were selected from patients referred for conventional magnetic resonance (MR) imaging. All children had absence of auditory impairment or mental retardation, and MR findings indicated that brain structure was normal. Sedation was achieved with pentobarbital (3-5 mg/kg) or chloral hydrate (75 mg/kg). Functional MR imaging was performed with a single-shot echo-planar blood oxygen-level-dependent technique and a passive block paradigm, in which the child listened to his or her mother's prerecorded voice. Statistical postprocessing of functional MR images was performed with the t test and cluster detection methods. Comparison between groups was performed depending on the type of data with a nonparametrical Mann-Whitney test, parametrical t test, or Fisher exact test. RESULTS: Five (83%) of the six children older than 3 years with speech delay had lateralized activation of functional MR imaging signal in the right hemisphere. Ten (71%) of 14 age-matched patients with normal speech had activation in the left hemisphere when exposed to the same passive listening tasks. When these groups were compared, this difference was statistically significant. (P =.036). No statistically significant lateralization was seen across all age groups in children with activation. CONCLUSION: Children older than 3 years with speech delay have activation in the right hemisphere more frequently than children older than 3 years with normal speech, who often have the expected finding of activation in the left hemisphere.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Byron Bernal, Nolan R Altman. 2003. Speech delay in children: a functional MR imaging study.. https://doi.org/10.1148/radiol.2293021746

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

A MAGIBU-based model for pediatric and juvenile CNS tumors: an in-house epigenetic decision-support framework compared with online DNA methylation classifiers.

Background: DNA methylation profiling is a tool that provides key support for central nervous system (CNS) tumor classification. However, diagnostically ambiguous pediatric cases may result in discordant outputs across classifiers. We developed MAGIBU, a cross-platform, projection-based framework that embeds individual methylomes into a fixed CNS reference landscape, ranking diagnostic entities by local epigenetic proximity to support clinician-led integrative diagnosis. Methods: As a proof-of-concept, we evaluated MAGIBU in eight morphologically challenging pediatric/juvenile CNS tumors with unresolved diagnoses after institutional and central pathology review. To establish a benchmark in the absence of a definitive histopathological ground truth, a consensus epigenetic reference was defined a priori for cases showing concordant results between the Heidelberg CNS Tumor Methylation Classifier and Methylscape Analysis. Comparisons were also performed with Epigenomic Digital Pathology (EpiDiP). To validate MAGIBU beyond this discovery cohort, performance was assessed at the family level across the CNS methylation spectrum (n = 678, 28 methylation families), on non-array platforms (whole-genome bisulfite sequencing and Oxford Nanopore), and in a focused analysis of the low-grade glioma and diffuse midline glioma compartment across four independent cohorts (n = 670). Results: In the discovery cohort, MAGIBU achieved high concordance with the consensus reference (Cohen's κ = 0.855), outperforming EpiDiP (κ = 0.278), which frequently placed low-grade tumors in proximity to higher-grade reference regions. Conclusions: MAGIBU provides a stable, quantitative differential diagnosis framework that mitigates the limitations of rigid categorical assignments. By leveraging a distance-based proximity metric, it offers a transparent decision-support tool that integrates effectively with clinical, radiological, and molecular data. While performance is inherently dependent on reference atlas composition, MAGIBU represents a robust complementary approach for the diagnostic workup of ambiguous CNS tumors.

Brain↗

1q21.1 distal copy number variants are associated with cerebral and cognitive alterations in humans.

Low-frequency 1q21.1 distal deletion and duplication copy number variant (CNV) carriers are predisposed to multiple neurodevelopmental disorders, including schizophrenia, autism and intellectual disability. Human carriers display a high prevalence of micro- and macrocephaly in deletion and duplication carriers, respectively. The underlying brain structural diversity remains largely unknown. We systematically called CNVs in 38 cohorts from the large-scale ENIGMA-CNV collaboration and the UK Biobank and identified 28 1q21.1 distal deletion and 22 duplication carriers and 37,088 non-carriers (48% male) derived from 15 distinct magnetic resonance imaging scanner sites. With standardized methods, we compared subcortical and cortical brain measures (all) and cognitive performance (UK Biobank only) between carrier groups also testing for mediation of brain structure on cognition. We identified positive dosage effects of copy number on intracranial volume (ICV) and total cortical surface area, with the largest effects in frontal and cingulate cortices, and negative dosage effects on caudate and hippocampal volumes. The carriers displayed distinct cognitive deficit profiles in cognitive tasks from the UK Biobank with intermediate decreases in duplication carriers and somewhat larger in deletion carriers-the latter potentially mediated by ICV or cortical surface area. These results shed light on pathobiological mechanisms of neurodevelopmental disorders, by demonstrating gene dose effect on specific brain structures and effect on cognitive function.

Brain↗