Purpose The primary purposes of this study were to examine the effects of hearing loss and respondent type (self- vs. parent-proxy report) on subjective fatigue in children. We also examined associations between child-specific factors and fatigue ratings. Method Subjective fatigue was assessed using the Pediatric Quality of Life Inventory Multidimensional Fatigue Scale (PedsQL-MFS; Varni, Burwinkle, Katz, Meeske, & Dickinson, 2002). We compared self- and parent-proxy ratings from 60 children with hearing loss (CHL) and 43 children with normal hearing (CNH). The children ranged in age from 6 to 12 years. Results School-age CHL experienced more overall and cognitive fatigue than CNH, although the differences were smaller than previously reported. Parent-proxy report was not strongly associated with child self-report, and parents tended to underestimate their child's fatigue, particularly sleep/rest fatigue. Language ability was also associated with subjective fatigue. For CHL and CNH, as language abilities increased, cognitive fatigue decreased. Conclusions School-age CHL experience more subjective fatigue than CNH. The poor association between parent-proxy and child reports suggests that the parent-proxy version of the PedsQL-MFS should not be used in isolation when assessing fatigue in school-age children. Future research should examine how language abilities may modulate fatigue and its potential academic consequences in CHL.

Objective The aim of the study was to conduct a meta-analysis of research examining the early speech and language functioning of young children, birth to age 8;11 (years;months), with nonsyndromic cleft lip and/or palate (NSCL/P) compared to their peers without NSCL/P. Method We conducted a random-effects metaregression using 241 effect sizes from 31 studies comparing 955 young children with NSCL/P to 938 typically developing peers on measures of speech and language functioning. Moderators were sample characteristics (i.e., age, cleft type, publication year, and study location) and measurement characteristics (i.e., speech sample material, language modality and domain, and assessment type). Results Young children with NSCL/P scored significantly lower on measures of speech and language compared to children without NSCL/P. Children with NSCL/P had smaller consonant inventories (standardized mean difference effect size [ES g ] = −1.24), less accurate articulation (ES g = −1.13), and more speech errors (ES g = 0.93) than their peers. Additionally, children with NSCL/P had poorer expressive (ES g = −0.57) and receptive (ES g = −0.59) language skills than their peers. Age and assessment type moderated effect sizes for expressive language. As children with NSCL/P aged, their expressive language performance became more similar to their peers. Expressive language effect sizes from parent reports and observational language measures (estimated effect size = −0.74) were significantly lower than those from standardized norm-referenced tests (estimated effect size = −0.45). Conclusions These findings suggest that young children with NSCL/P experience delays relative to their peers across multiple speech and language constructs. Differences between children with NSCL/P and their typically developing peers appear to decrease with age. Supplemental Material https://doi.org/10.23641/asha.11356904

Background: There is considerable variability in the presentation of developmental language disorder (DLD). Disagreement amongst professionals about how to characterize and interpret the variability complicates both the research on understanding the nature of DLD and the best clinical framework for diagnosing and treating children with DLD. We describe and statistically examine three primary possible models for characterizing the variability in presentation in DLD: predictable subtypes; individual differences; and continuum/spectrum. Aims: To test these three models of DLD in a population-based sample using two distinct types of cluster analyses. Methods & Procedures: This study included children with DLD (n = 505) from the US Epidemiological Study of Language Impairment database. All available language and cognitive measures were included. Two cluster methods were used: Ward’s method and K-means. Optimal cluster sizes were selected using Bayesian information criteria (BIC). Bootstrapping and permutation methods were used to evaluate randomness of clustering. Outcomes & Results: Both clustering analyses yielded more than 10 clusters, and the clusters did not have spatial distinction: many of these clusters were not clinically interpretable. However, tests of random clustering revealed that the cluster solutions obtained did not arise from random aggregation. Conclusions & Implications: Non-random clustering coupled with a large number of non-interpretable subtypes provides empirical support for the continuum/spectrum and individual differences models. Although there was substantial support for the continuum/spectrum model and weaker support for the individual differences model, additional research testing these models should be completed. Based on these results, clinicians working with children with DLD should focus on creating treatment plans that address the severity of functioning rather than seeking to identify and treat distinct subtypes. Additional consideration should be given to reconceptualizing DLD as a spectrum condition.

The purpose of this study was to investigate the hypothesis that individuals with dyslexia and individuals with childhood apraxia of speech share an underlying persisting deficit in processing sequential information. Levels of impairment (sensory encoding, memory, retrieval, motor planning/programming) were also investigated. Participants were 22 adults with dyslexia, 10 adults with a probable history of childhood apraxia of speech (phCAS), and 22 typical controls. All participants completed nonword repetition, multisyllabic real word repetition, and nonword decoding tasks. Using phonological process analysis, errors were classified as sequence or substitution errors. Adults with dyslexia and adults with phCAS showed evidence of persisting nonword repetition deficits. In all three tasks, the adults in the two disorder groups produced more errors of both classes than the controls, but disproportionally more sequencing than substitution errors during the nonword repetition task. During the real word repetition task, the phCAS produced the most sequencing errors, whereas during the nonword decoding task, the dyslexia group produced the most sequencing errors. Performance during multisyllabic motor speech tasks, relative to monosyllabic conditions, was correlated with the sequencing error component during nonword repetition. Results provide evidence for a shared persisting sequential processing deficit in the dyslexia and phCAS groups during linguistic and motor speech tasks. Evidence for impairments in sensory encoding, short-term memory, and motor planning/programming was found in both disorder groups. Future studies should investigate clinical applications regarding preventative and targeted interventions towards crossmodal treatment effects.

Interstitial and terminal 6q25 deletions are associated with developmental delays, hypotonia, eye pathologies, craniofacial dysmorphologies, and structural brain anomalies. In most cases, speech and language deficits are not described in detail. We report on a case (Patient 1, age 7 years) with a de novo 6q25.3-qter deletion, 11.1 Mb long and encompassing 108 genes, and a case (Patient 2, age 5 years) with an inherited interstitial 6q25.3 deletion, located within Patient 1's deletion region and 403 kb long, the smallest 6q25 deletion reported to date. Both children have hypotonia, motor speech disorders, and expressive language delays. Patient 1's speech was characterized by childhood apraxia of speech (CAS) and dysarthria. Other findings include developmental delay, ataxic cerebral palsy, optic nerve dysplagia, and atypical brain morphologies regarding the corpus callosum and gyration patterns, a clinical profile that closely matches a previously reported case with a nearly identical deletion. Patient 2 had speech characterized by CAS and typical nonverbal processing abilities. His father, a carrier, had typical speech and language but showed difficulties with complex motor speech and hand motor tasks, similar to other adults with residual signs of CAS. The small deletion in this family contains the IGF2R-AIRN-SLC22A2-SLC22A3 gene cluster, which is associated with imprinting and maternal-specific expression of Igf2R, Slc22a2, and Slc22a3 in mice, whereas imprinting in humans is a polymorphic trait. The shared phenotypes in the two patients might be associated with the deletion of the gene cluster.