Parent-Led Imitation Therapy for Non-Verbal Children with Suspected Autism

This study examined the results of Imitation Therapy conducted by parents of non-verbal children. Fifty-six parents were taught to engage in a specific form of imitation therapy with their child by speech-language pathologists (SLPs) who were familiar with the therapy. The SLPs oversaw the therapy via Zoom conferences and consultation with the parents. Parents who completed the study worked with their child for thirty minutes a day, five days a week, for four weeks. Measures of speech and language production were taken throughout the intervention period to determine progress. The children, ages two to five and a half, made significant increases in the number of different phonemes and the frequency of speech sounds they produced as well as their instances of imitation.  Eighty-five percent of them increased their word production. Most of the parents reported that the therapy had been effective in increasing their children’s language and imitation abilities. Children with mild autism symptoms showed more progress than those with severe symptoms. Some of the children who received fewer than the recommended twenty sessions progressed and those who received only two to three sessions did not demonstrate significant changes. Imitation therapy appears to provide an opportunity for parents to assist in children’s development of the sounds and imitative behaviors that are essential to language acquisition. Parent-led imitation therapy may offer an effective alternative when the availability of consistent speech therapy services is limited

Research Priorities for Childhood Apraxia of Speech: A Long View

This article introduces the Journal of Speech, Language, and Hearing Research Special Issue: Selected Papers From the 2022 Apraxia Kids Research Symposium. The field of childhood apraxia of speech (CAS) has developed significantly in the past 15 years, with key improvements in understanding of basic biology including genetics, neuroscience, and computational modelling; development of diagnostic tools and methods; diversity of evidence-based interventions with increasingly rigorous experimental designs; and understanding of impacts beyond impairment-level measures. Papers in this special issue not only review and synthesize the some of the substantial progress to date but also present novel findings addressing critical research gaps and adding to the overall body of knowledge. A second aim of this prologue is to report the current research needs in CAS, which arose from symposium discussions involving researchers, clinicians, and Apraxia Kids community members (including parents of children with CAS). Four primary areas of need emerged from discussions at the symposium. These were: (a) What questions should we ask? (b) Who should be in the research? (c) How do we conduct the research? and (d) How do we move from research to practice? Across themes, symposium attendees emphasized the need for CAS research to better account for the diversity of people with CAS and improve the timeliness of implementation of high-level evidence-based practice across the lifespan. It is our goal that the articles and prologue discussion in this special issue provide an appreciation of advancements in CAS research and an updated view of the most pressing needs for future research

Behind the Scenes of Noninvasive Brain– Computer Interfaces: A Review of Electroencephalography Signals, How They Are Recorded, and Why They Matter

Purpose: Brain–computer interface (BCI) techniques may provide computer access for individuals with severe physical impairments. However, the relatively hidden nature of BCI control obscures how BCI systems work behind the scenes, making it difficult to understand “how” electroencephalography (EEG) records the BCIrelated brain signals, “what” brain signals are recorded by EEG, and “why” these signals are targeted for BCI control. Furthermore, in the field of speech-languagehearing, signals targeted for BCI application have been of primary interest to clinicians and researchers in the area of augmentative and alternative communication (AAC). However, signals utilized for BCI control reflect sensory, cognitive, and motor processes, which are of interest to a range of related disciplines, including speech science. Method: This tutorial was developed by a multidisciplinary team emphasizing primary and secondary BCI-AAC–related signals of interest to speech-language-hearing. Results: An overview of BCI-AAC–related signals are provided discussing (a) “how” BCI signals are recorded via EEG; (b) “what” signals are targeted for noninvasive BCI control, including the P300, sensorimotor rhythms, steady-state evoked potentials, contingent negative variation, and the N400; and (c) “why” these signals are targeted. During tutorial creation, attention was given to help support EEG and BCI understanding for those without an engineering background. Conclusion: Tutorials highlighting how BCI-AAC signals are elicited and recorded can help increase interest and familiarity with EEG and BCI techniques and provide a framework for understanding key principles behind BCIAAC design and implementation

Auditory-cognitive interactions underlying interaural asymmetry in an adult listener: A case study

Objective: Abnormal interaural asymmetry on tests of dichotic listening is commonly observed in individuals suspected of auditory processing disorder (APD). Although a structural basis for the abnormality has been widely accepted, the influence of cognitive variables on the degree of observed asymmetry has gained increasing attention. To study this issue, we manipulated cognitive influences on interaural asymmetry in an adult with the auditory complaints typically associated with APD. Study sample: A 55 year-old woman with complaints of difficulty understanding speech in noisy environments despite normal audiometric levels. Design: Several experimental dichotic procedures were administered. Each procedure was characterized by the manipulation of cognitive task demands. Results: Interaural asymmetry was greatest when the demands on attention and/or memory were maximal. Electrophysiological data revealed interaural asymmetry on later stages of information processing. Conclusions: Results are discussed in relation to auditory-specific outcomes on clinical tests for APD

Behind the Scenes of Noninvasive Brain– Computer Interfaces: A Review of Electroencephalography Signals, How They Are Recorded, and Why They Matter

Purpose: Brain–computer interface (BCI) techniques may provide computer access for individuals with severe physical impairments. However, the relatively hidden nature of BCI control obscures how BCI systems work behind the scenes, making it difficult to understand “how” electroencephalography (EEG) records the BCIrelated brain signals, “what” brain signals are recorded by EEG, and “why” these signals are targeted for BCI control. Furthermore, in the field of speech-languagehearing, signals targeted for BCI application have been of primary interest to clinicians and researchers in the area of augmentative and alternative communication (AAC). However, signals utilized for BCI control reflect sensory, cognitive, and motor processes, which are of interest to a range of related disciplines, including speech science. Method: This tutorial was developed by a multidisciplinary team emphasizing primary and secondary BCI-AAC–related signals of interest to speech-language-hearing. Results: An overview of BCI-AAC–related signals are provided discussing (a) “how” BCI signals are recorded via EEG; (b) “what” signals are targeted for noninvasive BCI control, including the P300, sensorimotor rhythms, steady-state evoked potentials, contingent negative variation, and the N400; and (c) “why” these signals are targeted. During tutorial creation, attention was given to help support EEG and BCI understanding for those without an engineering background. Conclusion: Tutorials highlighting how BCI-AAC signals are elicited and recorded can help increase interest and familiarity with EEG and BCI techniques and provide a framework for understanding key principles behind BCIAAC design and implementation

Cerebral hypoperfusion in autism spectrum disorder

Cerebral hypoperfusion, or insufficient blood flow in the brain, occurs in many areas of the brain in patients diagnosed with autism spectrum disorder (ASD). Hypoperfusion was demonstrated in the brains of individuals with ASD when compared to normal healthy control brains either using positron emission tomography (PET) or single‑photon emission computed tomography (SPECT). The affected areas include, but are not limited to the: prefrontal, frontal, temporal, occipital, and parietal cortices; thalami; basal ganglia; cingulate cortex; caudate nucleus; the limbic system including the hippocampal area; putamen; substantia nigra; cerebellum; and associative cortices. Moreover, correlations between symptom scores and hypoperfusion in the brains of individuals diagnosed with an ASD were found indicating that the greater the autism symptom pathology, the more significant the cerebral hypoperfusion or vascular pathology in the brain. Evidence suggests that brain inflammation and vascular inflammation may explain a part of the hypoperfusion. There is also evidence of a lack of normal compensatory increase in blood flow when the subjects are challenged with a task. Some studies propose treatments that can address the hypoperfusion found among individuals diagnosed with an ASD, bringing symptom relief to some extent. This review will explore the evidence that indicates cerebral hypoperfusion in ASD, as well as the possible etiological aspects, complications, and treatments.publishedVersio

Cerebral hypoperfusion in autism spectrum disorder

Cerebral hypoperfusion, or insufficient blood flow in the brain, occurs in many areas of the brain in patients diagnosed with autism spectrum disorder (ASD). Hypoperfusion was demonstrated in the brains of individuals with ASD when compared to normal healthy control brains either using positron emission tomography (PET) or single-photon emission computed tomography (SPECT). The affected areas include, but are not limited to the: prefrontal, frontal, temporal, occipital, and parietal cortices; thalami; basal ganglia; cingulate cortex; caudate nucleus; the limbic system including the hippocampal area; putamen; substantia nigra; cerebellum; and associative cortices. Moreover, correlations between symptom scores and hypoperfusion in the brains of individuals diagnosed with an ASD were found indicating that the greater the autism symptom pathology, the more significant the cerebral hypoperfusion or vascular pathology in the brain. Evidence suggests that brain inflammation and vascular inflammation may explain a part of the hypoperfusion. There is also evidence of a lack of normal compensatory increase in blood flow when the subjects are challenged with a task. Some studies propose treatments that can address the hypoperfusion found among individuals diagnosed with an ASD, bringing symptom relief to some extent. This review will explore the evidence that indicates cerebral hypoperfusion in ASD, as well as the possible etiological aspects, complications, and treatments