El análisis pormenorizado del Childhood Autism Spectrum Test CAST permite diferenciar subtipos clínicos con dificultades en la comunicación social

European Journal of Education and Psychology ◽

10.32457/ejep.v14i2.1613 ◽

2021 ◽

pp. 1-20

Author(s):

Nerea Crespo Eguílaz ◽

Leire Gambra Echeverría ◽

Borja Laña ◽

Rocío Rocío Sánchez-Carpintero

Keyword(s):

Autism Spectrum ◽

Childhood Autism ◽

Discapacidad Intelectual

El Childhood Austism Spectrum Test-CAST (Scott et al., 2012a) es una prueba de screening del síndrome de Asperger o trastorno del espectro del autismo de grado 1 (TEA1). Se busca analizarla para precisar diferentes dimensiones en su contenido. para ello, se aplicó el CAST a 254 pacientes de nuestra Unidad de Neuropediatría, de 5 a 16 años, afectos de: TEA1 (n=17); trastorno de la comunicación social (n=43); trastorno de aprendizaje procedimental (n=60); trastorno por déficit de atención (n=44); discapacidad intelectual (n=30) y discapacidad intelectual y epilepsia (n=60). Los resultados con el uso tradicional del CAST en la muestra clínica se obtienen 47.1% y 33.75% de falsos negativos y positivos, respectivamente. Se realiza un análisis factorial de los 31 ítems del cuestionario. Con una buena adecuación de los datos (KMO=0,65 y MSA=0.47-0.88) se obtienen 7 factores, que explican el 63% de la varianza total. Se comprueba la fiabilidad y la validez. El análisis discriminante indica que esta nueva corrección e interpretación permite clasificar correctamente al 86.7% de nuestra casuística con o sin dificultades en el uso social del lenguaje. Se detallan las dimensiones alteradas con más frecuencia en cada grupo clínico. Este análisis pormenorizado del CAST aporta información relevante en el diagnóstico diferencial de trastornos del neurodesarrollo.

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Tactile cortical responses and association with tactile reactivity in young children on the autism spectrum

Molecular Autism ◽

10.1186/s13229-021-00435-9 ◽

2021 ◽

Vol 12 (1) ◽

Author(s):

Svenja Espenhahn ◽

Kate J. Godfrey ◽

Sakshi Kaur ◽

Maia Ross ◽

Niloy Nath ◽

...

Keyword(s):

Early Childhood ◽

Young Children ◽

Evoked Potentials ◽

Real World ◽

Somatosensory Evoked Potentials ◽

Children With Autism ◽

Autism Spectrum ◽

Childhood Autism ◽

Verbal Abilities ◽

Early Childhood Autism

Abstract Background Unusual behavioral reactions to sensory stimuli are frequently reported in individuals on the autism spectrum (AS). Despite the early emergence of sensory features (< age 3) and their potential impact on development and quality of life, little is known about the neural mechanisms underlying sensory reactivity in early childhood autism. Methods Here, we used electroencephalography (EEG) to investigate tactile cortical processing in young children aged 3–6 years with autism and in neurotypical (NT) children. Scalp EEG was recorded from 33 children with autism, including those with low cognitive and/or verbal abilities, and 45 age- and sex-matched NT children during passive tactile fingertip stimulation. We compared properties of early and later somatosensory-evoked potentials (SEPs) and their adaptation with repetitive stimulation between autistic and NT children and assessed whether these neural measures are linked to “real-world” parent-reported tactile reactivity. Results As expected, we found elevated tactile reactivity in children on the autism spectrum. Our findings indicated no differences in amplitude or latency of early and mid-latency somatosensory-evoked potentials (P50, N80, P100), nor adaptation between autistic and NT children. However, latency of later processing of tactile information (N140) was shorter in young children with autism compared to NT children, suggesting faster processing speed in young autistic children. Further, correlational analyses and exploratory analyses using tactile reactivity as a grouping variable found that enhanced early neural responses were associated with greater tactile reactivity in autism. Limitations The relatively small sample size and the inclusion of a broad range of autistic children (e.g., with low cognitive and/or verbal abilities) may have limited our power to detect subtle group differences and associations. Hence, replications are needed to verify these results. Conclusions Our findings suggest that electrophysiological somatosensory cortex processing measures may be indices of “real-world” tactile reactivity in early childhood autism. Together, these findings advance our understanding of the neurophysiological mechanisms underlying tactile reactivity in early childhood autism and, in the clinical context, may have therapeutic implications.

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Serum Tryptophan, Tryptophan Catabolites and Brain-derived Neurotrophic Factor in Subgroups of Youngsters with Autism Spectrum Disorders

CNS & Neurological Disorders - Drug Targets ◽

10.2174/1871527317666180720163221 ◽

2018 ◽

Vol 17 (8) ◽

pp. 626-639 ◽

Cited By ~ 7

Author(s):

Heidi Ormstad ◽

Vesna Bryn ◽

Robert Verkerk ◽

Ola H. Skjeldal ◽

Bente Halvorsen ◽

...

Keyword(s):

Autism Spectrum Disorders ◽

Neurotrophic Factor ◽

Serum Levels ◽

Brain Derived Neurotrophic Factor ◽

Autism Spectrum ◽

Childhood Autism ◽

Total Blood ◽

Healthy Control ◽

Tryptophan Catabolites ◽

Spectrum Disorders

Background: There is evidence that changes in neuro-immune responses coupled with dysfunctions in serotonin metabolism underpin the pathophysiology of autism spectrum disorders (ASD). Objective: This study aimed to delineate whether ASD subgroups or characteristics show aberrations in tryptophan and brain-derived neurotrophic factor (BDNF) metabolism. Methods: 65 individuals with ASD (diagnosed according to ICD criteria) and 30 healthy control patients were included. Measured were serum levels of tryptophan, kynurenine (KYN), kynurenic acid (KA), quinolinic acid (QA), BDNF and PRO-BDNF and total blood 5-HT and 5-OH-tryptophan (5-HTP). Results: Elevated BDNF levels and lower tryptophan and KA levels were characteristics of both childhood autism and intellectual disability disorder, whilst elevated tryptophan and lower 5-HT synthesis were hallmarks of Asperger syndrome. A pathological MRI was associated with elevated tryptophan and lowered KA. Abnormal EEG results and dysmorphology were both associated with an elevated BDNF/ PRO-BDNF ratio. Any brain pathology and gastro-intestinal symptoms were accompanied by lowered KA. Conclusions: Increased BDNF production and changes in the metabolism of tryptophan are associated with many ASD characteristics, showing particularly strong associations with childhood autism and Intellectual and Developmental Disabilities. Peripheral BDNF and tryptophan metabolism appear to take part in the pathophysiology of autism spectrum disorders and their phenotypes.

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