1. Albores-Gallo L, Fritsche-Garcia L, Miranda-Aguirre AP, Avila-Acosta M. {{Brief Report: Macrocephaly Phenotype and Psychiatric Comorbidity in a Clinical Sample of Mexican Children and Adolescents with Autism Spectrum Disorders}}. {J Autism Dev Disord}. 2017.
Autism spectrum disorders (ASD) may present with macrocephaly. Few studies have analyzed the association with psychiatric comorbidity. Participants were 94 children with any ASD with an age range from 2 to 16 years (Mdn 6 years), 82% were boys. It was found that 20% of the sample had macrocephaly and 1% microcephaly. There was no association between the presence of macrocephaly and subtype of ASD. The most associated comorbidity was attention-deficit/hyperactivity disorder (ADHD) 54.2%, followed by specific phobia 34%, dysthimia 29.7%, oppositional defiant disorder 13.83% motor tics 11.7%, separation anxiety 9.5% and Gilles de la Tourette 8.5%. In conclusion, macrocephaly and psychiatric comorbidity in this clinical sample of children with ASD is similar to the international literature results.
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2. Brenner J, Pan Z, Mazefsky C, Smith KA, Gabriels R. {{Behavioral Symptoms of Reported Abuse in Children and Adolescents with Autism Spectrum Disorder in Inpatient Settings}}. {J Autism Dev Disord}. 2017.
The objective of this study was to examine how behavioral manifestations of trauma due to abuse are expressed in youth with autism spectrum disorder (ASD). Analysis of covariance (ANCOVA) compared outcomes between patients with a caregiver reported history of abuse and those without. Findings indicate that patients with ASD and reported abuse (i.e. physical, sexual, and/or emotional) have more intrusive thoughts, distressing memories, loss of interest, irritability, and lethargy than those without reported maltreatment. Those with clinical diagnoses of posttraumatic stress disorder (PTSD) had more severe and externalized symptoms than those with reported abuse not diagnosed with PTSD. Results emphasize the need for trauma screening measures to guide evidence-based treatments for children with ASD.
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3. Campbell SB, Moore EL, Northrup J, Brownell CA. {{Developmental Changes in Empathic Concern and Self-Understanding in Toddlers at Genetic Risk for Autism Spectrum Disorder}}. {J Autism Dev Disord}. 2017.
Toddlers with an older sibling with autism spectrum disorder (ASD) and low risk (LR) toddlers were observed at 22, 28, and 34 months during two empathy probes: a crying baby and an adult who pretended to hurt her finger. Toddlers with a later ASD diagnosis showed less empathic concern and self-distress at each age on both empathy probes than LR toddlers. HR toddlers with no diagnosis showed growth in empathic concern between 22 and 34 months in response to the adult’s pain, differing from the children with ASD, but not the LR children, by 34 months. Developmental changes in parent-rated self-understanding showed a similar pattern. Results highlight individual differences in the social development of HR toddlers.
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4. Chee DY, Lee HC, Patomella AH, Falkmer T. {{Driving Behaviour Profile of Drivers with Autism Spectrum Disorder (ASD)}}. {J Autism Dev Disord}. 2017.
The symptomatology of autism spectrum disorder (ASD) can make driving risky, but little is known about the on-road driving behaviour of individuals with ASD. This study assessed and compared the on-road driving performance of drivers with and without ASD, and explored how the symptomatology of ASD hinders or facilitates on-road driving performance. Sixteen drivers with ASD and 21 typically-developed drivers participated in the study. Drivers with ASD underperformed in vehicle manoeuvring, especially at left-turns, right-turns and pedestrian crossings. However, drivers with ASD outperformed the TD group in aspects related to rule-following such as using the indicator at roundabouts and checking for cross-traffic when approaching intersections. Drivers with ASD in the current study presented with a range of capabilities and weaknesses during driving.
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5. Dillenburger K, Jordan JA, McKerr L, Lloyd K, Schubotz D. {{Autism awareness in children and young people: surveys of two populations}}. {J Intellect Disabil Res}. 2017.
BACKGROUND: Increasingly, pupils on the autism spectrum are educated in inclusive mainstream classrooms. However, they often experience social isolation and bullying, and raising the awareness of autism in peers has been suggested as a remedy. METHODS: In order to assess autism awareness in peers, autism-related questions were included in two large-scale surveys: the Kids Life and Times survey for 11-year olds and the Young Life and Times survey for 16-year olds; a total of n = 3353 children and young people completed the surveys. RESULTS: Autism awareness was higher for the teenagers (80%) than for the younger children (50%). Many of the children knew someone with autism (50%) and generally reported positive and supportive attitudes. Self-reported prevalence of autism was 3.1% for teenagers and 2.7% for the younger children. Peers recognised bullying as a problem and were willing to help. CONCLUSIONS: Children and young people have good levels of awareness and knowledge about autism and reported positive attitudes towards peers with autism and are willing to help those who are bullied. A higher than expected number of children and young people self-reported being on the autism spectrum. These findings bode well for peer-mediated support strategies for inclusive education.
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6. Emerson RW, Adams C, Nishino T, Hazlett HC, Wolff JJ, Zwaigenbaum L, Constantino JN, Shen MD, Swanson MR, Elison JT, Kandala S, Estes AM, Botteron KN, Collins L, Dager SR, Evans AC, Gerig G, Gu H, McKinstry RC, Paterson S, Schultz RT, Styner M, Schlaggar BL, Pruett JR, Jr., Piven J. {{Functional neuroimaging of high-risk 6-month-old infants predicts a diagnosis of autism at 24 months of age}}. {Sci Transl Med}. 2017; 9(393).
Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by social deficits and repetitive behaviors that typically emerge by 24 months of age. To develop effective early interventions that can potentially ameliorate the defining deficits of ASD and improve long-term outcomes, early detection is essential. Using prospective neuroimaging of 59 6-month-old infants with a high familial risk for ASD, we show that functional connectivity magnetic resonance imaging correctly identified which individual children would receive a research clinical best-estimate diagnosis of ASD at 24 months of age. Functional brain connections were defined in 6-month-old infants that correlated with 24-month scores on measures of social behavior, language, motor development, and repetitive behavior, which are all features common to the diagnosis of ASD. A fully cross-validated machine learning algorithm applied at age 6 months had a positive predictive value of 100% [95% confidence interval (CI), 62.9 to 100], correctly predicting 9 of 11 infants who received a diagnosis of ASD at 24 months (sensitivity, 81.8%; 95% CI, 47.8 to 96.8). All 48 6-month-old infants who were not diagnosed with ASD were correctly classified [specificity, 100% (95% CI, 90.8 to 100); negative predictive value, 96.0% (95% CI, 85.1 to 99.3)]. These findings have clinical implications for early risk assessment and the feasibility of developing early preventative interventions for ASD.
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7. Ethridge LE, White SP, Mosconi MW, Wang J, Pedapati EV, Erickson CA, Byerly MJ, Sweeney JA. {{Neural synchronization deficits linked to cortical hyper-excitability and auditory hypersensitivity in fragile X syndrome}}. {Mol Autism}. 2017; 8: 22.
BACKGROUND: Studies in the fmr1 KO mouse demonstrate hyper-excitability and increased high-frequency neuronal activity in sensory cortex. These abnormalities may contribute to prominent and distressing sensory hypersensitivities in patients with fragile X syndrome (FXS). The current study investigated functional properties of auditory cortex using a sensory entrainment task in FXS. METHODS: EEG recordings were obtained from 17 adolescents and adults with FXS and 17 age- and sex-matched healthy controls. Participants heard an auditory chirp stimulus generated using a 1000-Hz tone that was amplitude modulated by a sinusoid linearly increasing in frequency from 0-100 Hz over 2 s. RESULTS: Single trial time-frequency analyses revealed decreased gamma band phase-locking to the chirp stimulus in FXS, which was strongly coupled with broadband increases in gamma power. Abnormalities in gamma phase-locking and power were also associated with theta-gamma amplitude-amplitude coupling during the pre-stimulus period and with parent reports of heightened sensory sensitivities and social communication deficits. CONCLUSIONS: This represents the first demonstration of neural entrainment alterations in FXS patients and suggests that fast-spiking interneurons regulating synchronous high-frequency neural activity have reduced functionality. This reduced ability to synchronize high-frequency neural activity was related to the total power of background gamma band activity. These observations extend findings from fmr1 KO models of FXS, characterize a core pathophysiological aspect of FXS, and may provide a translational biomarker strategy for evaluating promising therapeutics.
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8. Fitzpatrick P, Romero V, Amaral JL, Duncan A, Barnard H, Richardson MJ, Schmidt RC. {{Evaluating the importance of social motor synchronization and motor skill for understanding autism}}. {Autism Res}. 2017.
Impairments in social interaction and communicating with others are core features of autism spectrum disorder (ASD), but the specific processes underlying such social competence impairments are not well understood. An important key for increasing our understanding of ASD-specific social deficits may lie with the social motor synchronization that takes place when we implicitly coordinate our bodies with others. Here, we tested whether dynamical measures of synchronization differentiate children with ASD from controls and further explored the relationships between synchronization ability and motor control problems. We found (a) that children with ASD exhibited different and less stable patterns of social synchronization ability than controls; (b) children with ASD performed motor movements that were slower and more variable in both spacing and timing; and (c) some social synchronization that involved motor timing was related to motor ability but less rhythmic synchronization was not. These findings raise the possibility that objective dynamical measures of synchronization ability and motor skill could provide new insights into understanding the social deficits in ASD that could ultimately aid clinical diagnosis and prognosis. Autism Res 2017. (c) 2017 International Society for Autism Research, Wiley Periodicals, Inc.
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9. Gaudissard J, Ginger M, Premoli M, Memo M, Frick A, Pietropaolo S. {{Behavioral abnormalities in the Fmr1-KO2 mouse model of fragile X syndrome: The relevance of early life phases}}. {Autism Res}. 2017.
Fragile X syndrome (FXS) is a developmental disorder caused by a mutation in the X-linked FMR1 gene, coding for the FMRP protein which is largely involved in synaptic function. FXS patients present several behavioral abnormalities, including hyperactivity, anxiety, sensory hyper-responsiveness, and cognitive deficits. Autistic symptoms, e.g., altered social interaction and communication, are also often observed: FXS is indeed the most common monogenic cause of autism. Mouse models of FXS are therefore of great interest for research on both FXS and autistic pathologies. The Fmr1-KO2 mouse line is the most recent FXS model, widely used for brain studies; surprisingly, little is known about the face validity of this model, i.e., its FXS-like behavioral phenotype. Furthermore, no data are available for the age-related expression of the pathological phenotypes in this mouse line, a critical issue for modelling neurodevelopmental disorders. Here we performed an extensive behavioral characterization of the KO2 model at infancy, adolescent and adult ages. Hyperactivity, altered emotionality, sensory hyper-responsiveness and memory deficits were already present in KO mice at adolescence and remained evident at adulthood. Alterations in social behaviors were instead observed only in young KO animals: during the first 2 weeks of life, KOs emitted longer ultrasonic vocalizations compared to their WT littermates and as adolescents they displayed more aggressive behaviors towards a conspecific. These results strongly support the face validity of the KO2 mouse as a model for FXS, at the same time demonstrating that its ability to recapitulate social autistic-relevant phenotypes depends on early testing ages. Autism Res 2017. (c) 2017 International Society for Autism Research, Wiley Periodicals, Inc.
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10. Lopata C, Rodgers JD, Donnelly JP, Thomeer ML, McDonald CA, Volker MA. {{Psychometric Properties of the Adapted Skillstreaming Checklist for High-functioning Children with ASD}}. {J Autism Dev Disord}. 2017.
This study examined the reliability and criterion-related validity of parent ratings on the Adapted Skillstreaming Checklist (ASC) for a sample of 275 high-functioning children, ages 6-12 years, with ASD. Internal consistency for the total sample was 0.92. For two subsamples, test-retest reliability was very good at the 6-week and good at the 9-month intervals. Child age, IQ, and language abilities were unrelated to the ASC score. The ASC total score was inversely and strongly related to parent ratings of ASD symptom severity. Significant positive correlations (moderate-to-high) were found between the ASC and prosocial skills scales and significant negative correlations (low-to-moderate) with problem behavior scales on a broad measure of child functioning. Implications and suggestions for future study are discussed.
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11. Mitra I, Tsang K, Ladd-Acosta C, Croen LA, Aldinger KA, Hendren RL, Traglia M, Lavillaureix A, Zaitlen N, Oldham MC, Levitt P, Nelson S, Amaral DG, Hertz-Picciotto I, Fallin MD, Weiss LA. {{Correction: Pleiotropic Mechanisms Indicated for Sex Differences in Autism}}. {PLoS Genet}. 2017; 13(6): e1006831.
[This corrects the article DOI: 10.1371/journal.pgen.1006425.].
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12. Novarino G. {{Rett syndrome modeling goes simian}}. {Sci Transl Med}. 2017; 9(393).
Rett syndrome modeling in monkey mirrors the human disorder.
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13. Saad K, Zahran AM, Elsayh KI, Abdel-Rahman AA, Al-Atram AA, Hussein A, El-Gendy YG. {{Frequency of Dendritic Cells and Their Expression of Costimulatory Molecules in Children with Autism Spectrum Disorders}}. {J Autism Dev Disord}. 2017.
The aim of our study was to evaluate the frequencies of myeloid dendritic cells (mDCs) and plasmacytoid dendritic cells (pDCs) in children with ASD. Subjects were 32 children with ASD and 30 healthy children as controls. The numbers of mDCs and pDCs and the expression of CD86 and CD80 on the entire DCs were detected by flow cytometry. ASD children had significantly higher percentages of mDCs and pDCs when compared to controls. We found significant inverse relationships between serum 25-hydroxyvitamin D levels and the frequencies of mDCs and pDCs in autistic children. Our data suggested that DCs could play a role in the clinical course of ASD. The relationship of DCs to immune disorders in ASD remains to be determined.
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14. Schiltz H, McIntyre N, Swain-Lerro L, Zajic M, Mundy P. {{The Stability of Self-Reported Anxiety in Youth with Autism Versus ADHD or Typical Development}}. {J Autism Dev Disord}. 2017.
Children with autism spectrum disorder (ASD) are at risk for anxiety symptoms. Few anxiety measures are validated for individuals with ASD, and the nature of ASD raises questions about reliability of self-reported anxiety. This study examined longitudinal stability and change of self-reported anxiety in higher functioning youth with ASD (HFASD) compared to youth with symptoms of attention deficit hyperactivity disorder and typical development (TD) using the Multidimensional Anxiety Scale for Children (March, 2012; March et al. J Am Acad Child Adolesc Psychiatry 36(4):554-565, 1997). Diagnostic groups demonstrated comparable evidence of stability for most dimensions of anxiety. The HFASD group displayed higher anxiety than both comparison groups, especially physical symptoms. These findings have implications for identification and measurement of anxiety in ASD.
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15. Shield A, Cooley F, Meier RP. {{Sign Language Echolalia in Deaf Children With Autism Spectrum Disorder}}. {J Speech Lang Hear Res}. 2017; 60(6): 1622-34.
Purpose: We present the first study of echolalia in deaf, signing children with autism spectrum disorder (ASD). We investigate the nature and prevalence of sign echolalia in native-signing children with ASD, the relationship between sign echolalia and receptive language, and potential modality differences between sign and speech. Method: Seventeen deaf children with ASD and 18 typically developing (TD) deaf children were video-recorded in a series of tasks. Data were coded for type of signs produced (spontaneous, elicited, echo, or nonecho repetition). Echoes were coded as pure or partial, and timing and reduplication of echoes were coded. Results: Seven of the 17 deaf children with ASD produced signed echoes, but none of the TD deaf children did. The echoic children had significantly lower receptive language scores than did both the nonechoic children with ASD and the TD children. Modality differences also were found in terms of the directionality, timing, and reduplication of echoes. Conclusions: Deaf children with ASD sometimes echo signs, just as hearing children with ASD sometimes echo words, and TD deaf children and those with ASD do so at similar stages of linguistic development, when comprehension is relatively low. The sign language modality might provide a powerful new framework for analyzing the purpose and function of echolalia in deaf children with ASD.
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16. Shroff G. {{Human Embryonic Stem Cells in the Treatment of Autism: A Case Series}}. {Innov Clin Neurosci}. 2017; 14(3-4): 12-6.
Background: Autism spectrum disorder is a neurodevelopmental disorder accompanied by weak immune system and neuroinflammation. Multiple factors contribute to etiology of autism spectrum disorder including genetic disorders, environmental substances/toxins, imbalanced immune system, encephalitis, and viral infections. Autism spectrum disorder is an incurable disease; however, it can be managed by educational and medical interventions. Human embryonic stem cell therapy has been shown to improve blood perfusion in the brain; thus, this therapy may be effective in improving motor skills, social skills, and cognition in patients with autism spectrum disorder. Method: Three pediatric patients with autism spectrum disorder were administered human embryonic stem cell therapy. Their treatment plan comprised 3 to 4 therapy sessions (T1, T2, T3, T4) that were 4 to 6 weeks in length, with 4- to 8-month gap phases separating each therapy session. Results: The patients showed improvements in eye coordination, writing, balancing, cognition, and speech and showed reduced hypersensitivity to noises and smells. Conclusion: The use of human embryonic stem cell therapy may be a safe and effective treatment for patients with autism spectrum disorder. Studies with larger sample sizes are needed to support the use of human embryonic stem cell therapy in this patient population.
17. Stafford LD, Tsang I, Lopez B, Severini M, Iacomini S. {{Autistic traits associated with food neophobia but not olfactory sensitivity}}. {Appetite}. 2017; 116: 584-8.
Food neophobia has been shown to be associated with a range of personality traits (including anxiety, lower sensation seeking) and additionally sensory aspects of food such as taste and texture. Running parallel to that work, research has demonstrated higher incidences of food neophobia in autistic populations and separately evidence of hypersensitivity in some sensory domains. The aim of the current study was to extend our understanding by exploring whether the broader aspects of autistic traits can predict food neophobia in a non-autistic population and whether this is mediated by differences in olfactory sensitivity. In the present study, student participants (N = 50) completed questionnaires measuring their food neophobia (FNS) and preferences for foreign cuisine, autistic traits (Autistic Quotient, AQ), and then completed an olfactory threshold test for a food related odour. The findings demonstrated a positive association between food neophobia and the magnitude of autistic traits and interestingly, an inverse relation between preference for foreign cuisine and olfactory sensitivity; those individuals less inclined toward foreign cuisine had poorer sensitivity to a food related odour. Since AQ was not related to olfactory sensitivity, these findings suggest the relation between autistic traits and food neophobia is unlikely to be mediated by olfactory sensitivity. More broadly however, our sense of smell is associated with experiencing a wider diet.
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18. Thurman AJ, Kover ST, Ted Brown W, Harvey DJ, Abbeduto L. {{Noncomprehension Signaling in Males and Females With Fragile X Syndrome}}. {J Speech Lang Hear Res}. 2017; 60(6): 1606-21.
Purpose: This study used a prospective longitudinal design to evaluate the trajectory and predictors of noncomprehension signaling in male and female youth with fragile X syndrome (FXS). Method: A direction-following task in which some of the directions were inadequate was administered. Participants were 52 youth (36 boys, 16 girls) with FXS. Upon study entry, participants ranged from 10 to 16 years. The average number of annual assessments per participant was 3.65 (range = 1-4), providing 198 data points for analysis. Results: Participants with FXS were less likely to signal noncomprehension than younger, typically developing, cognitively matched children. The average rate of change in noncomprehension signaling was not significantly different from 0 for either boys or girls, suggesting a plateau. Both FMRP and nonverbal IQ were significant independent predictors of noncomprehension signaling for boys. Variability in noncomprehension signaling among girls was not explained by any of the predictors, but trends similar to those observed for boys were observed. Conclusions: Noncomprehension signaling appears to be an area of weakness for individuals with FXS. Because the failure to signal noncomprehension can have negative, cumulative effects on comprehension, the results suggest a need for interventions targeting the requisite cognitive skills.
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19. Varghese M, Keshav N, Jacot-Descombes S, Warda T, Wicinski B, Dickstein DL, Harony-Nicolas H, De Rubeis S, Drapeau E, Buxbaum JD, Hof PR. {{Autism spectrum disorder: neuropathology and animal models}}. {Acta Neuropathol}. 2017.
Autism spectrum disorder (ASD) has a major impact on the development and social integration of affected individuals and is the most heritable of psychiatric disorders. An increase in the incidence of ASD cases has prompted a surge in research efforts on the underlying neuropathologic processes. We present an overview of current findings in neuropathology studies of ASD using two investigational approaches, postmortem human brains and ASD animal models, and discuss the overlap, limitations, and significance of each. Postmortem examination of ASD brains has revealed global changes including disorganized gray and white matter, increased number of neurons, decreased volume of neuronal soma, and increased neuropil, the last reflecting changes in densities of dendritic spines, cerebral vasculature and glia. Both cortical and non-cortical areas show region-specific abnormalities in neuronal morphology and cytoarchitectural organization, with consistent findings reported from the prefrontal cortex, fusiform gyrus, frontoinsular cortex, cingulate cortex, hippocampus, amygdala, cerebellum and brainstem. The paucity of postmortem human studies linking neuropathology to the underlying etiology has been partly addressed using animal models to explore the impact of genetic and non-genetic factors clinically relevant for the ASD phenotype. Genetically modified models include those based on well-studied monogenic ASD genes (NLGN3, NLGN4, NRXN1, CNTNAP2, SHANK3, MECP2, FMR1, TSC1/2), emerging risk genes (CHD8, SCN2A, SYNGAP1, ARID1B, GRIN2B, DSCAM, TBR1), and copy number variants (15q11-q13 deletion, 15q13.3 microdeletion, 15q11-13 duplication, 16p11.2 deletion and duplication, 22q11.2 deletion). Models of idiopathic ASD include inbred rodent strains that mimic ASD behaviors as well as models developed by environmental interventions such as prenatal exposure to sodium valproate, maternal autoantibodies, and maternal immune activation. In addition to replicating some of the neuropathologic features seen in postmortem studies, a common finding in several animal models of ASD is altered density of dendritic spines, with the direction of the change depending on the specific genetic modification, age and brain region. Overall, postmortem neuropathologic studies with larger sample sizes representative of the various ASD risk genes and diverse clinical phenotypes are warranted to clarify putative etiopathogenic pathways further and to promote the emergence of clinically relevant diagnostic and therapeutic tools. In addition, as genetic alterations may render certain individuals more vulnerable to developing the pathological changes at the synapse underlying the behavioral manifestations of ASD, neuropathologic investigation using genetically modified animal models will help to improve our understanding of the disease mechanisms and enhance the development of targeted treatments.
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20. Wilson US, Sadler KM, Hancock KE, Guinan JJ, Jr., Lichtenhan JT. {{Efferent inhibition strength is a Physiological Correlate of Hyperacusis in Children with Autism Spectrum Disorder}}. {J Neurophysiol}. 2017: jn 00142 2017.
Autism spectrum disorder (ASD) is a developmental disability that is poorly understood. ASD can influence communication, social interaction, and behavior. Children with ASD often have sensory hypersensitivities, including auditory hypersensitivity (hyperacusis). In adults with hyperacusis who are otherwise neurotypical, the medial olivocochlear (MOC) efferent reflex is stronger than usual. In children with ASD the MOC reflex has been measured, but without also assessing hyperacusis. We assessed the MOC reflex in children with ASD by measuring the strength of MOC-induced inhibition of transient-evoked otoacoustic emissions (TEOAEs), a non-invasive, physiological measure that reflects cochlear amplification. MOC activity was evoked by contralateral noise. Hyperacusis was assessed subjectively based on the children’s symptoms. We found a strong correlation between hyperacusis scores and MOC strength in children with ASD. When children were divided into ASD-with-severe-hyperacusis (ASDs), ASD-with-not-severe-hyperacusis (ASDns) and neurotypical (NT) groups, the last two groups had similar hyperacusis and MOC reflexes while the ASDs group, on average, had hyperacusis and MOC reflexes that were approximately twice as strong. The MOC inhibition of TEOAEs averaged larger at all frequencies in the ASDs compared to ASDns and NT groups. The results suggest that the MOC reflex can be used to estimate hyperacusis in children with ASD and might be used to validate future questionnaires to assess hyperacusis. Our results also provide evidence that strong MOC reflexes in children with ASD are associated with hyperacusis and that hyperacusis is a comorbid condition as opposed to being an integral part of the abnormal neural processing associated with ASD.
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21. Woodward ND, Giraldo-Chica M, Rogers B, Cascio CJ. {{Thalamocortical dysconnectivity in autism spectrum disorder: An analysis of the Autism Brain Imaging Data Exchange}}. {Biol Psychiatry Cogn Neurosci Neuroimaging}. 2017; 2(1): 76-84.
BACKGROUND: Individuals with autism spectrum disorder (ASD) exhibit differences in basic sensorimotor processing as well as general cortical excitability. These observations converge to implicate thalamocortical connectivity as a potential unifying neural mechanism. The goal of this study was to clarify mixed findings on thalamocortical functional connectivity in a large sample of individuals with ASD. METHODS: Using the Autism Brain Imaging Data Exchange (ABIDE), we examined thalamocortical functional connectivity in 228 individuals with ASD and a matched comparison group of 228 typically developing individuals. In order to fully characterize thalamocortical functional networks, we employed complementary seed-based approaches that examined connectivity of major cortical divisions (e.g. prefrontal cortex, temporal lobe) with the thalamus and whole-brain connectivity of specific thalamic sub-regions. RESULTS: Prefrontal cortex, temporal lobe, and sensorimotor cortex exhibited hyper-connectivity with the thalamus in ASD. In the whole-brain analysis, hyper-connectivity of several thalamic seeds included multiple cortical areas, but tended to converge in temporal cortical areas, including the temporoparietal junction. Follow-up analyses of age effects revealed that the connectivity abnormalities in ASD were more pronounced in adolescents compared to children and adults. CONCLUSIONS: These results confirm previous findings of temporal and motor thalamocortical hyper-connectivity in ASD, and extend them to include somatosensory and prefrontal cortex. While not directly addressable with the data available in ABIDE, this widespread hyper-connectivity could theoretically account for sensorimotor symptoms and general cortical excitability in ASD. Future studies should target comprehensive clinical and behavioral characterization in combination with functional connectivity in order to explore this possibility.
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22. Zantinge G, van Rijn S, Stockmann L, Swaab H. {{Physiological Arousal and Emotion Regulation Strategies in Young Children with Autism Spectrum Disorders}}. {J Autism Dev Disord}. 2017.
This study aimed to assess physiological arousal and behavioral regulation of emotion in the context of frustration in 29 children with Autism Spectrum Disorders (ASD) and 45 typically developing children (41-81 months). Heart rate was continuously measured and emotion strategies were coded, during a locked-box task. Results revealed increases in arousal followed by a decline during recovery, significant for both groups indicating that heart rate patterns between groups were identical. The ASD group deployed less constructive and more venting and avoidance strategies, which was related to language impairments. We conclude that rather than abnormal levels of emotional arousal, a key impairment in young children with ASD may be difficulties in behaviorally regulating and expressing experienced emotions to others.
