scholarly journals Behavioural and neural markers of tactile sensory processing in infants at elevated likelihood of autism spectrum disorder and/or attention deficit hyperactivity disorder

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Elena Serena Piccardi ◽  
◽  
Jannath Begum Ali ◽  
Emily J. H. Jones ◽  
Luke Mason ◽  
...  

Abstract Backgrounds Atypicalities in tactile processing are reported in autism spectrum disorder (ASD) and attention deficit hyperactivity disorder (ADHD) but it remains unknown if they precede and associate with the traits of these disorders emerging in childhood. We investigated behavioural and neural markers of tactile sensory processing in infants at elevated likelihood of ASD and/or ADHD compared to infants at typical likelihood of the disorders. Further, we assessed the specificity of associations between infant markers and later ASD or ADHD traits. Methods Ninety-one 10-month-old infants participated in the study (n = 44 infants at elevated likelihood of ASD; n = 20 infants at elevated likelihood of ADHD; n = 9 infants at elevated likelihood of ASD and ADHD; n = 18 infants at typical likelihood of the disorders). Behavioural and EEG responses to pairs of tactile stimuli were experimentally recorded and concurrent parental reports of tactile responsiveness were collected. ASD and ADHD traits were measured at 24 months through standardized assessment (ADOS-2) and parental report (ECBQ), respectively. Results There was no effect of infants’ likelihood status on behavioural markers of tactile sensory processing. Conversely, increased ASD likelihood associated with reduced neural repetition suppression to tactile input. Reduced neural repetition suppression at 10 months significantly predicted ASD (but not ADHD) traits at 24 months across the entire sample. Elevated tactile sensory seeking at 10 months moderated the relationship between early reduced neural repetition suppression and later ASD traits. Conclusions Reduced tactile neural repetition suppression is an early marker of later ASD traits in infants at elevated likelihood of ASD or ADHD, suggesting that a common pathway to later ASD traits exists despite different familial backgrounds. Elevated tactile sensory seeking may act as a protective factor, mitigating the relationship between early tactile neural repetition suppression and later ASD traits.

Autism ◽  
2021 ◽  
pp. 136236132199125
Author(s):  
Janina Neufeld ◽  
Mark J Taylor ◽  
Karl Lundin Remnélius ◽  
Johan Isaksson ◽  
Paul Lichtenstein ◽  
...  

Autism spectrum disorder is associated with sensory processing alterations, such as sensory hyper- and hypo-responsiveness. Twin studies are scarce in this field, but they are necessary in order to disentangle the genetic and environmental contributions to this association. Furthermore, it is unclear how different neurodevelopmental/psychiatric conditions contribute to altering sensory processing. We investigated the association between autistic traits/autism spectrum disorder diagnosis and sensory processing alterations in twins ( N = 269), using the adult/adolescent sensory profile, which differentiates four sub-domains: Low Registration, Sensation Seeking, Sensory Sensitivity, and Sensation Avoiding. While the associations between autistic traits and Low Registration and Sensation Avoiding persisted within monozygotic (genetically identical) twins, Sensory Sensitivity was only associated with autistic traits within dizygotic twins. In multivariate analyses with different neurodevelopmental/psychiatric diagnoses as predictor variables, autism spectrum disorder and attention deficit hyperactivity disorder were the strongest predictors for two adult/adolescent sensory profile sub-domains each. The results suggest that the association between autistic traits and Sensory Sensitivity is influenced by genetics while non-shared environmental factors influence the associations between autistic traits and Low Registration and Sensation Avoiding. They further indicate that altered sensory processing is not specific to autism spectrum disorder, while autism spectrum disorder is a strong predictor of certain sensory processing alterations, even when controlling for other (comorbid) neurodevelopmental/psychiatric conditions. Lay abstract Individuals diagnosed with autism often describe that they process sensory information differently from others, and many experience sensory issues as problematic. For instance, an increased sensitivity to smells or sounds can make participating in social settings challenging. While sensory issues are now part of the diagnostic criteria for autism, they also co-occur with other psychiatric diagnoses such as attention deficit hyperactivity disorder and anxiety disorders. It is unclear to what extent the relationship between autism and alterations in sensory processing are due to genetics or environment. In addition, more research is needed on how autism, as compared to other diagnoses, is associated with sensory issues. Using a twin study, we found that genetic factors influenced self-reported reactivity to sensory stimuli in autism while environmental factors influenced other sensory issues (e.g. difficulties in detecting or differentiating sensory input). Hence, sensory hyper-reactivity might be an early onset core feature of autism, while other domains of alterations in sensory processing might develop later, influenced by the environment. Moreover, autism was more strongly associated with sensory issues related to increased sensitivity/reactivity as compared to other psychiatric diagnoses. However, attention deficit hyperactivity disorder was more strongly related to deficits in detecting/differentiating sensory stimuli and with an increased drive to seek sensory input. Our results indicate that sensory issues are not specific to autism, but that some aspects of altered sensory processing are more relevant for autism than for other diagnoses.


2021 ◽  
Vol 162 (42) ◽  
pp. 1703-1708
Author(s):  
Nóra Kollárovics ◽  
Péter Nagy ◽  
Judit Balázs

Összefoglaló. Bár a figyelemhiányos hiperaktivitási zavar kezelése során alkalmazott metilfenidát-monoterápiával összefüggésben jelentkező gynaecomastiáról bizonyos nemkívánatos hatások adatbázisai beszámolnak, a szakirodalom áttekintése alapján ez idáig mindössze 5 esettanulmányt publikáltak a témában. Tanulmányunkban egy autizmusspektrum-zavarral és figyelemhiányos hiperaktivitási zavarral egyaránt diagnosztizált gyermek esetét mutatjuk be, akinél 6 hónapon át tartó, folyamatos metilfenidát-monoterápiájával összefüggésben kétoldali gynaecomastia kialakulását tapasztaltuk. A kezelés azonnali leállítása mellett 10 napos klomifénkezelés történt. A metilfenidát-terápia azonnali leállítását követően 14 nappal a gynaecomastia mindkét oldalon visszahúzódott. 3 hónapos, gyermekpszichiátriai szempontból gyógyszermentes időszakot követően a metilfenidát-terápia újraindítása történt, de 1 hónap elteltével a nem kívánt mellékhatás ismét jelentkezett. A metilfenidát-terápia és a gynaecomastia kialakulása közötti kapcsolat számos mechanizmussal kapcsolatban kérdéseket vet fel. Gyermekpszichiátriai szempontból érdekes kérdés, hogy releváns lehet-e a gyógyszeres terápia következményeként kialakuló nemkívánatos mellékhatás megjelenésében az autizmusspektrum-zavar és a figyelemhiányos hiperaktivitási zavar komorbid fennállása. A jelenség hátterében felmerül továbbá a neuroendokrin-immunológiai rendszer szabályozásának esetleges megváltozása. Esettanulmányunk felhívja a gyakorló orvoskollégák figyelmét a metilfenidát-terápia alkalmazása mellett potenciálisan kialakuló gynaecomastia monitorozására. Orv Hetil. 2021; 162(42): 1703–1708. Summary. Although gynecomastia associated with methylphenidate monotherapy in the treatment of attention deficit hyperactivity disorder has already been reported in some adverse event databases, based on a review of the literature it appears that only five case reports have been published. In our study, we present the case of a child diagnosed with both autism spectrum disorder and attention deficit/hyperactivity disorder, who developed bilateral gynecomastia in association with continuous methylphenidate monotherapy for 6 months. With immediate cessation of methylphenidate therapy, clomiphene treatment was given for 10 days. A total of 14 days after cessation of methylphenidate treatment gynecomastia receded on both sides. After a methylphenidate drug-free period of 3 months, methylphenidate therapy was restarted, but 1 month later the side effect reappeared. The relationship between methylphenidate and the development of gynecomastia raises questions about a number of mechanisms. From a child psychiatrist point of view, it is an interesting question whether the presence of comorbid autism spectrum disorder and attention deficit/hyperactivity disorder may be relevant in the onset of adverse events by medication. The phenomenon may also be caused by altered regulation of the neuroendocrine-immune system. Our case report draws the attention of practicing physicians to monitoring of potential gynecomastia during methylphenidate therapy. Orv Hetil. 2021; 162(42): 1703–1708.


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