scholarly journals Is a Negative Attentional Bias in Individuals with Autism Spectrum Disorder Explained by Comorbid Depression? An Eye-Tracking Study

Author(s):  
M. Annemiek Bergman ◽  
Janna N. Vrijsen ◽  
Mike Rinck ◽  
Iris van Oostrom ◽  
Cornelis C. Kan ◽  
...  

AbstractHeightened attention towards negative information is characteristic of depression. Evidence is emerging for a negative attentional bias in Autism spectrum disorder (ASD), perhaps driven by the high comorbidity between ASD and depression. We investigated whether ASD is characterised by a negative attentional bias and whether this can be explained by comorbid (sub) clinical depression. Participants (n = 116) with current (CD) or remitted depression (RD) and/or ASD, and 64 controls viewed positively and negatively valenced (non-)social pictures. Groups were compared on three components of visual attention using linear mixed models. Both CD individuals with and without ASD, but not remitted depressed and never-depressed ASD individuals showed a negative bias, suggesting that negative attentional bias might be a depressive state-specific marker for depression in ASD.

Children ◽  
2018 ◽  
Vol 5 (9) ◽  
pp. 112 ◽  
Author(s):  
Melissa DeFilippis

Autism spectrum disorder (ASD) has a high rate of psychiatric comorbidity. The prevalence of comorbid depression seems to correlate with higher functioning forms of ASD and increasing age. Adolescence is a time when youth struggle with identity and interpersonal relationships, and a diagnosis of ASD further complicates this process. Adolescents with ASD may be more aware of the social communication deficits that come with the diagnosis than children with ASD, and it is theorized that higher functioning adolescents may experience this more acutely. While this may be true, the lack of reliable rating and diagnostic scales for depression in individuals with ASD makes it difficult to accurately measure rates of depression among individuals with more severe verbal deficits. While some research has focused on the prevalence of comorbid depression in children and adolescents with ASD and on the associated risk factors, there is very little evidence guiding treatment, including no empirical studies on psychopharmacology for depression in this population. Available evidence exists only in psychosocial approaches to treatment at this time and is mostly limited to adult studies. Current evidence will be presented in this review, including prevalence rates of depression in youth with ASD, various risk and protective factors, the use of diagnostic rating scales, and treatment studies. The lack of evidence supporting various treatment approaches will be highlighted, including challenges specific to the treatment of depression in ASD, which are not addressed in the current treatment studies in typically developing youth with depression.


2017 ◽  
Vol 47 (12) ◽  
pp. 3714-3727 ◽  
Author(s):  
Bosiljka Milosavljevic ◽  
◽  
Elizabeth Shephard ◽  
Francesca G. Happé ◽  
Mark H. Johnson ◽  
...  

2012 ◽  
Author(s):  
C. Veness ◽  
M. Prior ◽  
E. Bavin ◽  
P. Eadie ◽  
E. Cini ◽  
...  

Emotion ◽  
2020 ◽  
Vol 20 (6) ◽  
pp. 980-992 ◽  
Author(s):  
Jennifer B. Wagner ◽  
Brandon Keehn ◽  
Helen Tager-Flusberg ◽  
Charles A. Nelson

2021 ◽  
Vol 15 ◽  
Author(s):  
Suk-Ling Ma ◽  
Lu Hua Chen ◽  
Chi-Chiu Lee ◽  
Kelly Y. C. Lai ◽  
Se-Fong Hung ◽  
...  

Background: Recent findings indicated a high comorbidity between attention-deficit/hyperactivity disorder (ADHD) and autism spectrum disorder (ASD), as well as shared genetic influences on them. The latter might contribute at least partly to the former clinical scenario. This study aimed at investigating whether SHANK genes were potential pleiotropic genes to the two said disorders, underlying their genetic overlap.Methods: This study recruited 298 boys with ADHD (including 256 family trios of 1 ADHD boy and his 2 biological parents), 134 boys with ASD, 109 boys with both ADHD and ASD, and 232 typically developing boys as community controls. They were aged between 6 and 11 years old.Results: There was no significant difference in allele frequency of a number of single nucleotide polymorphisms (SNPs) in SHANK2/SHANK3 between the three clinical groups (ADHD, ASD, and ADHD + ASD) and between the two control groups (community controls and pseudo-controls), respectively. The three clinical groups and the two control groups were thus, respectively, combined. A comparison between the two aggregated samples identified significant evidence of disease association for three SHANK2 SNPs with both ADHD and ASD, even after multiple testing correction: rs11236616 (OR = 0.762, permuted p = 0.0376), rs7106631 (OR = 0.720, permuted p = 0.0034), and rs9888288 (OR = 0.770, permuted p = 0.0407). Comparisons among individual groups pointed to a similar trend of findings.Conclusion:SHANK2 could be considered a potential pleiotropic gene underlying the genetic overlap between ADHD and ASD. This might contribute partly to their high comorbidity in the afflicted children.


PLoS ONE ◽  
2021 ◽  
Vol 16 (8) ◽  
pp. e0256780
Author(s):  
Toshiyuki Ohtani ◽  
Akio Wakabayashi ◽  
Chihiro Sutoh ◽  
Fumiyo Oshima ◽  
Yoshiyuki Hirano ◽  
...  

In clinical settings, autism spectrum disorder (ASD) with comorbid depression is often difficult to diagnose, and should be considered in treatment. However, to our knowledge, no functional imaging study has examined the difference between ASD adolescents with and without comorbid depression. We aimed to compare the characteristics and prefrontal brain function of ASD with and without depression in order to identify a biological marker that can be used to detect the difference. Twenty-eight drug-naïve adolescents with ASD (14 ASD with and 14 ASD without depression) and 14 age- and gender-matched adolescents with typical development were evaluated using several variables. These included intelligence quotient, autism quotient, depression severity using the Beck Depression Inventory 2nd edition (BDI-II), and level of social functioning using the Social Adaptation Self-evaluation Scale (SASS). In addition, frontotemporal hemodynamic responses during a verbal fluency task (VFT) were measured using functional near-infrared spectroscopy (fNIRS). The ASD group, including both of the ASD with and ASD without depression groups, showed smaller hemodynamic responses than the typical development group in portions of the left dorsolateral prefrontal cortex (DLPFC), bilateral ventrolateral prefrontal cortex (VLPFC) and anterior part of the temporal cortex (aTC) during the VFT. Moreover, the smaller hemodynamic responses in the right VLPFC during the VFT in the ASD group were associated with the worse BDI-II and SASS scores. Furthermore, the ASD with depression group showed smaller hemodynamic responses in the right VLPFC during the VFT than the ASD without depression group in a direct comparison. Adolescents with ASD showed reduced activation in broad frontotemporal regions during a cognitive task compared with those with typical development. More specifically, the right VLPFC activation reflected the level of self-estimated depression and social functioning in the ASD subjects, and could be used to discriminate between ASD adolescents with and without depression.


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