This study examines attentional biases in the presence of angry, happy and neutral faces using a modified eye tracking version of the dot probe task (DPT). Participants were 111 young children between 9 and 48 months. Children passively viewed an affective attention bias task that consisted of a face pairing (neutral paired with either neutral, angry or happy) for 500 ms that was followed by a 1,500-ms asterisk probe on 1 side of the screen. Congruent trials were trials in which the probe appeared on the same side of the screen as the emotional face and incongruent trials were trials in which the probe appeared on the opposite side of the emotional face. The latency to fixate on the probe, rather than the traditional task's button press latency, was measured for both types of trials and a bias score was calculated by subtracting the latency to the probe on congruent trials from that on incongruent trials. The results of the current study indicate positive internal reliability of this modified version of the DPT as well as the presence of a bias toward both angry and happy faces during the first 4 years of life. The successful use of the modified version of the DPT for use on the eye tracker presents a promising methodological tool for research on early attentional behavior and provides a tool for comprehensive longitudinal studies of identified risk factors for anxiety. (PsycINFO Database Record

Several researchers have proposed a causal relation between biased attention to threat and the development and maintenance of anxiety disorders in both children and adults. However, despite the widely documented correlation between attention bias to threat and anxiety, developmental research in this domain is limited. In this review, we highlight the importance of taking a developmental approach to studying attention biases to threat and anxiety. First, we discuss how recent developmental work on attention to threat fits into existing theoretical frameworks for the development of anxiety and how attention biases might interact with other risk factors across development. Then we review the developmental literature on attention bias to threat and anxiety and describe how classic methodologies can be modified to study attention biases in even the youngest infants. Finally, we discuss limitations and future directions in this domain, emphasizing the need for future longitudinal research beginning in early infancy that tracks concurrent developments in both biased attention and anxiety. Altogether, we hope that by highlighting the importance of development in the study of attention bias to threat and anxiety, we can provide a road map for how researchers might implement developmental approaches to studying a potential core mechanism in anxiety.

Collecting data with infants is notoriously difficult. As a result, many of our studies consist of small samples, with only a single measure, in a single age group, at a single time point. With renewed calls for greater academic rigor in data collection practices, using multiple outcome measures in infant research is one way to increase rigor, and, at the same time, enable us to more accurately interpret our data. Here, we illustrate the importance of using multiple measures in psychological research with examples from our own work on rapid threat detection and from the broader infancy literature. First, we describe our initial studies using a single outcome measure, and how this strategy caused us to nearly miss a rich and complex story about attention biases for threat and their development. We demonstrate how using converging measures can help researchers make inferences about infant behavior, and how using additional measures allows us to more deeply examine the mechanisms that drive developmental change. Finally, we provide practical and statistical recommendations for how researchers can use multiple measures in future work.

Mutations of the fragile X mental retardation 1 (FMR1) gene are the genetic cause of fragile X syndrome (FXS). The presence of significant socioemotional problems has been well documented in FXS although the brain basis of those deficits remains unspecified. Here, we investigated amygdala dysfunction and its relation to socioemotional deficits and FMR1 gene expression in children and adolescents on the FX spectrum (i.e., individuals whose trinucleotide CGG repeat expansion from 55 to over 200 places them somewhere within the fragile X diagnostic range from premutation to full mutation). Participants performed an fMRI task in which they viewed fearful, happy, and scrambled faces. Neuroimaging results demonstrated that FX participants revealed significantly attenuated amygdala activation in Fearful > Scrambled and Fearful > Happy contrasts compared with their neurotypical counterparts, while showing no differences in amygdala volume. Furthermore, we found significant relationships between FMR1 gene expression, anxiety/social dysfunction scores, and reduced amygdala activation in the FX group. In conclusion, we report novel evidence regarding a dosage response of the FMR1 gene on fear-specific functions of the amygdala, which is associated with socioemotional deficits in FXS.

BackgroundFragile X syndrome (FXS) results from a trinucleotide repeat expansion (full mutation >200 cytosine-guanine-guanine (CGG) repeats) in the FMR1 gene, leading to a reduction or absence of the gene’s protein product, fragile X mental retardation protein (FMRP), ultimately causing cognitive and behavioral impairments that are characteristic of the syndrome. In our previous work with infants and toddlers with FXS, we have been able to describe much about their cognitive and visual processing abilities. In light of recent work on the mild cognitive deficits and functional and structural brain differences that are present in adults with the fragile X (FX) premutation, in the present study we examined whether some of the low-level visual processing deficits we have observed in infants with FXS would also be present in infants with the FX premutation (55–200 CGG repeats).MethodsWe chose a contrast detection task using second-order motion stimuli on which infants with FXS previously showed significantly increased detection thresholds (Vision Res 48:1471–1478, 2008). Critically, we also included a developmental delay comparison group of infants with Down syndrome (DS), who were matched to infants with FXS on both chronological and mental age, to speak to the question of whether this second-order motion processing deficit is a FX-specific phenomenon.ResultsAs reported previously, infants with the FX full mutation showed motion contrast detection threshold levels that were significantly higher than age-matched typically developing control infants. Strikingly, the motion detection contrast levels of FX premutation infants were also significantly higher than typically developing (TD) infants and not significantly different from the group of infants with FXS or with DS.ConclusionsThese results, which are in keeping with a growing body of evidence on the mild cognitive and perceptual processing deficits and functional and structural brain differences that are present in adults and older children with the FX premutation, underscore the pressing need to study and describe the processing capabilities of infants and toddlers with the FX premutation.