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  • As some of the material

    2018-11-09

    As some of the material in this review is speculative, it is worth being more concrete about specific lines of research to follow up on our suggestions. First, it would be important to establish whether there is indeed a developmental moderation of risk for SAD. More precisely, here, we make the suggestion that certain cognitive risk factors for social anxiety, such as interpretation biases, only emerge at particular stages of development. The presence of these biases would be contingent on a more sophisticated understanding of social situations and increased kisspeptin complexity of social interactions. There is some suggestion that interpretation biases only influence social anxiety during the adolescent years, through cross-sectional comparison of findings. However, more systematic, longitudinal investigations in the same sample could be conducted, assessing whether interpretation biases only contribute toward social anxiety at particular stages of development. An even better strategy would be to derive indices of social-cognitive development or underlying kisspeptin maturation as an index of development rather than chronological age. A second exciting area of research is to establish whether plasticity and specifically responsiveness to particular external interventions are in fact greater in adolescence compared to children and adults – and moreover, whether within adolescence there are particular ‘hotspots’. In this review, we have discussed growing evidence that learning and flexibility may be greater during adolescence, but this data has yet to be extended to responsiveness to particular anxiety-reduction techniques or interventions. These data would carry important implications for when to administer interventions. Finally, as mentioned at the end of Section 4, developing versions of CBM and NF training (separately or in combined form) that are optimally effective, for example by using task stimuli that are motivationally salient for adolescents should be a priority.
    Conflict of interest
    Acknowledgements S. H. is supported by a studentship from the Medical Research Council. J. L. has received funding from the ESRC, Calleva Research Centre and British Academy to conduct research in this area. The work on NF was supported by the European Commission FP7 Braintrain grant (602186). G. S. is funded by a James S. McDonnell Foundation (Understanding Human Cognition) Scholar Award.
    Introduction There is much variability in the amount of description present in methods sections, with some providing detailed information (e.g., Zappasodi et al., 2001) whereas others do not include information such as attrition rate, number of trials present in final dataset or information about the stimuli (e.g., Eswaran et al., 2000). For those that do provide methodological information, there are variations in techniques, methods, and measures. It is possible that this is due to the focus of the field thus far being on the feasibility for delivering stimuli and recording a neural response in a foetal population. Consequently little has been done to address what could be causing variance in results between studies. For example, experimenters have instead focussed on different processing methods for reducing noise, which will contribute to variance (Samonas et al., 1997; Taulu et al., 2004; Vrba et al., 2004). Despite successes in processing methods, disparities in response rates and response latencies between studies remain in the literature. Many other factors can cause variance, which cannot be controlled in a typical within-subjects design, such as distance from stimuli and foetal state (Kiefer-Schmidt et al., 2013). Due to there being so much variation in factors that are difficult to control, such as foetal state, primary growth is even more imperative that we understand the potential variance that is present due to paradigm construction and stimuli.
    Methods
    Results