Our ability to differentiate between simple facial expressions of emotion develops between infancy and early adulthood, yet few studies have explored the developmental trajectory of emotion recognition using a single methodology across a wide age-range. We investigated the development of emotion recognition abilities through childhood and adolescence, testing the hypothesis that children’s ability to recognize simple emotions is modulated by chronological age, pubertal stage and gender. In order to establish norms, we assessed 478 children aged 6–16 years, using the Ekman-Friesen Pictures of Facial Affect. We then modeled these cross-sectional data in terms of competence in accurate recognition of the six emotions studied, when the positive correlation between emotion recognition and IQ was controlled. Significant linear trends were seen in children’s ability to recognize facial expressions of happiness, surprise, fear, and disgust; there was improvement with increasing age. In contrast, for sad and angry expressions there is little or no change in accuracy over the age range 6–16 years; near-adult levels of competence are established by middle-childhood. In a sampled subset, pubertal status influenced the ability to recognize facial expressions of disgust and anger; there was an increase in competence from mid to late puberty, which occurred independently of age. A small female advantage was found in the recognition of some facial expressions. The normative data provided in this study will aid clinicians and researchers in assessing the emotion recognition abilities of children and will facilitate the identification of abnormalities in a skill that is often impaired in neurodevelopmental disorders. If emotion recognition abilities are a good model with which to understand adolescent development, then these results could have implications for the education, mental health provision and legal treatment of teenagers.

The amygdala, which plays a critical role in emotional learning and social cognition, is structurally and functionally sexually dimorphic in humans. We used magnetic neuroimaging and molecular genetic analyses with healthy subjects and patients possessing X-chromosome anomalies to find dosage-sensitive genes that might influence amygdala development. If such X-linked genes lacked a homologue on the Y-chromosome they would be expressed in one copy in normal 46,XY males and two copies in normal 46,XX females. We showed by means of magnetic neuroimaging that 46,XY males possess significantly increased amygdala volumes relative to normal 46,XX females. However, females with Turner syndrome (45,X) have even larger amygdalae than 46,XY males. This finding implies that haploinsufficiency for one or more X-linked genes influences amygdala development irrespective of a direct or indirect (endocrinological) mechanism involving the Y-chromosome. 45,X females also have increased grey matter volume in the orbitofrontal cortex bilaterally, close to a region implicated in emotional learning. They are as poor as patients with bilateral amygdalectomies in the recognition of fear from facial expressions. We attempted to localize the gene(s) responsible for these deficits in X-monosomy by means of a deletion mapping strategy. We studied female patients possessing structural X-anomalies of the short arm. A genetic locus (no greater than 4.96 Mb in size) at Xp11.3 appears to play a key role in amygdala and orbitofrontal structural and (by implication) functional development. Females with partial X-chromosome deletions, in whom this critical locus is deleted, have normal intelligence. Their fear recognition is as poor as that of 45,X females and their amygdalae are correspondingly enlarged. This 4.96 Mb region contains, among others, the genes for monoamine oxidase A (MAOA) and B (MAOB), which are involved in the oxidative deamination of several neurotransmitters, including dopamine and serotonin. Abnormal activity of these neurotransmitters has been implicated in the aetiology of several neurodevelopmental disorders in which social cognitive deficits are prominent. These associated deficits include a specific lack of fear recognition from facial expressions. We show that the thrombocytic activity of MAOB is proportionate to the number of X-chromosomes, and hypothesize that haploinsufficiency of this enzyme in 45,X females predisposes to their deficits in social cognition.

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