The shared neural basis of empathy and facial imitation accuracy.

Empathy involves experiencing emotion vicariously, and understanding the reasons for those emotions. It may be served partly by a motor simulation function, and therefore share a neural basis with imitation (as opposed to mimicry), as both involve sensorimotor representations of intentions based on perceptions of others' actions. We recently showed a correlation between imitation accuracy and Empathy Quotient (EQ) using a facial imitation task and hypothesised that this relationship would be mediated by the human mirror neuron system. During functional Magnetic Resonance Imaging (fMRI), 20 adults observed novel 'blends' of facial emotional expressions. According to instruction, they either imitated (i.e. matched) the expressions or executed alternative, pre-prescribed mismatched actions as control. Outside the scanner we replicated the association between imitation accuracy and EQ. During fMRI, activity was greater during mismatch compared to imitation, particularly in the bilateral insula. Activity during imitation correlated with EQ in somatosensory cortex, intraparietal sulcus and premotor cortex. Imitation accuracy correlated with activity in insula and areas serving motor control. Overlapping voxels for the accuracy and EQ correlations occurred in premotor cortex. We suggest that both empathy and facial imitation rely on formation of action plans (or a simulation of others' intentions) in the premotor cortex, in connection with representations of emotional expressions based in the somatosensory cortex. In addition, the insula may play a key role in the social regulation of facial expression.

Deregulation of EIF4E: a novel mechanism for autism.

BACKGROUND: Autism is a common childhood onset neurodevelopmental disorder, characterised by severe and sustained impairment of social interaction and social communication, as well as a notably restricted repertoire of activities and interests. Its aetiology is multifactorial with a strong genetic basis. EIF4E is the rate limiting component of eukaryotic translation initiation, and plays a key role in learning and memory through its control of translation within the synapse. EIF4E mediated translation is the final common process modulated by the mammalian target of rapamycin (mTOR), PTEN and fragile X mental retardation protein (FMRP) pathways, which are implicated in autism. Linkage of autism to the EIF4E region on chromosome 4q has been found in genome wide linkage studies. METHODS AND RESULTS: The authors present evidence that directly implicates EIF4E in autism. In a boy with classic autism, the authors observed a de novo chromosome translocation between 4q and 5q and mapped the breakpoint site to within a proposed alternative transcript of EIF4E. They then screened 120 autism families for mutations and found two unrelated families where in each case both autistic siblings and one of the parents harboured the same single nucleotide insertion at position -25 in the basal element of the EIF4E promoter. Electrophoretic mobility shift assays and reporter gene studies show that this mutation enhances binding of a nuclear factor and EIF4E promoter activity. CONCLUSIONS: These observations implicate EIF4E, and more specifically control of EIF4E activity, directly in autism. The findings raise the exciting possibility that pharmacological manipulation of EIF4E may provide therapeutic benefit for those with autism caused by disturbance of the converging pathways controlling EIF4E activity.

Effects of treating postnatal depression on mother-infant interaction and child development: systematic review.

BACKGROUND: Postnatal depression has detrimental effects on the child's cognitive and emotional development. AIMS: To assess the benefits of treating postnatal depression for mother-infant interaction and child development. METHOD: A systematic search was made of 12 electronic bibliographic databases for randomised controlled trials and controlled clinical trials on treatment of mothers with postnatal depression, where outcomes were assessed in children; findings were assessed. RESULTS: Only eight trials met the inclusion criteria. Of those included, interventions varied widely but all involved therapies directed at the mother-infant relationship. One study with intensive and prolonged therapy showed cognitive improvement, whereas two others with briefer interventions improved maternal-infant relationships but did not affect the child's cognitive or behavioural development. All five studies assessing only mother-infant relationships showed improvements. CONCLUSIONS: Cognitive development in children of depressed mothers, along with better mother-infant relationships, might be improved with sustained interventions. Trials assessing treatments for postnatal depression would benefit from looking more closely at benefits for children as well as mothers, using validated objective measures.

Characteristics of fetal anticonvulsant syndrome associated autistic disorder.

The aim of this study was to evaluate the clinical features and frequency of autistic disorder or Asperger syndrome (AS; according to Diagnostic and Statistical Manual of Mental Disorders, 4th edition [DSM-IV] criteria) in children exposed to anticonvulsant medication in utero. During a 20-year study period, 626 children were born in Aberdeen to mothers taking antiepileptic drugs (AEDs). The study examined long-term effects of prenatal exposure to AEDs in 260 children (122 males, 138 females). Of these, 26 (16 males) were reported by parents to have social or behavioural difficulties. Eleven children (6 males, 5 females) fulfilled the DSM-IV criteria for autistic disorder and one (female) fulfilled the DSM-IV criteria for AS. These children comprised 4.6% of the exposed children studied, and 1.9% of all exposed children born during the study period. Mean age of these children at diagnosis was 5 years 4 months (SD 2y 11mo) and 9 years 10 months (SD 3y 10mo) at the time of this study. Other children from the group of 26 had difficulties in areas of speech and language development and social communication but did not meet the criteria for an autism spectrum disorder (ASD). Sodium valproate was the drug most commonly associated with autistic disorder, five of 56 (8.9%) of the study children exposed to sodium valproate alone had either autistic disorder or AS. It was concluded that prenatal exposure to anticonvulsant medication is a risk factor for the development of an ASD. Fetal anticonvulsant syndrome associated autistic disorder is characterized by an even sex ratio, absence of regression or skill loss, and language delay in the absence of global delay.

Second to fourth finger ratio and possible precursors of developmental psychopathology in preschool children.

BACKGROUND: The influence of sex steroids upon brain development has been suggested to mediate sex differences in developmental psychopathology. The ratio of the length of index finger or second finger to the ring finger or fourth finger (the 2D:4D ratio) appears to be a marker of early sex hormone exposure, with low 2D:4D associated with high prenatal testosterone and high 2D:4D associated with high prenatal oestrogen. This relationship allows a non-invasive measure of the long-term influence of prenatal sex steroids. Behaviours such as hyperactivity and poor social cognition are common in preschoolers. An association between 2D:4D and these possible precursors of psychopathology would be most readily identified in this group. AIM: To identify relationships between 2D:4D ratio and behaviours in preschool children which constitute possible precursors of developmental psychopathology. STUDY DESIGN: Population survey. METHOD: The 2D:4D ratio was measured in a group of preschool children and behavioural questionnaires were given to parents and teachers. RESULTS: Sex differences in behaviours were small, whilst correlations with 2D:4D were strong. Low 2D:4D was related to hyperactivity and poor social cognitive function in girls, and high 2D:4D with emotional symptoms in boys. CONCLUSIONS: We suggest that during early brain development androgens increase the probability of hyperactivity and poor social cognition in girls. Early oestrogens increase the probability of emotional problems in boys.