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Studies of adults with depression point to characteristic neurocognitive deficits, including differences in processing facial expressions. Few studies have examined face processing in juvenile depression, or taken account of other comorbid disorders. Three groups were compared: depressed children and adolescents with conduct disorder (n = 23), depressed children and adolescents without conduct disorder (n = 29) and children and adolescents without disorder (n = 37). A novel face emotion processing experiment presented faces with "happy", "sad", "angry", or "fearful" expressions of varying emotional intensity using morphed stimuli. Those with depression showed no overall or specific deficits in facial expression recognition accuracy. Instead, they showed biases affecting processing of low-intensity expressions, more often perceiving these as sad. In contrast, non-depressed controls more often misperceived low intensity negative emotions as happy. There were no differences between depressed children and adolescents with and without conduct disorder, or between children with comorbid depression/conduct disorder and controls. Face emotion processing biases rather than deficits appear to distinguish depressed from non-depressed children and adolescents.

Background There is a known strong genetic contribution to aggression in those with ADHD. In a previous investigation of a large population cohort, impaired 'emotional/social cognitive' processing, assessed by questionnaire, was observed to mediate the link between COMT Val158Met and aggression in individuals with ADHD. We set out to replicate and extend this finding in a clinical sample, using task-based and physiological assessments of emotional and cognitive processing. Our aim was to test the hypothesis that directly assessed emotional processing mediates the link between COMT Val158Met and aggression in young people with ADHD. Methods Males aged 10-17 years with ADHD were recruited from UK community clinics ( n = 194). Research diagnostic interviews (parent and child) were used to assess psychopathology and generate DSM- IV Conduct Disorder symptom scores. Participants completed tasks assessing executive function (response inhibition and set shifting), empathy for fear, sadness and happiness, and fear conditioning [measured using skin conductance responses ( SCR) to aversive stimuli]. Results COMT V al allele carriers showed poorer response inhibition ( F = 5.27, p = .02) and set shifting abilities ( F = 6.45, p = .01), reduced fear empathy ( F = 4.33, p = .04) and reduced autonomic responsiveness (lower SCRs) to the conditioned aversive stimulus ( F = 11.74, p = .001). COMT Val158Met did not predict impairments in recognising others' emotions or affective empathy for happiness or sadness. Mediation analysis revealed that impaired fear-related mechanisms indirectly mediated the link between COMT Val158Met and aggression. Conclusion Our findings suggest fear mechanisms as possible targets for psychological interventions to disrupt links between genetic risk and aggressive outcomes in ADHD. Our findings also reveal the potential of hypothesis-driven approaches for identifying neuropsychological mechanisms that mediate genetic risk effects on behaviour and psychopathology. [ABSTRACT FROM AUTHOR]

Aims and method In up to a quarter of patients, schizophrenia is resistant to standard treatments. We undertook a naturalistic study of 153 patients treated in the tertiary referral in-patient unit of the National Psychosis Service based at the Maudsley Hospital in London. A retrospective analysis of symptoms on admission and discharge was undertaken using the OPCRIT tool, along with preliminary economic modelling of potential costs related to changes in accommodation. Results In-patient treatment demonstrated statistically significant improvements in all symptom categories in patients already identified as having schizophrenia refractory to standard secondary care. The preliminary cost analysis showed net savings to referring authorities due to changes from pre- to post-discharge accommodation. Clinical implications Despite the enormous clinical, personal and societal burden of refractory psychotic illnesses, there is insufficient information on the outcomes of specialised tertiary-level care. Our pilot data support its utility in all domains measured. [ABSTRACT FROM AUTHOR]