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Negative biases in emotional processing are well recognised in people who are currently depressed but are less well described in those with a history of depression, where such biases may contribute to vulnerability to relapse.
To compare accuracy, discrimination and bias in face emotion recognition in those with current and remitted depression.
The sample comprised a control group (n = 101), a currently depressed group (n = 30) and a remitted depression group (n = 99). Participants provided valid data after receiving a computerised face emotion recognition task following standardised assessment of diagnosis and mood symptoms.
In the control group women were more accurate in recognising emotions than men owing to greater discrimination. Among participants with depression, those in remission correctly identified more emotions than controls owing to increased response bias, whereas those currently depressed recognised fewer emotions owing to decreased discrimination. These effects were most marked for anger, fear and sadness but there was no significant emotion × group interaction, and a similar pattern tended to be seen for happiness although not for surprise or disgust. These differences were confined to participants who were antidepressant-free, with those taking antidepressants having similar results to the control group.
Abnormalities in face emotion recognition differ between people with current depression and those in remission. Reduced discrimination in depressed participants may reflect withdrawal from the emotions of others, whereas the increased bias in those with a history of depression could contribute to vulnerability to relapse. The normal face emotion recognition seen in those taking medication may relate to the known effects of antidepressants on emotional processing and could contribute to their ability to protect against depressive relapse.
Drug-related stimuli reliably induce craving in experimental paradigms, yet are rarely cited by drug users as major precipitants of relapse. We examined the motivational significance of drug cues in opiate dependence, by exploring their impact on central attentional processes.
Fourteen methadone-maintained subjects and 14 matched controls were studied. Subjects performed a novel active visual oddball task, consisting of opiate-related and matched neutral pictures, some of which (the oddballs) included a white cup. Subjects were fitted with a 32-channel electrode cap. The P300 for each stimulus category was identified using temporal principal components analysis.
The P300 elicited by opiate stimuli was significantly larger than that elicited by neutral stimuli in the methadone-maintained group but not in the controls. There was also a non-significant trend for the opiate stimuli to elicit larger P300s than the oddball stimuli in the addicted group.
These results suggest that drug cues acquire motivational salience and automatically capture attentional resources in opiate addicts, even when engaged in a non-drug-related task. Enhanced P300s to drug cues may provide an important biological marker of crucial psychological mechanisms relevant to addiction.
Social adversity may be a risk factor for depression, by increasing Cortisol secretion, which impairs serotonin (5-HT) neurotransmission.
To examine this causal pathway in a community setting.
Women who were currently ICD–10 depressed (n=94), vulnerable to depression but not depressed (n=166) and non-vulnerable controls (n=177) were recruited. We assessed social adversity and vulnerability (Life Eventsand Difficulties Schedule; Self Evaluation and Social Support Scales) and psychiatric state (Schedules for Clinical Assessment in Neuropsychiatry). Salivary cortisol concentrations were measured at 09.00 and 23.00 h. Serotonin function was assessed using prolactin responses to dexfenfluramine.
Cortisol concentrations were not increased in the depressed or vulnerable. Morning salivary and serum cortisol were reduced in depression. Evening cortisol was increased after recent life events. Life events and depression were associated with increased prolactin responses.
The hypothalamic–pituitary–adrenal axis is sensitive to social stress but does not mediate vulnerability to depression. Exaggerated 5-HT2 receptor responsiveness to stress may play a role in the evolution of depression.
PET studies of verbal fluency in schizophrenia report a failure of ‘deactivation’ of left superior temporal gyrus (STG) in the presence of activation of left dorsolateral prefrontal cortex (DLPFC), which deficit has been attributed to underlying ‘functional disconnectivity’.
To test whether these findings provide trait-markers for schizophrenia.
We used H215O PET to examine verbal fluency in 10 obligate carriers of the predisposition to schizophrenia, 10 stable patients and 10 normal controls.
We found no evidence of a failure of left STG deactivation in carriers or patients. Instead, patients failed to deactivate the precuneus relative to other groups. We found no differences in functional connectivity between left DLPFC and left STG but patients exhibited significant disconnectivity between left DLPFC and anterior cingulate cortex.
Failure of left STG ‘deactivation’ and left fronto-temporal disconnectivity are not consistent findings in schizophrenia; neither are they trait-markers for genetic risk. Prefrontal functional disconnectivity here may characterise the schizophrenic phenotype.
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