Schizophrenia patients are impaired in empathic accuracy.

BACKGROUND: Empathy is crucial for successful social relationships. Despite its importance for social interactions, little is known about empathy in schizophrenia. This study investigated the degree to which schizophrenia patients can accurately infer the affective state of another person (i.e. empathic accuracy). METHOD: A group of 30 schizophrenia patients and 22 healthy controls performed an empathic accuracy task on which they continuously rated the affective state of another person shown in a video (referred to as the 'target'). These ratings were compared with the target's own continuous self-rating of affective state; empathic accuracy was defined as the correlation between participants' ratings and the targets' self-ratings. A separate line-tracking task was administered to measure motoric/attentional factors that could account for group differences in performance. Participants' self-rated empathy was measured using the Interpersonal Reactivity Index, and targets' self-rated emotional expressivity was measured using the Berkeley Expressivity Questionnaire. RESULTS: Compared with controls, schizophrenia patients showed lower empathic accuracy although they performed the motoric tracking task at high accuracy. There was a significant group×target expressivity interaction such that patients showed a smaller increase in empathic accuracy with higher levels of emotional expressivity by the target, compared with controls. Patients' empathic accuracy was uncorrelated with self-reported empathy or clinical symptoms. CONCLUSIONS: Schizophrenia patients showed lower empathic accuracy than controls, and their empathic accuracy was less influenced by the emotional expressivity of the target. These findings suggest that schizophrenia patients benefit less from social cues of another person when making an empathic judgement.

Individual differences in trait anhedonia: a structural and functional magnetic resonance imaging study in non-clinical subjects.

Anhedonia, the reduced capacity to gain pleasure from pleasurable experiences, is a key symptom of major depression and schizophrenia. Reduced hedonic capacity can also be measured as an enduring trait in non-clinical subjects. Such altered hedonic capacity is likely the result of a basic neuropsychophysiological dysfunction and a vulnerability marker that potentially precedes and contributes to the liability of developing psychiatric disorders. The characterization of the structural and functional neural correlates of trait anhedonia in non-clinical individuals may provide new insights for the early detection of such psychiatric diseases. Twenty-nine non-clinical subjects were scanned at the Montreal Neurological Institute. Trait anhedonia was measured using the Chapman Revised Physical Anhedonia Scale. Semi-automated and automated structural MRI segmentation techniques were used to explore structural correlates of trait anhedonia. Seventeen of the 29 subjects also underwent a functional imaging task where responses to the viewing of affective stimuli were examined to identify the functional correlates of trait anhedonia. Trait anhedonia was inversely related to anterior caudate volume, but positively related to ventromedial prefrontal cortex activity during the processing of positive information. These findings may reflect a specific kind of vulnerability for the development of psychiatric affective disorders and suggest that trait anhedonia may be linked to a volumetric reduction in the basal ganglia and to a prefrontal functional abnormality during hedonic processing.

Executive functions and updating of the contents of working memory in unipolar depression.

BACKGROUND: Depression is characterized by cognitive impairments, including executive dysfunctions. These executive deficits could reflect impairments of more basic executive processes, such as updating, set shifting and inhibition. While shifting and inhibition impairments are often reported, studies on depression have been somewhat obscure about specific deficits of the updating process. The main goal of that study was to assess the updating process in young in-patients with depression. METHODS: We used a verbal n-back task to assess updating process. Load and mental manipulation within working memory (WM) were incremented by using three different levels of complexity (1,2,3-back). Neuropsychological tests and an attentional task (0-back) were also administered to subjects. Twenty-two individuals meeting DSM-IV criteria for Major Unipolar Depression and 22 healthy control subjects, matched on age, verbal IQ and education, were included in the study. RESULTS: Subjects with depression showed significant deficits at the n-back task compared to control subjects. They were normal in tasks assessing the short-term maintenance in WM and attention. This suggests that depressed patients exhibit impairment in the updating process. Depressed patients also showed set shifting and inhibition deficits. Only the n-back task was correlated with the number of hospitalizations and the longitudinal course of the illness. CONCLUSIONS: Our results suggest that young depressed in-patients have widespread executive dysfunctions, including updating, shifting and inhibition processes. We also found a correlation between a longitudinal measure of depression severity and an updating task performance. We suggest that using multiple executive tasks gives the opportunity to distinguish the specific influence of various executive processes on clinical dimensions in depression.

Neurobehavioral changes in mice treated with methylmercury at two different stages of fetal development.

Pregnant C57BL/6 mice were orally given daily doses of 4 or 6 mg/kg of methylmercury chloride (MeHg) or vehicle during either gestational days 7-9 (GD7-9) or days 12-14 (GD12-14). Their female offspring were tested between 6 and 16 weeks of age on a variety of behavioral tasks. Motor coordination on the rotarod and visual discrimination learning in the Y maze were not affected by administration of MeHg either at GD7-9 or at GD12-14. In the open field, the total number of square crossings was lower in mice treated with 4 and 6 mg/kg of MeHg at GD12-14 than in control mice whether the environment was new or familiar, but prenatal administration of MeHg at GD7-9 had no effect on this measure. Administration of MeHg either at GD7-9 or at GD12-14 had no effect on the percentage of central square crossings or on the frequency of rearings in the open field. On spatial alternation training in the T maze, both treated groups in Condition GD7-9 and the group treated with 6 mg/kg at GD12-14 required more sessions to reach the learning criterion than their respective vehicle groups. When spatial alternation was tested with delays, treated groups did not differ from their respective control groups. In the radial arm maze, the performance of mice treated at GD7-9 was normal, but reference memory and working memory were impaired by administration of MeHg at GD12-14. In mice treated with 4 mg/kg of MeHg, reference memory was impaired only on the first block of trials, whereas in mice treated with 6 mg/kg, the deficit persisted on all blocks of trials. Overall, these results indicate that prenatal administration of MeHg at GD12-14 had more detrimental effects on behavioral performance than administration at GD7-9. It reduced locomotor activity and impaired reference memory for egocentric and allocentric spatial information as well as working memory for places.