Effect of risperidone versus haloperidol on emotional responding in schizophrenic patients.

CIC-UPCET et Pharmacologie Clinique, Hôpital de la Timone, UMR CNRS 6193 Institut des Neurosciences Cognitives de la Méditerranée, Marseille, France.
Psychopharmacology (Impact Factor: 3.99). 07/2008; 200(2):261-72. DOI: 10.1007/s00213-008-1203-y
Source: PubMed

ABSTRACT Studies on emotional processing report that schizophrenic patients present a specific pattern of emotional responding that usually includes deficits in emotional expressiveness, increased feelings of unpleasant emotion but decreased feelings of pleasant emotion, and increased physiological reactivity. However, studies have rarely controlled the nature of antipsychotic medication. Yet, the influence of these drugs on emotional response is uncertain and could vary depending on their pharmacological profile.
This prospective and randomized study aimed to compare the effects of an atypical antipsychotic, risperidone, to a typical one, haloperidol, on patients' emotional responding during an emotional induction task.
Twenty-five schizophrenic patients underwent two emotional and clinical evaluations: one before treatment initiation and a second 4 weeks after. Emotional states of fear, sadness, anger, joy, and disgust were induced, as well as a neutral baseline state. Video recordings of patients during the induction task allowed for assessment of emotional expressiveness. Self-reports and measures of skin conductance and heart rate were performed to determine both subjective and physiological reactions to emotional experience.
Compared to haloperidol, risperidone did not reduce patients' facial expressiveness, decreased physiological reactivity, and decreased experience of unpleasant emotion but maintained experience of pleasant emotion. Emotional expressiveness was negatively correlated to parkisonism.
Our preliminary results suggest that atypical antipsychotics allow for better-adapted patterns of emotional responding than typical ones do. We suggest that this effect is due to reduced striatal D2 blockade, therefore, attenuating akinesia, coupled with increased 5HT and DA levels in prefrontal cortex, which improves emotional regulation.


Available from: David Da Fonseca, Feb 02, 2015
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Objective: Deficit in facial affect recognition is a well-documented impairment in schizophrenia, closely connected to social outcome. This deficit could be related to psychopathology, but also to a broader dysfunction in processing facial information. In addition, patients with schizophrenia inadequately use configural information-a type of processing that relies on spatial relationships between facial features. To date, no study has specifically examined the link between symptoms and misuse of configural information in the deficit in facial affect recognition. Method: Unmedicated schizophrenia patients (n = 30) and matched healthy controls (n = 30) performed a facial affect recognition task and a face inversion task, which tests aptitude to rely on configural information. In patients, regressions were carried out between facial affect recognition, symptom dimensions and inversion effect. Results: Patients, compared with controls, showed a deficit in facial affect recognition and a lower inversion effect. Negative symptoms and lower inversion effect could account for 41.2% of the variance in facial affect recognition. Conclusion: This study confirms the presence of a deficit in facial affect recognition, and also of dysfunctional manipulation in configural information in antipsychotic-free patients. Negative symptoms and poor processing of configural information explained a substantial part of the deficient recognition of facial affect. We speculate that this deficit may be caused by several factors, among which independently stand psychopathology and failure in correctly manipulating configural information. (PsycINFO Database Record (c) 2014 APA, all rights reserved).
    Neuropsychology 09/2014; 29(2). DOI:10.1037/neu0000136 · 3.43 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Accumulating evidence suggests involvement of the endocannabinoid system in the pathophysiology of schizophrenia, which signifies a potential application for this system in the treatment of this disorder. However, before new research can focus on potential treatments that work by manipulating the endocannabinoid system, it needs to be elucidated how this system is involved in symptoms of schizophrenia. Here we review human studies that investigated acute effects of cannabis or ∆9-tetrahydrocannabinol (THC) on brain functions that are implicated in schizophrenia. Results suggest that the impact of THC administration depends on the difficulty of the task performed. Impaired performance of cognitive paradigms is reported on more challenging tasks, which is associated with both activity deficits in temporal and prefrontal areas and a failure to deactivate regions of the default mode network. Comparable reductions in prefrontal activity and impairments in deactivation of the default mode network are seen in patients during performance of cognitive paradigms. Normal performance levels after THC administration demonstrated for less demanding tasks are shown to be related to either increased neural effort in task-specific regions ('neurophysiological inefficiency'), or recruitment of alternative brain areas, which suggests a change in strategy to meet cognitive demands. Particularly a pattern of performance and brain activity corresponding with an inefficient working memory system is consistently demonstrated in patients. These similarities in brain function between intoxicated healthy volunteers and schizophrenia patients provide an argument for a role of the endocannabinoid system in symptoms of schizophrenia, and further emphasise this system as a potential novel target for treatment of these symptoms.
    Progress in Neuro-Psychopharmacology and Biological Psychiatry 12/2013; DOI:10.1016/j.pnpbp.2013.11.017 · 4.03 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Recent research has shown that patients with schizophrenia (SCZ) exhibit reduced directed forgetting (DF) for negative words, suggesting impaired ability to instantiate goal-directed inhibition in order to suppress a competing, emotion-driven responses (i.e., emotional memory enhancement). However, disrupted inhibition is not the only possible mechanism by which patients could manifest reduced emotional DF. Therefore, the primary objective of the current study was to use event-related brain potential (ERP) recordings to investigate alternative hypotheses. ERPs were recorded while patients and controls completed an item-method DF paradigm using negative and neutral words. The N2 indexed goal-directed inhibition of to-be-forgotten items. The late positive potential (LPP) indexed emotional memory enhancement for negative study items. The P300 indexed selective rehearsal of to-be-remembered items. The SCZ group exhibited a reduced DF effect overall, but this was not modulated by emotion. N2 amplitude at anterior sites was larger for forget versus remember cues in the control group only, but this effect was not modulated by emotion. LPP amplitude was greater for negative versus neutral words in both groups, independent of region. P300 amplitude at posterior sites was greater for remember versus forget cues in the control group only. These data suggest that reduced DF in SCZ may be due, in part, to both diminished goal-directed inhibition of to-be-forgotten items and reduced selective rehearsal of to-be-remembered items. However, these data do not support the hypothesis that goal-directed, inhibitory processes are disrupted by competing, emotion-driven processes in SCZ. Patients' ERP data also suggested that they did not exhibit disproportionately heightened encoding of emotional stimuli, nor did they have deficient selective rehearsal of to-be-remembered emotional items. Copyright © 2015. Published by Elsevier B.V.
    International journal of psychophysiology: official journal of the International Organization of Psychophysiology 01/2015; DOI:10.1016/j.ijpsycho.2015.01.006 · 2.65 Impact Factor