Impaired social cognition in schizophrenia during the Ultimatum Game: An EEG study

Schizophrenia has a core feature of cognitive dysfunctions. Since these deficits are predictive for patients' functional outcome, understanding their origin is of great importance to improve their daily lives. A specific component of the deficit involves social decision-making, which can be studied using the Ultimatum Game (UG). In this task, a “proposer” proposes a share of money to a “responder”, who can either accept or reject this offer. If the responder accepts the proposal, both win money. If the responder refuses, both players end up with nothing. Therefore, the UG evaluates decision-making strategies and social interaction.Methods: We compared the neuronal bases of schizophrenic patients with healthy controls, while performing the UG. Electroencephalography (EEG) was used to find differences in the event-related potential (ERP) components typical for the UG, namely the P2 and feedback-related negativity (FRN). Source reconstruction was further used to define the origin of these differences.Results: In the proposer condition, no differences were found in amplitude of the P2 and FRN components. In contrast, in the responder condition, significant differences were found for the amplitude of the FRN (p = 0.009). Using source reconstruction, a different activation in a border zone of the dorsolateral and the medial prefrontal cortex was revealed in schizophrenic patients to underlie this component.Conclusions: We suggest that the difference found in the FRN amplitude is associated with difficulties of patients in interpreting another's behavior. Although schizophrenic patients correctly activate neuronal bases in the proposer condition, they were not able to activate the same networks in the responder condition, thereby exposing their difficulties in social interaction

False memory production in schizophrenia: A neurophysiological investigation.

BACKGROUND: The topic of false memory in schizophrenia has been well documented in earlier research contributions. To date, there is no study exploring the implications of specific neural networks during this phenomenon in patients suffering from schizophrenia. METHODS: We compared 17 patients suffering from psychosis (SCZ) to 33 healthy controls (HC) performing a verbal memory task designed to produce false memories, i.e. the Deese-Roediger-McDermott paradigm (DRM). Electroencephalography was used to specifically analyze the P2 and N400 event-related potentials components. RESULTS: The SCZ patients showed a reduced ability to distinguish between true and false memories as assessed by the A index which was calculated based on the false and true memory rates. The morphology of the P2 differed in frontal electrode region with a lower amplitude in SCZ. In addition, the amplitude of N400 was more pronounced (more negative) in HC than in SCZ in centro-parietal electrode site. CONCLUSIONS: We suggest that the differences found in P2 amplitude are associated with difficulties of SCZ patients to efficiently compare item-specific features of a mnesic elements to incoming stimuli which impair the subsequent verbal memory information processing reflected by the N400 component amplitude decrease. These results are consistent with the idea that SCZ use a different strategy while they perform the DRM paradigm

False memory production in schizophrenia: A neurophysiological investigation

The topic of false memory in schizophrenia has been well documented in earlier research contributions. To date, there is no study exploring the implications of specific neural networks during this phenomenon in patients suffering from schizophrenia

Dépendances: nouveautés en médecine 2008 [Addiction]

L'actualité 2008 des dépendances est centrée sur l'avancée des neurosciences psychiatriques dans le domaine des addictions mais aussi sur les clarifications nécessaires face à la complexité des comorbidités psychiatriques des addictions, notamment en cas de schizophrénie. Enfin, le praticien trouvera des considérations utiles pour la prescription de traitements de substitution chez des patients VIH en trithérapie. The highlights 2008 in the addiction field are correlated to the progress of psychiatric neurosciences. Clarifications are also necessary towards the psychiatric comorbidities (schizophrenia) with the addictions. Then, useful considerations are given for the prescription of substitution treatment among HIV patients under tritherapy

Persistence of neuronal alterations in alcohol-dependent patients at conclusion of the gold standard withdrawal treatment ::evidence from ERPs

Background: One of the main challenges for clinicians is to ensure that alcohol withdrawal treatment is the most effective possible after discharge. To address this issue, we designed a pilot study to investigate the efficacy of the rehabilitation treatment on the main stages of information processing, using an electroencephalographic method. This topic is of main importance as relapse rates after alcohol withdrawal treatment remain very high, indicating that established treatment methods are not fully effective in all patients in the long run. Method: We examined in alcohol-dependent patients (ADP) the effects of the benzodiazepine-based standard detoxification program on event-related potential components at incoming (D0) and completion (D15) of the treatment, using tasks of increasing difficulty (with and without workload) during an auditory oddball target paradigm. Untreated non-alcohol-dependent-volunteers were used as matching controls. Results: At D0, ADP displayed significantly lower amplitude for all ERP components in both tasks, as compared to controls. At D15, this difference disappeared for the amplitude of the N1 component during the workload-free task, as well as the amplitude of the P3b for both tasks. Meanwhile, the amplitude of the N2 remained lower in both tasks for ADP. At D0, latencies of N2 and P3b in both task conditions were longer in ADP, as compared to controls, whilst the latency of N1 was unchanged. At D15, the N2 latency remained longer for the workload condition only, whereas the P3b latency remained longer for the workload-free task only. Conclusion: The present pilot results provide evidence for a persistence of impaired parameters of ERP components, especially the N2 component. This suggests that neural networks related to attention processing remain dysfunctional. Longitudinal long-term follow-up of these patients is mandatory for further assessment of a link between ERP alterations and a later risk of relapse

ABCB1 and cytochrome P450 genotypes and phenotypes: influence on methadone plasma levels and response to treatment

BACKGROUND AND OBJECTIVE: The in vivo implication of various cytochrome P450 (CYP) isoforms and of P-glycoprotein on methadone kinetics is unclear. We aimed to thoroughly examine the genetic factors influencing methadone kinetics and response to treatment. METHODS: Genotyping for CYP1A2, CYP2B6, CYP2C9, CYP2C19, CYP2D6, CYP3A4, CYP3A5, ABCB1, and UGT2B7 polymorphisms was performed in 245 patients undergoing methadone maintenance treatment. To assess CYP3A activity, the patients were phenotyped with midazolam. RESULTS: The patients with lower CYP3A activity presented higher steady-state trough (R,S)-methadone plasma levels (4.3, 3.0, and 2.3 ng/mL x mg for low, medium, and high activity, respectively; P = .0002). As previously reported, CYP2B6*6/*6 carriers had significantly higher trough (S)-methadone plasma levels (P = .0001) and a trend toward higher (R)-methadone plasma levels (P = .07). CYP2D6 ultrarapid metabolizers presented lower trough (R,S)-methadone plasma levels compared with the extensive or intermediate metabolizers (2.4 and 3.3 ng/mL x mg, respectively; P = .04), whereas CYP2D6 poor metabolizer status showed no influence. ABCB1 3435TT carriers presented lower trough (R,S)-methadone plasma levels (2.7 and 3.4 ng/mL . mg for 3435TT and 3435CC carriers, respectively; P = .01). The CYP1A2, CYP2C9, CYP2C19, CYP3A5, and UGT2B7 genotypes did not influence methadone plasma levels. Only CYP2B6 displayed a stereoselectivity in its activity. CONCLUSION: In vivo, CYP3A4 and CYP2B6 are the major CYP isoforms involved in methadone metabolism, with CYP2D6 contributing to a minor extent. ABCB1 genetic polymorphisms also contribute slightly to the interindividual variability of methadone kinetics. The genetic polymorphisms of these 4 proteins had no influence on the response to treatment and only a small influence on the dose requirement of methadone