The English version of the Mini-ICF-APP is a reliable and valid measure of disorders of capacity as defined by the International Classification of Functioning. Further work is necessary to establish whether the scale could be divided into sub scales which would allow the instrument to more sensitively measure an individual's specific impairments.
Positive changes of self-concept and action control features under methylphenidate treatment in this study may encourage therapists to treat adults with ADHD with stimulants, thus not being at risk to decrease their patients' self-efficacy. In combined pharmacological/psychotherapeutic approaches, self-concept scales could be used to predict treatment outcome, and in order to monitor interactions between ADHD symptom reduction and self concept.
IntroductionAbnormal EEG patterns are well known electrophysiological effects of the treatment with antipsychotic drugs, and the incidence of epileptic seizures is increased under psychopharmacotherapy [5]. In this respect the atypical antipsychotic drug clozapine carries the highest risk with a dose dependent cumulative one-year-incidence of seizures of up to 5 % [1,2,9]. Modern atypical antipsychotics are increasingly used in clinical practice, but have been studied less extensively in terms of electrophysiological aspects [3,7]. Nevertheless, the risk of the development of seizures is expected to be less pronounced [2]. In a retrospective investigation, Centorrino et al.[5] showed a particular high risk of EEG abnormalities with clozapine (47.1 %, n = 17) and olanzapine (38.5 %, n = 13), and a moderate risk for typical antipsychotics (14.5 %, n = 214). To further estimate the risk of EEG alterations including epileptiform activity under recently developed antipsychotics, we have analysed EEG recordings of all inpatients with schizophrenia within a two-year period, who were treated with the atypical antipsychotics olanzapine or amisulpride in monotherapy, in comparison to a control group under haloperidol. MethodsRoutine EEG recordings were obtained for at least 20 minutes including five minutes of hyperventilation, using a digital system (Neuroscan Synamps, 0.53 to 70 Hz, sample rate 250 Hz) with 21 electrodes, placed according to the 10/20-system. The data were digitally stored for off-line analysis. EEG data of all inpatients with the Abnormal EEG patterns are well known electrophysiological effects of treatment with antipsychotic drugs. To estimate the risk of EEG alterations including epileptiform activity under recently developed antipsychotics, we have analysed EEG recordings of all inpatients with schizophrenia medicated with atypical antipsychotics olanzapine or amisulpride in monotherapy, in comparison to a control group under haloperidol within a two-year period. EEG effects of olanzapine (n = 45) and amisulpride (n = 25) were retrospectively investigated and compared with the effects of haloperidol (n = 20) using digital EEG recordings, visually assessed by two independent investigators. Patients under olanzapine and amisulpride showed significantly higher rates of EEG abnormalities (46.7 and 44 %) as compared to haloperidol (10 %) (p < 0.01, and p < 0.05, respectively) and abnormal EEGs were associated with higher doses of medication. Epileptiform discharges were seen under olanzapine (15 %), and amisulpride (4 %), but not under haloperidol (statistical trend, p = 0.07). EEG abnormalities are frequent, and dose-dependent findings under treatment with olanzapine and amisulpride, and the occurrence of epileptiform activity has to be taken into account. Table 1 Demographic characteristics (mean SD) and EEG results, classified as normal/abnormal, with/without epileptiform activity (EA) of 90 patients with schizophrenia under monotherapy either with olanzapine, amisulpride or haloperidol Olanzapine Amis...
Since growing evidence suggests a significant role of chronic low-grade inflammation in the physiopathology of schizophrenia, we have hypothesized that functional genetic variant of the IFN gamma (IFN-γ; +874A/T; rs2430561) gene may be involved in the predisposition to schizophrenia. This research is based on a case-control study which aims to identify whether polymorphism of the IFN-γ gene is a risk factor for the development of schizophrenia. The RFLP-PCR genotyping of the IFN-γ gene was conducted on a Tunisian population composed of 218 patients and 162 controls. The IFN-γ (+874A/T) polymorphism analysis showed higher frequencies of minor homozygous genotype (TT) and allele (T) in all patients compared with controls (11.5 vs. 4.9%; p = 0.03, OR = 2.64 and 30.7 vs. 24.1%, p = 0.04, OR = 1.4, respectively). This correlation was confirmed for male but not for female patients. Also, the T allele was significantly more common among patients with paranoid schizophrenia when compared with controls (25.8 vs. 4.9%, p = 0.0001; OR = 6.7). Using the binary regression analysis to eliminate confounding factors as age and sex, only this last association remained significant (p = 0.03; OR = 1.76, CI = 1.05-2.93). In conclusion, our results showed a significant association between +874A/T polymorphism of IFN-γ and paranoid schizophrenia, suggesting that this single nucleotide polymorphism (SNP) or another at proximity could predispose to paranoid schizophrenia. Since the minor allele of this polymorphism was correlated with an increased expression of their product, our study validates the hypothesis of excessive pro-inflammatory cytokine in the physiopathology of paranoid schizophrenia.
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