5 research outputs found
Depersonalization: an exploratory factor analysis of the Italian version of the Cambridge Depersonalization Scale
Background: “Depersonalization” (DP) is a common symptom in the general population and psychiatric patients (Michal et al., 2011 [1]). DP is characterized by an alteration in the experience of the self, so that one feels detached from his or her own mental processes or body (or from the world), feeling as being an outside observer of his or her own self, and loosing the experience of unity and identity (American Psychiatric Association, 2013 [2]).
Aim: We performed an exploratory factor analysis of the Cambridge Depersonalization Scale Italian version (CDS-IV).
Methods: We enrolled 149 inpatients and outpatients of psychiatric services located in two Italian regions, Lazio and Campania. Patients were aged between 15 and 65 and diagnosed with schizophrenic, depressive or anxiety disorders.
Results: Four factors accounted for 97.4% of the variance. Factor 1 (10, 24, 26, 1, 13, 23, 9, 2, 5, and 11), called “Detachment from the Self”, captures experiences of detachment from actions and thoughts. Factor 2 (19, 20, 27, 3, 12, 23, 22, and 11), called “Anomalous bodily experiences”, refers to unusual bodily experiences. Factor 3 (7, 28, 25, 6, 9, and 2), named “Numbing”, describes the dampening of affects. Factor 4 (14, 17, and 16), named “Temporal blunting”, refers to the subjective experience of time. We did not find any specific factor that refers to derealization; this suggests that the constructs of depersonalization/derealization (DP/DR) were strongly related to each other. Conclusions: Our results show that the constructs of DP/DR subsume several psychopathological dimensions; moreover, the above mentioned factors were broadly consistent with prior literature
Chronic agomelatine treatment corrects the abnormalities in the circadian rhythm of motor activity and sleep/wake cycle induced by prenatal restraint stress in adult rats
Agomelatine is a novel antidepressant acting as an MT1/MT2 melatonin receptor agonist/5-HT2C serotonin receptor antagonist. Because of its peculiar pharmacological profile, this drug caters the potential to correct the abnormalities of circadian rhythms associated with mood disorders, including abnormalities of the sleep/wake cycle. Here, we examined the effect of chronic agomelatine treatment on sleep architecture and circadian rhythms of motor activity using the rat model of prenatal restraint stress (PRS) as a putative ‘aetiological’ model of depression. PRS was delivered to the mothers during the last 10 d of pregnancy. The adult progeny (‘PRS rats') showed a reduced duration of slow wave sleep, an increased duration of rapid eye movement (REM) sleep, an increased number of REM sleep events and an increase in motor activity before the beginning of the dark phase of the light/dark cycle. In addition, adult PRS rats showed an increased expression of the transcript of the primary response gene, c-Fos, in the hippocampus just prior to the beginning of the dark phase. All these changes were reversed by a chronic oral treatment with agomelatine (2000 ppm in the diet). The effect of agomelatine on sleep was largely attenuated by treatment with the MT1/MT2 melatonin receptor antagonist, S22153, which caused PRS-like sleep disturbances on its own. These data provide the first evidence that agomelatine corrects sleep architecture and restores circadian homeostasis in a preclinical model of depression and supports the value of agomelatine as a novel antidepressant that resynchronizes circadian rhythms under pathological conditions
Chronic agomelatine treatment corrects the anormalities in the circadian rhythm of motor activity andb sleep/wake cycle induced by prenatal restraint stress in adult rats
Agomelatine is a novel antidepressant acting as an MT1/MT2 melatonin receptor agonist/5-HT2C serotonin receptor antagonist. Because of its peculiar pharmacological profile, this drug caters the potential to correct the abnormalities of circadian rhythms associated with mood disorders, including abnormalities of the sleep/wake cycle. Here, we examined the effect of chronic agomelatine treatment on sleep architecture and circadian rhythms of motor activity using the rat model of prenatal restraint stress (PRS) as a putative 'aetiological' model of depression. PRS was delivered to the mothers during the last 10 d of pregnancy. The adult progeny ('PRS rats') showed a reduced duration of slow wave sleep, an increased duration of rapid eye movement (REM) sleep, an increased number of REM sleep events and an increase in motor activity before the beginning of the dark phase of the light/dark cycle. In addition, adult PRS rats showed an increased expression of the transcript of the primary response gene, c-Fos, in the hippocampus just prior to the beginning of the dark phase. All these changes were reversed by a chronic oral treatment with agomelatine (2000 ppm in the diet). The effect of agomelatine on sleep was largely attenuated by treatment with the MT1/MT2 melatonin receptor antagonist, S22153, which caused PRS-like sleep disturbances on its own. These data provide the first evidence that agomelatine corrects sleep architecture and restores circadian homeostasis in a preclinical model of depression and supports the value of agomelatine as a novel antidepressant that resynchronizes circadian rhythms under pathological conditions. © CINP 2012.SCOPUS: ar.jinfo:eu-repo/semantics/publishe
Study on psychoeducation enhancing results of adherence in patients with schizophrenia (SPERA-S): Study protocol for a randomized controlled trial
Background: Poor adherence to pharmacotherapy negatively affects the course and the outcome of schizophreniaspectrum psychoses, enhancing the risk of relapse. Falloon and coworkers developed a Psychoeducation Program aimed at improving communication and problem-solving abilities in patients and their families. This study set out to evaluate changes in adherence to pharmacotherapy in patients diagnosed with schizophrenia-spectrum psychoses, by comparing one group exposed to the Falloon Psychoeducation Program (FPP) with another group exposed to family supportive therapy with generic information on the disorders.Methods: 340 patients diagnosed with schizophrenia and related disorders according to standardized criteria from 10 participating units distributed throughout the Italian National Health System (NHS), will be enrolled with 1:1 allocation by the method of blocks of randomized permutations. Patients will be reassessed at 6, 12 and 18 months after start of treatment (duration: 6 months). The primary objective is to evaluate changes in adherence to pharmacotherapy after psychoeducation. Adherence will be assessed at three-month intervals by measuring blood levels of the primary prescribed drug using high pressure liquid chromatography, and via the Medication Adherence Questionnaire and a modified version of the Adherence Interview. Secondary objectives are changes in the frequency of relapse and readmission, as the main indicator of the course of the disorder. Enrolled patients will be allocated to the FPP (yes/no) randomly, 1:1, in a procedure controlled by the coordinating unit; codes will be masked until the conclusion of the protocol (or the occurrence of a severe negative event). The raters will be blind to treatment allocation and will be tested for blinding after treatment completion. Intention-to-treat will be applied in considering the primary and secondary outcomes. Multiple imputations will be applied to integrate the missing data. The study started recruitment in February 2013; the total duration of the study is 27 months.Discussion: If the psychoeducation program proves effective in improving adherence to pharmacotherapy and in reducing relapse and readmissions, its application could be proposed as a standard adjunctive psychosocial treatment within the Italian NHS. Trial registration: Protocol Registration System of ClinicalTrials.gov NCT01433094; registered on 20 August 2011; first patient was randomized on 12 February 2013. © 2013 Petretto et al.; licensee BioMed Central Ltd