Scielo RSS <![CDATA[The European Journal of Psychiatry]]> vol. 19 num. 4 lang. <![CDATA[SciELO Logo]]> <link></link> <description/> </item> <item> <title><![CDATA[<b>Response sets in self-report data and their associations with personality traits</b>]]> Objective: With a strong reliance on the use of self-report questionnaires in psychiatric research, appropriate attention should be given to the existence and correlates of response sets. We studied the presence of response tendencies by using an old research paradigm from psychology. Methods: We administered response options without questions to a sample of 91 second-year medical students, together with two personality questionnaires. Results: The scores of the respondents demonstrated the willingness of respondents to fill in a content-free questionnaire and revealed the presence of a general tendency towards positive responses. In psychometric theory, this would be referred to as a 'constant error'. More importantly, positive answers were significantly related to low neuroticism, high extraversion and high well-being. In psychometric theory, this would imply 'response bias' in which the self-reports are confounded by personality features. Conclusions: In the development and evaluation of questionnaires, researchers should be aware of the potential for this bias, particularly when asking questions about subjective health status. <![CDATA[<b>The enigmatic phenotype</b>: <b>Relevant signs and symptoms in schizophrenia</b>]]> Ever since schizophrenia was conceptualized by Kraepelin and Bleuler, attempts have been made to rearrange signs and symptoms in order to achieve an useful disease concept with consequences for outcome, prognosis, treatment response and etiology. Several procedures were used to describe relevant phenotypes of the disease. In the beginning, famous psychiatrists conceptualized definitions of schizophrenia which was followed by a consensus about the operational criteria of schizophrenia. Later, more emphasis was placed on the statistical analyses of symptoms present in patients with psychotic disorders which resulted in a great variety of symptom clusters. In another approach, investigators try to deconstruct psychiatric diagnoses in search for so called endophenotypes of which covert symptoms like cognitive deficits in schizophrenia, are an example. The value of all these endeavours ultimately depends on the external validity which means that a relationship has to be established with the etiology, treatment response and outcome. The premises of all these research efforts is, however, the idea that the pathogenic agent of schizophrenia or a subtype will be found. In this paper an outline of the literature about the ordening of overt and covert symptoms in schizophrenia is presented. It is concluded that the different approaches are essential analogue and that research into the delineation of cognitive deficits and their treatment is at present most promising. <![CDATA[<b>Structural effects of atypical antipsychotics</b>: <b>Implications for the meaning of cortical volume deficit in schizophrenia</b>]]> Patients with schizophrenia have a smaller volume of cortex than healthy controls. Nevertheless, the substrate of such deficit is not well understood A progressive loss of cortical GM in schizophrenia seemed supported by early studies with magnetic resonance imaging (MRI) in which patients received typical drugs between the baseline and final scans. However, recent MRI results challenge this notion and suggest that structural changes may depend, at least in part, on the type of treatment received. These data may be relevant for a correct interpretation of the substrate of cortical volume deficit in schizophrenia. If that deficit can be even reversed by treatment, as suggested by recent studies, a neuronal substrate seems unlikely. Several lines of evidence instead support that glia cells may have a role in cortical structural and functional deficits in schizophrenia, which would be also in agreement with recent longitudinal results with MRI in patients treated with atypical antipsychotics. These evidences are reviewed in this paper. <![CDATA[<b>Premorbid adjustment and previous personality in schizophrenic patients</b>]]> Psychosocial adjustment and premorbid personality are two factors that are frequently studied in order to elucidate the etiopathogenesis of schizophrenia. Premorbid adjustment alterations and personality disorders (principally those of the schizophrenia spectrum) have been considered vulnerability elements or have been linked with the early manifestations of a disease that is still underdeveloped (hypothesis of neurodevelopment). In this paper we review the literature. We also studied the relationship between premorbid adjustment (PAS scale) and previous personality disorders (SCID-II) in a sample of 40 patients with schizophrenia (DSM-III-R, DSM-IV, CIE-10), and statistically correlated them. The results show that premorbid adjustment correlates with avoidant, schizotypal and schizoid personality disorders: the more personality pathology found, the poorer is the premorbid psychosocial adjustment. Premorbid adjustment positively correlates with histrionic personality traits. The pathological traits of schizotypal and schizoid personalities account for up to 77% of the variance of the total premorbid adjustment in schizophrenic patients. Conclusion: The degrees of premorbid adjustment in schizophrenia are related to the different premorbid personality disorders of schizophrenic patients, which are mainly those most genetically related with schizophrenia, that is, the spectrum of the schizophrenia. <![CDATA[<b>Methamphetamine</b>: <b>A molecular and pathological exacerbate of HIV neurocognitive disorder</b>]]> The use of the recreational drug methamphetamine is becoming more widespread, and it is accompanied by unsafe sexual behaviours that increase the transmission of the human immunodeficiency virus (HIV). This article reviews the available literature of the effect of methamphetamine on the HIV infected brain, and in particular the molecular disturbances and neuropathology associated within this cohort. Our molecular research indicates that methamphetamine and HIV have a synergistic pathological impact on neuronal cell injury and death, which may be mediated by an upregulation of interferon inducible genes observed within this group, thereby contributing to the neurocognitive deficits observed in clinical populations of HIV infected methamphetamine abusers.