Scale for time and space experience in anxiety (STEA): Phenomenology and its clinical relevance.

Anxiety is a pervasive emotional state where, phenomenologically, subjects often report changes in their experience of time and space. However, a systematic and quantified examination of time and space experience in terms of a self-report scale is still missing which eventually could also be used for clinical differential diagnosis. Based on historical phenomenological literature and patients' subjective reports, we here introduce, in a first step, the Scale for Time and Space Experience of Anxiety (STEA) in a smaller sample of 19 subjects with anxiety disorders and, in a second step, validate its shorter clinical version (cSTEA) in a larger sample of 48 anxiety subjects. The main findings are (i) high convergent and divergent validity of STEA with both Beck Anxiety Inventory (BAI) (r = 0.7325; p < 0.001) and Beck Depression Inventory (BDI) (r = 0.7749; p < 0.0001), as well as with spontaneous mind wandering (MWS) (r = 0.7343; p < 0.001) and deliberate mind wandering (MWD) (r = 0.1152; p > 0.05), (ii) statistical feature selection shows 8 key items for future clinical usage (cSTEA) focusing on the experience of temporal and spatial constriction, (iii) the effects of time and space experience (i.e., for both STEA and cSTEA scores) on the level of anxiety (BAI) are mediated by the degree of spontaneous mind wandering (MWS), (iv) cSTEA allows for differentiating high levels of anxiety from the severity of comorbid depressive symptoms, and (v) significant reduction in the cSTEA scores after a therapeutic intervention (breathing therapy). Together, our study introduces a novel fully quantified and highly valid self-report instrument, the STEA, for measuring time-space experiences in anxiety. Further we develop a shorter clinical version (cSTEA) which allows assessing time space experience in a valid, quick, and simple way for diagnosis, differential diagnosis, and therapeutic monitoring of anxiety.

Scale for Space and Time Experience in Psychosis: Converging Phenomenological and Psychopathological Perspectives.

INTRODUCTION: Abnormalities in the experience of space and time are fundamental to understanding schizophrenia spectrum disorders, but the precise relation between such abnormalities and psychopathological symptoms is still unclear. Therefore, the aim of our study was to introduce a novel scale for space and time experience in psychosis (STEP), specifically devised to assess schizophrenia spectrum disorders. METHODS: The STEP scale is a semiquantitative instrument developed on the basis of several items from previous scales and phenomenological reports addressing the experience of space and time. We applied the STEP scale to three groups of subjects (patients with schizophrenia spectrum disorders, patients with predominant affective symptoms, and healthy control subjects), to whom we also applied other more general psychopathological scales, such as the Positive and Negative Syndrome Scale and the Ego-Psychopathology Inventory. RESULTS: Patients with schizophrenia spectrum disorders scored significantly higher on general psychopatho--logical scales relative to subjects belonging to the other groups. The STEP scale provided good psychometric properties regarding reliability. We also tested convergent and divergent validity of the STEP scale and found that space and time subscale scores of STEP significantly correlated with each other, as well as with the remaining general psychopathological scores. DISCUSSION/CONCLUSION: We introduced the STEP scale as a novel instrument for the assessment of experience of space and time. Its psychometric properties showed high validity and reliability to identify psychopathological symptoms and enabled to differentiate patients with predominantly psychotic symptoms from those with predominantly affective symptoms. The STEP scale provides a standardized measure for assessing disturbances in the experience of space and time. Furthermore, it probably represents a leap forward toward the establishment of an additional dimension of symptoms proposed as "spatiotemporal psychopathology."

Bleuler's Psychopathological Perspective on Schizophrenia Delusions: Towards New Tools in Psychotherapy Treatment.

The authors begin by addressing the historical evolution of the delusion concept and its different approaches, focusing afterwards mainly on the work of Bleuler, who stressed the proximity between delusions and the emotional life of patients with schizophrenia. I Therefore, the present work intends to review the main aspects of the theory of delusion formation in schizophrenia according to Bleuler's psychopathological perspective. For that purpose, first the role of delusions in the psychopathology of schizophrenia is explored in a close relation with the Bleuler's fundamental symptoms (Alogia, Autism, Ambivalence, and Affect Blunting) nowadays known as negative symptoms. Then, persecutory, grandiosity and sexual delusions in schizophrenia are described according to the tension between logic and affects, as well as, internal conflict, schizoid features, and auto-erotism as key psychopathological pathways. Thus, with this subjective perspective, it is intended to highlight Bleuler's psychopathological contribution to the affective and meaningful causality of delusions in schizophrenia. The former might be useful in the integration with other psychopathological phenomena (hallucinations and negative symptoms) and new forms of research and therapeutic approaches in this disorder that are complementary with the contemporary tendencies in psychopathology.

A Perspective on a Possible Relation Between the Psychopathology of the Schizophrenia/Schizoaffective Spectrum and Unconjugated Bilirubin: A Longitudinal Protocol Study.

Some authors suggest a relation between Unconjugated Bilirubin (UCB) plasma high levels and schizophrenia, as schizophrenia patients have been showing higher UCB levels when compared with other psychiatric patients and general population. These higher UCB levels have been already correlated with acute psychotic states, positive symptoms, and poor outcome in patients with schizophrenia. Schizophrenia and schizoaffective disorders share common symptoms but there aren't yet accepted biomarkers for their distinction. In our study protocol we propose an observational longitudinal study on a sample composed of two subgroups: patients with schizophrenia and patients with schizoaffective disorder. We will compare the UCB levels between groups, and search for a possible correlation with patient's psychopathology. For that purpose we will use nosological, psychopathological, neuropsychological, and psychosocial instruments. Thus we will be testing two different hypotheses: (1) Is UCB serum level a diagnosis indicator, with categorical distinction potential, between groups of patients with different psychotic disorders? (2) Is UCB serum level a severity indicator, with dimensional distinction potential, among groups of patients with the same psychotic disorder? We believe that UCB mean levels may contribute to some clarification of this controversy, as a potential biological indicator, facilitating the distinction between these two diagnostic categories and\or discriminating the dimensional severity among each of these psychotic conditions. Thus we may be opening a new opportunities for innovative and exciting biological psychiatry research regarding organic aspects in the schizophrenia spectrum.

[Seeking for biological markers in suicidal behaviour]. / A procura de marcadores biológicos no comportamento suicidário.

Suicidal behaviour still represents a serious public health problem. Although the existence of some consultations on this subject, their efficacy remains very far from what we wish. In that sense, the research on the biological markers of suicidal behaviour might be of considerable importance. The aim of this paper is to present the biological systems involved on suicidal behaviour and to discuss if they can be used as a group of biological tests which could help clinical interview in predicting and preventing this kind of behaviour. It was done a Medline search between 1989 and 2007, considering the key-words Neurobiology and Suicide and therefore forty original or review articles were selected after reading each abstract content. From all the biological systems studied the one which shows more convincing data about its involvement in suicide is the serotoninergic system. At this level, we can say that there is a decreased neurotransmission of this monoamine in the Central Nervous System and Platelets as well as a compensatory increased binding of ligands to the serotoninergic receptors. At the same time, we have an hyperactivation of the HPA axis with lack of normalization of the Dexametasone Supression Test, decrease of neurotrophic genes like CREB, NT-3 and BDNF on some regions of the brain and of molecules from the lipidic metabolism, all of them capable of down-regulating the serotoninergic neurotransmission. These results are found in different pathologies with suicidal features, which make us think about a specific Neurobiology of Suicide. On the other hand, genetic polymorphisms of genes like the serotonin transporter, Tryptophan hydroxilase and 5-HT2a receptor seem to be significantly associated to suicide. Others, like the dopaminergic and noradrenergic systems are possible candidates to play a role on this behaviour but these studies need further replication. Finally, we can say that about the endocannabinoid, thyroid hormones, glia and opioid receptors systems there are already the first results of their involvement on suicide but these are very preliminary data. In conclusion, we consider that as this is a largely heterogenous kind of behavior, clinical practice could, potentially, be assisted by a group of biological tests capable of making the clinical cases more objective, which in turn would allowed us to diagnose large nosographic groups of patients instead of specific categories. In other words, it would be possible to increase sensibility but at the same time decrease specificity.

[Depression and treatment. Apoptosis, neuroplasticity and antidepressants]. / Depressão e tratamento. Apoptose, neuroplasticidade e antidepressivos.

Depression's neurobiology begins to be better understood. The last decade data considers neuroplasticity and stress as implicated factors on the pathophisiology of depression. Because antidepressants have a lag-time on their action it is possible that inhibition of neurotransmitters recaptation is not sufficient to explain long term changes. For that purpose, neurogenesis increase, nervous fibers sprouting, new synapses and stabilization of the old ones can be responsible for those changes. AMPc-MAPcinases-CREB-BDNF cellular cascade can play a significant role in the mechanisms of dendritic restructuration, hippocampal neurogenesis increase and nervous cells survival. The aim of this article is to discuss if apoptosis could play a key role as an ethiopathogenic factor on the patogenesis of depression. It was done a medline search for references with apoptosis, stress, neuroplasticity, depression and antidepressants key-words. It were found 101 original or review references about these subjects. Stress plays a key role in the etiopathogeny of depression. Its deletery effects on apoptosis and neuroplasticity can be changed by antidepressants. Neurogenesis' increase is necessary for their action. This increase is reached with chronic antidepressant treatment and not with other psychotropic drugs which means some pharmacological specificity of antidepressants. AMPc, CREB, BDNF and Bcl-2 can be considered as target genes in antidepressant synthesis. At the level of this neurotrophic factors apoptosis might be included in the neuroplastic model of depression and play a prominent role in etiopathogeny of depression. To confirm that, we need more research on the field to know which are the mechanisms that trigger apoptosis and its biological significance. In relation to the last one, we can say that is possible to be physiological apoptosis in deteriorated neurons death which cannot make strong connections and pathological apoptosis because of stress via, namely, HPA axis.