Development and validity data of the Brazilian Internet Study on Temperament and Psychopathology (BRAINSTEP).

BACKGROUND: The internet provides a research opportunity for psychiatry and psychology. This article presents the development and preliminary data of a large web-survey created to study how temperament relates to other psychological measures, behavior and psychiatric disorders. METHODS: We used the Affective and Emotional Composite Temperament Scale (AFECTS) to evaluate temperament and we selected several self-report instruments to evaluate behavior, psychological constructs and mental disorders. The system provides anonymous psychological (phase 1) and psychiatric (phase 2) feedback and includes questions to assess the validity of the answers. Each phase has around 450 questions. This system was broadcast utilizing Brazilian media. RESULTS: After the exclusion of 21.5% of the volunteers (those who failed the validation questions), 41,427 participants concluded the first part of the system (mean age=31.2±10.5 yrs, 26.9% males), and 21,836 (mean age=32.5±10.9 yrs, 25.1% males) completed phase 2. Around 25% have received a psychiatric diagnosis from a mental health professional. Demographic and temperament profiles of those who completed either only 80 questions, only phase 1, or the whole system were similar. The rate of non-serious answers (e.g. on bizarre behaviors) was very low and congruency of answers was very high. The internal consistency of classical trait scales (TCI-R and PANAS) was high (Cronbach's alpha>0.80) for all dimensions. LIMITATIONS: Relatively high dropout rate due to the length of the process and an overrepresentation of female, young and well-educated subjects. CONCLUSIONS: The BRAINSTEP provides valid and abundant data on psychological and psychiatric measures.

The Affective and Emotional Composite Temperament (AFECT) model and scale: a system-based integrative approach.

UNLABELLED: Based on many temperament frameworks, here we propose an integration of emotional and affective temperaments (the AFECT model), forming a common substrate for mood, behavior, personality and part of cognition. Temperament is conceived as a self-regulated system with six emotional dimensions: volition, anger, inhibition, sensitivity, coping and control. The different combinations of these emotional dimensions result in 12 affective temperament types, namely depressive, anxious, apathetic, obsessive, cyclothymic, dysphoric, irritable, volatile, disinhibited, hyperthymic and euphoric. We also developed and validated a self-report scale to evaluate this construct, the Affective and Emotional Composite Temperament Scale (AFECTS). METHODS: Exploratory and confirmatory psychometric analyses were performed with the internet version of the AFECTS in 2947 subjects (72% females, 35±11years old). RESULTS: The factors interpreted as volition, anger, inhibition, sensitivity, coping and control showed very good Cronbach's alphas for 5 dimensions (0.87-0.90) and acceptable alpha for inhibition (0.75). Confirmatory factor analysis corroborated this 6-factor structure when considering inhibition as a second-order factor with fear and caution as first-order factors (SRMR=0.061; RMSEA=0.053). In the Affective section, all 12 categorical affective temperaments were selected in the categorical choice, with 99% of volunteers identifying at least one adequate description of their affective temperament. LIMITATIONS: Only the internet version was used in a general population sample. CONCLUSION: The AFECT model provides an integrated framework of temperament as a self-regulated system, with implications for mental health, psychiatric disorders and their treatment. The AFECTS showed good psychometric properties to further study this model.

Involvement of adenosine in the neurobiology of schizophrenia and its therapeutic implications.

Based on the neuromodulatory and homeostatic actions of adenosine, adenosine dysfunction may contribute to the neurobiological and clinical features of schizophrenia. The present model of adenosine dysfunction in schizophrenia takes into consideration the dopamine and glutamate hypotheses, since adenosine exerts neuromodulatory roles on these systems, and proposes that adenosine plays a role in the inhibitory deficit found in schizophrenia. Given the role of adenosine activation of adenosine A1 receptor (A1R) in mediating neurotoxicity in early stages of brain development, pre- and peri-natal complications leading to excessive adenosine release could induce primary brain changes (i.e., first hit). These events would lead to an adenosine inhibitory deficit through a partial loss of A1R that may emerge as reduced control of dopamine activity and increased vulnerability to excitotoxic glutamate action in the mature brain (i.e., second hit). Adenosine dysfunction is reasonably compatible with symptoms, gray and white matter abnormalities, progressive brain loss, pre- and peri-natal risk factors, age of onset, response to current treatments, impaired sensory gating and increased smoking in schizophrenia. Pharmacological treatments enhancing adenosine activity could be effective for symptom control and for alleviating deterioration in the course of the illness. Accordingly, allopurinol, which may indirectly increase adenosine, has been effective and well tolerated in the treatment of schizophrenia. Since much of the evidence for the adenosine hypothesis is preliminary and theoretical, further investigation in the field is warranted.

A clinical trial of adjuvant allopurinol therapy for moderately refractory schizophrenia.

OBJECTIVE: To evaluate the xanthine oxidase inhibitor allopurinol as an adjuvant treatment for patients with moderately refractory schizophrenia, with the objective of increasing the endogenous pool of purines, including the neuro-modulator adenosine. METHOD: A double-blind, placebo-controlled, crossover clinical trial of add-on allopurinol (300 mg b.i.d.) for poorly responsive schizophrenia or schizoaffective disorder (DSM-IV criteria) was conducted. Thirty-five patients were enrolled, of whom 22 completed the 12 weeks of the study. Eighteen of these patients also completed a P50 evoked potential evaluation. RESULTS: Allopurinol was well tolerated and produced significant improvement in Positive and Negative Syndrome Scale (PANSS) total, positive, negative, and general scores, particularly for positive symptoms compared with baseline and with placebo phase. Nine patients improved more than 20% in PANSS total score during allopurinol treatment, whereas none responded in the placebo phase. Responders had a shorter duration of illness than nonresponders. P50 auditory sensory gating failed to improve with allopurinol treatment. CONCLUSIONS: Allopurinol was an effective and well-tolerated adjuvant treatment for poorly responsive schizophrenia, especially for refractory positive symptoms.