ResumoContexto: A esquizofrenia é uma das mais intrigantes doenças psiquiátricas e, talvez por isso, a mais pesquisada, com grandes avanços sobre sua fisiopatologia no último século. Objetivo: Revisar os principais avanços na compreensão fisiopatológica da esquizofrenia. Método: Revisão da literatura para cada tópico proposto a partir de artigos levantados no Medline e/ou considerados importantes a partir da experiência dos autores. Resultados: A hipótese dopaminér-gica representa uma das primeiras teorias etiológicas e permanece até os dias atuais como uma das que apresenta evidências mais consistentes. No entanto, essa teoria falha em explicar a história natural, os prejuízos cognitivos e as alterações estruturais encontradas na esquizofrenia. A demonstração de estudos epidemiológicos de fatores de risco genéticos e ambientais, somados aos estudos neuropatológicos e de neuroimagem, sugerem um modelo interativo em que inúmeros fatores atuam conjuntamente para alterações mais globais do desenvolvimento cerebral. Conclusão: A compreensão fisiopatológica da esquizofrenia avançou bastante no último século, evoluindo de teorias etiológicas unicausais para modelos mais complexos que consideram a interação de inúmeros fatores genéticos e ambientais.Araripe Neto, A.G.A. et al. / Rev. Psiq. Clín. 34, supl 2; 198-203, 2007 Palavras-chave: Esquizofrenia, fisiopatologia, hipótese dopaminérgica, hipótese glutamatérgica, neurodesenvolvimento. AbstractBackground: schizophrenia is one of the most intriguing and studied psychiatric diseases and its physiopathology has advanced a lot in the last century. Objective: To review the most important advances in the physiopathology of schizophrenia. Method: Review of the literature of each proposed topic by articles searched in Medline and/or chosen accordingly the authors' experience. Results: The dopaminergic hypothesis was one of the first ethiological theories and until today is among the ones that presents the most consistent evidences. However, it fails to explain important features found in schizophrenia, such as the natural history, the cognitive impairments and the structural abnormalities. Evidences provided by epidemiological studies of genetic and environmental risk factors, associated with the findings of neuropathological and neuroimaging studies, suggest an interactive model with several factors acting together to create a global alteration of the brain development. Conclusion: The physiophatology of schizophrenia has advanced a lot in the last century, evolving from unicausal theories towards more complex models that consider the interaction among several genetic and environmental factors.
Background The study of individual negative symptoms is encouraged as they may have separate neurobiological substrates and require specific therapeutic strategies. Blunted affect is a decrease in the observed expression of emotion and may be more fluctuant than expected. We aim to investigate early trajectories of blunted affect in first episode schizophrenia (FES) patients without previous antipsychotic-treatment. Methods We included 82 first episode psychosis antipsychotic naïve patients meeting the DSM-IV criteria for schizophrenia, schizoaffective or schizophreniform disorder. All participant started risperidone (1-4mg) after the first assessment. Socioeconomic and demographic data were collected at baseline. Positive and Negative Syndrome Scale (PANSS) was applied at both assessments. PANSS negative component item N1 was used to access blunted affect. Participants were divided into three groups for each assessment according to their N1 score: (i) absence of symptoms - score 1 or 2; (ii) Mild intensity - score 3 or 4; and (iii) Severe intensity - score 5 to 7. Results Mean age was 25.77 (sd: ±7.27) years-old and 61% were male. Mean total PANSS was 92.74 (sd: ± 22.37) at baseline and 65.54 (sd: ± 20.42) at follow up. Mean risperidone dose at follow up was 3.71 (± 1.51). Forty three (52%) study participants had persistence of blunted affect at 10-week follow up regardless of symptom intensity. Sixteen (19.5%) patients never displayed blunted affect. In fact, the most common trajectories include participants who persists with the same symptom severity (n=48). Symptoms improved in 17 participants and got worse in 17 as well. Only one participant started the study without symptom and evolved to high intensity at follow up, while no participant started the study with high severity symptoms and evolved to absence of symptoms. Discussion Our study suggests that blunted affect exhibit different trajectories, but its intensity tends to remain stable over short-term follow up. Blunted affect may be unresponsive to risperidone at the beginning of treatment. Most of the previous studies addressed trajectories of negative symptoms as a group. Only few addressed the progression of blunted affect and, to the best of our knowledge, this is the first to use a sample of drug-naïve FES patients. Also, we selected only participants in use of risperidone after first assessment in order to reduce bias. A sample of drug naïve FES patients brings opportunities like assessing the course of blunted affect at an early phase of the condition and reducing confounders such as chronicity and exposure to antipsychotics.
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