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ObjectiveUnipolar mania is a clinical reality in our daily practice. Many authors suggested that bipolar patients can have only manic episodes without depressions. These findings lead us to explore more this particularity.MethodsWe conduct a retrospective, descriptive and comparative study including 173 patients, followed for bipolar disorder type I, according to the Diagnostic and Statistical Manual of Mental Disorders fifth edition criteria, during the period between January 2008 and December 2015. Two groups were identified. The first one was composed of 98 patients who had presented only manic episodes. The second group contained the rest of the sample. Unipolar mania was defined as the presence of three or more manic states without a depressive episode during the period of the study.ResultsOne hundred seventy three patients were included in the study. The average age of the sample was 43 years old. The first episode was manic in 129 patients (74.6%). The dominant polarity was manic in 90.8% of the cases. Seasonal characteristic and psychotic symptoms were observed in respectively 11.0% and 53.2% of the sample. Rapid cycling evolution was observed among 2.3% of patients. The unipolar manic profile accounted for 56.6% of the population. This result is equivalent to an annual incidence of 8%. Comparing the two groups, we did not find a significant difference concerning the sociodemographic and clinical variables except for the number of suicide attempts (p=0.014).ConclusionOur study shows that unipolar mania is clinical evidence. More studies should be conducted in order to understand its nosological and psychopathological foundations.

Research has provided strong evidence for oligodendrocyte and myelin-related genes dysfunction in schizophrenia. Several studies have suggested abnormalities in the expression of myelin-related genes including tumor necrosis factor receptor 2 (TNFR2) involved in the neurodegeneration and remyelination. In order to further assess the role of TNFR2 in schizophrenia, we examined a functional bi-allelic polymorphism associated with an impaired NF-KB signaling and cell survival. In the present case/control study, 220 patients with schizophrenia and 176 healthy controls were genotyped by RFLP-PCR for the T/G polymorphism at the position 676 in exon 6 of the TNFR2 gene. We found a trend towards over-representation of TNFR2 676G in the patients compared to the controls (p=0.19 and 0.09 respectively). Interestingly, when we evaluated the association between this genetic polymorphism and the clinical variables of schizophrenia, our findings indicated that the frequencies of the G/G genotype and the G allele were significantly higher in paranoid (p=0.014 and p=0.012 respectively) and adult-onset paranoid (p=0.004 and p=0.004 respectively) schizophrenia patient group compared to the controls. The potential association was confirmed by a logistic regression model only for development of the paranoid form of schizophrenia (p=0.022) indicating a substantially increased risk for paranoid schizophrenia with inheritance of the TNFR2(G) allele. In conclusion, this polymorphism in TNFR2 or a gene in proximity seems to be associated specifically with paranoid schizophrenia, at least in the Tunisian population. A replication of our findings in other and larger populations could be of particular importance to establish TNFR2 as one of the susceptibility genes of paranoid schizophrenia.

The IFNGR2Q64R polymorphism is correlated with male sex and paranoid schizophrenia. It is suggested that a chronic neuroinflammation may predispose to the paranoid schizophrenia development in men.

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