Temperament, Character, and Defense Mechanism Changes With Treatment in Depression: A 9-Month Naturalistic Follow-up.

The aim of this study was to evaluate the changes in temperament, character, and defense mechanisms with the treatment and remission in patients with major depressive disorder. The study was designed as a longitudinal observational follow-up study of patients with repeated measures at 0, 12, and 36 weeks. In baseline comparisons, the major depression group showed higher harm avoidance and novelty seeking scores and lower self-directness and mature defense styles scores compared with healthy controls. In the follow-up, temperament dimensions and neurotic defenses remained unchanged, mature defense styles and self-directness revealed significant increase, and immature defense styles revealed significant decrease. Although there was no significant difference in the defense styles, harm avoidance and novelty seeking scores remained higher in MDD patients compare with healthy controls in 36 weeks. Our findings regarding continuation of hierarchically upward improvement in defense mechanism after the remission may support importance of treatment after remission.

The relationship of Chlamydophila pneumoniae with schizophrenia: The role of brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3) in this relationship.

Several pathogens have been suspected of playing a role in the pathogenesis of schizophrenia. Chronic inflammation has been proposed to occur as a result of persistent infection caused by Chlamydophila pneumoniae cells that reside in brain endothelial cells for many years. It was recently hypothesized that brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3) may play prominent roles in the development of schizophrenia. NT-3 and BDNF levels have been suggested to change in response to various manifestations of infection. Therefore, we aimed to elucidate the roles of BDNF and NT3 in the schizophrenia-C. pneumoniae infection relationship. RT-PCR, immunofluorescence and ELISA methods were used. Fifty patients suffering from schizophrenia and 35 healthy individuals were included as the patient group (PG) and the healthy control group (HCG), respectively. We detected persistent infection in 14 of the 50 individuals in the PG and in 1 of the 35 individuals in the HCG. A significant difference was found between the two groups (p<0.05). Twenty-two individuals in the PG and 13 in the HCG showed seropositivity for past C. pneumoniae infection, and no difference was observed between the groups (p>0.05). C. pneumoniae DNA was not detected in any group. A significant difference in NT-3 levels was observed between the groups, with very low levels in the PG (p<0.001). A significant difference in BDNF levels was also found, with lower levels in the PG (p<0.05). The mean serum NT-3 level was higher in the PG cases with C. pneumoniae seropositivity than in seronegative cases; however, this difference was not statistically significant (p>0.05). In conclusion, we suggest that NT-3 levels during persistent C. pneumoniae infection may play a role in this relationship.

The role of latent toxoplasmosis in the aetiopathogenesis of schizophrenia--the risk factor or an indication of a contact with cat?

We assessed IgG antibody to Toxoplasma gondii in 300 inpatients with schizophrenia (SG), 150 outpatients with anxiety and depressive disorders (PCG), and 150 healthy blood donors (HCG). Seropositivity rates were 60.7% for SG, 36.7% for PCG, and 45.3% for HCG (p<0.001). The seropositivity rate for anti-Toxoplasma IgG antibodies in SG was significantly higher that in PCG (chi2 = 23.11, OR = 2.66, p = 0.001) and HCG (chi2 = 9.52, OR = 1.86, p = 0.002). Among SG, 85% of those who reported close cat contact had IgG antibodies to T. gondii. Close cat contacts were reported by 59% of SG, 6% of PCG, and 9% of HCG (p<0.001). There was a nonsignificant positive association between toxoplasmosis and schizophrenia for people with a contact with a cat (OR = 2.221, p = 0.127, CI95 = 0.796-6.192), and significant negative association between toxoplasmosis and schizophrenia for people without contact with a cat (OR = 0.532, p = 0.009, CI95 = 0.332-0.854). Close cat contact (OR = 2.679, p<0.001), 51-65-year age group (OR = 1.703, p<0.001) and education [illiterate+primary (OR = 6.146, p<0.001) and high school (OR = 1.974, p = 0.023)] were detected as independent risk factors in multivariate logistic regression. The effect of toxoplasmosis on risk of schizophrenia disappeared in the complex model analyzed with multivariate logistic regression. In conclusion, our data suggest that the toxoplasmosis has no direct effect on the risk of schizophrenia in Turkey but is just an indication of previous contacts with a cat.

[Phenomenological differences between adolescent and adult onset mania: a comparative study]. / Ergen ve eriskin baslangiçli maninin fenomenolojik farkliliklari: karsilastirmali bir calisma.

OBJECTIVE: The aim of this study is to determine the relationship between age of onset and phenomenology of bipolar affective disorder (mania). METHOD: The current and retrospective diagnoses of the patients were made according to DSM-IV Bipolar Affective Disorder (mania) criteria. Sociodemographic features, clinical features, type of episode, number and length of hospitalizations were investigated in three groups which were consisted of adolescent-onset adolescents (n=60), adolescent-onset adults (n=60) and adult-onset adults (n=60). The groups were determined according to age of onset and current age categories. All patients have been assessed by Structured Clinical Interview for DSM-IV-Clinical Version (SCID-I), Young Mania Rating Scale (YMRS), Hamilton Depression Rating Scale (HAM-D) and Scale for the Assessment of Positive Symptoms (SAPS). RESULTS: The groups were consisted of equal numbers of women and men. Rate of single (%51.7) and divorced patients (%21.7), rate of unemployment status (%70) were higher in adolescent-onset patients than adult-onsets. Adolescent-onset adolescents and adolescent-onset adults were different from adult-onset patients with respect to mixt episodes (%26.7, %15) and mood congruent or incongruent psychotic features (%35/%50, %31.7/%66.7) and length of hospitalization (23.9+/-4.8, 23.8+/-3.9). CONCLUSION: Adolescent-onset of illness causes higher probability of mixt episodes, psychotic features such as mood congruent or incongruent hallucinations and delusions. This study supports the hypothesis that adolescent-onset mania may be a different subtype than adult-onset mania with respect to type of episode, phenomenology, and clinical features.

Papel del factor neurotrófico de origen cerebral y de la neurotropina-3 en la relación de Chlamydophila pneumoniae con la esquizofrenia / The relationship of Chlamydophila pneumoniae with schizophrenia: The role of brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3) in this relationship

Several pathogens have been suspected of playing a role in the pathogenesis of schizophrenia. Chronic inflammation has been proposed to occur as a result of persistent infection caused by Chlamydophila pneumoniae cells that reside in brain endothelial cells for many years. It was recently hypothesized that brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3) may play prominent roles in the development of schizophrenia. NT-3 and BDNF levels have been suggested to change in response to various manifestations of infection. Therefore, we aimed to elucidate the roles of BDNF and NT3 in the schizophrenia-C. pneumoniae infection relationship. RT-PCR, immunofluorescence and ELISA methods were used. Fifty patients suffering from schizophrenia and 35 healthy individuals were included as the patient group (PG) and the healthy control group (HCG), respectively. We detected persistent infection in 14 of the 50 individuals in the PG and in 1 of the 35 individuals in the HCG. A significant difference was found between the two groups (p < 0.05). Twenty-two individuals in the PG and 13 in the HCG showed seropositivity for past C. pneumoniae infection, and no difference was observed between the groups (p > 0.05). C. pneumoniae DNA was not detected in any group. A significant difference in NT-3 levels was observed between the groups, with very low levels in the PG (p < 0.001). A significant difference in BDNF levels was also found, with lower levels in the PG (p < 0.05). The mean serum NT-3 level was higher in the PG cases with C. pneumoniae seropositivity than in seronegative cases; however, this difference was not statistically significant (p > 0.05). In conclusion, we suggest that NT-3 levels during persistent C. pneumoniae infection may play a role in this relationship.

Existe la sospecha de que algunos patógenos pueden desempeñar un papel en la patogénesis de la esquizofrenia; en ese contexto, se ha propuesto que la infección persistente causada por células de Chlamydophila pneumoniae presentes en las células endoteliales cerebrales durante muchos años lleva a la inflamación crónica. Recientemente se ha planteado la hipótesis de que el factor neurotrófico de origen cerebral (BDNF, por sus siglas en inglés) y la neurotropina-3 (NT-3) podrían estar implicados en el desarrollo de la esquizofrenia, y se ha sugerido que sus niveles se modifican en respuesta a diversas manifestaciones de la infección. En esta investigación intentamos esclarecer el papel que desempeñan el BDNF y la NT3 en la relación entre la esquizofrenia y la infección por C. pneumoniae. Se utilizaron métodos de RT-PCR, inmunofluorescencia y ELISA. Se incluyeron 50 pacientes con esquizofrenia y 35 individuos sanos como grupo de pacientes (GP) y grupo de controles sanos (GCS), respectivamente. Detectamos una infección persistente en 14 sujetos del GP y en 1 de los del GCS, lo que constituyó una diferencia significativa (p < 0,05). Veinte participantes del GP y 13 del GCS fueron seropositivos para una infección pasada por C. pneumoniae, diferencia no significativa (p > 0,05). No se detectó ADN de C. pneumoniae en ninguno de los dos grupos. Se observó una diferencia significativa entre los grupos en los niveles de NT-3, que fueron muy bajos en el GP (p < 0,001), y de BDNF, inferiores en el GP (p < 0,05). La concentración sérica media de NT-3 fue mayor en los individuos seropositivos para C. pneumoniae en comparación con los seronegativos, pero esta diferencia no alcanzó significación estadística (p > 0,05). Sugerimos que los niveles de NT-3 durante una infección persistente por C. pneumoniae pueden estar implicados en la relación de Chlamydophila pneumoniae con la esquizofrenia.

Antidepressant-associated mania or hypomania: a comparison with personality and bipolarity features of bipolar I disorder.

BACKGROUND: Hypomania/mania during antidepressant treatment is often neglected by clinicians. There are no specific diagnostic criteria for hypomania and mania associated by antidepressant treatment in the bipolar spectrum. The aim of this study is to compare various characteristics of bipolar I disorder and antidepressant-associated mania. METHOD: In this study, 76 bipolar patients who met DSM-IV criteria for bipolar disorder-type I in remission from mania or depression (Group 1; n = 44) and patients with major depression in remission, who had mania associated by antidepressant treatment (Group 2; n = 32), were admitted. All patients were assessed using the SCID I, Bipolarity Index (BI) and a patient data form. First-degree relatives of all patients were evaluated using the Mood Disorder Questionnaire (MDQ). RESULTS: Sociodemographic features of both groups were similar. The rate of major depression in the relatives of Group 2 was significantly higher than in Group 1. The severity of manic symptoms in Group 2 was significantly lower than in Group 1. Those in Group 2 who were diagnosed with their first episode had atypical depressive features. First-degree relatives of patients in Group 1 had higher positive scores on the MDQ. A statistically significant difference was found between the two groups on all dimensions of the BI except family history. LIMITATIONS: This is a cross-sectional study with a relatively small number of subjects. There is no control group of major depressive patients who did not develop mania during antidepressive treatment. CONCLUSIONS: Our results suggest that antidepressant-associated hypomania/mania could be a different subgroup in the bipolar spectrum.