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Aim: Even though numerous studies have focused on the effects of self-stigma on patients with schizophrenia, little is known about self-stigma of patients with bipolar disorder (BD). In this study, a self-administered scale of self-stigmatising attitudes of patients with BD and schizophrenia was used to explore these attitudes, examine the potential differences between the two groups and study the factors that influence stigma within groups., Methods: Self-stigma of 120 patients with schizophrenia and BD was assessed with the Self-stigma Questionnaire (SSQ) and the Stigma Inventory for Mental Illness (SIMI). Presence of clinical symptoms, overall functioning and level of self-esteem were also evaluated., Results: Self-stigma is present in both groups but differs in its intensity. Patients with BD experience self-stigma in a lesser degree without affecting their social life or overall functioning. Patients with schizophrenia adopt more intense self-stigmatising attitudes leading to social exclusion and lower level of overall functioning., Limitations: The results are limited by the small sample size, whereas the inclusion of other questionnaires would broaden our insight to self-stigma., Conclusions: Self-stigma has a direct effect on overall functioning of patients with BD and schizophrenia tampering the clinical outcome of therapeutic interventions. Therefore, it should be incorporated in every treatment plan and be addressed as a clinical symptom of the mental illness., (Copyright © 2015 Elsevier B.V. All rights reserved.)

Self-esteem (SE) and social adjustment (SA) are often impaired during the course of affective disorders; this impairment is associated with suicidal behaviour. The aim of the present study was to investigate SE and SA in unipolar or bipolar patients in relation to demographic and clinical characteristics, especially the presence of suicidality (ideation and/or attempt). Forty-four patients, 28 bipolar and 16 unipolar, in remission for at least 3 months, and 50 healthy individuals were examined through a structured clinical interview. SE and SA were assessed by the Rosenberg self-esteem scale and the social adjustment scale, respectively. The results have shown that bipolar patients did not differ from controls in terms of SE, while unipolar patients had lower SE than bipolars and controls. No significant differences in the mean SA scores were found between the three groups. Suicidality during depression was associated only in bipolar patients with lower SE at remission; similar but not as pronounced was the association of suicidality with SA. It is concluded that low SE lasting into remission seems to be related to the expression of suicidality during depressive episodes of bipolar patients, while no similar pattern is evident in unipolar patients.

There is accumulated evidence that the genes coding for the receptor of gamma aminobutyric acid (GABA), the most important inhibitory neurotransmitter in the CNS, may be involved in the pathogenesis of affective disorders. In a previous study, we have found a genetic association between the GABA-A receptor alpha5 subunit gene locus (GABRA5) on chromosome 15q11-of 13 and bipolar affective disorder. The aim of the present study was to examine the same subjects to see if there exists a genetic association between bipolar affective disorder and the GABA receptor beta3 subunit gene (GABRB3), which is located within 100 kb from GABRA5. The sample consisted of 48 bipolar patients compared to 44 controls (blood donors). All subjects were Greek, unrelated, and personally interviewed. Diagnosis was based on DSM-IV and ICD-10 criteria. The marker used was a dinucleotide (CA) repeat polymorphism with 12 alleles 179 to 201 bp long; genotyping was successful in all patients and 43 controls. The distribution of GABRB3 genotypes among the controls did not deviate significantly from the Hardy-Weinberg equilibrium. No differences in allelic frequencies between bipolar patients and controls were found for GABRB3, while this locus and GABRA5 did not seem to be in significant linkage disequilibrium. In conclusion, the GABRB3 CA-repeat polymorphism we investigated does not present the observed association between bipolar affective illness and GABRA5. This could be due to higher mutation rate in the GABRB3 CA-repeat polymorphism, but it might also signify that GABRA5 is the gene actually associated with the disease., (Copyright 2001 Wiley-Liss, Inc.)

Background: Being the rate-limiting enzyme in the biosynthesis of serotonin, the tryptophan hydroxylase gene (TPH) has been considered a possible candidate gene in bipolar and unipolar affective disorders (BPAD and UPAD). Several studies have investigated the possible role of TPH polymorphisms in affective disorders and suicidal behavior., Methods: The TPH A218C polymorphism has been investigated in 927 patients (527 BPAD and 400 UPAD) and their matched healthy control subjects collected within the European Collaborative Project on Affective Disorders., Results: No difference of genotype distribution or allele distribution was found in BPAD or UPAD. No statistically significant difference was observed for allele frequency and genotypes counts. In a genotype per genotype analysis in UPAD patients with a personal history of suicide attempt, the frequency of the C-C genotype (homozygosity for the short allele) was lower in UPAD patients (24%) than in control subjects (43%) (chi(2) = 4.67, p =.03). There was no difference in allele or genotype frequency between patients presenting violent suicidal behavior (n = 48) and their matched control subjects., Conclusions: We failed to detect an association between the A218C polymorphism of the TPH gene and BPAD and UPAD in a large European sample. Homozygosity for the short allele is significantly less frequent in a subgroup of UPAD patients with a history of suicide attempt than in control subjects.

Background: It has been suggested that the dopaminergic system is involved in the pathophysiology of mood disorders. We conducted a multicenter study of families with mood disorders, to investigate a possible linkage with genes coding for dopamine receptor D2, dopamine receptor D3 and tyrosine hydroxylase (TH)., Methods: Twenty three mood disorder pedigrees collected within the framework of the European Collaborative Project on Affective Disorders were analyzed with parametric and non-parametric linkage methods. Various potential phenotypes were considered, from a narrow (only bipolar as affected) to a broad (bipolar+major depressive+schizoaffective disorders) definition of affection status., Results: Parametric analyses excluded linkage for all the candidate genes, even though small positive LOD (Limit of Detection) scores were observed for TH in three families. Non-parametric analyses yielded negative results for all markers., Conclusion: The D2 and D3 dopamine receptors were, therefore, not a major liability factor for mood disorders in our sample, whereas TH may play a role in a subgroup of patients.

Genetic factors seem to play an important role in the pathogenesis of affective disorder. The candidate gene strategies are being used, among others, to identify the genes conferring vulnerability to the disease. The genes coding for the receptors of gamma-aminobutyric acid (GABA) have been proposed as candidates for affective disorder, since the GABA neurotransmitter system has been implicated in the pathogenesis of the illness. We examined the possible genetic association between the GABA(A) receptor alpha5 subunit gene locus (GABRA5) on chromosome 15 and affective disorder, in 48 bipolar patients (BP), 40 unipolar patients (UP), and 50 healthy individuals, age- and sex-matched to the patients. All patients and controls were unrelated Greeks. Diagnoses were made after direct interviews according to the DSM-IV and ICD-10 criteria. For the genotyping, a dinucleotide (CA) repeat marker was used. The polymerase chain reaction (PCR) products found were nine alleles with lengths between 272 and 290 base pairs (bp). The distribution of allelic frequencies of the GABRA5 locus differed significantly between BP patients and controls with the 282-bp allele found to be associated with BP affective disorder, while no such difference was observed between the groups of UP patients and controls nor between the two patient groups. The presence or absence of the 282-bp allele in the genotype of BP patients was not shown to influence the age of onset and the overall clinical severity, but was found to be associated with a preponderance of manic over depressive episodes in the course of the illness.

The effects of thyrotropin-releasing hormone (TRH) administration on electroconvulsive therapy (ECT)-induced prolactin (PRL) secretion and the duration of the seizure were studied in 14 depressed women. In a balanced order crossover design the patients were given 0.4 mg TRH or placebo intravenously 20 min before ECT during the first two sessions. In the third ECT session TRH was given just prior to ECT. ECT elicited the expected PRL response when given alone and when given 20 min after TRH when PRL plasma levels were high. During the coadministration design (third ECT session) PRL levels were raised not as a sum of the two stimuli but even significantly more. TRH failed to modify the duration of the seizure induced by ECT. Therefore, if TRH is involved in seizure modulation during ECT, our findings suggest a postictal rather than ictal role for TRH.

The main metabolites of noradrenalin, dopamine, and serotonin-3-methoxy-4-hydroxyphenylglycol (MHPG), homovanillic acid (HVA), and 5-hydroxyindoleacetic acid (5-HIAA), respectively--were estimated in plasma of 21 depressed patients before and after 2 and 4 weeks of treatment with the monoamine oxidase-type A (MAO-A) inhibitor moclobemide (mean final daily dose = 8.9 mg/kg body weight). The treatment caused significant mean reductions in plasma MHPG and HVA (46% and 30%, respectively), while plasma 5-HIAA was unchanged. Multiple regression analysis revealed associations between reductions in MHPG and changes on the anxiety-somatization factor of the Hamilton Rating Scale for Depression (HRSD), and between reductions in HVA and changes in the HRSD factors cognitive disturbance and retardation.

The therapeutic effect of total sleep deprivation (SD) given twice a week, for 4 weeks, was investigated in 16 drug-free patients with major affective disorders. The response was excellent in five patients, satisfactory in three and minimal in eight patients. Six of these patients were treated prophylactically once a week, and four had an excellent response. Additionally, out of five normothymic drug-free patients with affective illness treated prophylactically with SD, without prior therapeutic SD treatment, three had an excellent response. The majority of responders were rapid cycling patients. This method is worth applying to patients resistant to classical treatment.

Concentrations of cAMP and cGMP in plasma were measured in 20 drug-free melancholic patients during a simulated electroconvulsive treatment (SECT) and a bilateral ECT session. Blood samples were taken every 15 min beginning 15 min before and ending 60 min after the SECT or the ECT. Two-way ANOVA and paired t-test demonstrated a significant and greater fall in cAMP over time following SECT. ECT induced a marginal increase (P less than 0.05) at 45 min postictally. It is postulated that ECT causes an increase in cAMP levels which is masked by the decrease observed during SECT, caused presumably by the anaesthetic medication. The plasma cGMP levels were increased gradually and significantly after SECT and the same rise was observed during ECT. These effects are discussed in relation to changes in adrenergic-cholinergic activities induced by the medication and the electrical stimulus.

An electrooculographic (EOG) study was carried out in 20 depressed (12 with retarded and eight with agitated depression) and in 12 manic patients. Compared with controls, EOG ratios obtained from our patient's groups differed significantly and were low in depressive and high in manic patients. Appropriate treatment (tricyclics to depressives and haloperidol to manics) restored EOG ratio values to control levels. The observed EOG changes in manic-depressive illness are discussed in terms of their origin and the involvement of a neuroendocrine, dopamine-controlled, mechanism is postulated.

In a mixed bipolar disorder patient, DST-positive, treated with neuroleptics and antidepressants, the addition of clonidine (up to 0.6 mg/day) caused a rapid improvement in his psychopathology, without any significant side effects. The concentrations of the metabolites of noradrenaline, dopamine, and serotonin (MHPG, HVA, and 5-HIAA), the hormone prolactin and the activity of dopamine-beta-hydroxylase estimated in plasma during the clonidine trial are also reported.

Administration of prophylactic 36 h total sleep deprivation to 9 manic-depressive patients (5 bipolar and 4 unipolar depressives) reduced the frequency of relapses and increased the duration of normothymia in 5 patients, left the course of illness unchanged in 3 patients whilst in 1 patient the effect could not be evaluated. Sleep deprivation appeared to be more effective in women, 'rapid cyclers', patients with a positive family history of mental illness and patients with recurrent depression. These observations confirm previous impressions and suggest a possible prophylactic effect of sleep deprivation.

The postulated disturbance of cyclic AMP (cAMP) in manic-depressive illness was investigated by using plasma as the biological material. Cyclic AMP was measured by a protein-binding assay, which was found very satisfactory for the purpose of this study. In the drug-free state, depressed patients (n = 28) had significantly lower and manic patients (n = 9) significantly higher plasma concentrations of cAMP than controls. Unmedicated manic-depressive subjects had normal cAMP levels during normothymic phases (n = 7). Cyclic AMP was reduced by neuroleptics in mania and elevated by tricyclics in depression. Lithium exerted a normalizing effect on cAMP in both phases of the illness. It is concluded that manic-depressive illness is associated with a disturbance in the cAMP system. The use of plasma rather than urine for the investigation of the state of cAMP in psychiatric disorders is advocated.

Intense exercise for one hour induced a significant increase in plasma cyclic adenosine monophosphate (cAMP) in 5 healthy volunteers. In 44 manic-depressive patients, cAMP levels correlated more strongly with mood ratings than with activity scores. The authors conclude that physical activity is one of the factors which contribute to changes of cAMP levels in affective illness.

To investigate the effect of exposure to cannabis early in adolescence on subclinical positive and negative symptoms of psychosis.Cross-sectional survey in the context of an ongoing cohort study.Government-supported general population cohort study.A total of 3500 representative 19-year olds in Greece.Subjects filled in the 40-item Community Assessment of Psychic Experiences, measuring subclinical positive (paranoia, hallucinations, grandiosity, first-rank symptoms) and negative psychosis dimensions and depression. Drug use was also reported on.Use of cannabis was associated positively with both positive and negative dimensions of psychosis, independent of each other, and of depression. An association between cannabis and depression disappeared after adjustment for the negative psychosis dimensions. First use of cannabis below age 16 years was associated with a much stronger effect than first use after age 15 years, independent of life-time frequency of use. The association between cannabis and psychosis was not influenced by the distress associated with the experiences, indicating that self-medication may be an unlikely explanation for the entire association between cannabis and psychosis.These results add credence to the hypothesis that cannabis contributes to the population level of expression of psychosis. In particular, exposure early in adolescence may increase the risk for the subclinical positive and negative dimensions of psychosis, but not for depression. [ABSTRACT FROM AUTHOR]