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The aim of this article is to provide the reader, or anyone interested in creativity, a glimpse into the findings of existing psychological and psychiatric literature on manic depression, its occurrence in creative individuals, ways in which it manifests and affects their functioning and creative output (positively and negatively), and the lessons one can draw from these individuals attempts to creatively associate and even reconcile opposite positions. The literature from educational philosophy, psychology and psychiatry is used as a lens to examine mythological, biographical and autobiographical accounts of the lives of creative individuals, particularly frames or episodes of their mind. The construct of 'happiness' is deconstructed with didactical implications for education. [ABSTRACT FROM AUTHOR]

Linkage analyses of bipolar families have confirmed that there is a susceptibility locus near the telomere on chromosome 21q. To fine map this locus we carried out tests of allelic association using 30 genetic markers near the telomere at 21q22.3 in 600 bipolar research subjects and 450 ancestrally matched supernormal control subjects. We found significant allelic association with the microsatellite markers D21S171 (P=0.016) and two closely linked single-nucleotide polymorphisms, rs1556314 (P=0.008) and rs1785467 (P=0.025). A test of association with a three locus haplotype across the susceptibility region was significant with a permutation test of P=0.011. A two SNP haplotype was also significantly associated with bipolar disorder (P=0.01). Only two brain expressed genes, TRPM2 and C21ORF29 (TSPEAR), are present in the associated region. TRPM2 encodes a calcium channel receptor and TSPEAR encodes a peptide with repeats associated with epilepsy in the mouse. DNA from subjects who had inherited the associated marker alleles was sequenced. A base pair change (rs1556314) in exon 11 of TRPM2, which caused a change from an aspartic acid to a glutamic acid at peptide position 543 was found. This SNP showed the strongest association with bipolar disorder (P=0.008). Deletion of exon 11 of TRPM2 is known to cause dysregulation of cellular calcium homeostasis in response to oxidative stress. A second nonconservative change from arginine to cysteine at position 755 in TRPM2 (ss48297761) was also detected. A third nonconservative change from histidine to glutamic acid was found in exon 8 of TSPEAR. These changes need further investigation to establish any aetiological role in bipolar disorder.Molecular Psychiatry (2006) 11, 134–142. doi:10.1038/sj.mp.4001759; published online 4 October 2005 [ABSTRACT FROM AUTHOR]

The human serotonin transporter gene (5-HTT) is a candidate for the pathogenesis of mood disorders, including bipolar disorder (BPD). The 5-HTT gene has a 44-bp insertion/deletion polymorphism within the promoter region (5-HTTLPR) with 2 allelic forms, the long ( l) and the short ( s) variants, which affect transcriptional rates of the 5-HTT gene. Association between the low-activity s variant and BPD has been suggested but remains controversial, as replication has not been consistent. In the present study, we examined the frequency of this polymorphism in a group of 266 Brazilian BPD patients and 306 control subjects. Genotyping for the 5-HTTLPR was performed using PCR. The allele frequencies were found to differ between BPD patients and controls ( p=0.03), with a higher frequency of the l allele in the patients compared with the controls (60.5% vs 54.4%). The distribution of genotypes also differed significantly between cases and controls ( x 2=10.4, 2 df, p=0.005), with higher frequency of heterozygous l/s genotype in the BPD patient group (52.6% vs 44%). Because prior evidence from gene expression studies indicated that l/s and s/s genotypes are not distinguishable biochemically, we compared the distribution of the l/l genotype and the combined group l/s plus s/ s between case and controls, but there was no significant difference ( x 2=0.22). Likewise, a logistic regression model considering a dominant role for the s variant was not significant (OR=0.92, 95% CI 0.64–1.32). Our results suggest that the low-activity s variant does not influence susceptibility to BPD in our population. [ABSTRACT FROM AUTHOR]

Our previous results pointed to a putative gene for susceptibility to bipolar affective disorder located on the chromosomal region 12q23-q24 that segregated in the Saguenay-Lac-St-Jean population of Quebec. We report here results from a second genome-wide scan based on the analysis of 380 polymorphic microsatellite markers. For the purpose of this analysis, an additional 18 families were recruited from the Saguenay-Lac-St-Jean region and pooled to our previous sample to improve its statistical power, giving a total of 394 sampled individuals. This work confirms the presence of a susceptibility locus for affective disorder on chromosome 12q24 with parametric LOD score value of 3.35 at D12S378 when pedigrees were broken into nuclear families and analysed under a recessive segregation model. This result was supported by neighbouring markers and by a LOD score value of 5.05 at D12S378 under model-free analysis. Other regions of lower interest were indicated on chromosomes 2, 5, 7, 9, 10, 17 and 20.Molecular Psychiatry (2005) 10, 545-552. doi:10.1038/sj.mp.4001601 Published online 19 October 2004 [ABSTRACT FROM AUTHOR]

Once considered virtually nonexistent, bipolar disorder in children has recently received a great deal of attention from mental health professionals and the general public. This paper provides a current review of literature pertaining to the psychosocial treatment of children with early-onset bipolar spectrum disorder (EOBPSD). Commencing with evidence of the emerging interest in this topic, we then focus on terminology, the rationale for studying EOBPSD in children, current research and clinical progress, possible explanations for the recent increase in recognition, and essential issues that form the foundation of effective psychosocial treatment. Next we explore areas of research with direct implications for psychosocial treatment. These include biological and psychosocial risk factors associated with bipolar disorder; and the psychosocial treatment of adult-onset bipolar disorder, childhood-onset unipolar disorder, and anger management in children. Following this, we discuss treatments being developed and tested for children with EOBPSD. Finally, we conclude with recommendations for future studies needed to move the field forward. [ABSTRACT FROM AUTHOR]

The increased acceptance of stress-vulnerability models of severe mental disorders and of brief evidence-based psychological treatments in their treatment has finally led to increased interest in the role of psychotherapies in bipolar disorders. This paper reviews the results from randomised controlled trials of psychological therapies as an adjunct to standard medications. The evidence suggests that the addition of a psychological therapy may significantly reduce symptoms, enhance social adjustment and functioning, and reduce relapses and hospitalisations in patients with bipolar disorder. However, the methodological problems in the published randomised controlled trials and the heterogeneity in the outcomes achieved (some therapies reduce manic but not depressive relapses, others have the opposite effect) suggests that further studies are required to fully establish the place of these approaches in day to day practice. [ABSTRACT FROM AUTHOR]

Carbamazepine (CBZ), a drug with acute antimanic and prophylactic activity in the treatment of manic depressive psychosis, was administered to rats in their diet, resulting in plasma levels of 5-10 μg/ml, which is within the human therapeutic range. Chronic CBZ (14 days) did not increase hyperactivity stimulated by the dopamine agonist apomorphine (1.0 mg/kg or 0.5 mg/kg), or to methylamphetamine (0.75 mg/kg), a dopamine releasing agent. Chronic CBZ failed to attenuate the development of enhanced sensitivity to methylamphetamine (0.75 mg/kg) produced by chronic haloperidol (2 mg/kg daily), in contrast to the known attenuation produced by lithium. Pretreatment with CBZ attenuated the hypoactivity produced by apomorphine (0.08 mg/kg), suggesting possible decreased sensitivity of presynaptic dopamine auto-receptors inhibiting dopamine release. Pretreatment with CBZ for 14 days decreased accumulation of l-dopa after administration of NSD 1015 (100 mg/kg IP), an amino acid decarboxylase inhibitor, in the frontal cortex, suggesting decreased dopamine synthesis. These findings suggest that the anti-manic activity of CBZ is neither related to a dopamine blocking action similar to that of neuroleptics, or to an attenuation of dopamine regulatory mechanisms similar to that of lithium. However, chronic CBZ may have some effects on presynaptic dopamine function, indicated by reduced sensitivity of presynaptic dopamine receptors, which may be related to its therapeutic action. [ABSTRACT FROM AUTHOR]

Recent research has shown that there are X-linked and possibly chromosome 11-linked forms of manic depression as well as at least one other autosomal form. Segregation analyses of large affected families and the finding of genetic linkage between chromosome specific markers and manic depression mutations provide strong evidence that bipolar as well as unipolar forms of manic depression (MD) within the same family are inherited as a dominant gene disorder. This clarification of the etiology of certain types of depression should bring changed attitudes within psychiatry and may serve to stimulate discusssion of the role of evolutionary mechanisms. From a clinical point of view, it has now become possible to determine whether clinical (phenotypic) variation reflects the underlying genotypic heterogeneity of linkage. A preliminary analysis of data from four recent studies shows that there is no clear correlation between such clinical features as the ratio of unipolar to bipolar cases and the genotypic form of manic depression. Further recombinant DNA research, proven to be successful in other genetic diseases, can soon be applied to manic depression. The specific problems posed by manic depression for these techniques are discussed. [ABSTRACT FROM AUTHOR]