臨床的うつ病

Somatization might be defined as a process by which psychological, emotional pains and distress is expressed as physical symptoms without a known organic basis. This study aims to examining somatization symptoms among clinically depressed patients with White-American and Hispanic background. Participants diagnosed with major depressive disorder without psychotic features (DSM-V) completed self-report measures for somatization, depression, emotional expressivity (EE), and demographics. The findings suggest that patients low on emotional expressivity may tend to experience and report more bodily pains and complains than those who are emotionally expressive. No link between EE and depression was observed. Women scored higher on somatization then men in this study. In addition, Hispanics reported more somatization symptoms than their White American counterparts. The results of this study might contribute to provision of a clearer picture to distinguish between somatization syndrome and other actual physical conditions.

This article is an autobiographical study that relates my experiences, particularly my educational experiences, of living with dyslexia with the aim of elucidating its impact on the development of my selfhood. Examination of problems associated with dyslexia and evaluation on how my own experiences correlate to, or are disparate from, current knowledge about this specific learning difficulty (SpLD). The correlation between extreme stress, acting in a way to mask difficulties and depression is made as a negative impact upon selfhood.

This work makes an original contribution to knowledge as it is the study of the unique experiences of an individual and how dyslexia impacts upon his life. A single case can have considerable general illuminative utility. As such, the article is a link with others experiencing dyslexia, and therefore may help to inform them about ways to manage and cope with their SpLD in order to succeed in life. This autobiography may also be useful for those dealing with dyslexic individuals, such as parents and teachers, as they reflect on how they can support those in their care.

In this brief theoretical work, a new conceptual model is proposed to explain the psychosis of American chess player Bobby Fischer. Based on the pioneering work of psychoanalysts, we introduce the concept of sinthome, taken from the Lacanian topology of the Borromean knot, with its three registers: real, symbolic and imaginary [RSI], and its fourth stabilizer knot at the breaking of the symbolic. Here we call it chess-sinthome to designate the antipsychotic role fulfilled the ultra-competitive chess, in life and in the minds of some great players.

Major depressive disorder is a highly prevalent disease that is challenging to treat, often requiring medication and dose adjustments. Genetic factors play an important role in psychotropic medication responses. However, the translation of pharmacogenetics findings to clinical recommendations with regards to antidepressant responses is still in its early stages. We reviewed recent primary research articles, meta-analyses, and reviews on the pharmacogenetics of antidepressant treatment for major depressive disorder in different populations. We identified eight genes with likely associations with treatment responses and summarized genetic variants most likely to influence treatment responses. We determined the frequency of these variants in Caucasian, Asian, Hispanic, and African American populations. The genes are related to functions in drug metabolism, transport, signalling, stress response, and neuroplasticity. Clinical recommendations already exist for CYP2D6 and CYP2C19 cytochrome P450 drug metabolism genes. The other genes are: ABCB1 with single nucleotide polymorphisms (SNPs) rs2032583 and rs2235015; FKBP5 with SNPs rs1360780, rs3800373, and rs4713916; GNB3 with SNP rs5443; BDNF with SNP rs6265; HTR2A with SNPs rs7997012 and rs6313; and SLC6A4 with polymorphisms 5-HTTLPR and STin2. There is significant variability of the frequencies of these polymorphisms in the different populations we reviewed. There is also variability in the antidepressant responses between populations carrying the same polymorphism in some cases, indicating a likely polygenic influence. Future studies in the pharmacogenetics of antidepressants would benefit from including more subjects from underrepresented ethnic groups and stratifying results.