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Since 2014 premenstrual dysforic disorder (PMDD) has been included in the DSM-5. Although PMDD affects 3-8% of all fertile women, there is no psychiatric guideline on the treatment. Fortunately, there are multiple meta-analyses and gynecological guidelines to base the treatment on. We present a case of a woman with mood swings and irritability. Recognizing and treating the hormonal component of her complaints also helped her to deal with other problems. Psychiatrists and gynecologists use different approaches for similar symptoms. We compare the different classifications and suggest treatment recommendations. When treating women in the fertile age with mood symptoms, the influence of the menstrual cycle should always be considered.

In psychiatric disorders, the effect of genetic and environmental factors may converge on molecular pathways and brain circuits related to growth factor functioning. In this review, we describe how disturbances in fibroblast growth factors (FGFs) and their receptors influence behavior by affecting brain development. Recently, several studies reported associations of members of the FGF family with psychiatric disorders. FGFs are key candidates to modulate the impact of environmental factors, such as stress. Mutant mice for FGF receptor 1 show schizophrenia-like behaviors that are related to general loss of neurons and postnatal glia dysfunction. Mice lacking FGF2, a FGFR1 ligand, show similar reductions in brain volume and hyperactivity, as well as increased anxiety behaviors. FGFR2 and FGF17 are involved in the development of frontal brain regions and impairments in cognitive and social behaviors, respectively. Moreover, treatment with FGF2 was beneficial for depressive and cognitive measures in several animal studies and one human study. These findings indicate the importance of the FGF system with respect to developing novel etiology-directed treatments for psychopathology.

Background: Thousands of common single nucleotide polymorphisms (SNPs) are weakly associated with schizophrenia. It is likely that subsets of disease-associated SNPs are associated with distinct heritable disease-associated phenotypes. Therefore, we examined the shared genetic susceptibility modulating schizophrenia and brain volume., Methods: Odds ratios for genome-wide SNP data were calculated in the sample collected by the Psychiatric Genome-wide Association Study Consortium (8690 schizophrenia patients and 11,831 control subjects, excluding subjects from the present study). These were used to calculate individual polygenic schizophrenia (risk) scores in an independent sample of 152 schizophrenia patients and 142 healthy control subjects with available structural magnetic resonance imaging scans., Results: In the entire group, the polygenic schizophrenia score was significantly associated with total brain volume (R2 = .048, p = 1.6 × 10(-4)) and white matter volume (R2 = .051, p = 8.6 × 10(-5)) equally in patients and control subjects. The number of (independent) SNPs that substantially influenced both disease risk and white matter (n = 2020) was much smaller than the entire set of SNPs that modulated disease status (n = 14,751). From the set of 2020 SNPs, a group of 186 SNPs showed most evidence for association with white matter volume and an explorative functional analysis showed that these SNPs were located in genes with neuronal functions., Conclusions: These results indicate that a relatively small subset of schizophrenia genetic risk variants is related to the (normal) development of white matter. This, in turn, suggests that disruptions in white matter growth increase the susceptibility to develop schizophrenia., (Copyright © 2013 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.)

A large association study by O'Donovan et al recently suggested that genetic variation in fibroblast growth factor receptor (FGFR) 2 increases the risk for developing schizophrenia. Fibroblast growth factors (FGFs) are part of the family of glial growth factors; they control the growth and patterning of specific brain structures and regulate the maintenance and repair of neuronal tissues. In addition, a direct interaction was recently found between FGFRs and adenosine A(2A) receptors, leading to corticostriatal plasticity and antagonizing the signaling pathway of dopamine D(2) receptors. These findings make FGFs plausible candidate genes for schizophrenia. Here, we review the role of FGFs in schizophrenia and combine evidence from studies on variations in FGF genes, RNA expression, protein levels, and FGF administration, as well as the effects of medication and environmental risk factors for schizophrenia. These data suggest that changes in the FGF system contribute to schizophrenia and possibly to a wider range of psychiatric disorders. The role of FGFs in schizophrenia and related disorders needs to be studied in more detail.

We have used in situ hybridization to determine the distribution of pre-pro-neurotensin/neuromedin N (NT/N) mRNA in the brain of mice and rats. In rats and mice, expression was observed in the lateral septal nucleus, nucleus accumbens, medial preoptic area, bed nucleus of the stria terminalis, lateral hypothalamus, central amygdaloid nucleus and the subicilum. However, several differences in the NT/N mRNA distribution were observed between rats and mice in other brain areas. In mice, NT/N expression was detected in the subthalamic nucleus and geniculate nucleus, whereas expression was not observed in these brain areas in rats. Surprisingly, expression was not observed in mouse mesencephalic dopaminergic (mesDA) neurons and the CA1 area of the hippocampus, areas known to contain NT/N mRNA in the rat brain. Taken together, these results show that although the brain NT/N mRNA distribution largely overlaps in mice and rats, species differences exist in specific brain areas in rodents. Moreover, these data indicate that the distribution in mice resembles most that of primates than rats.