Early Neurological Outcome of Young Infants Exposed to Selective Serotonin Reuptake Inhibitors During Pregnancy: Results From the Observational SMOK Study.
Early Neurological Outcome of Young Infants Exposed to Selective Serotonin Reuptake Inhibitors during Pregnancy: Results from the Observational SMOK Study.
PLoS One. 2013; 8(5): e64654
de Vries NK, van der Veere CN, Reijneveld SA, Bos AF
Use of selective serotonin reuptake inhibitors (SSRI) during pregnancy is common while the effect on the infant’s neurological outcome is unknown. Our objective was to determine the effects of prenatal SSRI-exposure on the infants’ neurological functioning, adjusted for maternal mental health.A prospective observational study from May 2007 to April 2010. The study groups comprised 63 SSRI-exposed infants (SSRI group) and 44 non-exposed infants (non-SSRI group). Maternal depression and anxiety were measured using questionnaires. The main outcome measures during the first week after birth and at three to four months were the quality of the infants’ general movements (GMs) according to Prechtl and a detailed motor optimality score. We calculated odds ratios (ORs) and 95% confidence intervals (CIs) for abnormal GM quality in the SSRI and non-SSRI groups, and adjusted for maternal depression, anxiety, and other confounders. The study was registered under 53506435 in the ISRCTN.All infants were born around term. During the first week, abnormal GMs occurred more frequently in the SSRI group than in the non-SSRI group (59% versus 33%) and the median MOS was lower (13 versus 18). The OR for abnormal GMs in the SSRI versus the non-SSRI group was 3·0 (95% CI, 1.3 to 6.9) and increased after adjustment for confounders. At three to four months, more SSRI-exposed infants had monotonous movements (48% versus 20%) with lower median MOSs (26 versus 28). The OR for monotonous movements was 3·5 (95% CI, 1.5 to 8.6) and increased after adjusting for confounders.Prenatal exposure to SSRI had an adverse effect on early neurological functioning as reflected by GM quality, irrespective of maternal depression and anxiety, and other confounders. Physicians should take this into account in consultation with parents. HubMed – depression
Quest for biomarkers of treatment-resistant depression: shifting the paradigm toward risk.
Front Psychiatry. 2013; 4: 57
Smith DF
The search for potential biomarkers of psychiatric disorders is a central topic in biological psychiatry. This review concerns published studies on potential biomarkers of treatment-resistant depression (TRD). The search for biomarkers of TRD in the bloodstream has focused on cytokines and steroids as well as brain-derived neurotropic factor. Additional approaches to identifying biomarkers of TRD have dealt with cerebrospinal fluid analysis, magnetic resonance imaging, and positron emission tomography. Some studies have also investigated potential genetic and epigenetic factors in TRD. Most studies have, however, used a post hoc experimental design that failed to determine the association between biomarkers and the initial risk of TRD. Particular attention in future studies should be on shifting the experimental paradigm toward procedures that can determine the risk for developing treatment resistance in untreated depressed individuals. HubMed – depression
The cost of schizophrenia in Japan.
Neuropsychiatr Dis Treat. 2013; 9: 787-98
Sado M, Inagaki A, Koreki A, Knapp M, Kissane LA, Mimura M, Yoshimura K
Schizophrenia is a disorder that produces considerable burdens due to its often relapsing/remitting or chronic longitudinal course. This burden is felt not only by patients themselves, but also by their families and health care systems. Although the societal burden caused by this disorder has been evaluated in several countries, the magnitude of the societal cost of schizophrenia in Japan has never been estimated. The aim of this study is to clarify the societal burden of schizophrenia by estimating the cost of schizophrenia in Japan in 2008.A human capital approach was adopted to estimate the cost of schizophrenia. The total cost of schizophrenia was calculated as the sum of the direct, morbidity, and mortality costs. Schizophrenia was defined as disorders coded as F20.0-F20.9 according to the International Classification of Diseases-10. The data required to estimate the total cost was collected from publicly available statistics or previously reported studies.The total cost of schizophrenia in Japan in 2008 was JPY 2.77 trillion (USD 23.8 billion). While the direct cost was JPY 0.770 trillion (USD 6.59 billion), the morbidity and mortality costs were JPY 1.85 trillion (USD 15.8 billion) and JPY 0.155 trillion (USD 1.33 billion), respectively.The societal burden caused by schizophrenia is tremendous in Japan, similar to that in other developed countries where published data exist. Compared with other disorders, such as depression or anxiety disorders, the direct cost accounted for a relatively high proportion of the total cost. Furthermore, absolute costs arising from unemployment were larger, while the prevalence rate was smaller, than the corresponding results for depression or anxiety in Japan. HubMed – depression
Effects of pentoxifylline, 7-nitroindazole, and imipramine on tumor necrosis factor-? and indoleamine 2,3-dioxygenase enzyme activity in the hippocampus and frontal cortex of chronic mild-stress-exposed rats.
Neuropsychiatr Dis Treat. 2013; 9: 697-708
Mohamed BM, Aboul-Fotouh S, Ibrahim EA, Shehata H, Mansour AA, Yassin NA, El-Eraky W, Abdel-Tawab AM
This study aimed to investigate the role of tumor necrosis factor (TNF)-? and the neuronal nitric oxide synthase enzyme in dysregulation of indoleamine 2,3-dioxygenase (IDO) enzyme, and hence serotonin availability in chronic mild stress (CMS), an animal model of depression.RATS WERE DIVIDED INTO FIVE GROUPS: two control and CMS-exposed for 6 weeks, and another three groups exposed to CMS and administered pentoxifylline 50 mg/kg/day intraperitoneally, 7-nitroindazole 40 mg/kg/day subcutaneously, or imipramine 20 mg/kg/day intraperitoneally for the previous 3 CMS weeks. Rats were assessed for neurochemical and immunohistochemical abnormalities.Pentoxifylline-, 7-nitroindazole-, and imipramine-treated rats showed amelioration of CMS-induced behavioral deficits that was accompanied by significant reduction in kynurenine/serotonin molar ratio and nitrates/nitrites in frontal cortex and hippocampus. In the pentoxifylline and 7-nitroindazole groups, serum TNF-? was reduced relative to the CMS group (18.54 ± 0.85 and 19.16 ± 1.54 vs 26.20 ± 1.83 pg/mL, respectively; P < 0.05). Exposure to CMS increased TNF-? and IDO immunohistochemical staining scores in both hippocampus and midbrain raphe nuclei. 7-Nitroindazole and pentoxifylline significantly (P < 0.05) reduced TNF-? immunostaining in hippocampus and raphe nuclei, with significant (P < 0.01) reduction of IDO immunostaining in raphe nuclei. Likewise, imipramine reduced TNF-? immunostaining (P < 0.05) in hippocampus.Neuronal nitric oxide synthase and TNF-? may play a concerted role in modulating IDO enzyme activity in CMS-exposed rats and provide additional evidence for possible alternative approaches to switch the neurobiological processes in depression. HubMed – depression