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Subir??, Marta,Cano, Marta,de Wit, Stella J,Alonso, Pino,Cardoner, Narcí,s,Hoexter, Marcelo Q,Kwon, Jun Soo,Nakamae, Takashi,Lochner, Christine,Sato, Joã,o R,Jung, Wi Hoon,Narumoto, Jin,St JOURNAL OF PSYCHIATRY AND NEUROSCIENCE 2016 JOURNAL OF PSYCHIATRY AND NEUROSCIENCE Vol.41 No.2
<P>Frontostriatal and frontoamygdalar connectivity alterations in patients with obsessive-compulsive disorder (OCD) have been typically described in functional neuroimaging studies. However, structural covariance, or volumetric correlations across distant brain regions, also provides network-level information. Altered structural covariance has been described in patients with different psychiatric disorders, including OCD, but to our knowledge, alterations within frontostriatal and frontoamygdalar circuits have not been explored.</P>
Pae, Chi-Un,Wang, Sheng-Min,Han, Changsu,Lee, Soo-Jung,Patkar, Ashwin A,Masand, Praksh S,Serretti, Alessandro Journal of Psychiatry and Neuroscience] 2015 JOURNAL OF PSYCHIATRY AND NEUROSCIENCE Vol.40 No.3
<P>Vortioxetine was approved by the U.S. Food and Drug Administration (FDA) in September 2013 for treating major depressive disorder (MDD). Thus far, a number of randomized, double-blind, placebo-controlled clinical trials (RCTs) of vortioxetine have been conducted in patients with MDD. We performed a meta-analysis to increase the statistical power of these studies and enhance our current understanding of the role of vortioxetine in the treatment of MDD.</P>
Reduced cortical folding of the anterior cingulate cortex in obsessive-compulsive disorder.
Shim, Geumsook,Jung, Wi Hoon,Choi, Jung-Seok,Jung, Myung Hun,Jang, Joon Hwan,Park, Ji-Young,Choi, Chi-Hoon,Kang, Do-Hyung,Kwon, Jun Soo Journal of Psychiatry and Neuroscience] 2009 Journal of psychiatry & neuroscience Vol.34 No.6
<P>BACKGROUND: Anterior cingulate cortex (ACC) abnormalities have been implicated consistently in the pathophysiology of obsessive-compulsive disorder (OCD), yet it remains unclear whether these abnormalities originated during early neurodevelopment. In this study, we examined the ACC sulcal/gyral patterns to investigate whether neurodevelopmental anomalies of the ACC were present in patients with OCD. We hypothesized that patients with OCD would show reduced cortical folding of the ACC compared with controls. METHODS: We used magnetic resonance imaging (MRI) of 169 healthy volunteers and 110 patients with OCD to examine the paracingulate sulcus and cingulate sulcus. We assessed cortical folding patterns according to established classification criteria and constructed 3 categories of paracingulate sulcus morphology according to its presence and anteroposterior extent: 'prominent,' 'present' and 'absent.' We classified the cingulate sulcus as 'interrupted' or 'continuous' according to the interruptions in its course. In addition, we evaluated ACC sulcal asymmetry based on interhemispheric comparisons of paracingulate sulcus morphology. RESULTS: Analyses revealed that patients with OCD were significantly less likely than controls to show a well-developed left paracingulate sulcus: 50.0% of patients and 65.1% of controls showed a 'prominent' or 'present' paracingulate sulcus in the left hemisphere. However, there were no differences in regard to cingulate sulcus continuity, and patients also showed the same leftward ACC sulcal asymmetry as controls. LIMITATIONS: Our study was limited by the fact that we obtained the MRI scans from 2 different scanners, and we did not calculate cerebral fissurization as our study was restricted to 1 specific brain region. Moreover, patients and controls differed significantly in terms of sex ratio and IQ, although we controlled these variables as covariates. CONCLUSION: Our findings imply a subtle deviation in the early neurodevelopment of the ACC in patients with OCD, but the extent to which these anomalies contributed to the pathogenesis of OCD remains unclear. Further studies that link the ACC morphologic anomalies to the pathophysiology of OCD are recommended.</P>
Kim, Boong-Nyun,Kim, Jae-Won,Kang, Hyejin,Cho, Soo-Churl,Shin, Min-Sup,Yoo, Hee-Jeong,Hong, Soon-Beom,Lee, Dong Soo Journal of Psychiatry and Neuroscience] 2010 JOURNAL OF PSYCHIATRY AND NEUROSCIENCE Vol.35 No.5
<P>Background: Neurobiologic studies have suggested that dysregulation of central noradrenergic systems may be involved in the pathophysiology of attention deficit hyperactivity disorder (ADHD), and it has been hypothesized that genetic changes in the norepinephrine pathways might contribute to dysfunction of the prefrontal cortex circuits in ADHD. We previously reported decreased cerebral blood flow in the right lateral prefrontal cortex and both orbitofrontal cortices in children with ADHD. Genetic investigations have shown that the alpha-2A-adrenergic receptor gene (ADRA2A) is associated with ADHD. Our aim was to examine whether the presence of a risk allele of the ADRA2A MspI polymorphism is associated with differences in regional cerebral blood flow in boys with ADHD. Methods: We recruited 21 Korean boys with ADHD (mean age 9.9, standard deviation [SD] 2.7 yr) and 11 age- and sex-matched controls (mean age 10.6 [SD 2.1] yr). Each participant underwent technetium-99m-hexamethylpropylene amine oxime ((99m)Tc-HMPAO) single-photon emission computed tomography. We performed image analyses with voxe-wise t statistics using SPM2. Results: We found regional hypoperfusion in the prefrontal regions, including the right orbitofrontal and right medial gyri, and the bilateral putamen and cerebellum in boys with ADHD relative to controls (p < 0.0005, uncorrected for multiple comparisons). Boys with ADHD who carried the C allele (n = 13) at the ADRA2A MspI polymorphism had reduced perfusion in the bilateral orbitofrontal regions compared with those without the C allele (n = 8) (p < 0.0005, uncorrected for multiple comparisons). Limitations: This study was limited by the small sample size, and we did not obtain genetic data from the controls. Conclusion: Our findings suggest that regional differences in cerebral perfusion in the orbitofrontal cortex represent an intermediate neuroimaging phenotype associated with the ADRA2A MspI polymorphism; these data support the validity of the noradrenergic hypothesis regarding the pathophysiology of ADHD.</P>