دانلود مقاله ISI انگلیسی شماره 33230
ترجمه فارسی عنوان مقاله

تغییرات ماده سفید در اختلال اضطراب اجتماعی

عنوان انگلیسی
White matter alterations in social anxiety disorder
کد مقاله سال انتشار تعداد صفحات مقاله انگلیسی
33230 2011 7 صفحه PDF
منبع

Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)

Journal : Journal of Psychiatric Research, Volume 45, Issue 10, October 2011, Pages 1366–1372

ترجمه کلمات کلیدی
اختلال اضطراب اجتماعی - انتشار تصویر برداری تانسور - اتصال سفید مهم - ناهمسانگردی جزء به جزء -
کلمات کلیدی انگلیسی
Social anxiety disorder; Diffusion tensor imaging; White matter connectivity; Fractional anisotropy; Uncinate fasciculus; Trait anxiety
پیش نمایش مقاله
پیش نمایش مقاله  تغییرات ماده سفید در اختلال اضطراب اجتماعی

چکیده انگلیسی

White matter architecture in patients with social anxiety disorder (SAD) has rarely been investigated, but may yield insights with respect to altered structural brain connectivity. Initial evidence points to alterations in the uncinate fasciculus (UF). We applied diffusion tensor imaging in 25 patients with SAD and 25 matched healthy subjects. Whole-brain fractional anisotropy (FA) maps were used for group comparison and voxel-wise correlation with psychometric and clinical measures. Additionally, a region-of-interest analysis of the UF was performed. Patients with SAD had reduced FA compared to healthy subjects in or near the left UF and the left superior longitudinal fasciculus. There were no regions with increased FA in SAD. In the region-of-interest analysis, a negative correlation between FA and trait anxiety was identified in the left and right UF in patients, but not in healthy subjects. No correlations with social anxiety scores were observed. The present study partially confirms previous results pointing to frontal WM alterations in or near the UF in patients with SAD. SAD-specific dimensional associations of FA with trait anxiety might reflect general pathological and/or compensatory mechanisms as a function of symptom severity in patients. Future studies should disentangle in which way the identified WM alterations match functional alterations.

مقدمه انگلیسی

Social anxiety disorder (SAD) is a common anxiety disorder (Jefferys, 1997) with a life-time prevalence of about 10% (Kessler et al., 1994). It is characterized by exaggerated fear during the anticipation of or confrontation with evaluation by others. Since genetic factors are known to play a role in SAD (Mosing et al., 2009 and Stein and Stein, 2008) and based on the commonly early age of onset (Stein and Stein, 2008), manifestations in the brain’s structural architecture can be expected. Examination of white matter (WM) may yield insights into structural connectivity and complement functional neuroimaging studies. Until now, little is known about WM architecture in SAD. First evidence points to alterations in the uncinate fasciculus (UF) (Phan et al., 2009), a fiber bundle connecting inferior frontal cortices including orbitofrontal cortex with the anterior temporal lobe and the amygdala (Ebeling and von Cramon, 1992, Ghashghaei et al., 2007 and Petrides and Pandya, 2007). Since the amygdala mediates emotional arousal states (Davis and Whalen, 2001) and the orbitofrontal cortex is implicated in cognitive control of emotions (Ochsner and Gross, 2005), the UF may play a key role in the emergence or regulation of fear. Therefore, the UF represents a WM structure of interest for diffusion tensor imaging (DTI) studies related to fear and anxiety. Theories of SAD point to biases at different stages of cognitive-attentional processing (Hirsch and Clark, 2004), probably not mediated by the UF alone. Therefore, it can be expected that WM alterations are present in further brain areas mediating interpretative or associative processes. DTI is a magnetic resonance based technique allowing the examination of WM structural properties, such as microstructural anisotropic diffusion reflected by fractional anisotropy (FA) (Basser and Pierpaoli, 1996). In the present study, we assessed FA throughout the whole-brain in patients with SAD and in healthy control subjects. Additionally, we concentrated on FA within the UF in a region-of-interest approach. Given the results of related previous studies (Kim and Whalen, 2009 and Phan et al., 2009), which for the first time investigated associations between FA and anxiety, we expected that reduced rather than increased FA would be a characteristic of abnormal WM architecture in anxious individuals. First, we aimed at identifying altered WM structures in patients with SAD compared to healthy subjects. Specifically, we hypothesized reduced FA in the UF. Further, we sought to determine the dimensional impact of trait anxiety, social anxiety and SAD duration on FA.