توموگرافی تابش پوزیترون در زنان مبتلا به اختلال شخصیت مرزی
|کد مقاله||سال انتشار||مقاله انگلیسی||ترجمه فارسی||تعداد کلمات|
|33072||2003||7 صفحه PDF||سفارش دهید||محاسبه نشده|
Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)
Journal : Journal of Psychiatric Research, Volume 37, Issue 2, March–April 2003, Pages 109–115
The pathology of Borderline personality disorder (BPD) is poorly understood and its biological basis remains largely unknown. One functional brain imaging study using [18F]Deoxyglucose-PET previously reported frontal and prefrontal hypometabolism. We studied brain metabolism at baseline in 12 medication-free female patients with BPD without current substance abuse or depression and 12 healthy female controls by [18F]Deoxyglucose-PET and statistical parametric mapping. We found significant frontal and prefrontal hypermetabolism in patients with BPD relative to controls as well as significant hypometabolism in the hippocampus and cuneus. This study demonstrated limbic and prefrontal dysfunction under resting conditions in patients with BPD by FDG-PET. Dysfunction in this network of brain regions, which has been implicated in the regulation of emotion, may underlie symptoms of BPD.
American Psychiatric Association, 2000). Most researchers currently agree that a dysfunction of the emotional regulation system is a core component of the disorder (Linehan, 1993, Silk, 2000, Corrigan et al., 2000, Herpertz et al., 1999 and Stiglmayr et al., 2001). Currently, the etiology of BPD is poorly understood and its biological basis remains largely unknown. Preclinical research has revealed a network of regions involved in emotional regulation including prefrontal cortex, hippocampus, and amygdala (Davidson et al., 1999). The amygdala play a decisive role in the regulation of fear (Davis, 2001) and the hippocampus is involved in fear responses to the context of a stressful situation (Phillips and Le Doux 1992). Prefrontal cortex also regulates emotion and stress responses, including impulse control, inhibition of responses to external stimuli, and extinction of fear responses. The crucial function of these brain regions in the expression and modulation of emotion and impulsivity in both animals and humans has led to the hypothesis that dysfunctions in these regions may underlie some of the psychopathological symptoms seen in patients with BPD. One functional brain imaging study employing [18F]Deoxyglucose positron emission tomography (FDG-PET) under resting conditions revealed decreased metabolism in premotor and prefrontal areas, the anterior part of the cingulate cortex, and the thalamic, caudate and lenticular nuclei, in BPD patients as compared to controls (De la Fuente et al., 1997). In a pilot fenfluramine challenge study in five BPD patients and eight controls, Soloff et al. (2000) found greater FDG uptake in response to fenfluramine in medial and orbital regions of right prefrontal cortex (area 10), left middle and superior temporal gyri, left parietal lobe, and left caudate body in the control participants. There were no areas in which patients with BPD had greater relative regional uptake than controls. Herpertz et al. (2001) found elevated fMRI BOLD signals in the amygdala and prefrontal cortex of patients with BPD but not of controls during the presentation of emotionally aversive pictures of the International Affective Pictures System (IAPS). In the present study, we compared brain metabolism in patients with BPD in comparison to normal controls using FDG-PET under resting conditions. Since there is only one published study to date investigating baseline brain metabolism in BPD, we aimed at replicating the results of De la Fuente et al. (1997). Based on the preclinical studies and preliminary PET studies in BPD cited above we hypothesized alterations in function in prefrontal cortex, anterior cingulate, and hippocampus in BPD.