مغزی اختلالات حجمی در بیماران مبتلا به بی اشتهایی عصبی و پرخوری عصبی(بولیمیا): یک مطالعه مورفومتری مبتنی بر وکسل
|کد مقاله||سال انتشار||مقاله انگلیسی||ترجمه فارسی||تعداد کلمات|
|32566||2013||7 صفحه PDF||سفارش دهید||5748 کلمه|
Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)
Journal : Psychiatry Research: Neuroimaging, Volume 213, Issue 3, 30 September 2013, Pages 210–216
Recent studies focussing on neuroimaging features of eating disorders have observed that anorexia nervosa (AN) is characterized by significant grey matter (GM) atrophy in many brain regions, especially in the cerebellum and anterior cingulate cortex. To date, no studies have found GM atrophy in bulimia nervosa (BN) or have directly compared patients with AN and BN. We used voxel-based morphometry (VBM) to characterize brain abnormalities in AN and BN patients, comparing them with each other and with a control group, and correlating brain volume with clinical features. We recruited 17 AN, 13 BN and 14 healthy controls. All subjects underwent high-resolution magnetic resonance imaging (MRI) with a T1-weighted 3D image. VBM analysis was carried out with the FSL-VBM 4.1 tool. We found no global atrophy, but regional GM reduction in AN with respect to controls and BN in the cerebellum, fusiform area, supplementary motor area, and occipital cortex, and in the caudate in BN compared to AN and controls. Both groups of patients had a volumetric increase bilaterally in somatosensory regions with respect to controls, in areas that are typically involved in the sensory-motor integration of body stimuli and in mental representation of the body image. Our VBM study documented, for the first time in BN patients, the presence of volumetric alterations and replicated previous findings in AN patients. We evidenced morphological differences between AN and BN, demonstrating in the latter atrophy of the caudate nucleus, a region involved in reward mechanisms and processes of self-regulation, perhaps involved in the genesis of the binge-eating behaviors of this disorder.
Anorexia nervosa (AN) and bulimia nervosa (BN), the two principal DSM-IV eating disorders (ED) diagnoses, are complex psychiatric disorders in which biological, psychological, socio-cultural and environmental factors interact and coexist in different stages of development (Sadock et al., 2009). Recently, scientific research has focused on the study of the neurobiological basis of ED, aiming to identify biomarkers for the diagnosis and classification of these disorders, which are characterized by a high discrepancy between diagnostic criteria and clinical experience (Brooks et al., 2012). For this purpose, many studies have used both structural and functional neuroimaging techniques to analyze the brain regions involved in the pathophysiology of ED (Sadock et al., 2009). Observations of global cerebral and cerebellar atrophy in grey matter (GM) and white matter as well as ventricular enlargement in AN have led some authors to interpret these findings as representing a widespread cerebral vulnerability of this disorder (Artmann et al., 1985, Dolan et al., 1988, Krieg et al., 1988, Golden et al., 1996, Katzman et al., 1996, Lambe et al., 1997, Addolorato et al., 1998, Swayze et al., 2003 and Chui et al., 2008). Other studies, using a manual tracing approach on brain magnetic resonance imaging (MRI), have shown that some cerebral areas are particularly involved in AN, such as the thalamus, midbrain (Husain et al., 1992), paracentral lobule (Inui et al., 2002), hippocampus–amygdala complex (Giordano et al., 2001 and Connan et al., 2006) and anterior cingulate cortex (ACC) (McCormick et al., 2008). Voxel-based morphometry (VBM) is an unbiased automated technique based on high-resolution brain MRI sequences, and is widely used to measure structural differences across groups of subjects (Ashburner and Friston, 2000). A recent VBM study on AN patients found a significant reduction of total WM volume and focal GM atrophy in the cerebellum, hypothalamus, caudate nucleus, and frontal, parietal and temporal areas (Boghi et al., 2010). In another study, the authors found atrophy in the middle cingulate cortex, precuneus, and inferior and superior parietal lobules in restricting-type AN patients at an early stage of the disease, supporting the hypothesis of a regionally specific vulnerability in the areas that are involved in mental representation of self and body imagery (Gaudio et al., 2011). In recovered AN patients, a significant GM decrease in the ACC has been found, correlated with the lowest lifetime body mass index (BMI) (Muhlau et al., 2007). In another study, the authors found a volume reduction in the extrastriate body area in patients with AN which has been related to the body image distortion typical of this disorder (Suchan et al., 2010). In a recent work, Brooks and co-workers demonstrated a volumetric reduction of the insular cortex, parahippocampal and fusiform gyrus, cerebellum and posterior cingulate cortex in AN with respect to healthy controls. Moreover, the latter displayed an age-related volumetric decline of the dorsal-lateral prefrontal cortex that was absent in the patients, suggesting that restraint could spare the AN group from atrophy in this region (Brooks et al., 2011). VBM longitudinal studies in AN patients have suggested the reversibility of structural brain abnormalities in individuals with ED after nutritional recovery (Wagner et al., 2006), in particular GM alterations (Castro-Fornieles et al., 2010). Conversely, other studies have shown that GM volume restitution was incomplete in subjects who had been previously severely affected by AN (Joos et al., 2011). So far, only a few studies have focused their attention on brain changes in BN, finding that BN patients had decreased cortical mass, but that the decrease was less pronounced than in AN (Krieg et al., 1989). A recent VBM study, comparing AN and BN patients with controls, showed in AN a GM decrease in the ACC, frontal operculum, temporal-parietal regions and precuneus with respect to controls, while findings in BN did not show any difference from those in controls (Joos et al., 2010). Another study on AN and BN, which included long-term recovered patients, did not find differences with respect to controls except for an increased insular volume in BN (Wagner et al., 2006). A further study, which compared BN and binge-eating disorder patients, found that both had increased volume in the medial orbitofrontal cortex with respect to controls and BN displayed an enlargement of the ventral striatum, a brain structure involved in reward processes and self-regulation (Schäfer et al., 2010). However, the previous studies did not make direct comparisons between AN and BN, while in the majority of the current studies the authors included patients with symptoms of long duration. The aim of the present study was to use VBM to characterize brain abnormalities of AN and BN patients who had received their first diagnosis of an ED, comparing the groups with each other and with healthy controls, in order to investigate those brain abnormalities which could be specifically linked to each ED diagnosis and to correlate them with clinical and demographic features.