Functional anatomy of caloric fear in anorexia nervosa (Letter)
(Impact Factor: 45.22).
11/1998; 352(9135):1192. DOI: 10.1016/S0140-6736(05)60529-6
Available from: A.A. van Elburg
- "There are some caveats and limitations to this study. We did not find amygdala or OFC activation to food images in AN as shown in other studies (Ellison et al., 1998; Uher et al., 2003, 2004; Killgore and Yurgelun-Todd, 2005; Goldstone et al., 2009; Siep et al., 2009). This may be due to the small size of the amygdala, combined with low power due to our small sample size, and heterogeneity in AN patients, as we included both restrictive and purging AN individuals. "
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ABSTRACT: Anorexia Nervosa (AN) is a severe mental disorder characterized by food restriction and weight loss. This study aimed to test the model posed by Brooks et al. (2012), that women suffering from chronic AN show decreased food cue processing activity in brain regions associated with energy balance and food reward (bottom-up; BU) and increased activity in brain regions associated with cognitive control (top-down; TD) when compared to long term recovered AN (REC) and healthy controls (HC). Three groups of women, 15 AN (mean illness duration 7.8 ± 4.1 y), 14 REC (mean duration of recovery 4.7 ± 2.7 yr) and 15 HC viewed alternating blocks of food and non-food images preceded by a short instruction during functional magnetic resonance imaging (fMRI), after fasting overnight. Functional ROIs (fROIs) were defined in BU (e.g. striatum, hippocampus, amygdala, hypothalamus and cerebellum), TD (e.g. medial and lateral prefrontal cortex, anterior cingulate), the insula and visual processing areas (VPA). Food-cue processing activation was extracted from all fROIs and compared between the groups. In addition, functional connectivity between the fROIs was examined by modular partitioning of the correlation matrix of all fROIs. We could not confirm the hypothesis that BU areas are activated to a lesser extent in AN upon visual processing of food images. Among the BU areas the caudate showed higher activation in both patient groups compared to HC. In accordance with Brooks et al.’s model, we did find evidence for increased TD control in AN and REC. The functional connectivity analysis yielded two clusters in HC and REC, but three clusters in AN. In HC fROIs across BU, TD and VPA areas clustered, in AN one cluster span across BU, TD and insula, one across BU, TD and VPA areas and one was confined to the VPA network. In REC BU, TD and VPA or VPA and insula clustered. In conclusion, despite weight recovery, neural processing of food cues is also altered in recovered AN patient
Available from: Blake Woodside
- "Also, insular activity differs between patients and healthy controls, when viewing images of high calorie foods while in a hungry versus full state, with greater mPFC coactivation seen in patients versus controls (Gizewski et al., 2010). Other studies, in both currently ill and recovered patients, have linked insular activity to viewing aversive food stimuli (Ellison et al., 1998), to seeing pictures of one's self image (Sachdev, Mondraty, Wen, & Gulliford, 2008), to reflecting on one's appearance (McAdams & Krawczyk, 2012) and to evaluating one's shape relative to another person (Friederich et al., 2010). Anatomic and circuit models further support a central role for the insula in AN, which receives projections from ACC, OFC, DLPFC, as well as from SCC (Hamani et al., 2011). "
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ABSTRACT: Anorexia Nervosa (AN) is a serious psychiatric condition marked by firmly entrenched and maladaptive behaviours and beliefs about body, weight and food, as well as high rates of psychiatric comorbidity. The neural roots of AN are now beginning to emerge, and appear to be related to dysfunctional, primarily limbic, circuits driving pathological thoughts and behaviours. As a result, the significant physical symptoms of AN are increasingly being understood at least partially as a result of abnormal or dysregulated emotional processing. This paper reviews the nature of limbic dysfunction in AN, and how structural and functional imaging has implicated distinct emotional and perceptual neural circuits driving AN symptoms. We propose that top-down and bottom-up influences converge on key limbic modulatory structures, such as the subcallosal cingulate and insula, whose normal functioning is critical to affective regulation and emotional homeostasis. Dysfunctional activity in these structures, as is seen in AN, may lead to emotional processing deficits and psychiatric symptoms, which then drive maladaptive behaviours. Modulating limbic dysregulation may therefore be a potential treatment strategy in some AN patients.
Available from: PubMed Central
- "The mean BMI of patients with ED in the present study was equivalent to the lowest BMI of patients with ED included in previous NIRS studies [11-14], and lower than the BMI of patients with ED included in many studies using fMRI [54-64] or PET [65-72]. To the best of our knowledge, this study represents the first report of both brain activity and clinical features of patients with ED with extremely low body weight. "
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Functional neuroimaging techniques are widely used to elucidate changes in brain activity, and various questionnaires are used to investigate psychopathological features in patients with eating disorders (ED). It is well known that social skills and interpersonal difficulties are strongly associated with the psychopathology of patients with ED. However, few studies have examined the association between brain activity and social relationships in patients with ED, particularly in patients with extremely low body weight.
In this study, 22-channel near-infrared spectroscopy was used to quantify regional hemodynamic changes during a letter fluency task (LFT) in 20 female patients with ED with a mean body mass index of 14.0 kg/m2and 31 female controls (CTLs). Symptoms were assessed using the Eating Disorder Inventory-2 and Beck Depression Inventory. We hypothesized that frontal activity in patients with ED would be lower than in CTLs and would show different correlations with psychopathological features compared with CTLs.
The LFT performance and score on the social insecurity subscale of the Eating Disorder Inventory-2 were significantly higher in the ED group than in the CTL group. The mean change in oxygenated hemoglobin (oxy-Hb) in bilateral frontal regions during the LFT was significantly smaller in the ED group than in the CTL group. Social insecurity score was positively correlated with the concentration of oxy-Hb in the bilateral orbitofrontal cortex in the ED group but not in the CTL group.
These results suggest that activity of the orbitofrontal cortex is associated with social insecurity and disturbed in patients with ED. Therefore, disturbed orbitofrontal cortex activity may underlie the lack of insight and social isolation that is characteristic of patients with ED.
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