Brain Tissue Volume Changes Following Weight Gain in Adults with Anorexia Nervosa

Department of Psychology, Department of Epidemiology and Public Health, Yale University, New Haven, Connecticut 06520, USA.
International Journal of Eating Disorders (Impact Factor: 3.13). 07/2011; 44(5):406-11. DOI: 10.1002/eat.20840
Source: PubMed


To measure brain volume deficits among underweight patients with anorexia nervosa (AN) compared to control participants and evaluate the reversibility of these deficits with short-term weight restoration.
Brain volume changes in gray matter (GM), white matter (WM), and cerebrospinal fluid (CSF) were examined in 32 adult women with AN and compared to 21, age and body mass index-range matched control women.
Patients with AN had a significant increase in GM (p = .006, η(2) = 0.14) and WM volume (p = .001, η(2) = 0.19) following weight restoration. Patients on average had lower levels of GM at low weight (647.63 ± 62.07 ml) compared to controls (679.93 ± 53.31 ml), which increased with weight restoration (662.64 ± 69.71 ml), but did not fully normalize.
This study suggests that underweight adult patients with AN have reduced GM and WM volumes that increase with short-term weight restoration.

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Available from: Jordan Muraskin, Sep 16, 2014
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    • "Abnormalities in gray matter volume have been found previously in those recovered from AN [ Joos et al . , 2011 ; Katzman et al . , 1997 ; Roberto et al . , 2011 ] although this finding is not always reported [ Castro - Fornieles et al . , 2009 ; Wagner et al . , 2006b ] . To test whether altered func - tional connectivity in this study may be explained by dif - ferences between the groups in gray matter volume , voxel - based morphometry ( VBM ) analysis was run on the high - resolution T1 - we"
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    ABSTRACT: Functional brain imaging studies have shown abnormal neural activity in individuals recovered from anorexia nervosa (AN) during both cognitive and emotional task paradigms. It has been suggested that this abnormal activity which persists into recovery might underpin the neurobiology of the disorder and constitute a neural biomarker for AN. However, no study to date has assessed functional changes in neural networks in the absence of task-induced activity in those recovered from AN. Therefore, the aim of this study was to investigate whole brain resting state functional connectivity in nonmedicated women recovered from anorexia nervosa. Functional magnetic resonance imaging scans were obtained from 16 nonmedicated participants recovered from anorexia nervosa and 15 healthy control participants. Independent component analysis revealed functionally relevant resting state networks. Dual regression analysis revealed increased temporal correlation (coherence) in the default mode network (DMN) which is thought to be involved in self-referential processing. Specifically, compared to healthy control participants the recovered anorexia nervosa participants showed increased temporal coherence between the DMN and the precuneus and the dorsolateral prefrontal cortex/inferior frontal gyrus. The findings support the view that dysfunction in resting state functional connectivity in regions involved in self-referential processing and cognitive control might be a vulnerability marker for the development of anorexia nervosa. Hum Brain Mapp, 2012. © 2012 Wiley Periodicals, Inc.
    Full-text · Article · Feb 2014 · Human Brain Mapping
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    • "Diffusion tensor imaging was performed . AN vs HC : reduced fractional anisotropy in the bilateral fimbria - fornix , fronto - occipital fasciculus and posterior cingulum . Roberto et al . ( 2011 ) T1 : 32 AN , 21 HC T2 : 32 AN , 21 HC T1 : within 2 weeks of hospitalisation . T2 : before discharge ."
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    ABSTRACT: Objective: Recent advances in neuroimaging techniques have enabled a better understanding of the neurobiological underpinnings of anorexia nervosa (AN). The aim of this paper was to summarise our current understanding of the neurobiology of AN. Methods: The literature was searched using the electronic databases PubMed and Google Scholar, and by additional hand searches through reference lists and specialist eating disorders journals. Relevant studies were included if they were written in English, only used human participants, had a specific AN group, used clinical populations of AN, group comparisons were reported for AN compared to healthy controls and not merely AN compared to other eating disorders or other psychiatric groups, and were not case studies. Results: The systematic review summarises a number of structural and functional brain differences which are reported in individuals with AN, including differences in neurotransmitter function, regional cerebral blood flow, glucose metabolism, volumetrics and the blood oxygen level dependent response. Conclusion: Several structural and functional differences have been reported in AN, some of which reverse and others which persist following weight restoration. These findings have important implications for our understanding of the neurobiological underpinnings of AN, and further research in this field may provide new direction for the development of more effective treatments.
    Full-text · Article · Jan 2014 · Australian and New Zealand Journal of Psychiatry
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    • "On the other hand, if the smaller brain volumes that we observed in veterans with chronic PTSD were a consequence of having persistent PTSD over many years, then the lack of brain volume difference between veterans with remitted PTSD, those who never developed PTSD, and those who had not been exposed to trauma may be due to morphological restitution in the recovered veterans. Although the caudal anterior cingulate, insula, and corpus callosum are generally considered to have less capacity for neurogenesis than the hippocampus, there have been reports of suggestive of morphological restitution in non-hippocampal brain regions in elderly adults after six months of aerobic exercise training (Colcombe et al., 2006), in adults with anorexia nervosa following weight restoration (Roberto et al., 2011; Swayze et al., 1996), and in recovered alcoholics following abstinence (Bartsch et al., 2007; Gazdzinski et al., 2005,2010; ) that is not solely attributed to rehydration (Schroth et al., 1988; Trabert et al., 1995). Although it has been proposed that trauma exposure, even in the absence of PTSD, may be associated with reduced brain volume (Hedges and Woon, 2010; Sapolsky, 2000), one longitudinal study found no baseline hippocampal volume differences and no differences in the 6-month hippocampal atrophy rates of 10 trauma survivors who developed PTSD relative to 27 trauma survivors who did not develop PTSD. "
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    ABSTRACT: We previously reported that hippocampal volume was associated with current, but not lifetime posttraumatic stress disorder (PTSD) symptom severity. In the present study, we test the hypothesis that like the hippocampus, the volumes of other brain regions previously implicated in PTSD, are also negatively related to current, but not lifetime PTSD symptom severity. One hundred ninety-one veterans underwent structural magnetic resonance imaging (MRI) on a 4T scanner. Seventy-five veterans were trauma unexposed, 43 were trauma exposed without PTSD, 39 were trauma exposed with current PTSD, and 34 were trauma exposed veterans with remitted PTSD. Hippocampal, amygdala, rostral and caudal anterior cingulate, insula, and corpus callosum volumes, quantified with Freesurfer version 4.5, were analyzed by group using multivariate analysis of covariance. Veterans with PTSD had smaller hippocampal, caudal anterior cingulate, insula, and corpus callosum volumes than the unexposed controls (p≤0.009); smaller hippocampal, caudal anterior cingulate, insula (p≤0.009) and marginally smaller corpus callosum (p=0.06) than veterans with remitted PTSD; and smaller hippocampal and caudal anterior cingulate volumes than veterans without PTSD (p≤0.04). In contrast, there was no significant volume differences between veterans with remitted PTSD compared to those without PTSD or unexposed controls. The finding that current but not lifetime PTSD accounts for the volumes of multiple brain regions suggests that either smaller brain volume is a vulnerability factor that impedes recovery from PTSD or that recovery from PTSD is accompanied by a wide-spread restoration of brain tissue.
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