Uncovering neural pathways underlying bulimia nervosa: resting-state neural connectivity disruptions correlate with maladaptive eating behaviors.

PURPOSE: Bulimia nervosa (BN) is characterized by recurrent binge-eating episodes and inappropriate compensatory behaviors. This study investigated alterations in resting-state surface-based neural activity in BN patients and explored correlations between brain activity and eating behavior. METHODS: A total of 26 BN patients and 28 healthy controls were enrolled. Indirect measurement of cerebral cortical activity and functional connectivity (FC) analyses were performed in Surfstat. A principal component analysis (PCA) model was used to capture the commonalities within the behavioral questionnaires from the BN group. RESULTS: Compared with the healthy control group, the BN group showed decreased surface-based two-dimensional regional homogeneity in the right superior parietal lobule (SPL). Additionally, the BN group showed decreased FC between the right SPL and the bilateral lingual gyrus and increased FC between the right SPL and the left caudate nucleus and right putamen. In the FC-behavior association analysis, the second principal component (PC2) was negatively correlated with FC between the right SPL and the left caudate nucleus. The third principal component (PC3) was negatively correlated with FC between the right SPL and the left lingual gyrus and positively correlated with FC between the right SPL and the right lingual gyrus. CONCLUSION: We revealed that the right SPL undergoes reorganization with respect to specific brain regions at the whole-brain level in BN. In addition, our results suggest a correlation between brain reorganization and maladaptive eating behavior. These findings may provide useful information to better understand the neural mechanisms of BN. LEVEL OF EVIDENCE: V, descriptive study.

Fronto-temporal dysfunction in appetitive regulation of bulimia nervosa with affective disorders: A regional homogeneity and remote connectivity pattern analysis.

OBJECTIVE: The aim of this study was to assess brain functional alterations in BN patients with affective disorders and their association with maladaptive eating behaviors. METHODS: A total of 42 BN patients with affective disorders (anxiety and depression) and 47 healthy controls (HCs) were enrolled in this study. The resting-state fMRI data were analyzed for functional changes as indicated by regional homogeneity based on Kendall's coefficient of concordance (KCC-ReHo) and seed-based functional connectivity (FC). A principal component analysis (PCA) model was used to identify the commonalities within the behavioral questionnaires from the BN group. RESULTS: Patients in the BN group showed decreased ReHo in the bilateral middle frontal gyrus (MFG) and right supramarginal gyrus (SMG). Additionally, the BN group showed increased FC between the left MFG and the right inferior temporal gyrus (ITG); decreased FC between the right MFG and the bilateral insula and the left middle temporal gyrus (MTG); and decreased FC between the right SMG and the left superior temporal gyrus (STG) and right inferior frontal gyrus (IFG). In the FC-behavior association analysis, the second principal component (PC2) was negatively correlated with FC between the left MFG and the right ITG. CONCLUSION: Based on a brain functional analysis (ReHo and FC), this study revealed significant aberrant changes in the frontal-temporal regions of BN patients with affective disorders. These regions, which serve as fronto-temporal circuitry, are associated with restraint and emotional eating behaviors. Our findings shed new light on the neural mechanisms underlying the condition.

Characteristics of white matter alterations along fibres in patients with bulimia nervosa: A combined voxelwise and tractography study.

Accumulating evidence supports the hypothesis that white matter (WM) abnormalities are involved in the pathophysiology of bulimia nervosa (BN); however, findings from in vivo neuroimaging studies have been inconsistent. We aimed to investigate the possible brain WM alterations, including WM volume and microstructure, in patients with BN. We recruited 43 BN patients and 31 healthy controls (HCs). All participants underwent structural and diffusion tensor imaging. Differences in WM volume and microstructure were evaluated using voxel-based morphometry, tract-based spatial statistics, and automated fibre quantification analysis. Compared with HCs, BN patients showed significantly decreased fractional anisotropy in the middle part of the corpus callosum (nodes 31-32) and increased mean diffusivity in the right cranial nerve V (CN V) (nodes 27-33 and nodes 55-88) and vertical occipital fasciculus (VOF) (nodes 58-85). Moreover, we found decreased axial diffusivity in the right inferior fronto-occipital fasciculus (node 67) and increased radial diffusivity in the CN V (nodes 22-34 and nodes 52-89) and left VOF (nodes 60-66 and nodes 81-85). Meanwhile, WM microstructural changes were correlated with patients' clinical manifestations. We did not find any significant differences in WM volume and the main WM fibre bundle properties between BN patients and HCs. Taken together, these findings provide that BN shows significant brain WM reorganization, but primarily in microstructure (part of WM fibre bundle), which is not sufficient to cause changes in WM volume. The automated fibre quantification analysis could be more sensitive to detect the subtle pathological changes in a point or segment of the WM fibre bundle.

Exploration of the relationships between clinical traits and functional connectivity based on surface morphology abnormalities in bulimia nervosa.

BACKGROUND: Bulimia nervosa is a recurrent eating disorder with uncertain pathogenesis. Recently, there has been growing interest in using neuroimaging techniques to explore brain structural and functional alterations in bulimia nervosa, but the findings of previous studies have a great number of inconsistencies. METHODS: Here, we collected anatomical and resting-state functional magnetic resonance imaging data from 43 bulimia nervosa patients and 34 matched healthy controls (HCs). We applied a surface-based morphology analysis to explore brain cortical morphology differences and a novel surface-based functional connectivity (FC) analysis to investigate functional abnormalities. Principal component analysis was performed to analyze the behavioral data of the participants. We further analyzed the relationships between abnormalities in cortical characteristics or FC and clinical features. RESULTS: We observed increased greater sulcal depth in the right superior temporal gyrus (STG) and the right medial orbitofrontal cortex (mOFC) in bulimia nervosa patients than in the HCs. Additionally, the patients exhibited increased FC between the right STG and right ventral tegmental area but decreased function between the right mOFC and right putamen, which was significantly negatively correlated with the first principal component reflecting the severity of bulimia nervosa symptom. CONCLUSIONS: Our findings provide evidence of neuroanatomical and functional abnormalities in bulimia nervosa patients. Moreover, the FC between the right mOFC and right putamen was associated with symptom severity of bulimia nervosa, which may be a neural marker and involved in the neuropathological mechanism of bulimia nervosa.

Aberrant modular segregation of brain networks in female patients with bulimia nervosa.

OBJECTIVE: Bulimia nervosa (BN) is an eating disorder associated with the dysfunction of intrinsic brain networks. However, whether the network disruptions in BN patients manifest as dysconnectivity or imbalances of network modular segregation remains unclear. METHOD: We collected data from 41 women with BN and 41 matched healthy control (HC) women. We performed graph theory analysis based on resting-state functional magnetic resonance imaging (RS-fMRI) data; then, we computed the participation coefficient (PC) among brain modules to characterize the modular segregation for the BN and HC groups. The number of intra- and inter-modular connections was calculated to explain the PC changes. Additionally, we examined the potential associations of the measures mentioned above with clinical variables within the BN group. RESULTS: Compared with the HC group, the BN group showed significantly decreased PC in the fronto-parietal network (FPN), cingulo-opercular network (CON), and cerebellum (Cere). Additionally, the number of intra-modular connections of the default mode network (DMN) and the number of the inter-modular connections between the DMN and CON, FPN and Cere, and CON and Cere in the BN group were lower than those in the HC group. The nodal level analysis showed that the BN group had a decreased PC of the anterior prefrontal cortex (aPFC), dorsal frontal cortex (dFC), inferior parietal lobule (IPL), thalamus, and angular gyrus. Further, these metrics were significantly correlated with clinical variables in the BN group. DISCUSSION: These findings may provide novel insights to capture atypical topologies associated with pathophysiology mechanisms and clinical symptoms underlying BN.

Childhood maltreatment is associated with cortical thinning in people with eating disorders.

Childhood maltreatment (CM) is a non-specific risk factor for eating disorders (ED) and is associated with a greater severity in their clinical presentation and poorer treatment outcome. These data suggest that maltreated people with ED may be biologically other than clinically different from non-maltreated people. The aim of the present study was to investigate cortical thickness (CT), a possible biomarker of neurodevelopment, in people with ED with or without history of CM and in healthy women. Twenty-four healthy women, 26 with anorexia nervosa and 24 with bulimia nervosa underwent a 3T MRI scan. All participants filled in the childhood trauma questionnaire. All neuroimaging data were processed by FreeSurfer. Twenty-four participants with ED were identified as maltreated and 26 participants with ED as non-maltreated. All healthy women were non-maltreated. Compared to healthy women, maltreated people with ED showed lower CT in the left rostral anterior cingulate gyrus, while compared to people with ED without history of CM showed lower CT values in the left superior frontal and in right caudal middle frontal and superior parietal gyri. No significant differences emerged in CT measures between healthy women and people with ED without history of CM. The present findings show for the first time that in adult people with ED childhood maltreatment is associated with cortical thinning in areas implicated in the modulation of brain processes that are acknowledged to play a role in the psychopathology of ED.

Altered prefrontal activation during the inhibition of eating responses in women with bulimia nervosa.

BACKGROUND: The sense of 'loss of control' (LOC), or a feeling of being unable to stop eating or control what or how much one is eating, is the most salient aspect of binge eating. However, the neural alterations that may contribute to this experience and eating behavior remain poorly understood. METHODS: We used functional near-infrared spectroscopy (fNIRS) to measure activation in the prefrontal cortices of 23 women with bulimia nervosa (BN) and 23 healthy controls (HC) during two tasks: a novel go/no-go task requiring inhibition of eating responses, and a standard go/no-go task requiring inhibition of button-pressing responses. RESULTS: Women with BN made more commission errors on both tasks. BN subgroups with the most severe LOC eating (n = 12) and those who felt most strongly that they binge ate during the task (n = 12) showed abnormally reduced bilateral ventromedial prefrontal cortex (vmPFC) and right ventrolateral prefrontal cortex (vlPFC) activation associated with eating-response inhibition. In the entire BN sample, lower eating-task activation in right vlPFC was related to more frequent and severe LOC eating, but no group differences in activation were detected on either task when this full sample was compared with HC. BN severity was unrelated to standard-task activation. CONCLUSIONS: Results provide initial evidence that diminished PFC activation may directly contribute to more severe eating-specific control deficits in BN. Our findings support vmPFC and vlPFC dysfunction as promising treatment targets, and indicate that eating-specific tasks and fNIRS may be useful tools for identifying neural mechanisms underlying dysregulated eating.

Orbitofrontal cortex functional connectivity changes in patients with binge eating disorder and bulimia nervosa.

We aimed to define the shared and unshared functional neurobiological underpinnings of binge eating disorder (BED) and bulimia nervosa (BN). These disorders both involve loss of control over binge eating, but differ based on purging behavior and body image distortion. BED and BN have also been found to show differences in brain activation patterns in reward sensitivity. We enrolled 13 and 12 drug-naive and medication-free women with BED and BN, respectively, and 22 age- and sex-matched healthy controls. We performed an orbitofrontal cortex (OFC)-seeded resting-state whole brain functional connectivity (FC) analysis among the groups. In this study, BED patients exhibited significantly higher impulsivity than controls, whereas the difference in impulsivity between BN and controls was not significant. Participants with BED and BN showed weaker FC between the left lateral OFC and the right precuneus than controls. In the BED only group, the FC strength between these regions was negatively correlated with self-reported impulsivity. In both BED and BN, FC between the left lateral OFC and the right dorsolateral prefrontal cortex was weaker than that in controls. In BED, FC between the left medial OFC and the right cerebellar lobule IV was stronger than that of other groups. Our current results suggest similarities and differences between BED and BN in OFC-seeded FC with respect to reward processing. In particular, FC of the OFC in BED patients showed a significant correlation with their high impulsivity, which may reflect a decline in executive control over binge eating.

Striatal volumes as potential biomarkers in Eating Disorders: A pilot study.

INTRODUCTION: Differences in bulimic and impulsive behaviours in Eating Disorders (ED) have been associated with cortico-striatal circuit dysfunction at a neurobiological level. We sought to investigate neo-striatal volume as a biomarker in ED subgroups as well as the possible relationship with trauma history. MATERIAL AND METHODS: We studied 24 female patients: Anorexia Nervosa AN (n=8), Bulimia Nervosa BN (n=9), comorbid ED with borderline personality disorder (EDc; n=7), and a group of Healthy Controls (n=19). Binge eating behaviours and impulsivity scales were used to characterize our sample as well as Trauma Questionnaires and Magnetic resonance imaging (MRI) volumetric manual measurements of caudate and putamen nuclei (striatum). RESULTS: Our preliminary results showed a significantly larger left putaminal volume in AN compared to the other three groups [C (p=0.008), BN (p<.001) and EDc (p=.001)] and a smaller right putaminal volume in EDc compared to controls (p=.045) and AN (p=.039). Some negative correlations were found between bilateral putaminal volumes and self-reported general and early traumatization scores. CONCLUSION: This pilot study suggested that striatal volumes might differentiate AN from BN and EDc at a neurobiological level with implications for treatment strategies. Larger scale studies should be carried out that allow replication of these data.

Neural mechanisms underlying social recognition and theory of mind in adolescent patients with bulimia nervosa and transdiagnostic comparison with anorexia nervosa.

INTRODUCTION: Theory of mind (ToM) is important for social interactions and typical development and has been found to be impaired in patients with anorexia nervosa (AN) and bulimia nervosa (BN). Hypoactivation in frontotemporal brain regions seems to be the underlying neural mechanism in AN while whole-brain analyses in BN are lacking. METHODS: We used the well-validated social recognition task fMRI paradigm to assess ToM in a total of 72 female adolescents (16 BN, 18 AN and 38 matched healthy controls [HC]). RESULTS: Compared to HCBN , patients with BN showed hyperactivity during ToM-activity in the right frontal pole, middle temporal gyrus and left temporal pole and differed fundamentally from hypoactivation in these regions observed in patients with AN before and after short-term weight rehabilitation. Interaction and overlap analyses confirmed that similar regions were affected in opposite directions in both diseases. Hyperactivations in BN in the right middle temporal gyrus and right frontal pole were associated with clinical BN-severity markers binging and purging frequency. DISCUSSION: The hyperactivation in BN suggest different underlying neural mechanisms for ToM compared to AN. Hyperactivity might correspond to a different but also ineffective cognitive style in patients with BN when approaching social interactions. These important transdiagnostic differences are relevant for future brain-targeted therapeutic approaches.

Neural correlates associated with processing food stimuli in anorexia nervosa and bulimia nervosa: an activation likelihood estimation meta-analysis of fMRI studies.

PURPOSE: Various neurobiological models have utilised symptom categories to explore the underlying neural correlates in both anorexia nervosa (AN) and bulimia nervosa (BN). The aim of this research was to investigate the brain activity patterns associated with viewing food stimuli in anorexia nervosa and bulimia nervosa. METHODS: Electronic databases including PsycInfo and PubMed were systematically searched from data base inception until 1st of December 2020, identifying 14 suitable functional magnetic resonance imaging studies (fMRI), involving 470 participants. ALE meta-analysis was used to statistically analyse the overlap of activation foci from different fMRI studies in response to visual food stimuli. RESULTS: Comparing patients with AN with healthy control (HC), we detected hypoactivation in brain areas related to reward processing (i.e., amygdala and lentiform nucleus), and interoceptive processing (i.e., insula). In addition, patients with AN showed hyperactivations in cognitive control areas (i.e., prefrontal and anterior cingulate cortex). In contrast, patients with BN exhibited hyperactivations in brain areas related to reward processing (i.e., lentiform nucleus), and interoceptive processing (i.e., insula). Furthermore, patients with BN showed hypoactivations in brain regions associated with cognitive control (i.e., prefrontal and anterior cingulate cortex). CONCLUSIONS: Our study shows differing neural endotypes of the two types of eating disorders, that underpin their behavioural phenotypes. While exploratory in nature, these findings might be relevant for guiding new emerging therapies, including invasive and non-invasive neuromodulation techniques in treatment of eating disorders. LEVEL OF EVIDENCE: Level I, meta-analysis.

Changes in cognitive and behavioral control after lamotrigine and intensive dialectical behavioral therapy for severe, multi-impulsive bulimia nervosa: an fMRI case study.

PURPOSE: Adults with bulimia nervosa (BN) and co-occurring emotional dysregulation and multiple impulsive behaviors are less responsive to existing interventions. Initial data suggest that the combination of Dialectical Behavior Therapy (DBT) and a mood stabilizer, lamotrigine, significantly reduces symptoms of affective and behavioral dysregulation in these patients. Identifying candidate neurobiological mechanisms of change for this novel treatment combination may help guide future randomized controlled trials and inform new and targeted treatment development. Here, we examined neurocognitive and symptom changes in a female patient with BN and severe affective and behavioral dysregulation who received DBT and lamotrigine. METHODS: Go/no-go task performance data and resting-state functional MRI scans were acquired before the initiation of lamotrigine (after 6 weeks in an intensive DBT program), and again after reaching and maintaining a stable dose of lamotrigine. The patient completed a battery of symptom measures biweekly for 18 weeks over the course of treatment. RESULTS: After lamotrigine initiation, the patient made fewer errors on a response inhibition task and showed increased and new connectivity within frontoparietal and frontolimbic networks involved in behavioral and affective control. Accompanying this symptom improvement, the patient reported marked reductions in bulimic symptoms, behavioral dysregulation, and reactivity to negative affect, along with increases in DBT skills use. CONCLUSION: Improved response inhibition and cognitive control network connectivity should be further investigated as neurocognitive mechanisms of change with combined DBT and lamotrigine for eating disorders. Longitudinal, controlled trials integrating neuroimaging and symptom measures are needed to fully evaluate the effects of this treatment. LEVEL OF EVIDENCE: IV: Evidence obtained from multiple time series with or without the intervention, such as case studies.

Reward learning in unmedicated women with bulimia nervosa: A pilot investigation.

Bulimia nervosa (BN) is characterized by recurrent engagement in eating disorder behaviors despite negative consequences, potentially reflecting aberrant stimulus-response or reward-learning processes. Indeed, frontostriatal circuitry involved in reward learning is altered in persons with BN and preliminary research suggests reward learning is impaired in persons with BN. Additional research on reward learning in BN and its association with eating disorder symptom expression is warranted to further the field's understanding of potential pathophysiological mechanisms of BN. To this end, the probabilistic reward learning task (PRLT) was administered to unmedicated women with BN (n = 15) and demographically matched psychiatrically healthy women (n = 18). Contrary to our hypotheses, results demonstrated that women with BN showed greater reward learning during the PRLT relative to healthy comparison women when covarying for symptoms of depression, social anxiety, and mania. Exploratory analyses showed that binge-eating frequency was inversely associated with reward learning in women with BN; however, results should be interpreted with caution due to the small sample size. Together, results suggest that women with BN do not have deficits in implicit reward learning. Given the preliminary nature of this investigation, larger-scale studies are needed to further examine reward learning in current BN and could compare reward learning using general (e.g., monetary) and disorder-specific (e.g., food) reinforcers. Further work is needed to confirm the inverse association between reward learning and binge eating.

Increased anticipatory brain response to pleasant touch in women remitted from bulimia nervosa.

Bulimia nervosa (BN) is characterized by affective instability and dysregulated behaviors (binge eating, fasting, self-induced vomiting) that disrupt bodily homeostasis. Mechanisms underlying dysregulation in BN are unclear, although altered reward responsivity, anticipatory processing of environmental cues, and interoception (detection and integration of body-state signals to regulate behavior) have been implicated in BN pathophysiology. We aimed to determine whether BN is associated with ineffectively predicting body state or integrating predicted experience with actual experience by examining neural response to anticipation and experience of affective touch, a pleasant interoceptive stimulus that acts on sensory and emotional systems to guide behavior. During fMRI, we administered soft strokes to the palm and forearm in women remitted from BN (RBN; N = 23) and control women (CW; N = 25). A Group (RBN/CW) × Condition (anticipation/touch) interaction was found in the right dorsal caudate; both CW and RBN had increased activation during touch compared with anticipation, with RBN demonstrating marginally greater anticipatory response than CW. For RBN, those individuals who showed greater anticipatory response in the dorsal caudate also reported higher levels of harm avoidance. RBN individuals relative to CW showed greater activation in left putamen and insula during the anticipation but not when experiencing an affective touch. This increase during anticipation rather than the actual experience of the affective touch is consistent with a top-down preparatory process which is associated with harm avoidance and is similar to what has been observed in anxious individuals. This aberrant signal integration could disrupt feedback processing, serving to maintain disordered behavior.

Investigating resting brain perfusion abnormalities and disease target-engagement by intranasal oxytocin in women with bulimia nervosa and binge-eating disorder and healthy controls.

Advances in the treatment of bulimia nervosa and binge-eating disorder (BN/BED) have been marred by our limited understanding of the underpinning neurobiology. Here we measured regional cerebral blood flow (rCBF) to map resting perfusion abnormalities in women with BN/BED compared with healthy controls and investigate whether intranasal oxytocin (OT), proposed as a potential treatment, can restore perfusion in disorder-related brain circuits. Twenty-four women with BN/BED and 23 healthy women participated in a randomized, double-blind, crossover, placebo-controlled study. We used arterial spin labelling MRI to measure rCBF and the effects of an acute dose of intranasal OT (40 IU) or placebo over 18-26 min post dosing, as we have previously shown robust OT-induced changes in resting rCBF in men in a similar time-window (15-36 min post dosing). We tested for effects of treatment, diagnosis and their interaction on extracted rCBF values in anatomical regions-of-interest previously implicated in BN/BED by other neuroimaging modalities, and conducted exploratory whole-brain analyses to investigate previously unidentified brain regions. We demonstrated that women with BN/BED presented increased resting rCBF in the medial prefrontal and orbitofrontal cortices, anterior cingulate gyrus, posterior insula and middle/inferior temporal gyri bilaterally. Hyperperfusion in these areas specifically correlated with eating symptoms severity in patients. Our data did not support a normalizing effect of intranasal OT on perfusion abnormalities in these patients, at least for the specific dose (40 IU) and post-dosing interval (18-26 min) examined. Our findings enhance our understanding of resting brain abnormalities in BN/BED and identify resting rCBF as a non-invasive potential biomarker for disease-related changes and treatment monitoring. They also highlight the need for a comprehensive investigation of intranasal OT pharmacodynamics in women before we can fully ascertain its therapeutic value in disorders affecting predominantly this gender, such as BN/BED.

A broad-spectrum review on multimodal neuroimaging in bulimia nervosa and binge eating disorder.

Bulimia nervosa (BN) and binge eating disorder (BED) are psychiatric conditions marked by emotional disorders managed through the ingestion of great amount of food, with consequent vomiting for avoiding weight gain. Such behavioral habits are dysfunctional and severely impact both psychological and physical health, also compromising neurobiological processes. In the present review, we focus on recent neuroimaging findings (2010-2019) that provide insight into the neural bases of BN and BED. We describe the role of different neuroimaging techniques (magnetic resonance imaging, both structural and functional, positron emission tomography, single-photon emission computerized tomography, electroencephalography and magnetoencephalography) in the delineation of pathophysiological aspects of BN and BED. Results highlight the main involvement of the frontal system and its relationships with temporal areas for reward and self-regulatory processes modulation. The network that regulates food-stimuli control seems to be widespread across the brain, catching the insula, precentral gyrus, frontal cortex and extending until the visual cortex for processing of body image. These results demonstrate diffuse brain vulnerability associated with BN and BED and can confirm that symptomatology maintenance results from several neurostructural and neurofunctional alterations.

Eating disorders: Do PET and SPECT have a role? A systematic review of the literature.

A systematic review was implemented according to PRISMA guidelines on Pubmed, Psychinfo, Medline, Embase to fill the existing literature gap on the effectiveness of using Positron Emission Tomography (PET) and Single Photon Emission Computed Tomography (SPECT) in Anorexia Nervosa (AN), Bulimia Nervosa (BN) and Binge Eating Disorder (BED). Twenty-two articles were included. Four studies reported an increased density in 5-hydroxytryptamine receptor (5-HT1A) in fronto-temporo-parietal regions in both affected and recovered AN as well as in BN. The 5-HT transporter (5-HTT) binding was increased or diminished in different specific cortical areas and in relation to Eating Disorder (ED) subtypes. Some evidences of blunted Dopamine (DA) release in the putamen in BN patients suggest that their DA function might be impaired as in addictive behaviours. Studies estimating the regional Cerebral Blood Flow (rCBF) with SPECT demonstrated that temporal areas seem to play a key role in ED corroborating the hypothesis of a cingulate-temporal cortical dysfunction in AN. In addition, alterations of both parietal and prefrontal cortex provide a possible common neural substrate in AN. Studies included in this review are heterogeneous preventing robust conclusions, however, our findings add knowledge on some of the neurotransmitters involved in ED.

Disturbed Resting-State Whole-Brain Functional Connectivity of Striatal Subregions in Bulimia Nervosa.

BACKGROUND: Disturbed self-regulation, taste reward, as well as somatosensory and visuospatial processes were thought to drive binge eating and purging behaviors that characterize bulimia nervosa. Although studies have implicated a central role of the striatum in these dysfunctions, there have been no direct investigations on striatal functional connectivity in bulimia nervosa from a network perspective. METHODS: We calculated the functional connectivity of striatal subregions based on the resting-state functional Magnetic Resonance Imaging data of 51 bulimia nervosa patients and 53 healthy women. RESULTS: Compared with the healthy women, bulimia nervosa patients showed increased positive functional connectivity in bilateral striatal nuclei and thalamus for nearly all of the striatal subregions, and increased negative functional connectivity in bilateral primary sensorimotor cortex and occipital areas for both ventral striatum and putamen subregions. Only for the putamen subregions, we observed reduced negative functional connectivity in the prefrontal (bilateral superior and middle frontal gyri) and parietal (right inferior parietal lobe and precuneus) areas. Several striatal connectivities with occipital and primary sensorimotor cortex significantly correlated with the severity of bulimia. CONCLUSIONS: The findings indicate bulimia nervosa-related alterations in striatal functional connectivity with the dorsolateral prefrontal cortex supporting self-regulation, the subcortical striatum and thalamus involved in taste reward, as well as the visual occipital and sensorimotor regions mediating body image, which contribute to our understanding of neural circuitry of bulimia nervosa and encourage future therapeutic developments for bulimia nervosa by modulating striatal pathway.

Altered regional gray matter volume in Chinese female patients with bulimia nervosa.

BACKGROUND: Bulimia nervosa (BN) is a psychiatric disorder with unclear pathophysiology. Several studies have associated BN with structural and functional changes in the brain, but findings have been inconsistent. Here we explored this potential association in a small group of Chinese women with BN. METHODS: This retrospective study examined 34 women with BN and 34 age-matched healthy controls, all of whom underwent T1-weighted magnetic resonance imaging (MRI). Voxel-based morphometry was carried out to explore alterations in regional grey matter volume (GMV) that may be associated with BN. RESULTS: The BN group showed smaller GMV in the left medial superior frontal gyrus (SFGmed.L), right superior temporal gyrus (STG.R), right median cingulate and paracingulate gyri (DCG.R), left median cingulate and paracingulate gyri (DCG.L) and left dorsolateral superior frontal gyrus (SFGdor.L). No regions showing GMV increases in BN were identified. The GMV reduction did not correlate with body mass index, duration of illness, or patients' self-esteem or overall self-evaluation. GMV reduction correlated negatively with age in the SFGmed. L (r = - 0.516, P < 0.005), DCG. R (r = - 0.556, P < 0.005), DCG. L (r = - 0.576, P < 0.05) and SFGdor. L (r = - 0.576, P < 0.005). CONCLUSIONS: Women with BN show reduced GMV in several brain regions, but it is difficult to know whether these changes are the result of BN pathology or of binge-eating and compensatory behavior. These changes may be associated with impaired inhibitory control, body dissatisfaction and emotion dysregulation.

Abnormal structural brain network and hemisphere-specific changes in bulimia nervosa.

Bulimia nervosa (BN) is characterized by episodic binge eating and purging behaviors. Disrupted neural processes of self-regulation, taste-rewarding, and body image has been associated with the pathogenesis of BN. However, the structural basis for these behavioral and functional deficits remains largely unknown. We employed diffusion tensor imaging and graph theory approaches (including the nodal properties and network-based statistics (NBS)) to characterize the whole-brain structural network of 48 BN and 44 healthy women. For nodal measures of strength, local efficiency, and betweenness centrality, BN patients displayed abnormal increases in multiple left-lateralized nodes within the mesocorticolimbic reward circuitry (including the orbitofrontal cortex, anterior cingulate, insular, medial temporal, and subcortical areas), lateral temporal-occipital cortex, and precuneus, while reduced global efficiency was observed in the right-lateralized nodes within the dorsolateral prefrontal cortex, mesocorticolimbic circuitry, somatosensory and visuospatial system. Several mesocorticolimbic nodes significantly correlated with BN symptoms. At a network level, we found increased left-lateralized connections primarily within the orbitofrontal cortex and its connections to mesocorticolimbic and lateral temporal-occipital areas, but reduced right-lateralized connections across the inferior frontal gyrus and insula, as well as their connections to the lateral temporal cortex. This study revealed BN-related changes in white-matter connections across the prefrontal control, mesocorticolimbic reward, somatosensory and visuospatial systems. The hemispheric-specific change could be an important aspect of the pathophysiology of BN. By characterizing whole-brain structural network changes of BN, our study provides novel evidence for understanding the behavioral and functional deficits of the disorder.