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Introduction A fundamental question in anorexia nervosa (AN) research is to understand how patients resist food intake despite being life-threateningly underweight (1). Previous neuroscientific research has primarily focused on food [...], BACKGROUND. Given the heightened tolerance to self-starvation in anorexia nervosa (AN), a hypothalamic dysregulation of energy and glucose homeostasis has been hypothesized. Therefore, we investigated whether hypothalamic reactivity to glucose metabolism is impaired in AN. METHODS. Twenty-four participants with AN, 28 normal-weight participants, and 24 healthy participants with obesity underwent 2 MRI sessions in a single-blind, randomized, case-controlled crossover study. We used an intragastric infusion of glucose and water to bypass the cephalic phase of food intake. The responsivity of the hypothalamus and the crosstalk of the hypothalamus with reward-related brain regions were investigated using high-resolution MRI. RESULTS. Normal-weight control participants displayed the expected glucose-induced deactivation of hypothalamic activation, whereas patients with AN and participants with obesity showed blunted hypothalamic reactivity. Furthermore, patients with AN displayed blunted reactivity in the nucleus accumbens and amygdala. Compared with the normal-weight participants and control participants with obesity, the patients with AN failed to show functional connectivity between the hypothalamus and the reward-related brain regions during water infusion relative to glucose infusion. Finally, the patients with AN displayed typical baseline levels of peripheral appetite hormones during a negative energy balance. CONCLUSION. These results indicate that blunted hypothalamic glucose reactivity might be related to the pathophysiology of AN. This study provides insights for future research, as it is an extended perspective of the traditional primary nonhomeostatic understanding of the disease. FUNDING. This study was supported by a grant from the DFG (SI 2087/2-1).

Introduction Bulimia nervosa is a common mental disorder with heightened morbidity and all-cause mortality. (1) It is characterized by recurrent episodes of binge eating accompanied by a feeling of lack [...], Background: Impaired inhibitory control is considered a behavioural phenotype in patients with bulimia nervosa. However, the underlying neural correlates of impaired general and food-specific behavioural inhibition are largely unknown. Therefore, we investigated brain activation during the performance of behavioural inhibition to general and food-related stimuli in adults with bulimia nervosa. Methods: Women with bulimia and healthy control women underwent event-related fMRI while performing a general and a food-specific no-go task. Results: We included 28 women with bulimia nervosa and 29 healthy control women in our study. On a neuronal level, we observed significant group differences in response to general no-go stimuli in women with bulimia nervosa with high symptom severity; compared with healthy controls, the patients showed reduced activation in the right sensorimotor area (postcentral gyrus, precentral gyrus) and right dorsal striatum (caudate nucleus, putamen). Limitations: The present results are limited to adult women with bulimia nervosa. Furthermore, it remains unclear whether impaired behavioural inhibition in patients with this disorder are a cause or consequence of chronic illness. Conclusion: Our findings suggest that diminished frontostriatal brain activation in patients with bulimia nervosa contribute to the severity of binge eating symptoms. Gaining further insight into the neural mechanisms of behavioural inhibition problems in individuals with this disorder may inform brain-directed treatment approaches and the development of response inhibition training approaches to improve inhibitory control in patients with bulimia nervosa. The present study does not support greater behavioural and neural impairments to food-specific behavioural inhibition in these patients.

Background: Patients with Anorexia Nervosa (AN) show a moderate deficit in overall neuropsychological functioning. Since previous studies on memory performance mainly employed cross‐sectional designs, the present study aims to investigate changes in verbal memory following weight‐gain. Methods: Verbal memory was assessed with the Wechsler Memory Scale‐Revised (WMS‐R; 'logical memory'‐story‐recall‐subtest) and the California Verbal Learning Test‐II (CVLT‐II; 'verbal learning'). Included were 31 female patients with AN (18 restricting‐, 13 purging‐subtype; average disease duration: 5.1 years; average baseline BMI: 14.4 kg/m2) and 24 medication‐free normal‐weight healthy women adjusted for age at baseline (T0). In a post‐treatment assessment of approx. 6 weeks with weight increase (T1), 18 patients with AN and 20 healthy women were assessed again. Group differences in verbal memory (i.e., WMS‐R, CVLT‐II) were assessed for the baseline comparisons with a multivariate ANOVA and longitudinal data were analysed with repeated measures (RM) ANOVAs. Results: At baseline, patients with AN as compared to healthy women displayed deficits in logical memory. In the follow‐up assessment, patients with AN improved their logical memory significantly compared to healthy controls (p < 0.006). Furthermore, groups did not differ in verbal learning neither before nor after inpatient treatment. Conclusions: Enhanced logical memory in patients with AN following weight‐gain is probably due to the impaired memory as compared to healthy controls at T0. A survivorship bias could explain the improved memory performance in longitudinal data in contrast to cross‐sectional studies. Patients with AN with poorer memory performance before inpatient treatment are at higher risk to drop out and need support. Key points: Impaired logical memory before inpatient treatment improves in patients with anorexia nervosa (AN) during weight‐gain, while verbal learning seems to be intact before as well as after inpatient treatment as compared to healthy women.Drop‐out‐analyses revealed that patients with AN with poorer logical memory performance before inpatient treatment are at higher risk to drop out, and should receive further therapeutic support.Results imply, that therapeutic interventions using cognitive strategies may be overwhelming in severely ill patients with AN during early stages of the disease, while early cognitive interventions might be effective in a less sick, more motivated subgroup of patients with AN. [ABSTRACT FROM AUTHOR]

Background: Anorexia nervosa (AN) is characterized by an overgeneralization of food/body-related autobiographical memories (AM). This is regarded as an emotion regulation strategy with adverse long-term effects implicated in disorder maintenance and treatment resistance. Therefore, we aimed to examine neural correlates of food/body-related AM-recall in AN. Methods: Twenty-nine female patients with AN and 30 medication-free age-sex-matched normal-weight healthy controls (HC) underwent functional magnetic resonance imaging while recalling AMs in response to food/body-related and neutral cue words. To control for general knowledge retrieval, participants engaged in a semantic generation and riser detection task. Results: In comparison to HC, patients with AN generated fewer and less specific AMs in response to food/body-related words, but not for neutral cue words. Group comparisons revealed reduced activation in regions associated with self-referential processing and memory retrieval (precuneus and angular gyrus) during the retrieval of specific food/body-related AM in patients with AN. Brain connectivity in regions associated with memory functioning and executive control was reduced in patients with AN during the retrieval of specific food/body-related AM. Finally, resting-state functional connectivity analysis revealed no differences between groups, arguing against a general underlying disconnection of brain networks implicated in memory and emotional processing in AN. Conclusions: These results indicate impaired neural processing of food/body-related AM in AN, with a reduced involvement of regions involved in self-referential processing. Our findings are discussed as possible neuronal correlates of emotional avoidance in AN and provide new insights of AN-pathophysiology underscoring the importance of targeting dysfunctional emotion regulation strategies during treatment. [ABSTRACT FROM AUTHOR]

Despite a great diagnostic overlap, complex posttraumatic stress disorder (CPTSD) has been recognised by the ICD-11 as a new, discrete entity and recent empirical evidence points towards a distinction from simple posttraumatic stress disorder (PTSD) and borderline personality disorder (BPD). The development and maintenance of these disorders is sustained by neurobiological alterations and studies using functional magnetic resonance imaging (fMRI) may further contribute to a clear differentiation of CPTSD, PTSD and BPD. However, there are no existing fMRI studies directly comparing CPTSD, PTSD and BPD. In addition to a summarization of diagnostic differences and similarities, the current review aims to provide a qualitative comparison of neuroimaging findings on affective, attentional and memory processing in CPTSD, PTSD and BPD. Our narrative review alludes to an imbalance in limbic-frontal brain networks, which may be partially trans-diagnostically linked to the degree of trauma symptoms and their expression. Thus, CPTSD, PTSD and BPD may underlie a continuum where similar brain regions are involved but the direction of activation may constitute its distinct symptom expression. The neuronal alterations across these disorders may conceivably be better understood along a symptom-based continuum underlying CPTSD, PTSD and BPD. Further research is needed to amend for the heterogeneity in experimental paradigms and sample criteria. [ABSTRACT FROM AUTHOR]

Background: Restrictive food intake in anorexia nervosa (AN) has been related to an overactive cognitive control network inhibiting intuitive motivational responses to food stimuli. However, the influence of short-term homeostatic signaling on the neural regulation of cue-induced food craving in AN is still unclear. Methods: Twenty-five women with AN and 25 matched normal-weight women were examined on two occasions after receiving either glucose or water directly into their stomach using a nasogastric tube. Participants were blinded to the type of infusion. An event-related functional magnetic resonance imaging paradigm was used to investigate the effect of intestinal glucose load on neural processing during either simple viewing or distraction from food stimuli. Results: Neural differences between patients with AN and normal-weight participants were found during the distraction from food stimuli, but not during the viewing condition. When compared to controls, patients with AN displayed increased activation during food distraction in the left parietal lobule/precuneus and fusiform gyrus after water infusion and decreased activation in ventromedial prefrontal and cingulate regions after intestinal glucose load. Conclusions: Independent of the cephalic phase and the awareness of caloric intake, homeostatic influences trigger disorder-specific reactions in AN. Food distraction in patients with AN is associated with either excessive higher-order cognitive control during physiological hunger or decreased internally directed attention after intestinal glucose load. These findings suggest that food distraction plays an important role in the psychopathology of AN. This study was registered on clinicaltrials.gov with identifier: NCT03075371. [ABSTRACT FROM AUTHOR]

Objectives: Excess sugar consumption, particularly in the form of sweetened beverages, has been identified as a pivotal contributor to the epidemic of obesity and associated metabolic disorders. However, the impact of sugar-sweetened beverages on food craving is still inconclusive. Therefore, the present study aimed to specifically investigate the effects of an intestinal glucose load on neural processing of food cues. Methods: Using a single-blind fMRI design, 26 normal-weight women were scanned on two occasions, after receiving either a glucose or water infusion directly into the stomach using a nasogastric tube, without being aware of the type of infusion. Participants had to either view neutral and food images, or were asked to distract themselves from these images by solving an arithmetic task. Results: In response to viewing high-caloric food cues, we observed increased activation in reward-related brain areas. During food distraction, fronto-parietal brain regions were recruited, which are commonly related to attentional deployment and hedonic valuation. Furthermore, activity in the dorsolateral prefrontal cortex showed increased functional connectivity with the insula and was correlated with subjective craving levels to food cues. Despite an increase of blood glucose levels in response to the glucose compared to the water infusion, neither subjective food craving nor neural regulation of food craving showed significant differences. Conclusions: These findings support a decreased satiation effect of sweet beverages, as intestinal glucose ingestion and signalling showed no significant effect on cortical brain circuits associated with food craving. This trial was registered at clinicaltrials.gov as NCT03075371. [ABSTRACT FROM AUTHOR]

Background: Bipolar disorder I (BD-I) is defined by episodes of mania, depression and euthymic states. These episodes are among other symptoms characterized by altered reward processing and negative symptoms (NS), in particular apathy. However, the neural correlates of these deficits are not well understood. Methods: We first assessed the severity of NS in 25 euthymic BD-I patients compared with 25 healthy controls (HC) and 27 patients with schizophrenia (SZ). Then, we investigated ventral (VS) and dorsal striatal (DS) activation during reward anticipation in a Monetary Incentive Delayed Task and its association with NS. Results: In BD-I patients NS were clearly present and the severity of apathy was comparable to SZ patients. Apathy scores in the BD-I group but not in the SZ group correlated with sub-syndromal depression scores. At the neural level, we found significant VS and DS activation in BD-I patients and no group differences with HC or SZ patients. In contrast to patients with SZ, apathy did not correlate with striatal activation during reward anticipation. Explorative whole-brain analyses revealed reduced extra-striatal activation in BD-I patients compared with HC and an association between reduced activation of the inferior frontal gyrus and apathy. Conclusion: This study found that in BD-I patients apathy is present to an extent comparable to SZ, but is more strongly related to sub-syndromal depressive symptoms. The findings support the view of different pathophysiological mechanisms underlying apathy in the two disorders and suggest that extra-striatal dysfunction may contribute to impaired reward processing and apathy in BD-I. [ABSTRACT FROM AUTHOR]

Aim. Previous studies indicate the effectiveness of motor imagery training in stroke patients. To determine whether patients showing chronic visuospatial neglect symptoms may profit from motor imagery training, it is important to assess how the brain implements motor imagery when cortical systems involved in attentional control are impaired. Method. Therefore, in this pilot study, nine chronic neglect patients with right-hemispheric stroke performed motor imagery of a finger opposition task during functional magnetic resonance imaging (fMRI). Results. Imagery of unaffected hand movements was related to activations in the left primary somatosensory and premotor cortices as well as in the left supplementary motor area. During the imagery of the affected hand, patients displayed activations in the left premotor cortex and supplementary motor area as well as left dorsolateral prefrontal cortex. Furthermore, time since onset and visual imagery capacity were negatively related to activation in the supplementary motor area during the imagery of the affected hand. Conclusions. These initial results demonstrate motor imagery capacity in patients with chronic neglect via compensatory neural processing during motor imagery of the affected hand in ipsilateral brain regions, since we found that the supplementary motor area appears to be specifically related to neglect severity. Although our results must be treated with caution due to the small sample size and missing control group, they indicate that neglect is not necessarily an exclusion criterion for motor imagery training per se. [ABSTRACT FROM AUTHOR]