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Background Somnambulism, or sleepwalking (SW), is one of the most common forms of arousal parasomnias. It is characterized by different complex motor behaviors leading to unwanted movements in bed or walking during sleep. It can be the consequence of psychological stress, abnormal breathing during sleep, high fever, or drug adverse effects. There is evidence of an association between antipsychotic treatment, including olanzapine, and SW. Methods We present the case of a patient experiencing treatment-resistant anorexia nervosa whose somnambulism re-exacerbated after the addition of a low dose of olanzapine, following the CARE (CAse REport) Statement and Checklist. We also conducted a systematic review of the literature on olanzapine-induced somnambulism following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. PubMed, PsychINFO, and the Cochrane Library databases were independently reviewed up to January 2021 for articles reporting olanzapine-related somnambulism cases, without language or time restriction. Results We describe a case of somnambulism in a patient initially admitted to our hospital for anorexia nervosa and treated with a low dose of olanzapine. This is the first case of SW induced by olanzapine in eating disorders to be reported. Up-to-date olanzapine-related somnambulism was described in 8 patients experiencing psychiatric disorders (ie, schizophrenia and bipolar disorder). Conclusions To provide a reliable estimate of incidence and prevalence for olanzapine-related somnambulism, large-scale, pharmacovigilance studies are required, to allow for comparisons of overall clinical characteristics, outcomes, including time to recovery, between different treatment options. Clinician awareness should be enhanced, and attention should be given to such infrequent adverse effects associated with antipsychotics.

Background There is growing interest in new factors contributing to the genesis of eating disorders (EDs). Research recently focused on the study of microbiota. Dysbiosis, associated with a specific genetic susceptibility, may contribute to the development of anorexia nervosa (AN), bulimia nervosa, or binge eating disorder, and several putative mechanisms have already been identified. Diet seems to have an impact not only on modification of the gut microbiota, facilitating dysbiosis, but also on its recovery in patients with EDs. Methods This systematic review based on the PICO strategy searching into PubMed, EMBASE, PsychINFO, and Cochrane Library examined the literature on the role of altered microbiota in the pathogenesis and treatment of EDs. Results Sixteen studies were included, mostly regarding AN. Alpha diversity and short-chain fatty acid (SCFA) levels were lower in patients with AN, and affective symptoms and ED psychopathology seem related to changes in gut microbiota. Microbiota-derived proteins stimulated the autoimmune system, altering neuroendocrine control of mood and satiety in EDs. Microbial richness increased in AN after weight regain on fecal microbiota transplantation. Conclusions Microbiota homeostasis seems essential for a healthy communication network between gut and brain. Dysbiosis may promote intestinal inflammation, alter gut permeability, and trigger immune reactions in the hunger/satiety regulation center contributing to the pathophysiological development of EDs. A restored microbial balance may be a possible treatment target for EDs. A better and more in-depth characterization of gut microbiota and gut–brain crosstalk is required. Future studies may deepen the therapeutic and preventive role of microbiota in EDs.

Alterations of the immune system are known in eating disorders (EDs), however the importance of cytokine balance in this context has not been clarified. We compared cytokines and growth factors at opposite ends of BMI ranges, in 90 patients classified in relation to BMI, depressive and EDs comorbidities. Serum concentrations of interleukin (IL)-1&alpha, IL-1&beta, IL-2, IL-4, IL-6, IL-8, IL-10, interferon-gamma (IFN-&gamma, ), tumor necrosis factor-alpha (TNF-&alpha, ), monocyte chemoattractant protein-1 (MCP-1), vascular endothelial growth factor (VEGF), and epidermal growth factor (EGF) were determined by a biochip analyzer (Randox Labs). Differences were calculated through ANOVA. Possible predictors of higher cytokine levels were evaluated through regression analysis. IL-1&alpha, IL-10, EGF, and IFN-&gamma, were altered individuals with anorexia nervosa (AN) and binge eating disorder (BED). Night-eating was associated with IL-8 and EGF levels, IL-10 concentrations with post-dinner eating and negatively with sweet-eating, long fasting with higher IFN-&gamma, levels. IL-2 increase was not linked to EDs, but to the interaction of depression and BMI. Altogether, for the first time, IL-1&alpha, were shown to differ between AN and HCs, and between AN and individuals with obesity with or without BED. Only IL-2 was influenced by depression. Dysfunctional eating behaviors predicted abnormal concentrations of IL-10, EGF, IL-8 and IFN-&gamma