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Objective: Nocturnal eating behavior is shared by patients affected by a parasomnia, sleep-related eating disorder (SRED), and several eating disorders such as night eating syndrome (NES) and binge-eating disorder (BED); however, the differential clinical features of these patients have been poorly studied, with persisting difficulties in defining the borders between these pathologies. The aim of this study was to evaluate polysomnographic and personality characteristics of nocturnal eaters to further differentiate the syndromes., Methods: During a period of six months, consecutive patients complaining of nocturnal eating were asked to participate to the study. Twenty-four patients who were found to eat during the polysomnographic recording (PSG) study, and gender-matched control subjects were included. All subjects underwent a full-night video-PSG study and a psychometric assessment including the Eating Disorder Inventory (EDI-2), the self-rating Bulimic Investigatory Test-Edinburgh (BITE), the Temperament and Character Inventory (TCI), and the Barratt Impulsivity Scale (BIS)., Results: Nocturnal eaters showed a mild reduction in sleep efficiency and duration due to a moderate sleep fragmentation, whereas the percentage of each sleep stage was not significantly affected. Nocturnal eaters scored higher at many subscales of the EDI-2, at the BITE symptoms subscale, and at the BIS attentional impulsivity subscale., Conclusion: The psychological characteristics found in our patients with NES seem to be typical for patients affected by eating disorders, and support the hypothesis that the nocturnal behavior of these individuals is due to an eating disorder; however, specific traits also allow differentiation of NES from BED., (Copyright © 2014 Elsevier B.V. All rights reserved.)

Objectives: Nocturnal eating is a common symptom of two clinical conditions with different pathogenesis and needing different therapeutic approaches: Sleep Related Eating Disorder (SRED) and Night Eating Syndrome (NES). The first is considered a parasomnia while the second is an eating disorder; however, the distinction between SRED and NES is still a controversial matter. The aim of this study was to better define psychological, behavioral, and polysomnographic characteristics of the two syndromes., Methods: An eating disorders' specialist tested a group of 28 nocturnal eaters diagnosed as affected by SRED by a sleep expert, following the current criteria of the international classification of sleep disorders, to find out if any of them was affected by NES according to the criteria suggested by both sleep and eating disorders specialists during the first international meeting on Night Eating Syndrome (Minneapolis, 2009) and if they had specific psychological or polysomnographic characteristics., Results: Twenty-two subjects were diagnosed to be affected by NES. They scored higher on the physical tension subscale of the Sleep Disturbance Questionnaire (SDQ) and on the mood and sleep subscale of the Night Eating Questionnaire (NEQ), but there were no other significant differences between SRED and NES patients nor for age, Body Mass Index (BMI), or gender distribution., Conclusions: The overlap between the symptomatology and the polysomnographic characteristics of the two pathologies and the difficulty in making a differential diagnosis between NES and SRED indicate the need for an update of the diagnostic criteria for SRED, as was recently done for NES., (Copyright © 2012 Elsevier B.V. All rights reserved.)

The importance of d-norfenfluramine in regard to the indole-depleting action of d-fenfluramine has not been well studied in sensitive animal species. The present study therefore examined the intensity and time course of the neurochemical effects of i.p. injected d-fenfluramine (2.5 and 5 mg/kg) and d-norfenfluramine (2.5 mg/kg) in vehicle- and SKF-525A-pretreated rats, relating the effects to the brain concentration-time profiles of the drug and its active metabolite. At the lower dose d-fenfluramine caused only a small, short-lasting decrease in brain serotonin (5-HT) without affecting the 5-hydroxyindoleacetic acid (5-HIAA). Higher doses affected both 5-HT and 5-HIAA (50-60 and 30-40% reductions, respectively), the effect being maximal for at least 8 h. d-Norfenfluramine reduced the brain content of 5-HT and 5-HIAA less (by about 30%) than 5 mg/kg d-fenfluramine did. Brain concentrations of d-norfenfluramine at the time of the maximal depletion of indoles were close to those of the metabolite after 5 mg/kg d-fenfluramine, indicating that the acute indole-depleting effects did not depend solely on the brain concentrations of its nor-metabolite. SKF-525A changed the metabolite-to-parent drug ratios in brain without appreciably influencing the action of d-fenfluramine. However, the maximum decrease in indole content caused by 2.5 mg/kg d-fenfluramine in SKF-525A-pretreated rats was only 12% of the control level, although the brain concentration of unchanged drug was comparable to that after 5 mg/kg d-fenfluramine in vehicle-pretreated rats.(ABSTRACT TRUNCATED AT 250 WORDS)