Sleep-related Eating Disorder Research Articles

Treatment of sleep-related eating disorder.

Sleep-related eating disorder (SRED) is classified as an NREM-related parasomnia characterized by recurrent episodes of dysfunctional eating that occur after an arousal from the main sleep period with partial or complete amnesia for the event, resulting in weight gain from eating high calorie foods and causing various injuries due to consumption of inedible or toxic items. SRED can be idiopathic or commonly associated with other primary sleep disorders such as sleepwalking, restless legs syndrome (RLS), obstructive sleep apnea syndrome (OSAS), other clinical conditions, or use of sedative-hypnotic medications. First-line treatment of idiopathic SRED includes selective serotonin reuptake inhibitors (SSRIs) at mean dosages of 20 to 30mg/day. Topiramate at 100-300mg/day and clonazepam at 0.5-2.0mg/day can be valid alternative options. SRED related to other parasomnias or sleep disturbances that cause sleep fragmentation benefit most from treatment of the associated sleep disorder. In particular, RLS-related SRED is best treated with dopamine agonists such as pramipexole, while sleepwalking-related SRED benefits from low-dose benzodiazepines such as clonazepam. Different kinds of drug associations have been proposed in a limited number of cases, especially in the past. We strongly recommend that all patients suffering from SRED should undergo consistent and regular follow-up about 2-3 times per year or otherwise according to the physician's judgment, in order to assess the evolution of symptom severity and frequency and re-evaluate treatment efficacy and any side effects that may arise.

New data on psychological traits and sleep profiles of patients affected by nocturnal eating

ObjectiveNocturnal 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. MethodsDuring 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). ResultsNocturnal 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. ConclusionThe 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.

Sleep-related eating disorder and its associated conditions.

Sleep-related eating disorder (SRED) is a condition characterized by recurrent episodes of eating at the transition from night-time sleep to arousal. SRED patients describe eating in an out-of-control manner with preference for high-caloric foods and sometimes with inedible or toxic items. Level of consciousness during SRED episodes ranges from partial consciousness to dense unawareness typical of somnambulistic episodes. SRED is sometimes associated with psychotropic medication, in particular sedative hypnotics, and other sleep disorders, including parasomnias, narcolepsy, and restless legs syndrome. Night eating syndrome (NES) is another important condition in the disordered night-time eating spectrum showing hyperphagia episodes at full arousal from nocturnal sleep without accompanying amnesia. NES could be considered an abnormality in the circadian rhythm of meal timing with a normal circadian timing of sleep onset. The two conditions often overlap and possibly share a common pathophysiology. Studies have suggested that central nervous system serotonin modulation may lead to an effective treatment of NES, while the anti-seizure medication topiramate may be an effective SRED treatment.

Sleep-Related Eating Disorder Associated With Quetiapine

Sleep-Related Eating Disorder Associated With Quetiapine

O37: Clinical features of sleep-related eating disorder induced by hypnotics

O37: Clinical features of sleep-related eating disorder induced by hypnotics

Metabolic Consequences of Sleep and Circadian Disorders

Sleep and circadian rhythms modulate or control daily physiological patterns with importance for normal metabolic health. Sleep deficiencies associated with insufficient sleep schedules, insomnia with short-sleep duration, sleep apnea, narcolepsy, circadian misalignment, shift work, night eating syndrome, and sleep-related eating disorder may all contribute to metabolic dysregulation. Sleep deficiencies and circadian disruption associated with metabolic dysregulation may contribute to weight gain, obesity, and type 2 diabetes potentially by altering timing and amount of food intake, disrupting energy balance, inflammation, impairing glucose tolerance, and insulin sensitivity. Given the rapidly increasing prevalence of metabolic diseases, it is important to recognize the role of sleep and circadian disruption in the development, progression, and morbidity of metabolic disease. Some findings indicate sleep treatments and countermeasures improve metabolic health, but future clinical research investigating prevention and treatment of chronic metabolic disorders through treatment of sleep and circadian disruption is needed.

4:30 PM CHILDHOOD SLEEP DISTURBANCE AND RISK OF PSYCHOTIC EXPERIENCES IN A LARGE UK BIRTH COHORT

Parasomnias are unpleasant experiential or undesirable behavioral phenomena that occur during entry into sleep, during any stage of nonrapid eye movement (NREM) or rapid eye movement (REM) sleep, or on termination of sleep. All of sleep is vulnerable to parasomnias, which can occur spontaneously or linked with other sleep disorders, such as sleep apnea and restless legs syndrome. Our basic instincts can emerge pathologically with the parasomnias, including eating, sex, locomotion, and aggression. Parasomnias can affect people across the entire life span. Most parasomnias are diagnosable and treatable. Most are not the manifestation of psychopathology or psychiatric disorders. Parasomnias can be categorized as primary (disorders of the sleep states per se) and secondary (disorders of other organ systems that manifest themselves during sleep). The primary sleep parasomnias can be classified according to the sleep state of origin: REM sleep, NREM sleep, or miscellaneous (those not respecting sleep state). The secondary sleep parasomnias can be further classified by the organ system involved. The major primary parasomnias include disorders of arousal from NREM sleep (confusional arousals, including the variant sexsomnia, sleepwalking, and sleep terrors), REM sleep behavior disorder, and sleep-related eating disorder.

Disordered sleep characterized by disordered frontiers of sleep stages and wakefulness, with disorder motor control

Although the process of sleep is probably as old as the whole living world and although it occupies one third of our lives, and although it is a vital form of behavior whose purpose we do not fully understand - still, the first steps enabling us to enter some of the secrets of the process of sleep were made only in the past century. The first human electroencephalogram (EEG) was performed by the German neurologist Hans Berger in 1908. in Jenna. He published his discovery some twenty years later, in 1929. Formally the first school-textbook on sleep, with the title 'Sleep and Wakefulness', was published in Chicago (USA) in 1939. by professor Nathaniel Kleitmann. The dual nature of sleep was described by Eugen Aserinsky and Nathaniel Kleitmann in 1953. In Serbia, the first textbook on sleep with the title ; Wakefulness, sleep and dreaming' was written by the Academician professor Veselinka Susic in 1977. The last decades of the 20th century 'shook' the world of sleep with new discoveries. Several diseases were described (i.e., Sleep related eating disorder as NREM sleep, and REM sleep behavior disorder as REM sleep parasomnia) whose pathophysiology was comprehended. A CPAP apparatus was produced and perfected for the treatment of sleep apnea. The last decades of the past century with the discoveries of neurotransmitters hypocretin/orexin brought about the knowledge on the nature of narcolepsy whose therapy was significantly improved. The pathophysiology of NREM parasomnias (sleep walking or somnambulism and sleep terrors, confusional awakenings and nightmares, sleep related eating or sex) as well as some of the REM parasomnias (REM sleep behavior disorder) were explained in a novel manner. These fundamental discoveries threw new views on the nature of the process of sleep. They enabled us to better perceive the nature of the sleep process its physiology and pathology, and to better comprehend the processes called 'the dissociation of sleep stages'.

Restless Eating, Restless Legs, and Sleep Related Eating Disorder.

Restless legs syndrome (RLS) often presents with a primary complaint of sleep initiation difficulty with only ambiguous allusions to motor symptoms. This may result in the condition being misdiagnosed as a psychophysiological insomnia. Further, nocturnal eating is common in RLS and like the classic motor symptoms, patients will describe an inability to initiate sleep until their urge (to eat) is addressed. Restless nocturnal eating arises, intensifies, and subsides in parallel to motor symptoms. Once misdiagnosed as psychophysiological insomnia, RLS patients are frequently treated with benzodiazepine receptor agonists. The CNS actions of these sedating agents, suppression of memory and executive function, unleash predisposed amnestic behaviors. In the case of RLS this would be expected to include the inappropriate ambulatory and eating behaviors of sleep related eating disorder (SRED). The evidence and implications of a link between the restless eating of RLS and SRED is presented here.

Sleep-related eating disorder: a descriptive study in Chilean patients

ObjectivesWe aimed to describe a group of adults diagnosed with sleep-related eating disorder (SRED) at the Sleep Medicine Center of the Pontificia Universidad Catolica de Chile. MethodsWe performed a descriptive study of 34 consecutive patients who met the criteria of the International Classification of Sleep Disorders for SRED evaluated during a 3-year period who did not have an eating disorder according to the criteria of the Diagnostic and Statistical Manual of Mental Disorders, fourth edition. All patients had a structured clinical interview performed by a sleep specialist and completed the Beck Depression Inventory (BDI). Polysomnography (PSG) was performed when clinically indicated for ruling out other sleep-related disorders (18 patients; 52.9%). Patients’ demographic and clinical data, comorbidities, and treatment response also were analyzed. ResultsMost patients were women (n=23; 67.6%). The average age at the time of diagnosis was 39±13.8 (17–67years) and the latency since symptom onset was 8.3±8.8years. Most patients had several episodes per night (average, 2.6±1.6; 1–8) and all except one patient had partial or total amnesia of these events (n=33; 97%). Comorbidities were frequent and included insomnia (n=20; 58.8%), restless legs syndrome (RLS) (n=16; 47%), sleep-disordered breathing (SDB) (n=9; 26%), psychiatric disorders (n=13; 38.2%), and overweight or obesity (n=14; 41.1%). Most patients were hypnotic users (n=21; 61.7%) and reported weight-centered anxiety (n=23; 67.6%). Twenty patients (58.8%) were treated with topiramate, 17 of whom had adequate symptomatic responses. ConclusionOur SRED patients showed female preponderance, amnesia during the episodes, association with other sleep disorders, use of hypnotics, weight-centered anxiety, and positive response to topiramate. The presence of anxiety focused on weight in most patients may be an important element in the emergence of this behavior during sleep.

Comparison of clinical features between primary and secondary sleep-related eating syndrome

Introduction Sleep-related eating disorder (SRED) is a condition with recurrent episodes of involuntary eating and drinking during arousal from sleep resulting in problematic consequences. SRED is a syndrome in which pathophysiological features seem to be heterogeneous. The aim of this study is to ascertain the similarity and difference in the clinical characteristics between primary SRED and secondary SRED induced by medication of hypnotics or DSPT. Materials and methods This study was approved by the ethics committee of the Neuropsychiatric Research Institute. Eligible cases comprised a series of 52 consecutive patients with SRED, who visited outpatient clinic of the Japan Somnology Center. We retrospectively investigated demographics, and descriptive informations. The patients were classified into three types; primary SRED (n = 32), secondary SRED induced by DSPT (n = 10), and secondary SRED induced by hypnotics medication (n = 10). Results The demographic of the total 52 individuals diagnosed with SRED in our sample are as follows: the female ratio was 67.3%, mean age of onset of the symptoms 29.0 Materials and methods Primary SRED shows features as parasomnia, i.e. high ratio of history of sleepwalking during childhood, episode occurred at first half of sleep. Among secondary SRED induced by DSPT, time zone in which the episodes mainly occurred delayed. Among secondary SRED induced by hypnotics medication, onset age was older, and episode with total unconsciousness was high. In light of our results, we suggest there are different clinical features between primary and secondary SRED. Acknowledgement This study was supported by a Ministry of Education, Culture, Sports, Science and Technology grant, Japan.

Sleep related eating disorder (SRED) and night eating syndrome (NES): same or different disorders?

Introduction The last revision of the International Classification of Sleep Disorders ( ICDS-2) has considered SRED as a parasomnia and it has established precise diagnostic criteria in order to differentiate it from NES. The presence of a variable level of awareness during the nocturnal eating episodes, consumption of some peculiar food combinations or dangerous behaviors or sleep related-injuries during the night are more typical in SRED. However the overlap between the clinical and polysomnographic features of both disorders is evident and some authors have postulated that they are “opposite poles of a continuous clinical spectrum”. We expose the results of the study of 30 patients with recurrent involuntary eating episodes during the night. Materials and methods 6 males and 24 females. Age range: 19 −67 years. All subjects underwent a semi structured clinical and psychological interview. The behaviours and the severity of the compulsive nocturnal eating was measured using the Night Eating Questionnaire. A video – polysomnographic study ( v-PSG) was done placing a table with food and drinks at the bedside. Results 1. Variable number of nocturnal eating episodes per night (1–20) depending on the emotional state of the patient. Frequent association with depressive - anxious syndrome. 2. Involuntary eating with reward sensation. 3. Variable level of consciousness during the episodes within a single night and across the longitudinal course of the disorder. 4. Consumption of high caloric food but no inedible or toxic substances. Morning anorexia common. 5. 2/3 of the patients were night and evening eaters. 6. Insomnia (100%) and frequent comorbid sleep disorders. 7. Obstructive Sleep apnea treatment with CPAP failed to reduce the number of episodes. However some therapeutic benefit was achieved with dopaminergic agents in patients with concomitant Restless leg syndrome. Conclusion 1. Sleep, eating or mood disorder? Probable observation bias between different specialists. 2. At present there isn’t a clear-cut border between SRED and NES. Our results support the hypothesis that they are ends of a continuum with the same underlying pathophysiology. Acknowledgements All medical staff, nurses and technicians of our Multidisciplinary Marques de Valdecilla Sleep Unit. Thanks to my family.

Nocturnal eating is part of the clinical spectrum of restless legs syndrome and an underestimated risk factor for increased body mass index

ObjectivesWe aimed to investigate the prevalence of night eating syndrome (NES) in a large cohort of patients with restless legs syndrome (RLS). MethodsOur cross-sectional study included 120 patients examined at the University of Bologna Centre for Sleep Disorders, Bologna, Italy, and met all four International RLS criteria for the diagnosis of RLS. Each patient underwent a semistructured telephone interview investigating demographic data and general health status, RLS features and severity, presence of excessive daytime sleepiness, and presence of NES. ResultsThe sample included 37 men and 83 women with a mean age of 63.8±11.5years. There were 31% of patients who reported episodes of nocturnal eating (NE); among them, 17% fulfilled the new diagnostic criteria for NES. Comparing RLS patients with and without NE, there were no differences in RLS features. However, RLS patients with NE were older (67.2±11.6 vs 62.4±11; P=.038), were in a higher body mass index (BMI) range (27.7±3.8 vs 26.1±4.1kg/m2; P=.023), were taking more drugs for concomitant diseases (89% vs 72%; P=.031), were more likely to report insomnia (40% vs 23%; P=.041), and were using more hypnotic agents (37.8% vs 19.3%; P=.050) and dopaminergic drugs (65% vs 46%; P=.041). When comparing those RLS patients with NES diagnostic criteria and those without NES, no differences emerged in demographic, clinical, and RLS features; however, NES patients were in a higher BMI range (28.3±4.1 vs 26.2±3.9kg/m2, P=.037), were more frequently smokers (43% vs 17%; P=.027), and were more frequently using hypnotic agents (30% vs 24%; P=.025). Lastly, no differences were found when comparing patients with a NES diagnosis and those with NE not fitting the diagnostic criteria for NES, except for a higher use of benzodiazepine drugs (BDZ) in this latter subgroup (29% vs zero; P=.014). ConclusionsA nocturnal compulsion to eat seems to be an intrinsic part of the clinical spectrum of RLS manifestations and an odd risk factor for increases in BMI in RLS patients. However, it is still not clear if NE in RLS would fit in one of the two known categorized syndromes of NE (i.e., sleep-related eating disorder [SRED] or NES) or if it represents a different strictly RLS-related eating behavior.

Eating Disorders: Problems of Contemporary Civilisation – A Review

The eating disorders have been reviewed based on state-of-art of contemporary psychology, medicine and nutrition science, with a special emphasis put on different symptoms and forms, origins and testing methods. Among promoting eating disorders, bulimia nervosa, binge eating disorder, night eating disorder, sleep-related eating disorder are among offi cially approved and investigated. Among disorders resulting from lack of acceptance of own appearance, anorexia nervosa and bigorexia nervosa are the most serious improper ones. Disorders arising from health care include orthorexia nervosa and recently pregorexia. Different origins of eating disorders are considered, divided into three groups: social, psychological and pathological. The desire to possess a slim shapely silhouette and young appearance, usually under pressure of a social group, may result in disorders such as anorexia nervosa, pregorexia, ageorexia, and bigorexia nervosa. On the other hand, the focusing on eating mainly the biologically pure food, being a purely psychological and individual problem, may be a source of orthorexia nervosa. Majority of disorders have a psychological background constituting the escape and an answer to everyday life problems diffi cult to overcome. Recently, pathology is often considered as an additional and important determinant, which may cause or enhance the appearance of binge eating or night eating disorder. The eating disorders, if not subject to proper therapy and advising, can tend to incline and develop. The further research in order to properly recognise the eating disorders, and fi nd their roots, is necessary at a strict cooperation of psychologists, physicians and nutritionists or dietetics.

Zolpidem-Induced Compulsive Evening Eating Behavior

Zolpidem is associated with an amnestic sleep-related eating disorder, but not with compulsive eating behaviors. A 57-year-old woman receiving zolpidem for insomnia showed compulsive evening eating behavior under a wakeful state. Her compulsive evening eating behavior disappeared when zolpidem treatment was halted. Here, we report her case.

Sodium Oxybate Intolerance Associated with Familial Serum Acylcarnitine Elevation

Our case describes clinical features of two families defined by joint phenotypes: sodium oxybate intolerance and elevated serum acylcarnitines. Oxybate intolerance variably presents as either cervical dystonia or sleep-related eating disorder. Our objective is to identify biological markers which predict a poor response to sodium oxybate as a treatment for disturbed sleep. Familial inheritance pattern, genotype analysis, multiorgan system involvement, and response to treatment suggest the presence of a secondary cause of fatty oxidation defect, i.e., mitochondrial disorder. Our case report supports the possible conclusion that variance in human mitochondrial metabolism may affect sodium oxybate tolerability.

1740 – Psychometric properties of the night eating questionnare in a portuguese sample of overweight women

Introduction The Night Eating Questionnaire (NEQ; Allison et al, 2008) is the only validated instrument to assess the Night Eating Syndrome. It is composed of 14 Likert items and it enables to rule out for sleep-related eating disorder. Objectives To investigate the psychometric properties of the NEQ and to investigate its pattern of correlation with related variables in a sample of Portuguese overweight women. Methods The NEQ and the other self-report validated instruments to assess disordered eating, insomnia, daytime sleepiness, depressive symptoms and affect were administered to an outpatient sample of 276 women (Mean age=43.85±11.88; Mean BMI=32.82Kg/m2±5.43) attending a weight loss treatment consultation in a public hospital. Results The NEQ Coronach a was .60. A four factors structure (variance explained=57.62%) was selected: Factor (F)1 “Nocturnal ingestions” (α=.81); F2 “Evening hiperfagia” (α=.57); F3 “Mood/Sleep” (α=.42) and F4 “Morning anorexia” (α=.24). From the 23 participants (8.6%) who snacks when get up in the middle of the night, 6 (26.1%) had “not at all/a little” awareness of their eating; 3 (13.0%) had “none at all/a little” control over their eating while up at the night. NEQ total score significantly (p Conclusions The Portuguese version of NEQ presents reasonable internal consistency. The factorial structure overlaps with the original almost completely. The pattern of correlations with relevant variables was as expected. The NEQ could be very useful to clinical and epidemiological purposes.

Quetiapine-induced sleep-related eating disorder-like behavior: a case series

IntroductionSomnambulism or sleepwalking is a disorder of arousal from non-rapid eye movement sleep. The prevalence of sleep-related eating disorder has been found to be approximately between 1% and 5% among adults. Many cases of medication-related somnambulism and sleep-related eating disorder-like behavior have been reported in the literature. Quetiapine, an atypical antipsychotic medication, has been associated with somnambulism but has not yet been reported to be associated with sleep-related eating disorder.Case presentationCase 1 is a 51-year-old obese African American male veteran with a body mass index of 34.11kg/m2 and severe sleep apnea who has taken 150mg of quetiapine at bedtime for more than one year for depression. He developed sleepwalking three to four nights per week which resolved after stopping quetiapine while being compliant with bi-level positive pressure ventilation therapy. At one year follow-up, his body mass index was 32.57kg/m2.Case 2 is a 50-year-old African American female veteran with a body mass index of 30.5kg/m2 and mild sleep apnea who has taken 200mg of quetiapine daily for more than one year for depression. She was witnessed to sleepwalk three nights per week which resolved after discontinuing quetiapine while being treated with continuous positive airway pressure. At three months follow-up, her body mass index was 29.1kg/m2.ConclusionThese cases illustrate that quetiapine may precipitate complex motor behavior including sleep-related eating disorder and somnambulism in susceptible patients. Atypical antipsychotics are commonly used in psychiatric and primary care practice, which means the population at risk of developing parasomnia may often go unrecognized. It is important to recognize this potential adverse effect of quetiapine and, to prevent injury and worsening obesity, discuss this with the patients who are prescribed these medications.

Parasomnias: an updated review.

Parasomnias are abnormal behaviors emanating from or associated with sleep. Sleepwalking and related disorders result from an incomplete dissociation of wakefulness from nonrapid eye movement (NREM) sleep. Conditions that provoke repeated cortical arousals, or promote sleep inertia lead to NREM parasomnias by impairing normal arousal mechanisms. Changes in the cyclic alternating pattern, a biomarker of arousal instability in NREM sleep, are noted in sleepwalking disorders. Sleep-related eating disorder (SRED) is characterized by a disruption of the nocturnal fast with episodes of feeding after an arousal from sleep. SRED is often associated with the use of sedative-hypnotic medications; in particular, the widely prescribed benzodiazepine receptor agonists. Recently, compelling evidence suggests that nocturnal eating may in some cases be a nonmotor manifestation of Restless Legs Syndrome (RLS). rapid eye movement (REM) Sleep Behavior Disorder (RBD) is characterized by a loss of REM paralysis leading to potentially injurious dream enactment. The loss of atonia in RBD often predates the development of Parkinson's disease and other disorders of synuclein pathology. Parasomnia behaviors are related to an activation (in NREM parasomnias) or a disinhibition (in RBD) of central pattern generators (CPGs). Initial management should focus on decreasing the potential for sleep-related injury followed by treating comorbid sleep disorders. Clonazepam and melatonin appear to be effective therapies in RBD, whereas paroxetine has been reported effective in some cases of sleep terrors. At this point, pharmacotherapy for other parasomnias is less certain, and further investigations are necessary.

Restless Nocturnal Eating: A Common Feature of Willis-Ekbom Syndrome (RLS)

To determine the frequency of nocturnal eating (NE) and sleep related eating disorder (SRED) in restless legs syndrome (RLS) versus psychophysiological insomnia (INS), and the relationship of these conditions with dopaminergic and sedative-hypnotic medications. Prospective case series. Sleep disorders center. Newly diagnosed RLS or INS. RLS or INS pharmacotherapy with systematic follow up interview for NE/SRED. Patients presenting with RLS (n = 88) or INS (n = 42) were queried for the presence of NE and SRED. RLS patients described nocturnal eating (61%) and SRED (36%) more frequently than INS patients (12% and 0%; both p < 0.0001). These findings were not due to arousal frequency, as INS patients were more likely to have prolonged nightly awakenings (93%) than RLS patients (64%; p = 0.003). Among patients on sedative-hypnotics, amnestic SRED and sleepwalking were more common in the setting of RLS (80%) than INS (8%; p < 0.0001). Further, NE and SRED in RLS were not secondary to dopaminergic therapy, as RLS patients demonstrated a substantial drop (68% to 34%; p = 0.0026) in the frequency of NE after dopamine agents were initiated, and there were no cases of dopaminergic agents inducing novel NE or SRED. NE is common in RLS and not due to frequent nocturnal awakenings or dopaminergic agents. Amnestic SRED occurs predominantly in the setting of RLS mistreatment with sedating agents. In light of previous reports, these findings suggest that nocturnal eating is a non-motor manifestation of RLS with several clinical implications discussed here.