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

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

Post on 09-Dec-2016




0 download

Embed Size (px)


<ul><li><p>CASE REPORT Open Access</p><p>Quetiapine-induced sleep-related eating disorder-like behavior: a case seriesSadeka Tamanna1,2, M Iftekhar Ullah2,3*, Chelle R Pope3, Garland Holloman4 and Christian A Koch5,6,7</p><p>Abstract</p><p>Introduction: Somnambulism or sleepwalking is a disorder of arousal from non-rapid eye movement sleep. Theprevalence of sleep-related eating disorder has been found to be approximately between 1% and 5% amongadults. Many cases of medication-related somnambulism and sleep-related eating disorder-like behavior have beenreported in the literature. Quetiapine, an atypical antipsychotic medication, has been associated withsomnambulism but has not yet been reported to be associated with sleep-related eating disorder.</p><p>Case presentation: Case 1 is a 51-year-old obese African American male veteran with a body mass index of34.11kg/m2 and severe sleep apnea who has taken 150mg of quetiapine at bedtime for more than one year fordepression. He developed sleepwalking three to four nights per week which resolved after stopping quetiapinewhile being compliant with bi-level positive pressure ventilation therapy. At one year follow-up, his body massindex 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 sleepapnea who has taken 200mg of quetiapine daily for more than one year for depression. She was witnessed tosleepwalk three nights per week which resolved after discontinuing quetiapine while being treated with continuouspositive airway pressure. At three months follow-up, her body mass index was 29.1kg/m2.</p><p>Conclusion: These cases illustrate that quetiapine may precipitate complex motor behavior including sleep-relatedeating disorder and somnambulism in susceptible patients. Atypical antipsychotics are commonly used inpsychiatric and primary care practice, which means the population at risk of developing parasomnia may often gounrecognized. It is important to recognize this potential adverse effect of quetiapine and, to prevent injury andworsening obesity, discuss this with the patients who are prescribed these medications.</p><p>Keywords: Quetiapine, SRED, Somnambulism, Sleep eating, Sleepwalking, Obesity</p><p>IntroductionSleep-related eating disorder (SRED) represents recur-rent episodes of involuntary eating and drinking duringthe main sleep period with one or more features of con-sumption of peculiar foods, insomnia, sleep-related in-jury, dangerous behaviors performed while in pursuit offood, morning anorexia and adverse health conse-quences from recurrent binge eating of high caloric food[1-5]. Somnambulism or sleepwalking is a disorder of</p><p>arousal from non-rapid eye movement (NREM) sleepwhich often co-exists with SRED [3,6].Many cases of medication-related somnambulism and</p><p>SRED-like behavior have been reported in the literature.Zolpidem is one of the most commonly reported medi-cations associated with these conditions. Quetiapine(Seroquel), a piperazinyl-dibenzothiazepine analog ofclozapine, is an atypical antipsychotic medication fre-quently used for the treatment of schizophrenia, bipolardisorder and major depressive disorder as an adjunct toan antidepressant. It has been infrequently reported tobe associated with sleepwalking [7] and in one case, ithas actually been used to treat sleepwalking [8]. How-ever, to the best of our knowledge, quetiapine has notyet been reported to be associated with the developmentof SRED.</p><p>* Correspondence: mullah@umc.edu2Division of General Internal Medicine, Department of Medicine, University ofMississippi Medical Center, Jackson MS 39216, USA3Division of Pulmonary, Critical Care and Sleep medicine, Department ofMedicine, University of Mississippi Medical Center, Jackson MS 39216, USAFull list of author information is available at the end of the article</p><p>JOURNAL OF MEDICALCASE REPORTS</p><p> 2012 Tamanna et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the CreativeCommons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, andreproduction in any medium, provided the original work is properly cited.</p><p>Tamanna et al. Journal of Medical Case Reports 2012, 6:380http://www.jmedicalcasereports.com/content/6/1/380</p></li><li><p>We here report two cases of SRED which we believewere induced or aggravated by quetiapine because inboth cases the condition resolved completely after dis-continuation of the medication. In addition, bothpatients lost weight with a declining body mass index(BMI).</p><p>Case presentationCase 1A 51-year-old African American male veteran presentedto our sleep clinic, accompanied by his wife, with com-plaints of daytime sleepiness, sleepwalking and eatingduring sleep for more than a year. He reportedly walksand eats uncooked food from the refrigerator and mis-places things during sleep three to four nights per week.His wife saw him walking around inside the housedressed up in his best outfit in the middle of the nightcarrying the car key. The patient could not rememberany of these events after awakening.His past medical history included depression, hyper-</p><p>tension and mood disorder. There was no previous his-tory of seizure, childhood or family history ofparasomnia or alcohol abuse. His medications includedbupropion, quetiapine, lisinopril, hydrochlorothiazideand loratadine. He was diagnosed with major depressionabout eight years ago and received bupropion 150mgtwo times a day for treatment. He underwent a major fi-nancial crisis with job loss and had to move to hismothers house. His symptoms of depression were notimproving and quetiapine was added about six years agoto help improve his depression. The dose of quetiapinewas gradually titrated up to 150mg at bedtime by hispsychiatrist. It is not clear when his SRED first startedbecause the patient used to live alone until one year agowhen he got married. His physical examination was un-remarkable except for an elevated BMI of 34.11kg/m2</p><p>and poorly controlled hypertension. An overnight poly-somnography was performed which revealed severesleep apnea (apnea hypopnea index (AHI) of 86/hourwith an arousal index of 156/hour). No parasomnia orperiodic limb movements were noted during polysomno-graphy. During the overnight titration study, his sleepapnea responded well to bi-level positive pressure venti-lation (BiPAP) with optimal resolution of his apnea andhypopneas and there were not many treatment emergentcentral apneas. He was sent home on nightly BiPAPtherapy and was scheduled for a follow-up in threemonths.On his follow-up visit, he reported good compliance</p><p>with his BiPAP (99% compliance for &gt;4 hours per nightfor &gt;4 nights per week, verified by the memory card in-stalled in the BiPAP machine). His daytime sleepinessimproved significantly but his wife complained ofincreased frequency of sleepwalking and eating during</p><p>sleep almost every other night after starting him onBiPAP. Because quetiapine has been known to be asso-ciated with sleepwalking, he was advised to discontinueit. He returned for a follow-up in three months and, sur-prisingly, he did not have any further incidents of eitherSRED or sleepwalking. There was no change in anyother medication except discontinuation of his quetia-pine during this interval. He lost 0.91kg (2lb) during thisthree months follow-up. He was also followed up afterone year of stopping quetiapine and he reported restfulsleep without any further event of sleepwalking or eatingduring sleep. His BMI was 32.57kg/m2 and he had lost4.08kg (9lb). His serum quetiapine level had never beenmeasured.</p><p>Case 2A 50-year-old African American obese (BMI=30.5kg/m2)female veteran with a history of hypertension, asthma,major depressive disorder, migraine and obstructive sleepapnea presented to the clinic for follow-up. Her medica-tions included verapamil, lisinopril, hydrochlorothiazide,bupropion, venlafaxine, topiramate and quetiapine.She complained of walking in her sleep and eating</p><p>from the refrigerator while she was asleep. These inci-dents were observed and reported by her niece andbrother who lived in the same house. She was seen towalk and sit at the kitchen table with her eyes closed, eatcereal and go back to bed. They also mentioned that shestarted her electric coffee pot, putting water in it andwent to bed at 3 a.m. She was having these episodes twoto three nights per week. She was also diagnosed withobstructive sleep apnea after a baseline sleep study a fewyears back which showed obstructive sleep apnea(AHI = 10/hour) that was worse during REM sleep(REM AHI = 58/hour). She was prescribed continuouspositive airway pressure (CPAP) at 8cm after adequatetitration study but she was having trouble keeping hermask in place due to her sleepwalking episodes duringwhich she removed the mask.Over the past four years she was being treated with</p><p>quetiapine for depression. This medication was added asan adjunct therapy when other medications did not con-trol her symptoms adequately. Her quetiapine dose wasincreased to 200mg daily about a year ago for increasingdepression from work-related stress. She could not give acorrect history when the sleepwalking exactly started butit has been witnessed for six to eight months. As hermedication list shows, she was already on topiramate forher migraine headache which was continued after stop-ping quetiapine. Although topiramate has been shown tobe effective in SRED in a small trial [2], it did not help inher SRED symptoms. We tapered and eventually stoppedher quetiapine. After three months, she reported duringher follow up visit that she no longer had episodes of</p><p>Tamanna et al. Journal of Medical Case Reports 2012, 6:380 Page 2 of 4http://www.jmedicalcasereports.com/content/6/1/380</p></li><li><p>sleepwalking or sleep eating. There was no change in anyother medication except discontinuation of her quetia-pine during this interval. She could now use her CPAPevery night and felt rested after her sleep. Her BMI was29.1kg/m2 and she had lost 3.18kg (7lb).</p><p>DiscussionSRED is characterized by recurrent episodes of partialarousals with involuntary eating during the main sleep-ing period, usually within the first three hours of sleep.A strong association between somnambulism and SREDhas been reported. Somnambulism has been primarilylinked to NREM sleep instability, particularly an abnor-mality in regulation of slow wave sleep (SWS). It is com-monly precipitated by other factors including sleepdeprivation, presence of other primary sleep disorders(sleep apnea, periodic limb movement disorder) as wellas medications that raise the threshold for arousals [3].Our patients had a few important predisposing factors</p><p>for parasomnia including increased work-related stress,depression and severe sleep apnea with high arousalindex. If a patient with parasomnia has any other con-comitant primary sleep disorder, the treatment is initiallydirected towards that aspect which often resolves theparasomnia. Our first patient had severe sleep apnea thatwas treated adequately, but he continued to have sleep-walking and SRED despite good compliance with treat-ment probably because his SWS had increased afterusing BiPAP. Our second patient was not able to becompliant with the CPAP initially until she stopped tak-ing quetiapine.Sleepwalking and SRED have been commonly reported</p><p>after taking zolpidem as well as sodium oxybate [9,10].</p><p>However, one case report has proposed quetiapine as apotential treatment of somnambulism because itdecreases brain delta activity [8]. The somnambulismphenomenon from quetiapine may be explained by theserotonin hypothesis of parasomnia [11]. Quetiapine isfound to block 5-hydroxytryptamine-2A (5HT-2A) anddopamine receptors subtype 2 (D2) increasing corticaldopamine release by 5HT-1A agonism [12]. The seroto-nergic neurons of the dorsal raphe nucleus (DRN) in thebrain stem constitute an integral component for gener-ation of SWS. Among a variety of subtypes of serotoner-gic receptors, 5HT-2A receptors in the DRN are knownto regulate frequency and amplitude of SWS [13]. Theseneurons projecting into the ventrolateral preoptic areahelp maintain and increase the SWS. These serotonergicneurons are also thought to modulate the motor systemby dampening the sensory input and attenuating corticalactivation, which helps maintain the hypotonia of theantigravity muscles during SWS. Normally, maintenanceof SWS is well coordinated with motor inhibition so thatmotor activity does not happen without an arousal. Ablockade of serotonergic input can withdraw this motorinhibition, enabling the person to walk and performother motor activities. Quetiapine has been known toalter central serotonin activity by blocking the 5-HT ser-otonergic receptor which may, in turn, dissociate thesetwo components (state of sleep and muscle hypotonia)[12], leading to sleepwalking without a complete arousal.From the literature support described above, we</p><p>propose a potential mechanism of quetiapine-inducedSRED and somnambulism phenomenon explained inFigure 1. Sleepwalking aggravated by quetiapine may beexplained by the above hypothesis; however, how it may</p><p>5HT-2a receptor inRaphe nucleus</p><p>VLPO</p><p>Failure tomaintain SWS</p><p>Arousal</p><p>Prevention ofMotor hypotonia</p><p>Prevention of loss ofmuscle tone of theantigravity muscles</p><p>Enables walking</p><p>SRED, Somnambulism</p><p>5HT-2c receptor in Hypothalamus</p><p>Leptin receptor</p><p>Appetite</p><p>Hyperphagiasleep eating</p><p>Quetiapine</p><p>Figure 1 Potential mechanism of quetiapine-induced SRED and somnambulism. SRED: sleep-related eating disorder; SWS: slow wave sleep;VLPO: ventrolateral preoptic nucleus.</p><p>Tamanna et al. Journal of Medical Case Reports 2012, 6:380 Page 3 of 4http://www.jmedicalcasereports.com/content/6/1/380</p></li><li><p>also lead to eating during sleep is unclear. This may beagain related to its effect on another serotonin receptor:5HT-2C. The serotonin receptor 5HT-2C in the hypo-thalamus regulates mood, anxiety, feeding, and repro-ductive behavior [14]. Antagonism of the serotoninreceptor 5HT-2C by antipsychotic drugs, including que-tiapine, olanzapine and clozapine, increases appetiteleading to increased food intake and weight gain [15].Patients who are on these antipsychotic medications andgaining weight were also found to have elevated leptinlevels [16]. Because quetiapine blocks 5HT-2C, it maycause leptin resistance at the level of the hypothalamus,contributing to increased food intake and obesity(Figure 1). Often, an obese body shape is not even per-ceived to be a problem or stressful, as assessed by theperceived stress scale [17].</p><p>ConclusionQuetiapine may increase the potential of SRED-likecomplex motor behavior in susceptible patients. SRED ismore common than is generally recognized and theprevalence of SRED is high in the adult psychiatricpopulation [18]. Atypical antipsychotics are commonlyused in psychiatric and primary care practice, which putsthe population at risk of getting parasomnia that mayoften go unrecognized. It is important to discuss this po-tential adverse effect with patients who are o...</p></li></ul>


View more >