Nocturnal eating disorders are more common than previously thought. Sleep related eating disorder has been described in association with zolpidem. A review of the literature revealed the presence of 6 previously reported cases. In this presentation, the case of a 46-year-old female who developed sleep related eating disorder when she was treated with zolpidem for insomnia is reported. The patient recovered totally when zolpidem was stopped. Drug-induced sleep related eating disorders should be considered when evaluating patients with nocturnal eating.
Background and Objective: Excessive sleepiness is a common reason for a referral to sleep medicine clinics. The clinical picture and context usually suggest the underlying cause; however, all possibilities should be considered and only after sleep studies are done, one can determine the likely cause of the patient’s symptoms.
Case Report: We presented the case of a man who was referred for evaluation of hypersomnolence along with snoring and possible apnea during sleep. Obstructive sleep apnea (OSA) was suspected, so home sleep apnea test (HSAT) and later polysomnography (PSG) were performed and both ruled out this possibility. The PSG showed frequent periodic limb movements (PLMs), some associated with arousal; abnormal sleep structure suggested the effect of medication. The patient had been taking baclofen for musculoskeletal pain and it was concluded that baclofen was the cause of the patient’s somnolence and PLMs. The patient’s clinical presentation was compounded by his history of post-traumatic stress disorder (PTSD) and gastroesophageal reflux which probably caused increased arousals and the subjective feeling of poor sleep quality.
Conclusion: Treatment with medications that have sedative effects should be considered in all patients presenting with excessive daytime sleepiness even if the initial clinical picture suggests another possible cause. Baclofen can cause PLMs, sedation, changes in N3 stage, and reduction in rapid eye movement (REM) sleep.
Introduction
REM sleep behavior disorder (RBD) is a rare condition characterized by abnormal sleep behavior, such as dream enactment. Loss of atonia during REM sleep is noted in polysomnography (PSG). Failure to suppress spinal motor neurons is considered its pathophysiology. Etiologies include neurodegeneration, orexin deficiency, structural brain lesions, or medication effects. Although studies have shown that most patients with RBD develop neurodegenerative disorders, the variable etiologies suggest that prognosis of RBD can potentially be variable. We report a case of RBD with a significant family history without development of a neurodegenerative disorder.
Report of case(s)
A 64-year-old woman with hypertension, diabetes, body mass index of 29 kg/m2, and tobacco use presented with dream enactment for 10 years. She was referred by her neurologist, who she had seen for intermittent hand tremors but had no focal abnormalities on her neurological exam. She complained of snoring, daytime sleepiness, and unrefreshed sleep. Her medications were aspirin, hydrochlorothiazide-valsartan, metformin, and pantoprazole. She denied any traumatic experience. Family history was relevant for dream enactment in her younger sister and both parents, with an age of onset in their early 50s in all. None of these relatives had any reported neurological issues. Labs revealed abnormal SPEP, an IgG kappa band, which can an early presentation of monoclonal gammopathy of undetermined significance (MGUS). She had PSG with an extended electroencephalogram (EEG) monitor, which showed REM atonia consistent with RBD. She shouted, talked, and moved limbs during REM sleep. No evidence of sleep apnea was seen. She took melatonin 3 mg without any improvement. A trial of clonazepam 0.25 mg reduced the frequency of dream enactment and helped her anxiety. We plan to increase melatonin dosing and observe her response.
Conclusion
Our patient had dream enactment for over 10 years but has not developed any neurological abnormalities to date. She has a family history of dream reenactment with the age of onset in early 50s without any neurological associations. Due to variable etiologies of RBD, this case may be a subtype of RBD with a benign clinical course.
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