Excessive daytime sleepiness in childhood might be abnormal phenomenon and often related to the sleep disorders or insufficient sleep duration. The most common cause of excessive daytime sleepiness would be insufficient sleep. However, narcolepsy, idiopathic hypersomnia, circadian rhythm sleep disorders, medication, medical illness and other sleep disorders that could cause insomnia and poor quality of sleep also result in excessive daytime sleepiness. The misdiagnosed and untreated excessive daytime sleepiness in childhood can lead to serious developmental and educational problem.
Child ; Humans ; Hypersomnolence, Idiopathic ; Narcolepsy ; Sleep Wake Disorders ; Sleep Wake Disorders, Circadian Rhythm ; Sleep Initiation and Maintenance Disorders

Narcolepsy is a sleep disorder, which is characterized by excessive daytime sleepiness (EDS) that is typically associated with cataplexy, sleep fragmentation and other REM sleep-related phenomenon such as sleep paralysis and hypnagogic hallucination. Narcoleptic symptoms can be developed from various medical or neurological disorders. A 17-year-old male patient admitted for the evaluation of EDS which started three-month ago. He slept more than 18 hours a day with cataplexy and hypnagogic hallucination. He was obese with body mass index (BMI) of 30.4 kg/m2. After admission he was newly diagnosed to the thyrotoxicosis. T3 391.2 ng/dL (60-181), free T4 4.38 ng/dL (0.89-1.76), TSH <0.01 microIU/mL (0.35-5.5) were measured. His pulse rate ranged 70-90 beats per minute and blood pressure ranged 150/100-120/70 mmHg. Polysomnography revealed many fragmentations in sleep with many positional changes (81 times/h). Sleep onset latency was 33.5 min, sleep efficiency was 47.9%, and REM latency from sleep onset was delayed to 153.6 min. REM sleep percent was increased to 27.1%. Periodic limb movement index was 13.4/h. In the multiple sleep latency test (MSLT), average sleep latency was 0.4 min and there were noted 3 SOREMPs (Sleep Onset REM sleep period) on 5 trials. We couldn't discriminate the obvious sleep-wake pattern in the actigraph and his HLA DQB1 *0602 type was negative. His thyroid function improved following treatment with methimazole and propranolol. Vital sign maintained within normal range. Cataplexy was controlled with venlafaxine 75 mg. Subjective night sleep continuity and PLMS were improved with clonazepam 0.5 mg, but the EDS were partially improved with modafinil 200-400 mg. Thyrotoxicosis might give confounding role when we were evaluating the EDS, though sleep fragmentation was one of the major symptoms of narcolepsy, but enormous amount of it made us think of the influence of thyroid hormone. The loss of sleep-wake cycle, limited improvement of EDS to the stimulant treatment, and the cataplexy not supported by HLA DQB1 *0602 should be answered further. We still should rule out idiopathic hypersomnia and measuring CSF hypocretin level would be helpful.
Adolescent ; Benzhydryl Compounds ; Blood Pressure ; Body Mass Index ; Cataplexy ; Clonazepam ; Cyclohexanols ; Extremities ; Hallucinations ; Heart Rate ; HLA-DQ beta-Chains ; Humans ; Hypersomnolence, Idiopathic ; Intracellular Signaling Peptides and Proteins ; Male ; Methimazole ; Narcolepsy ; Nervous System Diseases ; Neuropeptides ; Polysomnography ; Propranolol ; Reference Values ; Sleep Deprivation ; Sleep Paralysis ; Sleep, REM ; Thyroid Gland ; Thyrotoxicosis ; Vital Signs ; Orexins ; Venlafaxine Hydrochloride