• Sleep Medicine and Psychophysiology
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• v.13 no.2
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• pp.67-74
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• 2006

Introduction: Excessive daytime sleepiness and cataplexy are key features of narcolepsy. Modafinil is psychostimulant used in the treatment of narcolepsy. In this study, we evaluated effects of modafinil on nocturnal sleep structure and sleep latency in multiple sleep latency test and clinical features. Methods: Twelve narcoleptic patients (7 male, age: $22.9{\pm}2.6\;yrs$) were participated in the study. All of them had done nocturnal polysomnography (nPSG), multiple sleep latency test (MSLT), clinical symptoms scales and have repeated same procedure after taking 200 mg of modafinil. We have done linear mixed model analysis to describe effects of group, medication and nap time on these measures. Results: Modafinil did not affect clinical scales except PSQI which had been reduced after medication. In this study, Modafinil reduced total sleep time, sleep efficiency and increased wake after sleep onset and percent of arousal during sleep in nocturnal polysomnography and prolonged mean sleep latency in multiple sleep latency tests in both group. Discussion: Modafinil has stimulant effect of central nervous system but its effect on night sleep is less than other psychostimulants such as methylphenidate. We ascertained that modafinil affected total sleep time, sleep efficiency and percent of wake during sleep but did not effect on sleep structure. Modafinil was effective in the management of day time sleepiness. Modafinil can enhance alertness of control group without day time sleepiness.

• Sleep Medicine and Psychophysiology
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• v.18 no.1
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• pp.40-44
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• 2011

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/$m^2$. 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 ${\mu}IU$/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 treatmen, 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.

• Sleep Medicine and Psychophysiology
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• v.12 no.2
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• pp.122-132
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• 2005

Objectives: The objective of this study is to assess cognitive functions and their relationship with sleep symptoms in young narcoleptic patients. Methods: Eighteen young narcolepsy patients and 18 normal controls (age: 17-35 years old) were recruited. All narcolepsy patients had HLA $DQB_1$ *0602 allele and cataplexy. Several important areas of cognition were assessed by a battery of neuropsychological tests consisting of 13 tests: executive functions (e.g. cognitive set shifting, inhibition, and selective attention) through Wisconsin card sorting test, Trail Making A/B, Stroop test, Ruff test, Digit Symbol, Controlled Oral Word Association and Boston Naming Test; alertness and sustained attention through paced auditory serial addition test; verbal/nonverbal short-term memory and working memory through Digit Span and Spatial Span; visuospatial memory through Rey-Osterrieth complex figure test; verbal learning and memory through California verbal learning test; and fine motor activity through grooved pegboard test. Sleep symptoms in narcolepsy patients were assessed with Epworth sleepiness scale, Ullanlinna narcolepsy scale, multiple sleep latency test, and nocturnal polysomnography. Relationship between cognitive functions and sleep symptoms in narcolepsy patients was also explored. Results: Compared with normal controls, narcolepsy patients showed poor performance in paced auditory serial addition (2.0 s and 2.4 s), digit symbol tests, and spatial span (forward)(t=3.86, p<0.01; t=-2.47, p=0.02; t=-3.95, p<0.01; t=-2.22, p=0.03, respectively). There were no significant between-group differences in other neuropsychological tests. In addition, results of neuropsychological test in narcolepsy patients were not correlated with Epworth sleepiness scale score, Ullanlinna narcolepsy scale score and sleep variables in multiple sleep latency test or nocturnal polysomnography. Conclusion: The current findings suggest that young narcolepsy patients have impaired attention. In addition, impairment of attention in narcolepsy might not be solely due to sleep symptoms such as excessive daytime sleepiness.