• 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.7 no.2
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• pp.115-119
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• 2000

Objectives Summary: A 20-year-old man was presented with a history of difficult waking for 10 years. He suffered from morning headache, chronic fatigue and mild daytime sleepiness but had no history of irresistible sleep attack, cataplexy, hypnagogic hallucination or sleep paralysis. Methods: Night polysomnography (PSG), multiple sleep latency test (MSLT) and HLA-typing were carried out. Results: The PSG showed short sleep latency (4.0 min) and REM latency (2.5 min), increased arousal index (15.7/hour), periodic limb movements during sleep (PLMS index=8.1/hr) with movement arousal index 2.1/hr and normal sleep efficiency (97.5%). The MSLT revealed normal sleep latency (15 min 21 sec) and 4 times sleep-onset REM (SOREM). HLA-typing showed DQ6- positive, that corresponded at the genomic level to the subregion DQB1*0601, which was different from the usual locus in narcolepsy patients (DQB1*0602 and DQA1*0102). Conclusion: Differential diagnosis should be made with circadian rhythm disorder and other causes of primary waking disorder. The possibility of a variant type of narcolepsy could be suggested with an unusual clinical manifestation and a new genetic marker.

• Sleep Medicine and Psychophysiology
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• v.16 no.1
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• pp.5-9
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• 2009

Relatively little is known about the neurobiology of insomnia, despite its wide prevalence and broad medical impact. Although much is still to be learned about the pathophysiology of the disorder, identification, systematic assessment, and appropriate treatment are clearly beneficial to patients. Recent research, using quantitative EEG, polysomnography (PSG), multiple sleep latency test (MSLT) and neuroimaging techniques, suggests that some broad areas can be identified as possible pathophysiological models. Sleep-wake homeostat model hypothesizes a failure in homeostatic regulation of sleep, an attenuated increase in sleep drive with time awake, and/or defective sensing of sleep need. Circadian clock model hypothesizes a dysfunctional circadian clock, resulting in changes in the timing of sleep-wake propensity that are incompatible with normal sleep. Intrinsic sleep-wake state mechanism model suggests that abnormal function of insomnia comprises the systems responsible for expression of the sleep states themselves. Extrinsic over-ride mechanism (stress-response) model suggests that insomnia reflects the consequences of overactivity of one of the systems considered "extrinsic" to normal sleep-wake control. Many current therapies for insomnia are based on these physiological models. Several attempts have been made to create a physiological model that would explain this disorder and could be used as a foundation for treatment. However, it appeared that no model can fully explain and clarify all aspects of insomnia. Future research should be necessary to expand our knowledge on the biological dimensions of insomnia.

• Sleep Medicine and Psychophysiology
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• v.4 no.1
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• pp.89-95
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• 1997

The authors studied 5 cases of idiopathic CNS hypersomnia who visited Division of Sleep Studies, Seoul National University Hospital in 1995. Detailed medical history was taken and nocturnal polysomnography(NPSG), multiple sleep latency test(MSLT) and human leukocyte antigen(HLA) typing were performed. Neither cataplexy nor hypnagogic hallucination was reported in all cases and in NPSGs, there were tendencies of increased sleep period time and decreased slow wave sleep time. In MSLT, all the subjects showed average sleep latencies less than 8 minutes without sleep-onset rapid eye movement period(SOREMP). In HLA typing, some correlation between idiopathic CNS hypersomnia and HLA DR4 was observed. In contrast to previous reports, overall treatment response with methylphenidate was remarkable. Therefore, the authors suggest that patients suspected of idiopathic CNS hypersomnia be actively evaluated and treated with rather optimistic perspective.

• Journal of the Korean Academy of Child and Adolescent Psychiatry
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• v.4 no.1
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• pp.173-178
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• 1993

Narcolepsy's age at onset is reported to be relatively homogeneous, occuring usually after the onset of puberty, although most cases are diagnosed when the patients are in their late teens to late 20s. It is very unusual for a patient to develop narcolepsy before 15 years of age or after 30 years of age. A 11-year old boy who has developed excessive daytime sleepiness since age of 7 and has all the four major features of narcolepsy by the time of evaluation is presented. On polysomnographic examination, the patient showed two sleep onset REM periods in the three latency test of the multiple sleep latency test and the nocturnal polysomnogram. In addition, the findings of typing HLA class I and II of the patient's family are presented. Reports of pediatric narcolepsy previously reported are reviewed.

• Sleep Medicine and Psychophysiology
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• v.1 no.2
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• pp.125-144
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• 1994

Recently excessive daytime sleepiness was found to have relations with various social, occupational, and health problems. This condition is common symptom of several sleep disorders, among which sleep apnea syndrome is most contributive. It is essential to assess daytime sleepiness exactly for the diagnosis of such sleep disorders. Multiple sleep latency test which is a valid and objective measurement technique of sleepiness is time and cost consuming, and so there is increasing need of scales measuring general level of daytime sleepiness which are quick and simple to perform for clinical and research purpose. And also, there have been a lot of sleep researches viewing sleep as a chronobiological process, especially in the study of circadian type of shift workers. In these studies they used various techniques of multiple demensions to assess sleepiness or circadian rhythm which concerns various psychological variables. Of these measurement techniques circadian type questionnaires might have some problems in their psychometric properties. So some of these morningness-eveningness questionnaires have been revised and more valid scales are being suggested by different authors. The author briefly reviewed various measurement techniques of sleepiness and circadian rhythm and introduced recently developed scales which are more valid allegedly, and finally discussed psychometric properties of these morningness-eveningness questionnaires.

• 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.

• Korean Journal of Clinical Laboratory Science
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• v.47 no.4
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• pp.216-224
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• 2015

This study aims to identify the prevalence of sleep related disease in those who experienced car accidents caused by drowsy driving. To this end, a survey of usual sleep habits, polysomnography, and multiple sleep latency tests were conducted in 34 persons who experienced an accident after normal sleep (Group 1), 22 persons who experienced an accident after abnormal sleep (Group 2), and 17 persons who was proven to be normal as a result of polysomnography and had no accident (Group 3). In all, 192 persons responded to the preliminary survey and the results were compared and analyzed. Crossover analysis was conducted to test the homogeneity of statistical characteristics, and the physical characteristics by age were analyzed. In the survey of sleeping habits, there was a significance between groups in how often they woke up while asleep (p<0.01), how difficult it was to go back to sleep again after waking up from sleep (p<0.05), how early they woke up in the morning (p<0.05), how difficult it was to get up in the morning (p<0.05), how sleepy they felt in the daytime (p<0.01), and how tired they felt in the daytime (p<0.01). Furthermore, among 56 subjects who had an accident during drowsy driving, 94.6% (53 persons) were found to have sleep related diseases. This suggests that car accidents during drowsy driving is not simply caused by temporary lack of sleep but by sleep related diseases even when sleep is adequate, leading to car accidents. Therefore, this study is significant identifying the association between car accidents during drowsy driving and sleep related disorders. Furthermore, the data would be considered basic to prepare social measures against drowsy driving related to such sleep related disorders.

• Proceedings of the KOR-BRONCHOESO Conference
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• 1991.06a
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• pp.23-23
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• 1991

구개인두성형술이 코골음과 수면무호흡증에 유용한 수술적 방법으로 널리 이용되고 있으나 코골음과 수면무호흡증의 유발기전이 어리기지 복합적인 원인에 의하므로 구개인두성형술의 적응증을 결정하는데 많은 어려움이 있어, 수술전에 이 방법의 적응이 되는 환자를 보다 정확히 선택함이 중요하므로 많은 사람들에 의하여 주된 병변부위를 검시하는 방법들이 시행되어 왔다. 예를 들면 Mueller maneuver 중 내시경검사, Cephalometrics, polysomnogram, Multiple sleep latency test, CT scan 등의 방법이 환자선택에 이용되었다. 저자들은 비교적 쉽고 경비가 들지 않는 술전 검사법으로 양 후구치봉선(retromolar raphe)을 연결하는 선상에서 구인두궁 (soft palate arch)의 길이를 비교하는 방법을 총 89례에 적용 시행하여 그중 추적관찰이 가능한 46례에서 코골음은 86%, 수면무호흡증은 82%에서 자각적 증상의 개선이 있었기에 구개인두성형술을 시행함에 있어 양 후구치봉선거리와 구인두궁 거리를 비교하는 방법이 간단하고 경제적인 술전 진단방법으로 사료되어 문헌고찰과 함께 보고하는 바이다.

• Sleep Medicine and Psychophysiology
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• v.8 no.2
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• pp.107-112
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• 2001

Introduction: Narcolepsy, a sleep disorder characterized by excessive daytime sleepiness and cataplexy, is known to be closely associated with the human leukocyte antigen (HLA) DQB1*0602. Several studies have suggested that HLA-DQB1*0602 is strongly linked with narcolepsy-cataplexy. However, no studies have yet been made on whether HLA DQB1*0602 is associated with Korean patients with narcolepsy. This study was designed to investigate the frequency of HLA-DQB1*0602 of Korean patients with narcolepsy. Methods: Twenty patients were selected (mean age: $28.2{\pm}3.0$, 11 men and 9 women). The patients were confirmed to have narcolepsy by the overnight polysomnography and multiple sleep latency test (MSLT) in addition to their clinical history and symptoms at St. Vincent's Hospital and Korea University Hospital Sleep Disorders Clinic. Any subjects co-morbid with other hypersomnic sleep disorders such as sleep apnea or periodic limb movements during sleep were excluded. Clinical data was collected through a semi-structured interview for narcoleptic patients. All patients and 21 control did HLA typing for the presence of DQB1*0602. Results Obtained were as Follows: 1) Mean sleep latency was 2.4 (${\pm}2.0$ minutes) and mean frequency of sleep-onset REM period was 3.0 (${\pm}1.6$) by MSLT. 2) Characteristic symptoms of narcolepsy investigated were as follows: excessive daytime sleepiness (100%), cataplexy (100%), sleep paralysis (60%), hypnagogic hallucination (70%) and disrupted nocturnal sleep (75%). 3) Strong emotional expression such as laughing (80%) and joking (70%) triggered cataplexy which affects the knee and leg region (80%) and jaw region (30%). 4) HLA-DR2 was found in 90% of patients and 35% in controls. The frequency of HLA-DQB1*0602 in patients and controls was 90%, and 24%, respectively. Conclusions: These results, which exhibit high HLA-DQB1*0602 expression in Korean patients with narcolepsy, suggest that HLADQB1*0602 could be a strong genetic marker in narcolepsy.