• Sleep Medicine and Psychophysiology
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• v.2 no.2
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• pp.146-155
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• 1995

Jet lag can be defined as the cumulative physiological and psychological effects of rapid air travel across multiple time zone. The consequences of jet lag include fatigue, general malaise, sleep disturbances, and reductions of cognitive and psychomotor performance, all of which have been documented in experimental biological and air crew personnel studies. Thus authors tried to study the jet lag of natural travellers by modified self reporting sleep log. Total 61 healthy travellers was studied for 3 days before and 7 days after jet-flights across seven to ten time zone. The eastbound travelling group was 38 persons, aged 19 -70 and westbound travelling group was 23 persons, aged 13 - 69. Sleep onset time, wake-up time, sleep latency, awakening frequency on night sleep, awakening duration on night sleep, sleepiness at wake-up and nap length were evaluated. Our results suggested that the 7 to 10 time zone shift gave significant influence to traveller's sleep-wake cycles. The date which subjective physical condition was recovered on was $5.16{\pm}1.50$ day after arrivals for eastbound, while for westbound, $4.91{\pm}1.62$ day. In eastbound travelling, sleep onset time became later than baselines and could not recover until 7th day. But in westbound, it became earlier than baseline and could recover until 6th day. The mean score of 24-hour sleepiness was greater in eastboumd than westbound. Therefore the eastbound travelling caused more sleep-wake cycle disturbance and daytime dysfunction than westbound travelling. In other parameters, there was no definite difference between east and westbound. From our results, it was suggested that the symptom severity of jet lag was dependent on the travelling direction. To demonstrate more definite evidence, large sized data collections and comparision by age difference were needed.

• Sleep Medicine and Psychophysiology
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• v.23 no.1
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• pp.10-15
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• 2016

Since its development in the early 70s, actigraphy has been widely used in sleep research and clinical sleep medicine as an assessment tool of sleep and sleep-wake cycles. The validation and reliability of actigraphic measures have been reasonably examined in healthy normal individuals with good sleep patterns. Recent literature suggests that the use of actigraphy could be further extended to monitor insomnia and circadian sleep-wake disturbances, and detect sleep changes associated with drug treatments and non-pharmacologic interventions, although it is generally recommended to use complementary assessments such as sleep diaries and overnight polysomnography when possible. The development of actigraphy includes its improved hardware sensors for better detection of movements and advanced algorithms to score sleep and wake epochs. In this paper, we briefly review the quantitative analysis methods of actigraphy and its potential applications in sleep research.

• Sleep Medicine and Psychophysiology
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• v.3 no.2
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• pp.18-31
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• 1996

Jet-lag can be defined as the cumulative physiological and psychological effects of rapid air travel across multiple time zones. Many reports have suggested that age-related changes in sleep reflect fundamental changes in the circadian system and in significant declines in slow wave sleep. Jet lag is a dramatic situation in which the changes of the phase of circadian process and homeostatic process of sleep occur. Thus the authors evaluatead the changes of sleep-wake cycle from jet lag by age. Thirty-eight healthy travellers were studied for 3 days before and 7 days after jet-flights across seven to ten time zone. They were aged 19-70, They trareled eastbound, Seoul to North America (USA, Canada). Sleep onset time, wake-up time, sleep latency, awakening frequency on night sleep, awakening duration on night sleep, sleepiness at wake-up and nap length were evaluated. Our results suggest that by the 7 to 10 time zone shift, the old age group was significantly influenced in sleep-wake cycles. The date on which subjective physical condition was recovered was $6.23{\pm}83$ day after arrivals for old age group, while for young and middle age group, $4.46{\pm}1.50$ day and $4.83{\pm}1.52$ day, respectively. In old age group, sleep onset time was later than baselines and could not recover untill 7th day. But in other groups, the recovery was within 5th day. Nap dura fion was longer in old age group through jet lag than younger age group. In other parameters, there was no definite difference among three age groups. Our results suggested that the old age was significantly influenced by the disharmony between internal body clock and sleep-wake cycle needed at the travel site. Thus we proved that recovery ability from jet lag was age-dependent as well as travelling direction-dependent. To demonstrate more definite evidence, EEG monitoring and staging of sleep were funthun encouraged.

• Sleep Medicine and Psychophysiology
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• v.4 no.2
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• pp.147-155
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• 1997

To assess the reliability of chronobiological models of sleep/wake regulation, it is necerssary that the models predict the data which has been studied in sleep research, and they should be generalized across all ages. To date, many adult human data on such models have accumulated, yet it is evident that a comprehensive theory of the biorhythmic aspects of sleep/wake states has not established. Circadian rhythms such as the time going to bed, sleep onset, slow wave sleep pressure, periodicity of REM sleep, daytime performance, and early evening alertness are resumed everyday. Even in adult humans, sleep is inherently polyphasic. In both the disentrained and entrained states, naps when allowed tend to recur in a temporally lawful manner. The monophasic sleep pattern of most industrial societies therefore appears to be purely of social origin. The endogenous biorhythmic nature of circasemidian sleep tendency is supported by the ubiquity of the phenomenon across all ages. The NREM/REM sleep cycle within sleep with its inherent physiological, endocrine, and neurochemical fluctuations represents the best-documented ultradian sleep rhythms. Also, a daytime ultradian variation in sleepiness with a periodicity similar to nocturnal NREM/REM cycle(BRAC hypothesis) is suggested. This review article provides a brief synoptic review of the evidences for circadian, circasemidian, and ultradian sleep/wake rhythms, and then the authour will suggest the issues which expedite fuller modeling of sleep/wake system, to be further discussed.

• Journal of mucopolysaccharidosis and rare diseases
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• v.1 no.2
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• pp.35-39
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• 2015

Sleep problems occur frequently among patients with Prader-Willi syndrome (PWS). The most common problem is excessive daytime sleepiness (EDS) that are closely related to of sleep-related breathing disorder (SRBD) such as obstructive sleep apnea (OSA) and congenital hypoventilation syndrome. Obesity, craniofacial dysmorphism and muscular hypotonia of patients with PWS may increase the risk of SRBD. Sleep apneas can interrupt the continuity of sleep, and these disruptions result in a decrease in both the quality and quantity of sleep. In addition to SRBD, other sleep disorders have been reported, such as hypersomnia, a primary abnormality of the rapid eye movement (REM) sleep and narcolepsy traits at sleep onset REM sleep. Patients with PWS have intrinsic abnormalities of sleep-wake cycles due to hypothalamic dysfunction. The treatment of EDS and other sleep disorders in PWS are similar to standard treatments. Correction of sleep hygiene such as sufficient amount of sleep, maintenance of regular sleep-wake rhythm, and planned naps are important. After comprehensive evaluation of sleep disturbances, CPAP or surgery should be recommended for treatment of SRBD. Remaining EDS or narcolepsy-like syndrome are controlled by stimulant medication. Bright light therapy might be beneficial for disturbed circadian sleep-wake rhythm caused by hypothalamic dysfunction.

• Journal of Ginseng Research
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• v.36 no.4
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• pp.403-410
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• 2012

The current inquiry was conducted to assess the change in sleep architecture after long periods of administration to determine whether ginseng can be used in the therapy of sleeplessness. Following post-surgical recovery, red ginseng extract (RGE, 200 mg/kg) was orally administrated to rats for 9 d. Data were gathered on the 1st, 5th, and 9th day, and an electroencephalogram was recorded 24 h after RGE administration. Polygraphic signs of unobstructed sleep-wake activities were simultaneously recorded with sleep-wake recording electrodes from 11:00 a.m. to 5:00 p.m. for 6 h. Rodents were generally tamed to freely moving polygraphic recording conditions. Although the 1st and 5th day of RGE treatment showed no effect on power densities in nonrapid eye movement (NREM) and rapid eye movement (REM) sleep, the 9th day of RGE administration showed augmented ${\alpha}$-wave (8.0 to 13.0 Hz) power densities in NREM and REM sleep. RGE increased total sleep and NREM sleep. The total percentage of wakefulness was only decreased on the 9th day, and the number of sleep-wake cycles was reduced after the repeated administration of RGE. Thus, the repeated administration of RGE increased NREM sleep in rats. The ${\alpha}$-wave activities in the cortical electroencephalograms were increased in sleep architecture by RGE. Moreover, the levels of both ${\alpha}$- and ${\beta}$-subunits of the ${\gamma}$-aminobutyric acid $(GABA)_A$ receptor were reduced in the hypothalamus of the RGE-treated groups. The level of glutamic acid decarboxylase was over-expressed in the hypothalamus. These results demonstrate that RGE increases NREM sleep via $GABA_A$ergic systems.

• Clinical and Experimental Pediatrics
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• v.50 no.8
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• pp.711-717
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• 2007

Sleep is a vital, highly organized process regulated by complex systems of neuronal networks and neurotransmitters. Normal sleep comprises non-rapid eye movement (NREM) and REM periods that alternate through the night. Sleep usually begins in NREM and progresses through deeper NREM stages (2, 3, and 4 stages), but newborns enter REM sleep (active sleep) first before NREM (quiet sleep). A period of NREM and REM sleep cycle is approximately 90 minutes, but newborn have a shorter sleep cycle (50 minutes). As children mature, sleep changes as an adult pattern: shorter sleep duration, longer sleep cycles and less daytime sleep. REM sleep is approximately 50% of total sleep in newborn and dramatically decreases over the first 2 years into adulthood (20% to 25%). An initial predominant of slow wave sleep (stage 3 and 4) that peaks in early childhood, drops off abruptly after adolescence by 40% from preteen years, and then declines over the life span. The hypothalamus is recognized as a key area of brain involved in regulation of sleep and wakefulness. The basic function of sleep largely remains elusive, but it is clear that sleep plays an important role in the regulation of CNS and body physiologic processes. Understanding of the architecture of sleep and basic mechanisms that regulate sleep and wake cycle are essential to evaluate normal or abnormal development of sleep pattern changes with age. Reduction or disruption of sleep can have a significant impact on daytime functioning and development, including learning, growth, behavior, and emotional regulation.

• Biomolecules & Therapeutics
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• v.26 no.3
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• pp.268-273
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• 2018

Sleep is the most basic and essential physiological requirement for mental health, and sleep disorders pose potential risks of metabolic and neurodegenerative diseases. Tryptic hydrolysate of ${\alpha}_{S1}$-casein (${\alpha}_{S1}-CH$) has been shown to possess stress relieving and sleep promoting effects. However, the differential effects of ${\alpha}_{S1}-CH$ on electroencephalographic wave patterns and its effects on the protein levels of ${\gamma}$-aminobutyric acid A ($GABA_A$) receptor subtypes in hypothalamic neurons are not well understood. We found ${\alpha}_{S1}-CH$ (120, 240 mg/kg) increased sleep duration in mice and reduced sleep-wake cycle numbers in rats. While ${\alpha}_{S1}-CH$ (300 mg/kg) increased total sleeping time in rats, it significantly decreased wakefulness. In addition, electroencephalographic theta (${\theta}$) power densities were increased whereas alpha (${\alpha}$) power densities were decreased by ${\alpha}_{S1}-CH$ (300 mg/kg) during sleep-wake cycles. Furthermore, protein expressions of $GABA_A$ receptor ${\beta}_1$ subtypes were elevated in rat hypothalamus by ${\alpha}_{S1}-CH$. These results suggest ${\alpha}_{S1}-CH$, through $GABA_A$ receptor modulation, might be useful for treating sleep disorders.

• Natural Product Sciences
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• v.22 no.4
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• pp.263-269
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• 2016

Rhynchophylline (RP) is a major tetracyclic oxindole alkaloid of Uncariae Ramulus et Uncus which has been used to treat hypertension, seizures, pain and anxiety in the oriental countries. A recent report revealed that RP attenuated ischemia-induced neuronal damage and kainite-induced convulsions in animals. This study was performed to investigate whether RP enhances pentobarbital-induced sleep behaviors and modulates sleep architecture in mice. Locomotor activity was significantly inhibited by RP at 0.25 and 0.5 mg/kg, similar to 2 mg/kg diazepam (a benzodiazepine agonist) in mice. RP shortened sleep latency and increased total sleep time in a dose-dependent manner when administrated with pentobarbital (42 mg/kg, i.p.). RP also increased the number of sleeping mice and total sleep time by concomitant administration with the sub-hypnotic dosage of pentobarbital (28 mg/kg, i.p.). On the other hand, RP (0.25 mg/kg, p.o.) itself significantly inhibited sleep-wake cycles, prolonged total sleep time, and rapid eye movement in rats. In addition, RP also increased chloride influx in the primary cultured hypothalamic neuronal cells. In addition, we found that glutamic acid decarboxylase ($GAD_{65/67}$) was activated by RP. In conclusion, RP augments pentobarbital-induced sleeping behaviors, and can be a candidate for treating insomnia.

• Natural Product Sciences
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• v.23 no.1
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• pp.53-60
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• 2017

Perillae Herba has been traditionally used for the sedation in the oriental countries. Therefore, this study was conducted to determine whether Perillae Herba ethanol extract (PHEE) enhances pentobarbital-induced sleeping behaviors in animals. In addition, the possible mechanisms are demonstrated. PHEE (12.5, 25 and 50 mg/kg. p.o.) reduced the locomotor activity in mice. PHEE reduced sleep latency and augmented the total sleep time in pentobarbital (42 mg/kg, i.p.)-induced sleep in mice. Furthermore, the number of sleeping mice treated with sub-hypnotic pentobarbital (28 mg/kg, i.p.) increased. PHEE (50 mg/kg. p.o.) decreased the sleep/wake cycles and wakefulness, and increased total sleeping time and NREM sleep in electroencephalogram (EEG) of rats. In addition, PHEE (0.1, 1.0 and $10{\mu}g/ml$) increased the intracellular $Cl^-$ level through the GABA receptors in the hypothalamus of rats. Moreover, the protein of glutamate decarboxylase (GAD) was overexpressed by PFEE. It was found that PHEE enhanced pentobarbital-induced sleeping behaviors through $GABA_A-ergic$ transmissions.